Major Systems and Physiology
The skeletal and muscular shell of the thorax encloses the heart and lungs, powers breathing, and is the mechanical platform for arm and neck motion. It is bounded anteriorly by the sternum and ribs, laterally and posteriorly by the ribs, and supported posteriorly by the spine. The inferior boundary is the diaphragm and rib margins. Superiorly, it is bounded by the clavicles and soft tissues of the neck. The thoracic wall includes the bodies of the 12 thoracic vertebrae, the 12 pairs of ribs, and the sternum.
The thorax resembles a truncated cone, each pair of ribs having a greater diameter than that above, so the rib cage is much smaller at the top than at the base. The ribs are separated by intercostal spaces numbered from the rib above. The first rib slopes slightly downward from back to front; each succeeding rib has a greater slope so the intercostal spaces widen from top to bottom.
The sternum (Fig. 8-1) consists of the manubrium, the gladiolus, and the xiphoid cartilage. There is a fibrocartilage (rarely synovial) joint between the manubrium and the gladiolus; mobility is slight. The xiphoid is lance shaped or bifid and usually calcifies in later life. When angulated forward it may be mistaken for an abdominal mass.
The Bony Thorax
The left clavicle is removed exposing the underlying first rib. The cartilages of the xiphoid and ribs are stippled. Note the surface landmarks: the suprasternal notch, the angle of Louis, and the infrasternal notch. The two lower rib margins form the intercostal angle.
Each rib is a flattened arch. Each typical rib has two connections with the vertebral column. Each rib articulates with two adjacent vertebrae and their intervertebral disk at a gliding synovial joint, and with the transverse process of the upper vertebra by a second synovial joint. The sternal rib ends continue as costal cartilages. The first to seventh ribs are true ribs since their costal cartilages join the sternum. The costal cartilage of the first rib connects to the manubrium at a fibrous joint. The other six true ribs attach to the sternum by synovial joints. The second rib attaches to both the manubrium and the gladiolus with two synovial joints. The first, tenth, eleventh, and twelfth ribs are atypical, each articulating with a single vertebra. The eighth to twelfth ribs are false ribs. The eight, ninth, and tenth ribs are vertebrochondral, each costal cartilage usually joining the cartilage of the rib above; many variations are found. The 11th and 12th ribs are vertebral or floating ribs.
The intercostal spaces contain the internal and external intercostal muscles that attach to adjacent rib margins; contraction draws the bones together. When the first rib is fixed by contraction of the scaleni, contraction of the intercostals, the levatores costarum, and the serratus posterior superior pull the ribs upward. When the last rib is fixed by contraction of the quadratus lumborum, the subcostales and the transversus thoracis draw the ribs downward.
The thoracic respiratory system is composed of the trachea entering superiorly, the lungs with their branching airways, arterial, venous and lymphatic vascular channels, and the pleura, which lines both the lung (visceral pleura) and the chest wall and mediastinum (parietal pleura).
Respiratory excursions of the thorax
At end expiration thoracic volume is at its normal minimum; inspiration increases the thoracic dimensions anteroposteriorly, transversely, and vertically, expanding lung volume. It is important to remember that volume varies as the third power of changes in linear dimension. Therefore, relatively small changes in the height, width, and depth of the thoracic cavity lead to large volume changes. Expiration is largely passive relying elastic recoil of the lungs and the chest wall; forced expiration by contraction of abdominal and chest wall muscles greatly accelerates airflow.
Increasing the anterior–posterior diameter of the thorax
The chest is like a cylindrical pail with its wire handle bowed in a semicircle of slightly greater diameter than the cylinder (Fig. 8-2A). When the handle hangs obliquely, the distance from its center to the cylindric axis is the radius of the pail. Raising the handle toward the horizontal moves it away from the side of the pail. In the model in Figure 8-2B, a straight piece of wood represents the thoracic spine, a vertical stick is the sternum in the position of expiration (dotted), and the dotted hoop is a pair of ribs. When the sternum and the first rib are pulled upward, the costal ring rotates pushing the sternum forward and upward. This happens when the sternum and the first rib are fixed by the scaleni while intercostal muscle contraction narrows the interspaces: the ribs are pulled upward and the sternum moves forward, increasing the anteroposterior dimension of the thoracic cavity.
Models Illustrating Thoracic Respiratory Movements
A. At rest, the handle of a cylindric paint can hangs obliquely, so its center and the side of the pail are equidistant from the central axis of the cylinder. When the handle is raised to the horizontal, the center of the handle diverges from the side increasing the distance from the central axis. B. In this model, two parallel rigid hoops pierce two vertical sticks. Elevation of the front stick (representing the sternum) will increase the distance between it and the other stick (representing the spine). The differences in the points of the arrows show this change in the anteroposterior diameter. C. The semicircular ribs hang from the sternum and the spine, like the hoops in B and the bucket handle in A. The ribs move in such a way that elevation of the sternum and the lateral bows of the ribs during inspiration increases both the transverse (as in A) and the anteroposterior (as in B) diameters of the thorax. D. Inspiratory volume further augmented by depression of the diaphragm.
Increasing the transverse diameter of the thorax
In a similar model (Fig. 8-2C) the sternum and the first rib are fixed. Each rib of a pair is a separate semicircle rotating on an anteroposterior axis. During expiration, the planes of the hoops slant downward on either side of the axis. When the hoops are pulled upward toward the horizontal, each hoop acts as a pail handle by moving further from the center, increasing the transverse dimension. Similarly, the narrowing the interspaces by intercostal muscle contraction elevates the ribs increasing the transverse diameter of the thorax. Thus, fixation of the first rib and manubrium and narrowing the interspaces cause rotation of each rib, except the first, on both an anteroposterior and a transverse axis, expanding the dimensions of the thoracic cavity. Because the lower ribs are longer and more oblique, and the interspaces are wider, movement is greater in the lower thorax.
Increasing the vertical dimension of the thorax
The diaphragm is an elliptic muscular sheet with a central fibrous aponeurosis. Its edges are fixed to the lower ribs, whereas the center domes into the thorax. At end expiration, the dome is high and the thoracic walls are close together (Fig. 8-2D). During inspiration, the walls diverge and the muscular diaphragm contracts lowering its dome thereby elongating the vertical dimension of the thoracic cavity and further increasing its volume.
The airways include the nasal passages and nasopharynx, the mouth and oropharynx, the larynx, the trachea, and the branches of the bronchial tree supplying the pulmonary alveoli. The larynx is a frequent site of obstruction, either from intrinsic swelling or by paralysis of its vocal cords.
The trachea bifurcates asymmetrically into the right and left mainstem bronchii at the carina. The left bronchus diverges at a greater angle from the trachea than the right bronchus; this is why foreign bodies are more likely to lodge in the right main stem bronchus. The right bronchus sends a lobar bronchus to each of the three pulmonary lobes; the left bronchus forms two lobar bronchi. Each first branch of a lobar bronchus supplies a bronchopulmonary lung segment. The heart lies in front of the tracheal bifurcation and the aorta arches from front to back over the left mainstem bronchus. Interposed between the aorta and the bronchus is the left recurrent laryngeal nerve, which descends in front of the aortic arch, loops under it, and ascends beside the trachea to the neck. The dilated aorta may produce a tracheal tug by pulsating against the left bronchus, or it may compress the left recurrent laryngeal nerve against the left bronchus, with resulting paralysis of the left vocal cord.
Think of the lungs as clusters of pulmonary alveoli around the subdivisions of the bronchial tree. The right lung has upper, middle, and lower lobes. The left lung has upper and lower lobes. The lobes are separated by an infolded visceral pleura; the lobar fissures. The shape of the lungs is molded by the rib cage; the medial edge of the left lung has an inferior-anterior indentation, the cardiac notch. Each lobe is divided into bronchopulmonary segments consisting of the cluster of alveoli supplied by a single first branch of the lobar bronchus (Figs. 8-3 and 8-4). Segments are not demarcated by fissures. However, if present, extra fissures do follow these boundaries. The lingula of the left upper lobe is homologous with the right middle lobe.
The Lobes of the Lungs
The transparent diagram shows the anterior aspects of the pulmonary lobes and their main bronchi. Note the three divisions of the right main bronchus and the more direct line with the trachea on the right side. The dotted line shows the posterior extent of the lower lobes.
Each lobe is divided into segments. The thick lines are the anatomical fissures, readily identified on inspection of the lung and often in radiographs. The thinner lines are established only by careful dissections of injected preparations. In the abbreviations the first capital letter designates right or left; the second, upper, middle, or lower the third L is for lobe. Note that the lingula, composed of the superior and inferior segments of the left upper lobe, is near the heart and corresponds in many respects to the right middle lobe.
The relation of each lung to its pleura can be visualized by imagining a sphere of thin plastic material from which the air is being evacuated (Fig. 8-5). As the sphere collapses, one part invaginates to form a hollow hemisphere with convex and concave layers in apposition. The convex layer, representing the parietal pleura, is cemented to the inside of the thoracic cavity. The lung fills the concavity, which represents the visceral pleura. The parietal pleura is adherent to the thoracic wall; the visceral pleura is fixed to the lung surface and also lines the interlobar fissures. The two apposing layers form the pleural cavity, containing only enough fluid for lubrication. The parietal pleura has the greater area, extending inferiorly on the ribs and diaphragm some distance below the lower tip of the lung to form the costophrenic sinus. This permits the lungs to move within the thoracic cavity, each descending part way into this sinus during deep inspiration. Between the two layers of pleura is a potential space, normally with a negative pressure relative to the atmospheric. This negative pressure maintains lung distention and transfers the inspiratory forces of diaphragm flattening and chest expansion to the lung. Introduction of air into this space (pneumothorax) destroys mechanical coupling of chest motion to lung expansion. The parietal pleura contains sensory nerve endings, but the visceral pleura is anesthetic.
Modeling the Relationship of the Pleura and Lung
Deflate a rubber or plastic sphere so that it assumes a hemisphere with a concave and convex surface. Place a model lung in the concavity and cement the lung surface to the inner surface of the hemisphere. On the right, in cross section, the parietal pleura is represented by the convex surface of the hemisphere; the cemented layers represent the visceral pleura. To complete the model, exhaust the hemisphere of air, replacing it with a little fluid to lubricate the inner surface. This geometry should be visualized in the examination of the chest and when looking at X-ray films, remembering that the pleural surfaces are anterior, lateral, medial, and inferior.
Mechanics of the lung and pleura
When a normal lung is removed it partially collapses from its elastic recoil becoming much smaller than its hemithorax. Because it adheres to the thoracic wall by the apposition of the parietal and visceral pleurae, normal lung volume is much greater. Atmospheric pressure resists any force tending to separate the pleural layers. During expiration, about negative 25 cm of water intrapleural pressure is generated by the elastic recoil of the lung and thorax. During inspiration, the negative pressure increases to approximately 215 cm of water because additional elastic recoil is produced by stretching the lung as the thorax expands.
The Cardiovascular System
The circulatory system includes the heart, the blood and its conducting vessels, the lymph and its ducts, and the vessel walls. Since the heart and much of the aorta are intrathoracic, consideration of the circulatory system starts in the chest. Blood returning from the extremities enters the chest from the abdomen and lower extremities via the inferior vena cava (IVC), and from the arms and head via the axillary and jugular veins, which merge into the brachiocephalic veins and superior vena cava (SVC) in the mediastinum. The heart is suspended from the great vessels (aorta, pulmonary artery, pulmonary veins, IVC, and SVC) within the pericardium, which allows free motion of the heart during ventricular contraction.
The cardiac conduction system
The heart’s normal pacemaker is the sinoatrial (SA) node located in the right atrial wall near the entrance of the SVC (Fig. 4-1). It originates rhythmic waves of excitation that spread quickly through both atria until they reach the atrioventricular (AV) node near the posterior margin of the interatrial septum. The AV node delays conduction during atrial systole. The impulse then passes down the bundle of His, which divides into right and left bundle branches to the muscle of the right and left ventricles via the Purkinje network. Conduction is normally very rapid, arriving nearly simultaneously in both atria, and, after AV delay, in both ventricles. Deviations in the timing or pathways taken by these electrical waves cause changes in rate, rhythm, and electrical pattern of the P, QRS, and T waves of the electrocardiogram (ECG). Normal cardiac function results when these electrical signals trigger mechanical muscular contraction via the cellular process of electrical–mechanical coupling.
Heart movement and function
The myocardial muscle fibers form a complete spiral, so contraction produces a decrease in all diameters during systole. The apex rotates forward and to the right, approaching the chest wall and frequently causing a visible and palpable thrust, the apical impulse. Occurring early in systole, this thrust is a marker for the onset of cardiac contraction. The heart has extremely high oxygen and energy requirements and the highest oxygen extraction of any organ. As a result, it is particularly sensitive to decreases in blood supply. Blood flow within the heart and lungs is dependent upon complete functional separation of the cardiac chambers by intact interatrial and interventricular septa and functional valves. Valve closure, turbulent blood flow, and contraction of the heart can be felt and auscultated through the chest wall.
Blood is distributed to the body through the major branches of the aorta, which are easily examined where they leave the chest (carotid and axillary arteries) or abdomen (femoral arteries). Measurement of blood pressure and estimates of the blood flow are easily performed on physical examination.
Knowledge of the normal functional anatomy of the leg veins is essential. The great saphenous vein begins at the mediodorsal side of the foot continuing upward along the medial edge of the tibia, passing the knee behind the medial femoral condyle. In the thigh, it runs subcutaneously to the femoral canal, emptying into the femoral vein. The small saphenous vein begins at the lateral side of the foot, curving under and behind the lateral malleolus, continuing upward in the posterior midline, and finally diving into the popliteal vein. Valved communicating veins connect the saphenous veins to the deep calf veins and the great saphenous to the femoral vein. Normal flow is from superficial to deep veins and thence proximally driven by skeletal muscle contraction compressing the veins within the muscle compartments (the muscle pump). Antegrade flow is assured by competent venous valves.
Superficial Thoracic Anatomy
The subcutaneous anterior surface of the sternum has landmarks for inspection and palpation. The heads of the clavicles form the sides of the suprasternal notch; its base is the superior edge of the manubrium (Figs. 8-1 and 8-6). The junction of the manubrium and the gladiolus, where the second rib articulates, forms the angle of Louis (sternal angle), a useful landmark for identifying ribs and interspaces. At the inferior end of the gladiolus a slight depression, the infrasternal notch, is formed by the junction of the 7th rib costal cartilages. The xiphoid cartilage may be felt below this notch.
The Angle of Louis
The adjacent edges of the manubrium and gladiolus form the angle of Louis. This is a landmark for counting ribs anteriorly because the second rib abuts the junction that forms the angle. The costicartilage of the second rib articulates with the fibrocartilage between the manubrium and the gladiolus and with the edges of both bones.
The bony thorax is a truncated cone narrowing superiorly. This narrowing is partially obscured by the overlying clavicles, the shoulders, and muscles of the upper chest and arms, which give the body its broad shouldered, squared-off contour. The clavicles, sternum, and lower ribs are palpable throughout their extent; portions of most other ribs can be seen or palpated. The first rib is overlaid by the clavicle. The pectoralis major and the female breasts obscure palpation of parts of the ribs anteriorly; the latissimus dorsi covers some ribs in the axillary line. Posteriorly, the scapulae overlie the posterior chest wall lateral to the spine covering parts of the second through seventh ribs. With the arms at the sides, the inferior border of the scapula is usually at the seventh or eighth intercostal space, serving as the usual landmark for counting ribs in the back (Fig. 8-7). The inferior margins of the seventh, eighth, and ninth costal cartilages on the two sides meet in the midline to form the infrasternal angle (intercostal angle). An oblique line drawn from the head of the clavicle to the anterior axillary line on the ninth rib approximately locates the costochondral junctions of the second to tenth ribs. The lower ribs with large radii, superficial location, and extensive anterior cartilage are vulnerable to injury; the upper ribs are much less susceptible to mechanical injury because of their smaller radius of curvature and overlying muscles.
Surface Landmarks of the Posterior Thorax
Note the relation of the scapulae to the ribs. The inferior angle of the scapula is usually at the eighth interspace; this allows one to identify the eighth rib posteriorly to count ribs in the back.
The scapula is overlaid with skeletal muscle and glides on the chest wall. Its medial border, inferior angle, lateral border, spine, acromion, and coracoid process are easily palpable. The lungs extend to the thoracic apex and may extend superiorly into the base of the neck where they are vulnerable to penetrating injury. The pleural spaces coapt in the anterior superior mediastinum but are separated posteriorly by the spine and mediastinum and anteriorly and inferiorly by the pericardial sack and heart. The heart lies retrosternally and to the left with the right ventricle in the retrosternal position and the left ventricle left lateral and posterior. The liver and spleen are positioned inferior to the diaphragm deep to the inferior ribs. Deep inspiration with flattening of the diaphragm pushes them toward the costal margins where the normal liver and enlarged spleen can be palpated. The axillary folds are formed by the pectoralis major anteriorly and the subscapularis and latissimus dorsi posteriorly.
The topography of the five lung lobes has some clinical applications. In Figure 8-8, note that the anterior aspect of the right lung is formed almost entirely of the right upper and middle lobes; the posterior aspect contains only the upper and lower lobes. In the left lung, the upper and lower lobes present both back and front.
Topography of the Five Lobes of the Lungs
The solid lines are the pulmonary fissures; the broken lines are projections. The boundary of the lingula (L) is hypothetical.
The anterior surface of the chest over the heart and aorta is termed the precordium. Normally, this area extends vertically from the second to the fifth intercostal space, transversely from the right border of the sternum to the left midclavicular line in the fifth and sixth interspaces. The upper epigastrium is occasionally included. When the heart is enlarged or displaced, the boundaries of the precordium shift accordingly. In dextrocardia, all signs described herein are located in the opposite hemithorax.
The projections of the normal heart upon the precordium are depicted in Figure 8-9 and their projections on a chest radiograph are depicted in Figure 8-10. Behind the manubrium are the aortic arch and other mediastinal structures. The right border of the heart corresponds roughly to the right edge of the sternum from the third to fifth interspaces. The right atrium forms the right border with the right ventricle anterior under the sternum and left lower ribs. The left ventricle forms the cardiac apex and a slender area of the left border and sits posteriorly to the right ventricle. Thus, the right ventricle forms most of the heart’s anterior surface but neither right or left heart border.
Precordial Projections of the Anterior Surface of the Heart
The entire central area of the precordium is a projection of the right ventricle. The left border and apex are formed by the left ventricle; the right atrium is the right border.
X-ray Silhouettes of the Heart
The positions are named for the aspect of the patient’s thorax that faces the cassette (except for the PA view). Angles are measured between the direction of the X-ray beam and the plane of the patient’s back. The heavy lines on the silhouettes indicate distinctive segments used in diagnosis.
Physical Examination of the Chest and Major Vessels
Inspection of the Rib Cage and Thoracic Musculature
Examination of the Chest and Major Vessels: Rib Cage, Thoracic Musculature, Lungs, Pleura, Heart, and Precordium
Inspect for structural deformities of the thorax and skin lesions that might restrict respiratory excursion. Observe several respiratory cycles noting the movements of the chest and respiratory rate, amplitude, and rhythm. Look for labored inspiration, intercostal retraction, and forced expiration, while noting cough or noisy breathing. Palpate with the palms of the hands to confirm areas of dyskinetic chest wall motion. Inspect the chest wall of the supine patient from the foot of the bed.
Have the patient stand or sit; inspect the profile of the spine from the side for kyphosis, lordosis, and gibbus. From the back, look for lateral deviation of the spinous processes indicating scoliosis. To detect scoliosis when the patient is obese, palpate and mark each spinous process. Observe for exaggerated thoracic kyphosis or kyphoscoliosis. The complete spinal examination is described in Chapter 13.
Palpation of the Rib Cage and Thoracic Musculature
To check for a deviated trachea, place your index finger in the suprasternal notch and feel the space between the clavicles and the lateral tracheal borders. Alternatively, feel for the tracheal rings in the middle of the suprasternal notch. If the apex of the rings touches the middle of the finger tip, the trachea is in the midline.
Palpation is indicated if there is chest pain, a mass seen on inspection, breast masses, or draining sinuses. Examine the soft tissues and the large thoracic muscles for tenderness; if tender, identify the movements that cause pain. Feel for soft-tissue crepitus. Palpate the intercostal spaces for tenderness and masses. Examine the costal cartilages and palpate the costochondral junctions and xiphisternal joint for tenderness. Palpate the ribs for point tenderness, swelling, crepitus, and pain on chest compression.
Testing excursion of the upper thorax
Place a hand on each side of the patient’s neck with palms against the upper anterior thoracic wall. Curl the fingers firmly over the superior edges of the trapezii. Move the palms downward against the skin, to provide slack, until the palms lie in the infraclavicular fossae. Then extend your thumbs so their tips meet in the midline (Fig. 8-11A). Have the patient inspire deeply permitting your palms to move freely with the chest while your fingers are anchored on the trapezii. The upper four ribs move forward with inspiration, so your thumbs diverge from the midline. Normally, the thumbs move laterally for equal distances. Asymmetric excursions suggest a lesion on the lagging side in the chest wall, the pleura, or the upper lobe of the lung.
Testing Thoracic Movement
A. The upper anterior thorax. B. Expansion of the anterior mid-thorax. C. Expansion of the posterior thorax. D. Movement of costal margins.
Testing excursion of the anterior middle thorax
With your fingers high in each axilla and your thumbs abducted, place the palms on the anterior chest. Move the hands medially, dragging skin to provide slack, until the thumb tips meet in the midline at the level of the sixth ribs (Fig. 8-11B). Have the patient inspire deeply letting your hands follow the chest movements. The thumbs should move apart. A unilateral lag indicates a nearby lesion in the wall, pleura, middle lobe of the right lung, or lingula of the left lung.
Testing excursion of the posterior lower chest
Have the patient sit or stand with his back toward you. Place your fingers in each axilla, with the palms applied firmly to the patient’s chest, so your forefingers are one or two ribs below the inferior angles of the scapulae. To provide slack, press the soft tissues and pull your hands medially until your thumbs meet over the vertebral spines (Fig. 8-11C). Have the patient inspire deeply, following the lateral movements of the chest with your hands; your thumbs should move apart. A unilateral lag indicates a lesion in the nearby wall, pleura, or lower lobes.
Testing excursion of the costal margins
With the patient supine, place your hands so the extended thumbs lie along the inferior edges of the costal margins, with their tips nearly touching (Fig. 8-11D). Have the patient inspire deeply, letting your thumbs follow the costal margins. Normally, the thumbs diverge. Diminished divergence or convergence indicates flattening of the diaphragm.
Examination of the Lungs and Pleura
Some argue that physical examination of the lungs and pleura is no longer necessary, because X-ray examination is readily available and discloses many lesions without physical signs. Although the usefulness of X-ray examination is acknowledged, it does not replace the physical examination. Physical examination is rapid, can be performed in all clinical situations, and does not require additional equipment or remove caregivers from the patient. In addition, some clinical conditions are diagnosed only by physical examination or may be apparent on examination before radiographic signs appear: for example, early pneumonia can be diagnosed by the clinician before radiographic signs appear; a fractured rib may be obvious to palpation weeks before callus is evident with radiographs; the radiologist cannot diagnose asthma; the friction rub of pleurisy can appear and subside without radiographic signs; and pulmonary emphysema may be evident clinically before the radiologist can recognize it.
The physical examination of the pleura seeks to detect evidence of pleural inflammation, pleural adhesions, increases in pleural thickness, and the presence of air or excessive fluid in the pleural cavity. The lungs are examined to judge their volume, distensibility, density, changes in airway caliber, and abnormal secretions in the airways. Inspection and tactile palpation give some information. Vibratory qualities of the thorax and its contents yield significant information. Some vibrations are palpated; others are heard by the unaided ear, as in sonorous and definitive percussion, or through the stethoscope in auscultation. Vibrations are produced by the patient’s spoken voice and by the examiner tapping the patient’s chest. The caliber of the airways and their contained secretions modify the breath sounds or produce extraneous noises heard through the stethoscope.
Vibratory palpation of the lungs and pleura
Vibratory palpation uses the examiner’s vibratory sense, which is most acute over the joints. To test this, apply the handle of a vibrating tuning fork first to the fingertip and then to volar surface of the metacarpophalangeal joint; this demonstrates the superior sensitivity of the basal part of the finger to vibrations (Fig. 8-12).
Vibratory Acuity in Various Parts of the Hand
Place the handle of a vibrating tuning fork sequentially on the fingertip and the palmar aspect of the metacarpophalangeal joint: the palmar base is more sensitive. This part of the hand should be applied to the precordium to detect thrills.
Speech produces vibrations in the bronchial air column that are conducted to the chest wall through the lung septa where they are felt by vibratory palpation as vocal fremitus. Diminished vocal fremitus can be caused by airway obstruction, by fluid or air sound screens in the pleural cavity, or by pleural fibrosis. Increased vocal fremitus occurs with lung consolidation; the density of the tissues is determined by percussion (see Percussion.). To compare vocal fremitus in different regions of the chest, each test word must be spoken with equal pitch and loudness. Vocal fremitus is normally more intense in the parasternal region in the right second interspace where it is closest to the bronchial bifurcation. The interscapular region is also near the bronchi and registers increased fremitus. Use the same technique to feel for pleural friction rubs (friction fremitus).
Procedure for vibratory palpation
If able, have the patient sit or stand. Place the palmar bases of the fingers on to the interspaces (Fig. 8-13). Alternatively, the ulnar side of the hand and fifth finger may be used. Ask the patient to repeat the test words “ninety-nine” or “one–two–three,” using the same pitch and intensity of voice each time. If vibrations are not felt, have the patient lower the pitch of their voice. Compare symmetrical parts of the chest sequentially with the same hand. It is better to compare two sensations sequentially with the same hand than to compare simultaneous sensations from two hands. When the lower thorax is reached, ascertain the point at which fremitus is lost. In the absence of a pleural lesion, this indicates the lung bases. Compare this with the position obtained by percussion and auscultation.
Detection of Vocal Fremitus by Vibratory Palpation
Symmetrical points on the chest are palpated sequentially with the same hand and the strength of vocal fremitus is compared in different regions. The palpating hand is applied firmly to the chest wall with palm in contact with the wall, and vibrations are sensed with the bases of the fingers.
Percussion of the lungs and pleura: thoracic percussion
See Chapter 3 for a discussion of percussion techniques. For best results, press the pleximeter finger into the intercostal spaces parallel to the ribs, then strike a series of blows with the plexor. Percuss the back with the patient sitting and the anterior chest with the patient sitting and supine. Both sonorous and definitive percussion are used on the back (Fig. 8-14). When the patient is unable to sit, he must be examined in the right and left lateral decubitus position which introduces problems in the interpretation of percussion sounds (see Vibratory Palpation and Fig. 8-31).
Percussion Map of the Thorax
The entire lung surface is normally resonant. At the apices, a band of resonance, known as the Krönig isthmus, runs over the shoulders like shoulder straps. Hepatic dullness ranges downward from the right sixth rib to merge into hepatic flatness. The Traube semilunar space of tympany extends downward from the left sixth rib; it is variable in extent, depending upon the amount of gas in the stomach. Posteriorly, the dullness below the lung bases begins at about the tenth rib.
Definitive chest percussion
Definitive thoracic percussion is used to outline the borders between lung resonance and dullness of the heart, the spleen, the upper border of the liver, and the lumbar muscles below the lung bases. The boundary between resonant lung and tympanitic gastric bubble outlines the Traube space. The Krönig isthmus over the lung apices is defined by percussing the area of resonance in the supraclavicular fossae.
Use sonorous percussion with heavy indirect bimanual percussion. Starting under the clavicles, compare the percussion sound from each interspace sequentially with that from the contralateral region. Work downward to the region of hepatic dullness on the right and the Traube space on the left (Fig. 8-14). Also, percuss the lateral thorax. Except for cardiac dullness, the anterior chest should be resonant.
The domed superior aspect of the liver normally produces a transverse zone of dullness from the fourth to the sixth interspaces in the right midclavicular line. If a wedge of lung lies between the upper liver border and the chest wall, the transition from lung resonance to hepatic flatness is more gradual.
The stomach usually contains an air bubble that produces tympany in the Traube space. Because the left diaphragm is lower, the upper tympanitic border is somewhat lower than the upper border of liver flatness on the right.
The spleen produces an oval of dullness between the ninth and eleventh ribs in the left midaxillary line. Gastric or colonic tympany often obscures it completely. Dullness in this region may be enlarged by solid or liquid contents of the stomach or colon or by pleural effusion. An enlarged spleen is seldom obscured by gas. Enlarged splenic dullness or dullness in Traube space requires careful palpation for the spleen.
The lung apices extend slightly above the clavicles, producing a band of resonance over each shoulder, widening at its scapular and clavicular ends. The narrowest part, the Krönig isthmus, lies atop the shoulder. Reproducibility of this finding is low. With the patient sitting or standing, sound each supraclavicular fossa. On the right place the examiner’s left thumb in the right supraclavicular fossa (Fig. 8-15A) where it is struck by the plexor finger of the right hand. For the pleximeter in the left fossa, the examiner’s left arm is put around the patient’s back, and the left long finger is curled anteriorly over the trapezius muscle into the fossa (Fig. 8-15B). Fibrosis or infiltration of the lung narrows or obliterates the resonance.
Percussion of the Lung Apices
Bimanual indirect percussion is applied in the usual fashion, except for the use of the pleximeter. See the text for descriptions.
Posterior lung and diaphragm excursion
Use sonorous percussion with the patient sitting or standing, the spine slightly flexed and the shoulders pulled forward. Begin at the top and work downward comparing right to left sequentially. The scapula and muscles impair resonance in proportion to their mass so asymmetry is the notable finding. The inferior lung margins are usually at about the ninth rib on the left and the eighth interspace on the right (Fig. 8-14). The transition between lung resonance and muscle dullness (or flatness) is gradual. Light percussion is required. Mark the lung bases, during quiet respiration, then have the patient inspire deeply and hold the breath while you percuss the full inspiratory level. The bases should move downward 5 or 6 cm reflecting flattening of the diaphragm.
Auscultation of the lungs and pleura
Movement of air in the tracheobronchial tree produces vibrations perceived as sounds. Lung and heart sounds have a frequency between 60 and 3000 cycles per second. Sounds are produced by turbulent air movement in normal, dilated, or constricted airways from secretions, or from the vocal cords. The absence of the normal sounds indicates airway obstruction or pleural disease.
If possible, have the patient sit. When recumbent, the back should be examined by turning the patient from side to side. While the patient breathes through the mouth, deeper and slightly more forcefully than usual, listen with the stethoscope’s diaphragm anteriorly at the apices and work downward, comparing right to left sequentially. Then, listen to the back, again starting at the apices and working downward. Compare the lower lung margins as determined by auscultation, percussion, and fremitus.
Breath sounds are described as vesicular, bronchovesicular, bronchial, asthmatic, cavernous, or absent. Note also their quality and pitch and the relative duration of inspiration and expiration (Fig. 8-16). If crackles are heard, note whether they persist or disappear after a few deep breaths. If crackles are not heard, test for posttussive crackles by listening after a cough, particularly at the end of expiration. If an abnormality is found, test front and back for whispered pectoriloquy by having the patient whisper test words, such as “one–two–three” (Asthmatic or obstructive breathing). Test similarly with the spoken voice for bronchophony (Asthmatic or obstructive breathing). Be alert for friction rubs, bone crepitus, and other unusual sounds.
Breath Sounds Map in the Normal Chest
The areas of the lungs that are unlabeled have normal vesicular breathing.
Bedside inspection of the sputum
Collect sputum from a productive cough in a clear plastic cup. Note the color, viscosity, presence of blood, or odor and estimate the daily volume. Look for caseous masses, mucous plugs, Curschmann spirals, bronchial casts, and concretions.
Physical Examination of the Heart and Precordium
Despite advances in diagnostic technology, the cardiovascular physical examination remains an essential skill for the expert physician. Practice with mentoring by an expert is critical to learn heart examination; simulation technology facilitates this training [Issenberg SB, McGaghie WC, Hart IR, et al. Simulation technology for health care professional skills, training, and assessment. JAMA. 1999;282:861–866]. The physical examination is both sensitive and relatively specific for the diagnosis of valvular heart disease [Roldan CA, Shively BK, Crawford MH. Value of the cardiovascular physical examination for detecting valvular heart disease in asymptomatic subjects. Am J Cardiol. 1996;77:1327–1331].
The cardiovascular examination is presented here in a convenient sequence with emphasis on the precordium and careful examination of the neck and extremities. A complete cardiovascular evaluation also requires, if indicated, supplementary procedures such as electrocardiography, echocardiography, CT, MRI, scintigraphy, and catheterization.
Stand or sit at the patient’s right side. Shine a light across the anterior chest surface toward the examiner preferably from the left side. When possible, examine the patient while erect. Look for the apical impulse which is visible in 20% of normal people. With your line of sight across the sternum look for precordial heaves.
Pulsations, lifts, heaves, and thrills can be felt in the precordium. Palpate with the palm of the hand, first examining areas of visible pulsations. Even when not visible try to identify the apical impulse in approximately the left fifth interspace 7 to 9 cm from the midline; it should be no larger than 2 cm in diameter. The impulse is synchronous with early ventricular systole. Palpate the entire precordium for the presence and strength of right and left ventricular (LV) thrusts. When a thrill or friction rub is identified it must be described as systolic or diastolic by its relation to the apical impulse.
Percuss the precordium to identify the borders of cardiac dullness (definitive percussion). With the left arm abducted locate the left border of cardiac dullness (LBCD) by percussing in the fifth, fourth, and third interspaces, starting over resonant lung near the axilla and moving medially until cardiac dullness is encountered (Fig. 8-17). Measure the distance from the midline to the LBCD in the fifth interspace. The right border of cardiac dullness (RBCD) is normally behind the sternum so its position is not certain; it may even be displaced leftward. When the heart border is displaced rightward, the RBCD can be identified. No conclusion about heart size can be drawn by percussing only the LBCD. With hydrothorax or thickened pleura, percussion of the heart border may be impossible. Measure the width of the retromanubrial dullness; in the adult a width exceeding 6 cm suggests an anterior mediastinal mass.
Pattern of Precordial Percussion
The fifth, fourth, and third intercostal spaces on the left are percussed sequentially, as indicated by the arrows, starting near the axilla and moving medially until cardiac dullness is encountered.
Proper use of the stethoscope is described in Chapter 3 on Use of the stethoscope. The same principles apply to auscultation of the heart as to lung auscultation. Listen in each of the primary valve areas (Fig. 8-18). Timing of cardiac sounds is especially important; use the apical impulse, or, if absent, the carotid upstroke to mark the onset of ventricular systole. Map the radiation of abnormal sounds on the precordium.
Cardiac Valve Areas for Precordial Auscultation
These are the areas where the sounds originating from each valve are best heard; the areas are not necessarily closest to the anatomic location of the valves.
Auscultation for cardiac rate and rhythm
Auscultate the apical ventricular rate and compare it with a peripheral arterial pulse. If the rate is regular and not very slow, counting for 15 seconds and multiplying by 4 is sufficiently accurate. Any difference between the auscultated apical and palpated arterial rates is a pulse deficit. Pulse deficit occurs whenever ventricular systole generates a stroke volume insufficient to produce an arterial pulse wave; it is frequent with premature beats, bigeminal rhythm, and atrial fibrillation. The ECG is the gold standard for heart rate, as not all electrical events produce an audible mechanical event, especially at high heart rates. After counting the heart rate, listen carefully for an irregularity of rhythm. Dysrhythmias are harder to detect when the diastolic intervals are either very long or very short, that is, with particularly slow or fast heart rates. Determine if an irregularity has a relation to respirations and if there is a repeating pattern of beats.
Auscultation of the heart sounds: S1 and S2
Normally, auscultation reveals paired sounds, usually distinct in intensity and pitch, with each cardiac cycle (Fig. 8-19). Identification of the first (S1) and second heart (S2) sounds is essential because they mark the beginning and end of ventricular systole. The sound synchronous with an apical impulse is S1. Without an apical impulse, palpate the carotid pulse, allowing for a slight interval between the onset of cardiac systole and the wave’s arrival in the neck. The radial pulse is too far from the heart to reliably distinguish the heart sounds. At ventricular rates less than 100 bpm, diastole is longer than systole, so the first of the pair can be accepted as S1. When the rate is more than 100 bpm try to slow the heart for a few beats with a Valsalva maneuver or by gently massaging either carotid sinus. The initial sound after a long pause must be the first sound. Finally, the second sound is almost invariably louder than the first at the base of the heart.
Relation of the Heart Sounds to Other Events in the Cardiac Cycle
Of all these phenomena, only one visible and one audible sign are produced.
After identifying S1 and S2 at the apex, move the stethoscope short distances along the left sternal border and toward the base (inching) tracing each sound across the precordium. Use separate passes concentrating sequentially on the intensity (accentuated or diminished), the quality, the duration, and the presence of splitting of the sounds. Prolonged sounds can be differentiated from murmurs by their abrupt beginning and ending; murmurs have a gradual onset and end. A sound that begins abruptly but ends gradually is probably a heart sound followed by a murmur. Cardiac auscultation is difficult to master. It requires mentored practice listening to many normal and abnormal hearts to recognize the range of normal and correctly identify abnormal sounds.
Auscultation of heart murmurs
Listen for cardiac murmurs only after S1 and S2 have been positively identified. Decide whether a sound of abnormal length is a split heart sound or a heart sound and murmur. Now turn your attention to the systolic interval between S1 and S2. Decide if there is any audible sound in this interval by assuming that a heart sound is the shortest perceptible sound and that anything appreciably longer may be heart sound and murmur. A prolonged sound starting abruptly and dwindling is probably a heart sound followed by murmur; one developing gradually and ending abruptly is likely murmur and heart sound. Carefully examine each valve area using the diaphragm and listen at the apex and lower left sternal border with the bell. Cover the intervening spaces by moving the stethoscope short distances each time, “inching.” Once a murmur is identified, ascertain its characteristics: Timing: Determine in what part of the cardiac cycle the murmur occurs, and whether it is early, middle, or late in the interval, by reference to the first and second heart sounds. Location: Ascertain where on the precordium the murmur exhibits maximum intensity. Intensity: Grade intensity by the following scale: Grade I, barely audible with greatest difficulty; Grade II, faint but heard immediately upon listening. Grades III, IV, V, and VI are progressively louder: Grade IV the presence of a thrill; Grade V, loud enough to be heard with the stethoscope placed on its edge; Grade V, so loud it can be heard with the stethoscope off the chest. The grade should be recorded as, for instance, III/VI to show the scale being used. Pattern or Configuration: Decide if the murmur is uniform in intensity throughout or whether the loudness increases (crescendo), or diminishes (decrescendo), or both (crescendo-decrescendo). The term diamond-shaped murmur is taken from the graphic depiction with the maximum intensity in mid systole, with a crescendo preceding and decrescendo following the peak. Pitch: Determine whether the murmur is high or low pitched. Is the murmur is better heard with the bell (low pitched) or the diaphragm (high pitched)? Remember, the bell should be applied lightly and the diaphragm should be pressed firmly against the skin. Is the pitch more like a murmur or a friction rub? Rubs are frequently misdiagnosed as murmurs; they are distinguished by the quality of the sound. Posture and Exercise: When possible, auscultate the heart in both the supine and erect positions. Listen in the left lateral decubitus position at the cardiac apex to detect the murmur of mitral stenosis and gallop rhythms. After the systolic interval has been thoroughly explored, listen in the diastolic interval carrying out the same procedures while asking the same questions.
Listening for extra systolic sounds
After identifying systole and diastole, and noting any murmurs, listen for extra sounds in the systolic interval. Any abnormal sound must be either a murmur or a systolic click (Fig. 8-20).
Timing of Heart Sounds, Clicks, Opening Snap, and Murmurs Within the Cardiac Cycle
ICS, intercostal space; SB, sternal border; S2-A, S2-in aortic area; S2-P, S2 in pulmonic area.
Listening for diastolic sounds
After examining the systolic interval, listen in diastole, between S2 and S1, for a murmur, opening snap, third heart sound (S3), fourth heart sound (S4), or pericardial knock (Fig. 8-20).
Physical Examination of the Blood Vessels
Clinicians must be familiar with the accessible arteries and veins. These arteries are usually palpable: temporal, common and external carotid, axillary, brachial, radial, ulnar, common iliac, femoral, popliteal, dorsalis pedis, and posterior tibial (Fig. 4-2). The abdominal aorta may be palpable. Visible veins are the external jugular, cephalic, basilic, median basilic, great saphenous, and veins on the hands and feet.
Measurement of arterial blood pressure
Central venous pressure (CVP) is measured at the level of the right atrium. When erect, this is at the anterior fourth intercostal space. Proximal and superior to the RA are, in order, the SVC, the two subclavian veins, and the two subcutaneous external jugular veins in the neck above the clavicles. The vertical height of the blood column above the RA is the CVP, normally about 10 cm (Fig. 8-21A). Peripheral veins below CVP level are filled with blood; those above are collapsed. In adults, the upper clavicle border is about 13 to 18 cm above the RA, so the external jugular veins collapse when the patient is erect (Fig. 8-21C). As the thorax reclines blood rises into the neck veins becoming visible in the jugular veins (Fig. 8-21B). The arm and forearm veins distend to the same level as the SVC. In the horizontal position, all peripheral veins are filled (Fig. 8-21A). Raising the arm above the CVP height collapses the distal veins. Transient distention of the jugular veins is seen with increased intrathoracic pressure as with coughing, laughing, crying, and Valsalva. Also, a large cervical or retrosternal goiter may cause venous obstruction.
Response of the Jugular Blood Column to Changes in Posture
The anteroposterior diameter of the thorax at the fourth interspace is 20 cm; from this point, the vertical distance to the superior border of the clavicle is 15 cm in the erect position. The right atrium is located at the midpoint of an anteroposterior line from the fourth interspace to the back. In any posture, a horizontal plane through this point is the zero pressure level. In this figure, a slightly elevated venous pressure of 12.3 cm is assumed. A. With the patient supine, the horizontal plane 12.3 cm above the zero level is above the neck; at normal venous pressure the jugular vein is filled. B. With the thorax at 45 degrees, the blood column extends midway up the jugular, so the head of the column is visible. C. In the erect position, the head of the column is concealed within the thorax, 2.7 cm below the upper border of the clavicle.
The vertical distance in centimeters from the head of the jugular blood column to the right atrium is an approximate measure of CVP. When identifiable, the internal jugular vein provides a more accurate estimate than the external jugular veins; the veins on the right are more reliable than those on the left. When sitting or standing, distended external jugular veins indicate an increased CVP (assuming no SVC obstruction). The presence of jugular venous waves excludes central obstruction. Tense venous distention may prevent visualization of the venous waves.
Indirect measurement of CVP
If the jugular veins are collapsed in the vertical position, slowly lower the thorax until the head of the blood column appears. The right atrial position is estimated by running an imaginary anteroposterior line from the anterior fourth interspace halfway to the back; a horizontal plane through this point is the zero level for measuring venous pressure (Fig. 8-21B). The vertical distance in centimeters from this plane to the head of the blood column is the approximate CVP. The angle of Louis (sternal angle) is another reference point for estimating CVP. It is approximately 6 cm above the RA in most positions, though not always [Seth R, Magner P, Matzinger F, van Walraven C. How far is the sternal angle from the mid-right atrium? J Gen Intern Med. 2002;17:852–856]. Jugular venous pulsations >3 cm vertically above this landmark indicate elevated venous pressure [McGee SR. Physical examination of venous pressure: a critical review. Am Heart J. 1998;136:10–18].
Alternate indirect measurement of CVP
Place the patient supine with an arm hanging over the bedside. Raise the arm slowly until the distended arm or hand veins collapse. The vertical distance from the zero level to the point of collapse estimates the CVP. Select a vein as close to the heart, for example, the cephalic, basilic, or median basilic veins (Fig. 8-22). There is great variation in the caliber and superficiality of the arm veins.
Visible Veins and Venous Pressure Measurements
A. Veins of the neck. B. Veins of the arm. C. Veins of the thigh and leg.
The venous pulse wave is a normal phenomenon that can be demonstrated in the external jugular veins but visibility depends on the amount of overlying tissue. Venous pulsation is readily distinguished from an arterial pulse by being impalpable. There are three upward components to the venous pulse wave (Fig. 8-23) and two prominent descents. The “a” wave results from right atrial systole; the “c” wave is principally caused by expansion of the underlying carotid artery and is usually not visible. The “a” wave peak is followed by an “x” descent, initially because of atrial relaxation and later of downward movement of the tricuspid valve with right ventricular systole. The rising “v” wave is produced by right atrial filling with the tricuspid valve closed. The peak of the “v” wave is followed by the y descent associated with tricuspid valve opening at onset of right ventricular diastole. Correctly identifying the waves and descents requires careful correlation with the cardiac cycle. The rapid descents are usually better appreciated than the slowly rising waves. The “x” descent is normally the most readily observed portion of the jugular pulse, and its nadir is approximated by S2. The peak of “a” wave is normally the most prominent wave and occurs at about S1.
Jugular Venous Pulse Waves
Heart action is reflected in the jugular vein. The waves should be timed with the apical impulse or heart sounds, remembering that a perceptible time elapses between cardiac events and their signs in the neck. The “a” wave is the rebound from atrial systole. The bulging of the tricuspid valve cusps early in ventricular systole produces the c deflection. The “v” wave results from atrial filling while the valve is closed, together with an upward movement of the AV valve ring at the end of ventricular systole. The x descent comes with atrial relaxation and the y descent with opening of the tricuspid valve.
Venous pulsations can also be seen as lateral expansion of the neck occurring with filling and collapse of the internal jugular veins and their tributaries. This is best seen from the foot of the bed. In a few persons, pulsations occur in the superficial veins of the arms, forearms, and hands. Occasionally, a disproportion in the number of “a” waves and ventricular systoles gives direct indication of a dysrhythmia; but the waves are difficult to see consistently. Failure to identify an expected venous pulse may indicate obstruction of the veins proximal to the right atrium.
Press down on the tip of a fingernail until the distal third of the nailbed blanches. With each heartbeat, the border of pink extends and recedes. This a prominent sign in aortic regurgitation known as Quincke pulse, but, to a lesser degree, it can be seen in many normal persons.
Examination of the Arterial Circulation in the Extremities
Large arteries are named and normally have visible or palpable pulses. Their occlusion is recognized by regional ischemia. In the complete physical examination, assess the circulation by (1) bilateral palpation of the pulse volume in brachial, radial, femoral, dorsalis pedis, and posterior tibial arteries; (2) palpation for skin temperature changes; (3) inspection for varicose veins, edema, pallor, cyanosis, and ulceration of the arms and legs; and (4) inspection of the retinal vessels. Complaints of pain, coolness, or numbness in an extremity or signs of enlarged veins, masses, swellings, localized pallor, redness, or cyanosis lead to special examinations of the peripheral circulation. The cause of a circulatory deficit is suggested by the history, the distribution of the deficit, and the state of the vessel wall.
Skin examination for circulation
When an affected part is below heart level, pooled venous blood obscures evidence of arterial flow. Venous pressure rarely exceeds 30 cm above that of the right atrium, whereas the systolic arterial pressure is more than 150 cm above the same reference point. Thus, when the hand or foot is lifted above the right atrium to a height exceeding the venous pressure, the masking venous blood pool is drained, permitting evaluation of the tissue color produced by the arterial inflow. The most reliable signs of a regional perfusion abnormality are a temperature or perfusion discrepancy between symmetrical parts at the same external temperature.
It is imparted by the blood in the venules of the subpapillary layer and the melanin content of the skin. Examination for circulatory changes in dark-skinned individuals is difficult; focus attention on the mucous membranes, nail beds, and palms. When the arterial flow is nil and the veins empty, the skin is chalky white. Partial but inadequate arterial supply may produce red or cyanotic skin, depending on the effect of external temperature and amount of pooled blood in the venules.
Temperature is a reliable indicator of skin perfusion. Normal flow is principally governed by arteriolar constriction or dilatation. Internal body temperature is maintained within narrow limits, partly by heat dissipation from the skin. In clothed persons, the skin of the head, neck, and trunk is warmer than that of the extremities, and the digits are cooler than the proximal hands and feet. Peculiarly, normal digits adjust their temperature to only one of the two levels. The fingers are somewhat cooler (32°C [90°F]) than blood temperature (37°C [98°F]) when the air temperature exceeds 20°C (68°F). If the air temperature is below 16°C (60°F), finger temperatures drop to approximately 22°C (72°F); no intermediate level is maintained.
Skin examination for arterial deficit
In a draft-less room at approximately 22°C (72°F) expose the extremities for 10 minutes. If the room temperature much exceeds 26°C (78°F), coldness in the skin will not be demonstrable. Have the patient sit, hanging the legs from the table or bed; compare the skin color of both feet looking for pallor, deep redness, pale blueness, deep blueness, or a violaceous color (Fig. 8-24A). With the back of your hand or fingers, feel the skin temperature from the feet up the legs. Compare similar sites on each leg in sequence noting whether the increase in temperature is gradual or sharply demarcated. Have the patient lie supine. Grasp the patient’s ankles and elevate the feet more than 30 cm (12 inch) above the right atrium. Note any change in skin color (Fig. 8-24C). If the color does not change, have the patient dorsiflex the feet five or six times, wait several minutes, then observe the feet for color changes induced by exercise. Allow the feet to hang down again and note the time for the color to return. Note how quickly color returns to an area blanched by finger pressure. Inspect the feet carefully for evidence of malnutrition, for example, atrophy of the skin, loss of lanugo hair on the dorsa of the toes, thickening or transverse ridging of the nails, and ulceration or patches of gangrene. Examine the arms similarly by exposing them for 10 minutes and then observing the color in dependency and when elevated well above heart level (Fig. 8-24B). Repetitively open and close the fists to disclose latent color changes. Note the time of return of color in dependency. Look for evidence of dermal malnutrition.
Circulation of the Skin in Extremities
A. The legs are dependent to observe the color of the skin and nail beds. Arterial deficit produces a violaceous color from pooling of the blood in the venules because of loss of venomotor tone as a result of hypoxia. B. While the patient is supine, the foot is elevated above the level of venous pressure (15 cm [6 in.] above the right heart or 25 cm [10 in.] above the table when the patient is supine). Elevation drains the foot of venous blood so the skin color reflects only the presence of arterial blood. The elevated leg is compared with the opposite extremity. C. The hand is raised above the heart level so the skin color is produced exclusively by arterial blood.
Examination of large arm and leg arteries
Palpate the walls of accessible arteries for increased thickness, tortuosity, and beading. A spastic artery feels like a small cord. Compare the pulse volume at symmetric arterial levels.
Listen for a bruit in the supraclavicular fossa over the subclavian artery. The arteries in the arm and forearm are palpable only at the brachial artery in the upper arm and the radial and ulnar arteries in the wrist. With the forearm in about 90 degrees of flexion, palpate the brachial artery on the medial aspect of the arm in the groove between the biceps and triceps muscles (Fig. 8-25A). Feel the radial artery on the flexor surface of the wrist just medial to the radial styloid. Palpate the ulnar artery on the flexor surface of the wrist just medial to the distal ulna; it lies deeper than the radial artery and may not be palpable. Examine for patency of the radial and ulnar arteries with the Allen test (Fig. 8-25B). Have the patient sit with her hands supinated on her knees; stand at the patient’s side with your fingers around her right wrist and your thumbs on its flexor surface. Have the patient make a tight fist, then compress both the radial and ulnar arteries with your thumbs. Have the patient open the hand; the skin should be pale and remain so if both arteries are compressed. Take your thumb off the radial artery; the palm and fingers should quickly turn pink as flow returns. Delayed flush or no flush indicates partial or complete obstruction of the radial artery. Repeat the process, this time removing pressure from the ulnar artery. Return of flow is normally somewhat slower from the ulnar artery, but absence of flush is pathologic. Repeat this sequence on the other hand.
Testing Patency Arm Arteries
A. Palpable segments of the arm arteries (segments in solid black). Frequently the ulnar pulse is not palpable in normal persons. B. Allen test. See the text for details.
Palpate the abdominal aorta deeply between the xiphoid and the umbilicus. Palpate the common femoral arteries just below the inguinal ligaments, equidistant between the anterior superior iliac spines and the pubic tubercles (Fig. 8-26). Feel for popliteal artery pulsation with the patient supine and the legs extended. Place a hand on each side of the patient’s knee with your thumbs anteriorly near the patella and the fingers curling around so the tips rest in the popliteal fossa. Firmly press the fingers against the lower end of the femur or the upper part of the tibia; feel for the arterial pulsation. A normal popliteal artery may not be palpable. For the pulse of the posterior tibial artery, feel in the groove between the medial malleolus and the Achilles tendon. It may be more accessible with passive dorsiflexion of the foot. Locate the dorsalis pedis artery on the dorsum of the foot, just lateral to and parallel with the tendon of the extensor hallucis longus. In normal persons older than age 45 years, either the dorsalis pedis or the posterior tibial pulse frequently will be impalpable, but not both in the same foot. Do not mistake the pulse in your finger for that of the patient. Check the ankle-brachial index (ABI) by measuring the systolic blood pressure in the brachial artery and the posterior tibial and/or the dorsalis pedis artery. The ABI is the ratio of the ankle systolic pressure to the brachial systolic pressure. Normal is >0.9, 0.75 to 0.9 is mild, 0.6 to 0.75 is moderate, and <0.6 is severe ischemia. ABI <0.5 is limb threatening. Use of a Doppler may be necessary.
Palpable Lower Limb Arteries
The palpable segments of the arteries are in solid black. The femoral artery is palpable only a short distance below the inguinal ligament at the midpoint between the anterior superior iliac spine and the pubic tubercle. The popliteal artery lies vertically in the popliteal fossa; it can be felt only by compressing the contents of the fossa from behind against the bone. The posterior tibial artery can be felt as it curls forward and under the medial malleolus. The palpable segment of the dorsalis pedis artery lies just lateral to the most medial of the dorsal tendons of the foot (the flexor of the great toe) over the arch of the foot.
Doppler ultrasound examination
Small portable instruments for use at the bedside make it possible to evaluate the arterial circulation more precisely, especially when the pulses are not readily palpable.
Examination of the Large Limb Veins
Adequate drainage of blood from the extremities requires (1) patency of the veins, (2) voluntary muscle contractions to pump blood proximally by compressing the veins, and (3) competent valves in the perforating and deep veins so that vein compression moves the blood proximally. A defect in any of these may result in venous stasis with increased filtration pressure in the distal capillaries and post-capillary venules producing edema, stasis pigmentation, and/or skin ulceration.
Examination of the large arm and leg veins
With the patient supine, look for signs of venous stasis. Have the patient stand and look for dilated veins in the arms and legs. Elevate each extremity to determine how rapidly the veins collapse; failure to promptly empty indicates obstruction. If occlusion is present, palpate the venous walls for hard plugs of thrombus or hard cords of fibrosis. If patent varicose veins are present, use the special tests for incompetency of valves.
Laboratory examination of the large limb veins
Techniques such as Doppler ultrasound, impedance plethysmography, venography, and MRI can determine the patency and valve competence of the large limb veins.
Chest, Cardiovascular, and Respiratory Symptoms
Thoracic pain has many causes and, unless obviously the result of minor trauma, is often accompanied by fear of heart disease. Chest pain can occur without physical signs, so diagnostic accuracy requires careful attention to history, especially the attributes of pain (PQRST: provocative-palliative factors, quality, region-referral, severity, and timing). Always have the patient demonstrate the entire area where they perceive pain and the location of maximal intensity. The diagnostic approach is twofold: first to assess the risk for major vascular disease and acute coronary events, and second, to develop the differential diagnosis of noncardiovascular explanations [Lee TH, Goldman L. Evaluation of the patient with acute chest pain. N Engl J Med. 2000;342:1187–1195]. Careful risk factor assessment and a high index of suspicion is necessary. Reassurance after exclusion of cardiovascular disease is often the most effective therapy [Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA. 2005;294:2623–2629]. See Six-Dermatome Pain Syndromes.
Deep retrosternal or precordial pain and the six-dermatome band
Dermatomes T1 to T6 cover the thoracic surface from the neck to beneath the xiphoid process and extend down the anteromedial aspects of the arms and forearms (Fig. 8-27). The upper four spinal segments are supplied by sensory afferent fibers from the dorsal roots of T1 to T4 and the lower cervical and upper thoracic sympathetic ganglia. In the ganglia and spinal cord, the fibers communicate with one another superiorly and inferiorly. The mediastinal, thoracic, and abdominal organs are also supplied by sensory afferents and parasympathetic efferents via the vagus nerve (CNX). Practically, all the thoracic viscera are served by sensory fibers in these pathways: myocardium, pericardium, aorta, pulmonary artery, esophagus, and mediastinum. Lesions in any of these structures produce pain of the same quality: deep, visceral, and poorly localized. Spinal segments T5 and T6 receive sensory fibers from the lower thoracic wall, the diaphragm and its peritoneal surface, the gallbladder, the pancreas, the duodenum, and the stomach. Inflammation in these structures causes deep, visceral, poorly localized pain very similar in quality to that of the upper band. Deep visceral pain behind the sternum in the precordial region or epigastrium is typical for pain from the entire region supplied by spinal segments T1 to T6, including the sympathetics. It is not specific for heart disorders. The neuroanatomy of the region explains the structural basis for this clinical observation. Usually pain arising from T1 to T4 is maximal in the retrosternal region or the precordium; it often extends with lesser intensity upward into the neck and downward on the anteromedial aspects of one or both arms and forearms. Pain arising in T5 or T6 is maximally intense in the xiphoid region and in the back, inferior to the right scapula, but the pain may extend to the upper band of T1 to T4 through posterior connections in the sympathetics, so that the pattern may be indistinguishable from that arising above the diaphragm. The location of pain only indicates that its source is somewhere in the six-dermatome band (the myocardium, pericardium, aorta, pulmonary artery, mediastinum, esophagus, gallbladder, pancreas, duodenum, stomach, or subphrenic region). Have the patient rate the pain intensity on a scale of 1 to 10. Shorten the list of possible etiologies by carefully searching for provocative-palliative factors and timing to activities. CLINICAL OCCURRENCE: Congenital: hypertrophic cardiomyopathy; Endocrine: retrosternal thyroid; Idiopathic: esophageal spasm, gastroesophageal reflux; Inflammatory/Immune: esophagitis, pericarditis, pleuritis, myocarditis, postcardiotomy syndrome, pancreatitis, cholecystitis, gastritis; Infectious: infectious pericarditis and pleuritis, myocarditis, subphrenic abscess; Metabolic/Toxic: acid or alkali ingestion; Mechanical/Trauma: pneumothorax, esophageal rupture, esophageal obstruction (extrinsic, foreign body, neoplasm, web, or ring), esophageal diverticulum, gastric perforation; Neoplastic: carcinoma (primary or metastatic) of the esophagus, pericardium, lung, mediastinum, pleura; lymphoma; thymoma; teratoma; testicular cancer; Neurologic: postherpetic neuralgia, diabetic radiculopathy, intercostal neuritis; Psychosocial: somatization disorder, panic attack, hypochondriasis, malingering, Munchausen syndrome; Vascular: myocardial ischemia (coronary atherosclerosis, spasm, embolism, thrombosis, vasculitis), central pulmonary embolism (PE) and infarction, aortic dissection.
The Six-Dermatome Band
Dermatomes T1 to T6 form a band that covers most of the thorax and extends down the anteromedial aspect of the arms and forearms. Sensory pathways from the viscera of this entire region are so interconnected axially that stimulation of any part can produce the same patterns of chest pain.
Shortness of breath—dyspnea
Dyspnea results from abnormalities of gas exchange (decreased oxygenation, hypoventilation, hyperventilation), and increased work of breathing because of changes in respiratory mechanics and/or anxiety. Dyspnea means difficult breathing; it is both a symptom and a sign. The patient’s complaint is likely to be “shortness of breath,” “run out of breath,” “can’t take a deep breath,” “smothering,” or “tightness in the chest.” Dyspnea is often accompanied by tachypnea, increased respiratory excursions (hyperpnea), tensing of the scaleni and sternocleidomastoidei, flaring of the alae nasi, and facial expressions of distress. Sometimes, the patient seems unaware of dyspnea despite having to pause for breath in the middle of a sentence. It is essential to identify associations of dyspnea such as exertional dyspnea versus dyspnea at rest and dyspnea on standing or lying down. A diagnostic classification of dyspnea can be based on anatomic or physiologic criteria. Often more than one mechanism is involved, for example, pneumonia causes hypoxia and increases the work of breathing. Patients may complain of dyspnea disproportionate to identifiable physiologic or anatomic abnormalities; anxiety with hyperventilation or unsuspected decreases in respiratory muscle strength or chest compliance should be suspected. CLINICAL OCCURRENCE: Decreased Fraction of Inspired Oxygen: high altitudes; Airway Obstruction: Larynx and Trachea infections (laryngeal diphtheria, acute laryngitis, epiglottitis, Ludwig angina), angioedema, trauma (hematoma or laryngeal edema), neuropathic (abductor paralysis of vocal cords), foreign body, tumors of the neck (goiter, carcinoma, lymphoma, aortic aneurysm), ankylosis of the cricoarytenoid joints; Bronchi and Bronchioles acute and chronic bronchitis, asthma, retrosternal goiter, aspirated foreign bodies, extensive bronchiectasis, bronchial stenosis. Abnormal Alveoli: Alveolar Filling pulmonary edema, pulmonary infiltration (infectious and aspiration pneumonia, carcinoma, sarcoidosis, pneumoconioses), pulmonary hemorrhage, pulmonary alveolar proteinosis; Alveolar Destruction pulmonary emphysema, pulmonary fibrosis, cystic disease of the lungs; Compression of the Alveoli atelectasis, pneumothorax, hydrothorax, abdominal distention; Restrictive Chest and Lung Disease: paralysis of the respiratory muscles (especially the intercostals and the diaphragm), myasthenia gravis thoracic deformities (kyphoscoliosis, thoracoplasty), scleroderma or burns of the thoracic wall, pulmonary fibrosis; Abnormal Pulmonary Circulation: pericardial tamponade, pulmonary artery stenosis, arteriovenous shunts in heart and lungs, pulmonary thromboembolism and infarction, other emboli (fat, air, amniotic fluid), arteriolar stenosis (primary pulmonary hypertension, irradiation); Oxyhemoglobin Deficiency: anemia, carbon monoxide poisoning (carboxyhemoglobinemia), methemoglobinemia and sulfhemoglobinemia, cyanide and cobalt poisoning; Abnormal Respiratory Stimuli: pain from respiratory movements, exaggerated consciousness of respiration (effort syndrome), hyperventilation syndrome, secondary respiratory alkalosis (increased intracranial pressure, metabolic acidosis).
A transient increase in pulmonary capillary pressure is caused by redistribution of fluid from edematous extremities to the lungs with recumbency, or ischemia-induced transient decreases in LV performance. Sudden paroxysms of breathlessness often occur with recumbency or exertion. When sleep is interrupted, it is termed paroxysmal nocturnal dyspnea which may be accompanied by orthopnea and coughing. The patient often finds that sitting or walking for a few minutes relieves the dyspnea permitting sleep to resume.
Shortness of breath when lying down—orthopnea
Redistribution of extracellular fluid from the periphery to the lungs, elevation of the diaphragm from obesity or ascites, and muscular weakness all contribute to dyspnea when lying flat. The patient assumes a resting position with the head and chest elevated; the severity is estimated by the number of pillows required to achieve a comfortable sleeping position. Many patients awaken from sleep in the supine position severely short of breath (paroxysmal nocturnal dyspnea). Orthopnea may be overlooked if not specifically ask about or if the patient is not observed for some time while supine.
Shortness of breath when standing up—platypnea
Enlargement of pulmonary arteriovenous shunts leads to increased right to left shunting with standing. The results are decreased oxygen saturation on standing (orthodeoxia) and shortness of breath. This is part of the hepatopulmonary syndrome (see Hepatopulmonary syndrome) seen in patients with advanced liver disease. Patients complain of shortness of breath and weakness on standing, relieved by sitting or lying. They have stigmata of advanced liver disease including cutaneous spiders and ascites caused by portal hypertension.
Chest pain with tenderness
Lung and Pleural Symptoms
Shortness of breath—dyspnea
Respiratory pain—intercostal neuralgia
Irritation of an intercostal nerve produces sharp, lancinating, stabbing pain along the nerve’s course. The pain is frequently intensified by respiratory motion, trunk movements, or exposure to cold. Tenderness along the nerve is diagnostic. Pain is greatest near the vertebral foramen, in the axilla, or at the parasternal line, corresponding to its major cutaneous branches. CLINICAL OCCURRENCE: Herpes zoster, diabetes mellitus, tabes dorsalis, mediastinal neoplasm, neurofibroma (an intercostal mass may be felt), Tarlov cyst, vertebral tuberculosis, or obesity with nerve stretching.
Cough is a sudden, forceful, noisy expulsion of air from the lungs. The three stages of coughing are preliminary inspiration, glottal closure and contraction of respiratory muscles, followed by sudden glottal opening to produce the outward blast of air. The sensory nerve endings for the cough reflex are branches of the vagus (CN-X) in the larynx, trachea, and bronchi. Cough may also be induced by external acoustic meatus stimulation via the auricular nerve, a branch of the vagus, and from esophageal stimulation by acid reflux. Stimuli for coughing include exudates in the pharynx or bronchial tree, irritation of foreign bodies, and inflammation. Coughing may be voluntary or involuntary, single or paroxysmal. A productive cough raises sputum. Chronic unexplained coughs are most commonly caused by chronic post-nasal drip, gastroesophageal reflux, or cough-variant asthma [Irwin RS, Madison JM. The diagnosis and treatment of cough. N Engl J Med. 2000;343:1715–1721]. DDX: A brassy cough is nonproductive with a strident quality; it occurs with narrowing of the trachea or glottal space, most commonly laryngitis or epiglottitis, but also laryngeal paralysis, vocal cord neoplasm, or aortic aneurysm. In pertussis the cough is preceded by a long strident inspiratory noise, a whoop. CLINICAL OCCURRENCE: Congenital: tracheoesophageal fistula, mediastinal teratoma; Endocrine substernal thyroid; Idiopathic: emphysema; Inflammatory/Immune: inhaled allergens, asthma, chronic bronchitis, vasculitis, Goodpasture syndrome, relapsing polychondritis, endobronchial amyloidoma; Infectious: sinusitis, pharyngitis, laryngitis, epiglottitis, tracheobronchitis, pneumonia, bronchiectasis, lung abscess, subphrenic abscess, typhoid; Metabolic/Toxic: tobacco smoking, inhaled irritants, angiotensin-converting enzyme inhibitors; Mechanical/Trauma: cervical osteophytes, inhaled foreign bodies, acute and chronic aspiration, mediastinal mass and lymphadenopathy; Neoplastic: cancer of the larynx and lung, endobronchial adenoma, thymoma, mediastinal lymphoma, metastases to the lung; Neurologic: gastroesophageal reflux, tympanic membrane irritation; Psychosocial: cough tics and habits; Vascular: congestive heart failure (CHF), vasculitis (Wegener, Churg–Straus), aortic aneurysm, PE and infarction, pulmonary hemorrhage.
Chest pain intensified by breathing
Awareness of heart action, whether fast or slow, regular or irregular, is palpitation. The sensation may be described as “pounding,” “fluttering,” “flip-flopping,” “skipping a beat,” “missing a beat,” “stopping,” “jumping,” or “turning over.” The frequency, regularity, rate, and intensity depend on the underlying cause. Ask whether the sensation is a single extra beat, a pause, or a series of beats. If the latter, ask whether it starts and ends abruptly or gradually, whether it is fast or slow, and whether it is regular or irregular. Have them tap out the rhythm with their finger. Identify precipitating circumstances and associated symptoms that precede, accompany, or follow the palpitations. Next, perform a physical examination and obtain an ECG. Ambulatory monitoring is recommended for patients who tolerate the palpitations poorly, have heart disease, or sustained palpitations.
Exertional limb pain—claudication
Exercising muscle has high oxygen and energy requirements; energy is stored, but oxygen must be continuously delivered to meet the increased demand. Inability to increase blood flow during exertion produces ischemic muscle pain relieved by rest. Anemia increases symptoms by loss of oxygen-carrying capacity, whereas polycythemia increases blood viscosity slowing capillary flow. The patient usually complains of calf pain at a fixed distance of walking that requires him/her to stop or sit for relief. It is consistently reproducible. Claudication can occur in any exercising muscle; be alert for reproducible exertional extremity or gluteal pain. Pulses are usually diminished or absent in the popliteal, dorsalis pedis, and/or posterior tibial arteries of the affected leg. CLINICAL OCCURRENCE: Atherosclerotic, thrombotic or embolic obstruction of major arteries to the legs is most common. Exertional buttock and/or thigh pain may be true claudication or pseudoclaudication from spinal stenosis. Predisposing factors are tobacco use and diabetes.
Unilateral claudication in the young—popliteal artery entrapment syndrome
Entrapment of the popliteal artery by the medial head of the gastrocnemius muscle is a congenital anomaly. A young person develops unilateral claudication, with absence of or diminished pulses in the ipsilateral popliteal and dorsalis pedis arteries.
This common problem is caused by regional vasoconstriction to conserve heat. Examine carefully for decreased peripheral pulses or skin changes suggesting ischemia.
Chest, Trachea, and Respiratory Signs
Abnormalities of the thoracic spine
See Musculoskeletal Signs, Chapter 13 for a complete discussion. Thoracic spine and chest wall deformities may decrease chest compliance, severely limit respiratory excursions, and increase the work of breathing. In either curved or angular kyphosis (Fig. 8-28A), the spinal flexion may fix the thorax in the inspiratory position with increased AP diameter and horizontal ribs. Although the thoracic distortion is identical to the barrel chest of pulmonary emphysema, the auscultatory signs of emphysema are absent. Conversely, accentuation of the lumbar curve throws the thoracic spine backward and the thoracic cage becomes flattened from the pull of the abdomen, causing an expiratory position to be assumed (Fig. 8-28B). Lateral curvature of the thoracic spine is usually accompanied by some rotation of the vertebral bodies, but only the lateral deviations of the spinous processes are visible (Fig. 8-28C). Minor functional scoliosis forms a single lateral curve, usually with convexity to the right. With structural changes, the lateral curve in the thorax produces an opposite compensatory curve inferiorly, so the line of spinous processes forms an S-shaped curve. The spinous processes always rotate toward the concave side. On the convex side, rotation of the vertebral bodies causes flattening of the ribs anteriorly and bulging of the chest posteriorly, lifting the shoulder and lowering the hip. Viewed from the patient’s back, the posterior bulge is augmented with anteflexion of the spine.
Curvatures of the Spine Affecting the Thorax
A. Kyphotic thorax. B. Lordotic thorax. C. Scoliotic thorax. Note the narrowing of the rib interspaces on the right and the accentuation of the interspaces, posterior humping of the chest, and elevation of the shoulder on the left.
Abnormalities of the rib cage
Deformities of the rib cage can be congenital or acquired from nutritional disorders, trauma, or adaptive responses of the muscles and ribs to changes in the heart, lungs, and diaphragm.
Some causes of masses on ribs are callus around an old fracture or fibrous dysplasia, neoplasm (e.g., chondrosarcoma), myeloma, desmoid tumor, metastasis of carcinoma, angioma, eosinophilic granuloma, and bone cysts, including osteitis fibrosa cystica. An intercostal nerve neurofibroma causes swelling near the neck of the rib.
Pigeon breast (pectus carinatum)
The sternum protrudes from the narrowed thorax like the keel of a ship (Fig. 8-29B); the cause can be congenital or acquired. In rickets, the softened upper ribs bend inward, forcing the sternum forward increasing the AP dimension at the expense of the width. Vertical grooves are formed in the line of the costochondral junctions. This deformity persists after healing of the rickets. Pigeon breast also occurs in Marfan syndrome. A similar but asymmetric deformity occurs in severe primary kyphoscoliosis.
Deformities of the Thorax
A. Rachitic rosary. B. Pigeon breast. C. Harrison grooves. D. Funnel breast. E. Barrel chest.
Harrison groove (Harrison sulcus)
During active rickets, the protuberant rachitic abdomen pushes the plastic lower ribs outward on a fulcrum formed by the costal attachments of the diaphragm. The line of bending forms a groove or sulcus in the rib cage, extending laterally from the xiphoid process, with flaring of the cage below the groove (Fig. 8-29C). The deformity remains when the rickets heals.
Funnel breast (pectus excavatum)
The reverse of the pigeon breast, the lower costal cartilages, inferior sternum, and xiphoid process are retracted toward the spine. Its most mild form is an oval pit near the infrasternal notch. When the entire lower sternum sinks, significantly diminishing the AP thoracic dimension, a more extensive deformity forms (Fig. 8-29D). Rickets and Marfan syndrome are causes, but many cases are unexplained.
Emphysema causes increased residual volume leading to increased AP chest diameter, horizontal ribs, and a depressed diaphragm. Since both the AP and the transverse chest dimensions enlarge, the ribs become nearly perfect circles (Fig. 8-29E).
The sternal ends of rachitic ribs bulge at their costochondral junctions. In severe cases of rickets, the outward bulging produces knobs at the costochondral junctions (Fig. 8-29A). The condition resolves completely with treatment.
Chest and respiratory pain with tenderness
The distinction between respiratory pain with tenderness and chest pain with tenderness is artificial; many conditions present in either manner, or with both pain at rest and with respirations. The patient may recognize the pain as superficial, sharp, and well localized. Almost always this type of pain is accompanied by localized tenderness. The structures involved are the skin and subcutaneous tissues, the fat, skeleton, or the breasts. Careful chest examination can localize the pain to specific structures.
Skin and subcutaneous structures
Inflammation, trauma, and neoplasm in these tissues offer no special diagnostic problems, provided they are considered and searched for. The presence of bruises, lacerations, ulcers, hematomas, masses, trigger points, or tenderness is usually diagnostic.
Have the patient point to the site of pain. Next, perform four maneuvers: (1) Palpate the chest wall for tenderness by applying firm, steady pressure to the sternum, costosternal junctions, intercostal spaces, ribs, and pectoralis major muscles and their insertions; (2) adduct the arms horizontally by lifting one arm after the other by the elbow and pulling it across the chest toward the contralateral side, with the head rotated toward the ipsilateral side; (3) extend the neck as the arms are pulled backward and slightly upward; and (4) exert vertical pressure on the head. If any of these tests reproduces the patient’s pain, the problem is in the chest wall.
Costochondritis and Tietze syndrome
This is a common cause of chest pain. The onset may be sudden or gradual. The pain is usually dull and may be intensified by respiratory motion and shoulder movements. The sole physical sign is tenderness at the costochondral junction. There is no swelling and there are no X-ray findings. In Tietze syndrome, the pain is accompanied by tender, fusiform swelling of one or more costal cartilages, often that of the second rib. The overlying skin is reddened. Pain may radiate to the shoulder, neck, or arm. There is no lymphadenopathy. The pain may subside in a few weeks or persist for months, whereas the swelling may persist after the pain and tenderness subside. The cause is unknown and the condition must be distinguished from osteitis, periostitis, rheumatic chondritis, and neoplasm of the ribs.
Movement of rib fragments causes well-localized, sharp, lancinating pain. The patient complains of chest pain with breathing. Usually there is a history of thoracic trauma. Without this history symptoms can suggest pleurisy. Ask about recent severe coughing. Inspiration is limited and palpation discloses point tenderness on a rib. The fracture and/or crepitation may be felt. With one hand supporting the back, compression of the sternum with the other elicits pain at the untouched fracture site (Fig. 8-30A).
Examining for Rib Pain
A. Compression test for rib fracture. When the site of suspected rib fracture is located by point tenderness, the sternum is pushed toward the spine with one hand whereas the other hand supports the patient’s back. The maneuver will elicit pain at the untouched fracture site. B. Slipping tenth rib. When the tenth rib lacks an anterior attachment, it can slip forward upon the ninth rib during respiratory movements and cause pain.
Any rib from the second to the eleventh, most commonly the sixth, may break. The fracture is caused by a shearing force on the rib anterior to the serratus anterior attachment that pulls the rib upward, and posterior to the abdominal external oblique attachment that pulls the rib downward. Fracture results from structural fatigue (stress fracture) from repeated coughing. A patient who has been coughing for some time begins to experience pain with respiratory movements and coughing. The typical signs of fracture of a rib are present. If rib palpation is not performed, the condition may be misdiagnosed as pleurisy [Hanak V, Hartman TE, Ryu JH. Cough-induced rib fractures. Mayo Clin Proc. 2005;80:879–882].
The pain is reproduced by palpation of the xiphoid cartilage.
The ligament between two ribs, commonly between the ninth and tenth costal cartilages, is weak or ruptured. The tenth rib overrides the nineth with breathing or movement which may produce an audible or palpable click (Fig. 8-30B). The slipping rib may cause pain falsely attributed to intraabdominal disease.
Palpable pleural friction rub
The inflamed pleural surfaces lose their lubricating fluid (“dry pleurisy”) and rub together during breathing producing vibrations similar to two pieces of dry leather rubbing together. The rub is also heard with the stethoscope or the unaided ear as a creaking sound.
Inspiratory retraction of interspaces
Airway obstruction or decreased lung compliance leads to excessively negative inspiratory intrapleural pressure and collapse of the intercostal spaces. The inward movement is usually most evident in the lower chest. Sudden, violent retractions occur in tracheal obstruction and severe paroxysms of asthma.
Diminished local excursion of the thorax
This points to a lesion in the underlying chest wall, pleura, or lung; causes include pain, fibrosis, or consolidation. The restricted movement may be best observed from the foot of the bed.
Localized bulging of the thorax during expiration—flail chest
Fracture of several contiguous ribs or the separation of several contiguous costal cartilages results in loss of chest wall integrity. The negative intrathoracic pressure during inspiration pulls the injured segment inward, whereas the rise in intrathoracic pressure during expiration causes it to bulge outward. The paradoxical chest movements decrease minute ventilation and may produce respiratory failure.
Inspiratory convergence of costal margins
When the dome of the diaphragm is flattened, the direction of its pull on the costal margins is changed from upward to inward. The degree of outward flare of the lower costal margins is decreased or pulled inward. A flattened diaphragm can be caused by pulmonary emphysema or fluid or air in the pleural space.
Fluctuant intercostal masses and sinuses
This is usually an abscess. A cold abscess lacking surrounding inflammation is usually tuberculosis in a nearby rib. Actinomycosis frequently produces abscesses in the lung that burrow through the chest wall. An abscess may result when an untreated pleural empyema points through the interspaces.
Subcutaneous and mediastinal emphysema
Air can invade the chest wall from the neck, from esophageal rupture, or directly from the lung. Rupture of alveoli permits air to travel beneath the visceral pleura to the hilum of the lung, then along the trachea to the neck. The thoracic wall is involved secondarily by migration from the neck. When a fractured rib or penetrating foreign-body punctures the pleura, air travels across the pleura to the thoracic wall causing emphysema in the deep muscle layers and later the subcutaneous tissues. Crepitus is a sensation imparted to the pressing finger by small globules of air moving in the tissues. Soft-tissue crepitus may be the first clue to rupture of the alveoli, pleura, or esophagus. The air may invade the mediastinum producing a distinctive systolic precordial crunch known as Hamman sign. Soft tissue compression in the neck can produce massive neck and face swelling accompanied by cyanosis.
Pulsating sternoclavicular joint
There is an enlarged major vascular structure impinging posteriorly on the manubrium. It is seen with dissection of the aortic arch, ruptured saccular aortic aneurysm, persistent right aortic arch or fusiform aneurysms of the innominate, carotid, or subclavian artery.
Lateral deviations of the trachea
Lateral tracheal deviation at the level of the suprasternal notch can be caused by a mass higher in the neck, such as cervical goiter or enlarged lymph nodes (Fig. 7-55), or by mediastinal shifts within the chest. Below the suprasternal notch, an eccentric retrosternal goiter may push the trachea to one side. The trachea and mediastinum deviate to the opposite side with pleural effusion and tension pneumothorax. Displacement of the trachea to the ipsilateral side occurs in pulmonary atelectasis or fibrosis of the lung or pleura reducing lung volume.
Palpate the cricoid cartilage or tracheal rings with the thumb and index finger and ask the patient to swallow. Normally, the larynx and trachea rise cephalad. Grasp the trachea gently and move it side to side; usually, it is easily mobile. Fixation of the trachea occurs normally when the neck is dorsiflexed, and abnormally in pulmonary emphysema, adhesive mediastinitis, aortic aneurysm, and mediastinal neoplasm.
Lung, Pleura, and Respiratory Signs
Hiccup is a sudden involuntary diaphragmatic contraction producing an inspiration interrupted by glottal closure causing a characteristic sharp sound. It is thought to be mediated centrally through the phrenic nerve, by direct stimulation of the phrenic nerve, or by direct irritation of the diaphragm. The contractions occur two or three times each minute. A variety of clinical conditions are associated with hiccup. CLINICAL OCCURRENCE: Hiccough Without Organic Disease: excessive laughter, tickling, aerophagia, tobacco smoking,intake of alcohol, hysteria (persisting for weeks, but ceasing during sleep); Diseases of the Central Nervous System: encephalitis, meningitis, vertebrobasilar ischemia, intracranial hemorrhage, intracranial tumor, uremia, degenerative changes in brain and medulla, tabes dorsalis; Mediastinal Disorders: trauma to phrenic nerve, enlargement of mediastinal lymph nodes (tuberculosis, malignant neoplasm, fibrosis), bronchial obstruction, adherent pericardium, cardiac enlargement, myocardial infarction (MI), esophageal obstruction; Pleural Irritation: pneumonia with pleurisy; Diaphragm and Abdominal Disorders: diaphragmatic hernia of stomach, subphrenic abscess, subphrenic peritonitis, hepatic neoplasm, gumma or abscess, stomach carcinoma, splenic infarction, acute intestinal obstruction, acute hemorrhagic pancreatitis, after upper abdomen operations, diaphragm stimulation by cardiac pacemaker.
Cough productive of blood is hemoptysis. The bleeding lesion may be anywhere from the nose to the alveoli. Expectorated blood usually comes from the upper respiratory tract while blood in the bronchial tree induces coughing. Patients may not distinguish which is occurring, so upper and lower respiratory tract disorders must be considered. CLINICAL OCCURRENCE: Upper Respiratory Tract: epistaxis, bleeding from the oropharynx, gum bleeding, laryngitis, laryngeal carcinoma, hereditary hemorrhagic telangiectasia; Tracheobronchial Tree: acute and chronic bronchitis, trauma from coughing, bronchiectasis, bronchial carcinoma, broncholiths, foreign-body aspiration, erosion by aortic aneurysms; Lungs: infections (pneumonia, especially caused by Klebsiella, lung abscess, tuberculosis, fungal infections, amebiasis, hydatid cyst), PE with infarction, trauma, pulmonary hemorrhage (vasculitis especially Wegener, Goodpasture syndrome), idiopathic pulmonary hemosiderosis, lipoid pneumonia; Cardiovascular: mitral stenosis, CHF, arteriovenous fistula, anomalous pulmonary artery, hypertension; Hematologic: thrombocytopenia, leukemia, hemophilia.
Snoring is produced by vibrations of the lax soft palate during sleep, often in association with obstructive sleep apnea. A similar sound results from uncleared secretions in the upper respiratory tract. When this occurs during severe illness, it is frequently a grave prognostic sign, the “death rattle.”
A high-pitched whistling or crowing sound is caused by inspiration through a narrow glottis. It occurs with vocal cord edema, neoplasm, diphtheritic membrane, pharyngeal abscess, and foreign body in the larynx or trachea. It may signal impending airway closure and asphyxiation.
Diminished or absent vocal fremitus
The interposition of vibration dampers such as thickened pleura, pleural effusion, pneumothorax, or loss of lung parenchyma (e.g., emphysema) reduces transmission of vibrations to the chest wall diminished or absent vocal fremitus.
Tension in the lung septae increases transmission of vibrations. Consolidated tissue in pneumonia or inflammation around a lung abscess, when in contact with a bronchus or cavity in the lung, transmits bronchotracheal vibrations more efficiently than air-filled alveoli increasing vocal fremitus.
Normal dullness in the lateral decubitus position
When the patient cannot sit, percuss the back with the patient on one side then the other. The position is not optimal because it is difficult to interpret the percussion sounds. The damping effect of the mattress causes a band of dullness in the thorax nearest the bed (Fig. 8-31). Directly above this band is an irregular area of dullness caused by compression of the downward lung by the body weight. If there is a lengthwise sag of the mattress from the body weight, it flexes the spine laterally compressing the thoracic wall and lung in the upward hemithorax, producing another area of dullness.
Areas of Percussion Dullness Created by the Lateral Decubitus Position
The lowest blue-shaded area is dull from compression of the thorax against the mattress. Immediately above, dullness is produced by compression of the lung from the body weight. In the opposite lung, dullness results by lateral deviation of the spine as it follows the sag in the mattress and compresses the lung.
Abnormal sonorous percussion
An abnormal distribution of sounds of normal quality can be pathologic. The lung is normally resonant. As consolidation occurs its density increases producing, successively, impaired resonance, dullness, and flatness. The normal pleura contributes little to the percussion note, but a thickened pleura produces dullness. Fluid in the pleural cavity gives dullness to flatness in a dependent distribution. Dullness Replacing Resonance in the Upper Lung: This suggests neoplasm, atelectasis, or consolidation. Dullness Replacing Resonance in the Lower Lung: Pleural effusion, pleural thickening, and elevation of the diaphragm are specific to this area; neoplasm, atelectasis, and consolidation are other causes. Flatness Replacing Resonance or Dullness: Almost invariably, flatness results from massive pleural effusion. Hyperresonance Replacing Resonance or Dullness: When hyperresonance replaces resonance or the area of hepatic and cardiac dullness is resonant or hyper-resonant, emphysema, pneumothorax, or the interposition of gas-filled gut are suggested. Tympany Replacing Resonance: This occurs almost exclusively with a large pneumothorax.
Auscultation of Breath Sounds
Several types of breath sounds with distinctive qualities are recognized. All are characterized by rising pitch during inspiration and falling pitch during expiration (Doppler effect). The duration and force of inspiration and expiration affect the breath sounds.
Normal breath sounds—vesicular breathing
Tidal breathing during quiet respirations produces breath sounds with a longer inspiratory than expiratory phase (Fig. 8-32). They are heard normally over the entire lung surface, except beneath the manubrium and in the upper interscapular region, where we hear bronchovesicular sounds. The breath sounds are faintest over the thinner portions of the lungs.
Distinguishing Features of Breath Sounds
In the diagrams, the vertical component indicates rising and falling pitch, the thickness of the lines indicates loudness, and the horizontal distance represents duration. Inspiration is longer in vesicular breathing, expiration in bronchial breathing. Bronchovesicular breathing is a mixture of the two. Normally vesicular breathing is heard over most of the lungs, except that bronchovesicular breathing occurs over the thoracic portion of the trachea, anteriorly and posteriorly. Bronchial breathing does not occur in the normal lung. In cogwheel breathing, the inspiratory sound is interrupted with multiple breaks. Asthmatic breathing is characterized by a much prolonged and higher-pitched expiratory sound than is found in bronchial breathing. Asthmatic breathing is usually, but not always, accompanied by wheezes.
This is identical with vesicular breathing except that the inspiratory phase is broken by short pauses, giving the impression of jerkiness (Fig. 8-32). The pauses are attributed to irregular inflation of the alveoli; it has no pathologic significance.
Bronchovesicular breathing is pathologic and indicates partial pulmonary consolidation or compression transmitting airway sounds with increased efficiency. This is intermediate between vesicular and bronchial breathing. The two respiratory phases are about equal in duration (Fig. 8-32), although expiration may be a bit longer. It is normal over the manubrium and in the upper interscapular region. As the compression or consolidation increases breath sounds become bronchial.
Bronchial breathing (tubular breathing)
This results from consolidation or compression of lung facilitating sound transmission from the bronchi. In contrast to vesicular breathing, bronchial breath sounds have a shorter inspiratory than expiratory phase (Fig. 8-32) and they are usually louder. Bronchial breathing does not occur in the normal lung.
Tracheal breathing is heard in the suprasternal notch and over the sixth and seventh cervical spines; it is harsher and hollower than bronchial breathing.
Wheezes arise from turbulent airflow and the vibration of small airways in which there is partial obstruction to airflow. Wheezes are heard predominantly during expiration. They occur when airways are narrowed by bronchospasm, edema, collapse, or by intraluminal secretions, neoplasm, or foreign body. They are diffuse in asthma and bronchitis, usually accompanying a prolonged expiratory phase. An isolated wheeze may signal bronchial obstruction by a tumor or foreign body. Wheezing is neither sensitive nor specific for detecting airflow obstruction.
Asthmatic or obstructive breathing
As in bronchial breathing, inspiration is short and expiration prolonged, but there is no confusing the two (Fig. 8-33). In asthma, the expiratory phase is several times longer than in bronchial breathing, and the pitch is much higher. Expiration is active, not passive, and may require significant effort. Frequently, but not always, asthmatic breathing is accompanied by wheezes audible without the stethoscope. Emphysema produces a similar pattern of breath sounds, but wheezing is absent and the sound intensity is diminished.
Thoracic Disorders with Dullness and Diminished Vibration
○, absent; ∨, diminished; ∧, increased; ←, direction of deviation.
Crackles result from the opening and closing of alveoli and small airways during respiration. In pulmonary edema fine crackles may be produced by air bubbling through fluid in the distal small airways. Inspiratory crackles resemble the sound of several hairs being rubbed together. They are heard in the bases with interstitial lung disease, fibrosing alveolitis, atelectasis, pneumonia, bronchiectasis, and pulmonary edema, and often in the apices with tuberculosis.
Rhonchi are low-pitched gurgling sounds produced by liquid within the larger airways. They clear or change significantly after an effective cough.
This is produced by a large empty superficial cavity communicating with a bronchus or an open pneumothorax. Amphoric breath sounds resemble blowing air over the mouth of a large bottle.
Auscultation of Voice Sounds
In normal lungs whispered words are faint and the syllables indistinct, except over the main bronchi. Louder and more distinct words indicate consolidation, atelectasis, or fibrosis, all of which improve sound transmission. Because of their pitch and loudness, whispered and spoken voice sounds are more useful than breath sounds in detecting pulmonary consolidation, infarction, and atelectasis. Spoken voice sounds are not as useful as whispered sounds since they are too loud for subtle discrimination.
Consolidated lung transmits whispered syllables distinctly, even when the pathologic process is too small to produce bronchial breathing. This is particularly valuable in detecting early pneumonia, infarction, and atelectasis.
Spoken syllables are normally heard indistinctly. With lung consolidation syllables are distinct and sound close to the ear.
This is a form of bronchophony in which the spoken “Eee” is changed to “Ay,” with a peculiar nasal or bleating quality. This arises from compressed lung below a pleural effusion, and occasionally with lung consolidation.
Auscultation of Abnormal Sounds
Rubs (pleural friction rub)
The continuous murmur of a pulmonary arteriovenous fistula increases in intensity with inspiration. In patients with coarctation of the aorta, continuous murmurs may be heard below the left scapula and over the intercostal and internal mammary arteries from the collateral circulation.
Systolic crunching sounds
Interpretation of Pulmonary and Pleural Signs
The findings of thoracic inspection, palpation, percussion, and auscultation must be synthesized to suggest a pathophysiologic process or diagnosis. The signs of altered lung density are the starting point for differential diagnosis. It is useful to draw a chest diagram like those in Figures 8-33 and 8-34 to depict your findings and hypotheses.
Dullness and diminished vibrations—pleural effusion or pleural thickening
Unless the fluid is loculated, dullness occurs in the lowermost chest (Fig. 8-33, left). Because the costophrenic sulcus is higher in front, the dull region is a transverse band broadest posteriorly and laterally. The superior border of the dullness may be difficult to percuss accurately because the fluid layer is an upward-pointing wedge. Shifting dullness is not usually demonstrable. Since air is absent, there is no succession splash. With a small amount of fluid respiratory excursions are normal. In pleurisy an antecedent friction rub disappears when an effusion forms. Pleural fluid damps vibrations from the bronchotracheal air column, so vocal fremitus, breath sounds, and whispered and spoken voice are transmitted poorly. The mediastinum is not shifted with small pleural effusions. Because pleural fibrosis results from the organization of pleural effusion, the distribution of dullness is the same. The thicker it is, the more it obstructs sound transmission and the more the percussion note indicates denseness. Extensive fibrosis may pull the trachea to the affected side. Any longstanding pleural effusion may organize. Neoplasm, asbestosis, and mesothelioma can cause thickened pleura.
Dullness and diminished vibrations—pleural fluid
Fluid accumulates in the pleural space because of transudation of fluid from the pleural and pulmonary vessels (increased venous hydrostatic pressure, decreased oncotic pressure, capillary leak), increased production of pleural fluid (inflamed pleura or pleural neoplasm), decreased pleural absorption of fluid (lymphatic obstruction, systemic venous hypertension), or by bleeding into the pleural space. The pleural fluid produces a dull or flat note to percussion. The lung immediately over the fluid may be hyperresonant (skodaic resonance) from distention of the alveoli above a compressed region. The distribution of dullness is dependent. With large amounts of fluid the trachea may be pushed to the unaffected side (Fig. 8-34). Vocal fremitus is absent. Occasionally, loud bronchial breathing is heard through the fluid from the compressed lung, the unwary mistake it for consolidation. Fluid is distinguished from consolidation by noting diminished breath sounds and absence of fremitus with fluid, and bronchial breath sounds with “E” to “A” changes in consolidation. Massive pleural effusion obscures the lung fields on radiographs, so that no appraisal of the parenchyma is possible. With a hydropneumothorax, when the patient stands, the fluid level falls below much of the lung, permitting visualization of the lung (Fig. 8-35) [Case with differential diagnosis: Quing DA, Mark EJ. Case 8-2002–A 56 year-old woman with a persistent left-sided pleural effusion. N Engl J Med. 2002;346:843–850]. CLINICAL OCCURRENCE: Increased Transudation: CHF, hypoalbuminemia (cirrhosis, nephrotic syndrome), PE, SVC syndrome; Increased Production: mesothelioma, metastatic cancer, infections (bacteria, mycobacteria, viral, parasites, fungi), pulmonary infarction, pancreatitis, mediastinitis, collagen-vascular diseases (e.g., RA, systemic lupus erythematosus [SLE], drug-induced lupus, vasculitis), after heart or lung surgery, uremia, Meigs syndrome, pleuropericarditis peritoneal dialysis; Decreased Absorption: lymphatic obstruction (lymphoma, lymphatic carcinomatosis, irradiation, surgical injury), CHF, SVC syndrome; Bleeding: ruptured aortic aneurysm or dissection, trauma, postoperative.
Thoracic Disorders with Dullness and Accentuated Vibration
○, absent; N, normal; +, present; ∧ increased; →, direction of deviation.
Models Illustrating Pleural Effusion and Pneumothorax
A. Suspend a plastic bag filled with water, noting its contour. B. When air is introduced, a fluid level forms, the contour changes, and a succussion splash occurs with shaking. C. An uncomplicated pleural effusion: note the tapering upper wedge, or meniscus, of fluid. D. Hydropneumothorax: when air is introduced, a fluid level forms and the meniscus largely disappears.
Dullness and diminished vibration—pulmonary consolidation with bronchial plugging
Consolidated lung produces dullness. Bronchial plugging blocks vibrations from the air column, so there is absence of vocal fremitus, breath sounds, whispered and spoken voice (Fig. 8-33, middle right). The trachea is not displaced. Plugging of a bronchus is usually a transitory occurrence in lobar pneumonia, recognized by the sudden loss of air transmission. Imaging can distinguish between pleural effusion and pulmonary consolidation. If the dullness is in the upper chest, effusion is excluded by physical examination.
Dullness with diminished vibration—atelectasis with bronchial plug
The volume of atelectatic lung is diminished; with considerable lung involvement the dense mass is pulled toward the chest wall by the negative intrapleural pressure shifting the trachea to the affected side. The collapsed lung is dull because its density is increased. The bronchial plug prevents transmission of air vibration, so vocal fremitus and breath and voice sounds are absent (Fig. 8-33, right). The tracheal deviation distinguishes atelectasis from consolidation with bronchial plug and from pleural effusion. Often, atelectasis is accompanied by fever that distinguishes it from thickened pleura with fibrotic traction on the mediastinum. Similar dullness and decreased breath sounds at the left scapular tip can be caused by a large pericardial effusion compressing the LLL (Ewart sign).
Dullness with accentuated vibration—pneumonia with small consolidation
A small, deeply placed region of consolidation may produce impaired resonance or dullness, depending on its size and depth from the chest wall. The dense lung transmits airway sounds with increased efficiency, so vocal fremitus is increased and bronchovesicular or bronchial breathing and crackles may be heard (Fig. 8-34, left). Fever, chills, and productive cough are accompanied by tachypnea and tachycardia. Whispered pectoriloquy and bronchophony are produced by the consolidation. Small regions of consolidation must be distinguished from a small cavity lying near a bronchus. Imaging is required for definitive diagnosis. Pneumonia, granulomatous infiltrates of the lung, neoplasm about a bronchus, rheumatoid arthritis (RA), and sarcoidosis may all produce these findings.
Dullness with accentuated vibration—pneumonia with lobar consolidation
The dense lung causes dullness or flatness on percussion. Consolidated lung in contact with a bronchus transmits vibrations with increased efficiency so vocal fremitus is pronounced, there is bronchial breathing, and whispered and spoken voice produce pectoriloquy and bronchophony (Fig. 8-34, middle right). Crackles (rales) are frequently present. The lung volume is unchanged, so the trachea remains in the midline. These finding are seen classically in lobar pneumonia but occasionally in lung neoplasms and pulmonary infarction. Consolidation may be confused with a thick-walled cavity and the distinction is made by imaging. Massive pleural effusion gives dullness and may transmit loud bronchial breath sounds above the effusion, but the trachea is usually displaced to the unaffected side.
Dullness with accentuated vibration—thick-walled cavity
Signs of consolidation are present: dullness, increased vocal fremitus, bronchovesicular breathing, and pectoriloquy (Fig. 8-34, middle left). Amphoric breathing or cracked-pot resonance is rarely heard, but even these signs may occur in consolidation without cavity.
Resonance and hyperresonance—pulmonary emphysema
Loss of interstitial elasticity and interalveolar septa leads to air trapping, so the lung volume is increased. The air trapping holds the chest in the inspiratory position producing a barrel chest. The diaphragm is flattened, so the costal margins move out sluggishly or actually converge during inspiration (Fig. 8-36, left). The lungs are hyperresonant throughout because of their low density. Air pockets are poor transmitters of vibrations; thus vocal fremitus, breath sounds, heart sounds, and whispered and spoken voice are impaired or absent. When the breath sounds are audible, they are faint and harsh, distinctively lacking the rustling quality of vesicular breathing; this may antedate recognizable X-ray evidence of emphysema. The expiratory phase of respiration usually exceeds the inspiratory phase. Rales are not necessarily present and wheezes are not heard. The elevated clavicles and flattened diaphragm give rise to two signs: the thyroid cartilage appears to be low in a shortened neck and it descends less than 4 cm toward the suprasternal notch with full inspiration. The thyroid is often in a retrosternal position and not palpable.
Thoracic Disorders with Resonance Impaired Vibration
○, absent; ∨, diminished; +, present; →, direction of deviation.
Resonance or hyperresonance—closed pneumothorax
When the air leak between lung and pleura becomes sealed, a closed pneumothorax is formed. If the volume of enclosed air is small, the lung remains partially inflated, and the mediastinum is not displaced (Fig. 8-36, middle left). A similar situation may be created with an open pneumothorax by pleural adhesions that prevent collapse of the lung and displacement of the trachea. Vocal fremitus, breath sounds, and whispered and spoken voice are usually inaudible or impaired. The chest is resonant or hyperresonant. Frequently, pneumothorax cannot be distinguished from a normal or emphysematous chest by percussion. A disparity between the breath sounds on the two sides suggests pneumothorax on the quieter side. There may be a pendular deviation of the trachea toward the affected side during inspiration. The pleural tear may be spontaneous or the result of trauma [Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl J Med. 2000;342:868–874].
Resonance or hyperresonance—open pneumothorax
In open pneumothorax there is continual communication between lung and pleural cavity and the pneumothorax is at atmospheric pressure. The affected lung is completely collapsed and the mediastinum may be drawn toward the unaffected side by the contraction of the normal lung. Overlying the pneumothorax, the chest wall is hyperresonant or tympanitic. Fremitus and breath and voice sounds are absent. Usually, the patient is severely dyspneic and may be cyanotic.
Resonance or hyperresonance—tension pneumothorax
A one-way tissue valve permits air to enter the pleural space during inspiration and prevents its expulsion during expiration. Thus, the pressure in the cavity builds up above atmospheric pressure. The affected lung is collapsed and the increasing intrapleural pressure causes extreme tracheal deviation, compression of the unaffected lung, and decreased venous return to the heart (Fig. 8-36, middle left). Decreased respiratory excursion, a distended tympanic hemithorax, and tracheal deviation away from the immobile side are diagnostic of tension pneumothorax. There is deep cyanosis, severe dyspnea, and shock; release of air from the pleural cavity is lifesaving.
Resonance and hyperresonance—hydropneumothorax
Hyperresonance or tympany in the upper thorax with dullness inferiorly suggests hydropneumothorax or a massive pleural effusion (Fig. 8-36, right). In either case, the trachea may be displaced to the unaffected side. In hydropneumothorax, the hyperresonant region does not transmit fremitus, breath sounds, or voice sounds. The lung over a simple hydrothorax transmits well. When hydropneumothorax is present, the fluid level can be sharply demarcated by percussion; the level is vague in simple effusion. Shifting dullness is readily demonstrated by percussion with hydropneumothorax. The air-filled cavity carries bell tympany, and a succession splash may be demonstrated.
Special sounds in hydropneumothorax
Fluid movement is silent in a cavity devoid of air. When the cavity contains both air and fluid, body movements cause a succussion splash, audible to the patient and the examiner. Grasp the patient’s shoulders shaking the thorax while listening with and without a stethoscope. An abdominal succussion splash is present in the normal and dilated stomach. A thoracic succussion splash suggests a hydropneumothorax, but a fluid-filled stomach herniating into the thorax through a diaphragmatic hernia may also produce the splash. Occasionally, one hears a falling-drop sound, resembling a drop of water hitting the surface of fluid. A metallic tinkle may be heard when air bubbles emerge through a small bronchopleural fistula below the fluid level; when the fistula is larger, the air may gurgle, a lung-fistula sound.
Blood in the sputum usually brings patients to the physician. First identify the anatomic site of hemorrhage. Blood-Streaked Sputum is usually caused by inflammation in the nose, nasopharynx, gums, larynx, or bronchi. Sometimes it occurs only after severe paroxysms of coughing and is attributed minor airway trauma. Pink Sputum results from blood mixing with secretions in the alveoli or smaller bronchioles; it is most characteristic of pneumonia and pulmonary edema. Massive Bleeding occurs with erosion of a bronchial artery by cavitary tuberculosis, aspergilloma, lung abscess, bronchiectasis, embolism with infarction, bronchogenic carcinoma, or a broncholith. Alveolar Hemorrhage does not produce bloody sputum in all cases; it results from pulmonary vasculitis of any cause and blunt chest trauma.
Bloody gelatinous (Currant-Jelly) sputum
Copious tenacious, bloody sputum are prominent in pneumonia caused by Klebsiella pneumoniae or Streptococcus pneumoniae.
Purulent sputum containing degraded blood pigment is typical of pneumococcal pneumonia but it is frequently preceded by small amounts of frank blood.
Frothy sputum—pulmonary edema
Alveoli are flooded with fluid from the capillaries producing thin secretions containing air bubbles, frequently colored with hemoglobin. This is typical of pulmonary edema of any cause.
Inflammatory cells, predominately polymorphonuclear leukocytes, enter the airways and alveoli in response to lower airway infection. The exudate may be yellow, green, or dirty gray. Small amounts are typical of acute bronchitis, resolving pneumonia, small tuberculous cavities, or lung abscess. Copious purulent sputum occurs with lung abscess, bronchiectasis, or bronchopleural fistula communicating with an empyema. Fetid sputum is characteristic of anaerobic infection and/or lung abscess. Many lung abscesses are not associated with much sputum since their connection to the airways does not allow complete drainage.
Increased mucous production and mucous plugs occur in asthma; during resolution retained mucous and mucous plugs are mobilized.
Calcified particles in the sputum are usually broncholiths coming from calcified lymph nodes eroding the bronchi or from calcareous granulomas in silicosis, tuberculosis, or histoplasmosis. They may explain the source of pulmonary hemorrhage [Harris NL, McNeely WF, et al. Case 14--2002. Case records of the Massachusetts General Hospital. N Engl J Med. 2002;346:1475–1482].
Interpretation of physical signs from inspection, palpation, and percussion of the precordium depend on relatively normal anatomic relations of the heart and chest wall. With thoracic deformity, for example, kyphoscoliosis and pectus excavatum, caution is advised.
Dyspnea (shortness of breath)
Extracellular fluid (saline) is partitioned between blood and interstitial tissues by a net equilibrium between hydrostatic and oncotic pressures. Normally, fluid flows into the extravascular interstitial space in response to hydrostatic pressure in the precapillary arterioles and capillaries (intravascular > interstitial), which is only partially offset by the opposing oncotic pressure (intravascular > interstitial). In the postcapillary venules, the lowered intravascular hydrostatic pressure is more than compensated by the intravascular oncotic pressure, resulting in return of interstitial saline to the intravascular space. Interstitial fluid, proteins, and cells are also removed from the interstitial space and, ultimately, returned to the blood through the lymphatics. Alteration of any of these forces upsets the equilibrium. Increasing venous pressure in CHF produces dependent edema; occlusion of a vein may result in localized edema. Obstruction of lymphatic channels produces lymphedema. Reduction in the plasma albumin (the plasma protein contributing most to oncotic pressure) lowers the plasma oncotic pressure, permitting edema to form; this type of edema may first appear in areas of decreased tissue pressure such as the periorbital tissues. Increased capillary permeability may cause edema that is not dependent. Tissue inflammation by bacterial, chemical, thermal, or mechanical means increases capillary permeability to make localized edema. Excessive accumulation of interstitial fluid, either localized or generalized, is termed edema. When generalized edema is extensive, it is known as anasarca. In the adult, approximately 4.5 kg (10 lb) of fluid must accumulate in adults before pitting edema is produced. To detect edema, gently press a thumb into the skin against a bony surface, such as the anterior tibia, dorsum of the foot, or sacrum. When the thumb is withdrawn, an indentation persists.
The distribution of edema must be noted. Dependent edema responds to gravity so it first appears in the feet and ankles or over the posterior calves or sacrum in a supine patient. As the amount of dependent fluid increases, a fluid level may be detected; seldom does dependent edema rise higher than the heart. Anasarca can be recognized at a glance by the obliteration of subcutaneous superficial landmarks. Chronic edema leads to fibrosis of the subcutaneous tissues and skin, so they no longer pit on pressure; this is sometimes called brawny edema. Symmetric edema affecting both legs suggests a problem in the pelvis or more proximally, whereas edema limited to the arms and head suggests SVC obstruction.
Edema limited to one extremity suggests a local problem with vascular channels or local inflammation. Edema formation is the same whether it is generalized or local. To evaluate local edema, the examiner must consider the local anatomy of the arteries, veins, lymphatics and soft tissues, the presence of any inflammatory or structural disease, and then form hypotheses as to the likely mechanism and anatomic site of the problem.
Exclusive dependence upon clinical information may overlook cardiovascular causes of bilateral leg edema, so consider measurement of BNP and/or echocardiography with estimation of right heart pressures, RV and LV size and function, and tricuspid valve function [Blankfield RP, Finkelhor RS, Alexander JJ, et al. Etiology and diagnosis of bilateral leg edema in primary care. Am J Med. 1998;105:192–197]. The following approach, based upon the anatomic distribution of edema, is diagnostically useful. CLINICAL OCCURRENCE: Localized Edema: Inflammation infection, angioedema, contact allergy; Metabolic Causes gout; Insufficiency of Venous Valves (with or without varicosities); Venous Thrombosis postoperative, prolonged air or automobile travel; Venous or Lymphatic Compression malignancies, constricting garments; Chemical or Physical Injuries burns, irritants and corrosives, frostbite, chilblain, envenomation (insects, snakes, spiders); Congenital amniotic bands, arteriovenous fistulas, Milroy disease; Bilateral Edema Above the Diaphragm: SVC obstruction; Bilateral Edema Below the Diaphragm: CHF with elevated jugular venous pressure, including elevated pulmonary artery pressure caused by left heart abnormalities, intrinsic pulmonary disorders, right heart abnormalities, and constrictive pericarditis; Portal Vein Hypertension or Obstruction cirrhosis, portal vein thrombosis, schistosomiasis; IVC Obstruction thrombosis, extrinsic compression, pregnancy; Loss of Venous Tone drugs (calcium channel blockers, angiotensin-converting enzyme inhibitors, other vasodilators), convalescence, lack of exercise; Generalized Edema: Hypoalbuminemia nephrotic syndrome, cirrhosis, chronic liver disease, protein losing conditions (e.g., enteropathy, burns, fistulas); Renal Retention of Salt and Water corticosteroids, NSAIDs; Increased Capillary Permeability sepsis, systemic inflammatory response syndrome, interleukin-2, idiopathic capillary leak syndrome.
Recurrent and chronic edema occurs in women in the third to fifth decades without heart, liver, or kidney disease or venous or lymphatic obstruction. Affective disorders and obesity may coexist. Possible mechanisms include mild persistent precapillary arteriolor dilatation, exaggerated capillary leakage on assuming the upright posture, and inappropriate chronic diuretic administration often started for minor degrees of peripheral edema (diuretic-induced edema). Each mechanism probably leads to inappropriate activation of renin–aldosterone leading to salt and water retention.
Pitting ankle edema often occurs in normal adults within 48 h of arriving in the tropics from a temperate climate, or in temperate zones when weather changes from cool and dry to warm and humid. It spontaneously resolves with acclimatization.
Painless subcutaneous soft-tissue edema begins abruptly and spreads to involve several centimeters of tissue with diffuse borders. Erythema is not prominent. Angioedema often involves the face, lips, or tongue and is life threatening when the larynx is involved. Causes include hereditary absence of C1 esterase, exposure to allergen, and angiotensin-converting enzyme inhibitors.
Careful examination of the apical impulse yields useful information about the heart size, force of LV contraction, obstruction to LV ejection, and stroke volume.
Increased force of LV contraction increases the apical impulse amplitude. This can be caused by LV hypertrophy (arterial hypertension, aortic stenosis, aortic regurgitation, mitral regurgitation (MR)) and increased contractility (exertion, emotion, hyperthyroidism).
Enlarged, sustained apical impulse
Left ventricular ejection against increased afterload prolongs the ejection time. Aortic valve stenosis and systemic hypertension produce an enlarged sustained impulse rather than the normal brief tap.
LV volume overload will produce LV dilation with normal ejection; the PMI is enlarged, brisk, and displaced laterally, but is not sustained. This occurs with aortic or mitral regurgitation and intracardiac shunts. Reduced contractility weakens the PMI, whereas LV dilatation may make it more diffuse. Other causes of left displacement are right pneumothorax, left pleural adhesions, or left lung volume loss.
This is seen with left pneumothorax, right pleural adhesions, volume loss of the right lung, and dextrocardia.
Severe emphysema flattens the diaphragm pulling the heart and mediastinum downward. The PMI may be felt just inferior to the xiphoid.
Right ventricular impulse
Right ventricle contraction of normal hearts does not produce a palpable impulse. A dilated, hypertrophied or forward displaced RV may produce a palpable impulse. A palpable precordial impulse near the left edge of the sternum in the third, fourth or fifth interspace and medial to the apex impulse almost always is the result of right ventricular pressure or volume overload. It is nearly always abnormal; an exception is with severe mitral insufficiency where expanding the left atrium produces a sternal or parasternal impulse. The latter peaks with S2, whereas true right ventricular impulses peak during systole. Slight impulses only move the interspaces; with more advanced disease the lower sternum lifts with each beat. CLINICAL OCCURRENCE: Right Ventricular Hypertrophy (Pressure Overload): pulmonic stenosis, pulmonary hypertension, mitral stenosis; Right Ventricular Dilation (Volume Overload): tricuspid or pulmonary valve insufficiency, left-to-right intracardiac shunts; Forward Displacement of the Heart: tumors behind the heart, enlarged left atrium; Protuberance of the Right Ventricle: aneurysm of the right ventricular wall; Hyperdynamic Circulation: exertion, emotion, hyperthyroidism.
Epigastric Pulsation: This is normal, especially in thin people after exertion. It can appear if the heart is displaced inferiorly in emphysema. Most frequently, it reflects the normal aortic pulsation. Abdominal aortic aneurysm (AAA) should be considered. Pulsations at the Base: In pulmonary hypertension and/or with increased pulmonary blood flow from a large left to right shunt, an impulse may be felt just to the left of the sternum in the second or third interspace over the pulmonary conus. Pulsations in the right second interspace may occur from an ascending aortic aneurysm.
Turbulent blood flow produces audible murmurs and palpable thrills when transmitted to peripheral structures. The vibrations feel similar to the sensation of holding a purring cat. Since auscultation is more sensitive than palpation, thrills are associated with murmurs and indicate greater intensity (grade IV/VI). Thrills must be localized and timed to the cardiac cycle. DDX: In mitral stenosis, diastolic and presystolic thrills may be felt at the apex. Severe aortic stenosis causes a systolic thrill in the second right interspace and carotid arteries. The thrill from a ventricular septal defect (VSD) is felt in the fourth and fifth interspaces near the sternum.
Palpable friction rubs (friction fremitus)
Occasionally a pleural (Rib fracture) or pericardial (Acute Pericarditis) friction rub is palpable.
Shifted borders of cardiac dullness
Although precordial percussion can estimate the distance of the cardiac apex from the midsternal line (MSL) in the fifth interspace with fair accuracy, only gross changes in cardiac size can be detected.
Left border shifted to left
The LBCD is normally 7 to 9 cm to the left of the MSL. DDX: Causes of a leftward shift include dilatation of the left ventricle (RBCD normally placed or shifted to right), pericardial effusion (RBCD shifted to right, muffled heart sounds, paradoxical pulse), and displacement of a normal-sized heart to left by right pneumothorax, right hydrothorax, left pleural adhesions, or atelectasis of left lung with mediastinal shift to left.
Left border shifted to right
Consider pulmonary emphysema with a normal heart in the midline, a prominent lingula anterior to the heart preventing accurate percussion of LBCD, and displacement rightward from right lung fibrosis or atelectasis, left pneumothorax, or left hydrothorax.
Right border shifted to right
Causes include cardiac dilatation, pericardial effusion, left pneumothorax, left hydrothorax, right lung atelectasis, right pleural adhesions, and dextrocardia.
Right border shifted to left
Causes include left lung atelectasis, left pleural adhesions, right pneumothorax, and right hydrothorax.
Enlarged area of cardiac dullness
The area of cardiac dullness is expanded when there is lateral displacement of the right or left border with the other normally situated, or displacement of both borders in opposite directions. This is caused by either cardiac dilatation or pericardial effusion. Indirect definitive percussion is accurate when compared to CT [Heckerling PS, Weiner SL, Wolfkiel CJ, et al. Accuracy and reproducibility of precordial percussion and palpation for detecting increased left ventricular end-diastolic volume and mass. JAMA. 1993;270:1943–1948].
Widened retromanubrial dullness
Width in excess of 6 cm suggests aortic aneurysm, retrosternal goiter, thymic tumor, lymphoma, or metastatic carcinoma.
Auscultation of Heart Sounds
Much of this section is derived from the papers [Shaver JL, Leonard JJ, Leon DF. Examination of the Heart, Part IV: Auscultation of the Heart. Dallas, TX: American Heart Association; 1990; Perloff JK. The physiologic mechanisms of cardiac and vascular physical signs. J Am Coll Cardiol. 1983;1:184–198].
First (S1) and second (S2) heart sounds
With onset of ventricular systole, ventricular contraction rapidly increases intraventricular pressure, closing the AV valves (mitral and tricuspid) and, shortly thereafter, opening the aortic and pulmonic valves (Fig. 8-19). Tensing of the AV valves is associated with S1; tensing of the aortic and pulmonic valves is associated with S2. The normal heart sounds are NOT caused by slapping together of the leaflets. Rather, the high-frequency components of these sounds are probably caused by tensing of the closed valves producing abrupt deceleration of blood vibrating the heart, vessels, and blood column. Ventricular contraction forces blood silently into the aorta and pulmonary artery until the ventricles relax and the intraventricular pressure falls. Initial apposition of the aortic and pulmonic valve leaflets occurs prior to the high-frequency components of the second heart sound. The gradient of pressure between the artery and the more rapidly declining intraventricular pressures leads to an abrupt stretching of the elastic leaflet tissue producing the second heart sound. The sound occurs when flow in the artery has fallen to near zero but just before brief retrograde flow occurs [Sabbah HN, Stein PD. Investigation of the theory and mechanism of the origin of the second heart sound. Circ Res. 1976;39:874–882]. The heart sounds are usually loudest on the precordium nearest their origin: S1 from the AV valves at the apex and lower left sternal border; S2 from the semilunar valves at the base. The second sound is louder than the first at the base. Occasionally, S2 at the apex may be as loud or louder than S1. The intensity of the sounds varies with the stress on the valve leaflets.
Prosthetic heart valves are very common. It is advisable for the clinician to be familiar with the various types of valves and their auscultatory features [Vongpatanasin W, Hillis LD, Lange RA. Prosthetic heart valves. N Engl J Med. 1996;335:407–416].
First heart sound, S1—onset of ventricular systole
S1 marks the beginning of ventricular systole, approximately synchronous with the apical impulse. S1 is usually louder than S2 at the cardiac apex, but can be heard throughout the precordium. At the base, S1 is fainter than S2.
S1 splits when tensing of the tricuspid and mitral valves is asynchronous. Slight splitting of S1 is a common normal finding. Wide splitting occurs with right bundle-branch block, which delays onset of right ventricular contraction.
Thickening with preserved mobility of the mitral valve leaflets or increased force of LV contraction accentuates S1. This occurs in mitral stenosis, tachycardia from fever, hyperthyroidism, exercise, emotion, and hypertension.
When the mitral and tricuspid valves are more closely approximated at the onset of systole, their tensing is less forceful. Attenuation of heart sounds by chest wall soft tissues also diminishes S1. This occurs with obesity, emphysema, and pericardial and/or pleural effusion. Other causes include weak ventricular contraction, aortic insufficiency, prolonged PR interval, and heavily calcified mitral valve leaflets.
Variable and intermittently very loud S1 (Bruit de Canon)
Variable ventricular diastolic filling and asynchronous atrial and ventricular contraction change the intensity of S1 from beat to beat. Atrial fibrillation, atrial flutter with varying block, complete AV block, frequent premature beats, and ventricular tachycardia can each be a cause.
Second heart sound, S2—onset of ventricular diastole
Tensing of the closed semilunar aortic (A2) and pulmonic (P2) valves produces S2; normally, A2 slightly precedes P2. The more compliant or distensible an artery is, the less faithfully the pressure in the artery will follow temporally the rise and fall of the pressure in the ventricle ejecting into that artery, a phenomenon known as hangout [Curtiss EI, Matthews RF, Shaver JA. Mechanism of normal splitting of the second heart sound. Circulation. 1975;51:157–164]. Thus, the lower aorta compliance compared with greater PA compliance causes the interval between the completion of LV systole and A2 to be much shorter than that between the completion of RV systole and P2; therefore, A2 precedes P2 (Fig. 8-37). The intensity of A2 should be greater than P2. This follows from the much higher aortic pressure distending the AV leaflets compared with the PA pressure. To judge the relative intensities of A2 and P2 compare them in the second left intercostal space. In adults, only A2 is heard at the apex; if both components are heard, it suggests that P2 is abnormally loud. Respiratory Effect: The pulmonary valve closes later during inspiration than during expiration because of increased venous return to the right heart and changes in pulmonary compliance created by the negative intrathoracic pressure. This produces inspiratory splitting of S2. In children and adolescents, the normal respiratory splitting of S2 is wider than in older adults, probably because of reduced aortic compliance. In recumbent young persons, S2 may not fuse into a single sound with expiration. Fusion should occur during expiration when sitting; failure to fuse suggests unusually wide splitting. With advancing age, the inspiratory splitting of S2 may not be detectable even in recumbency because of the narrow normal split.
Normal Physiologic Variations in the Heart Sounds
Duration is represented on the horizontal axis, and intensity of the heart sounds on the vertical axis. The S1 is prolonged during inspiration. The aortic component of the second sound (A2) is audible over the entire precordium, but (P2) the weaker pulmonic component is heard only in the left second intercostal space. During expiration, the aortic and pulmonic components of are fused. With inspiration the splitting of S2 widens. Splitting of S2 is normal only in this pulmonic area; it is pathologic elsewhere.
Increased pressure on the closed aortic valve increases A2. Arterial hypertension is most common, but it can occur with ascending aortic aneurysm.
A2 is decreased when the valve is rigid and immobile or the pressure on the valve and aortic root at end systole is lower. Arterial hypotension and a heavily calcified AV in aortic stenosis diminish A2.
P2 is accentuated in primary or secondary pulmonary hypertension, atrial septal defect (ASD), truncus arteriosus, and in adolescence (Fig. 8-21A).
Diminished pulmonary artery pressure reduces tension on the pulmonic valve. Pulmonic stenosis is the most common cause (Fig. 8-38).
Pathologic Variations in the Heart Sounds
Pulmonary hypertension causes an increased P2. Right bundle-branch block delays right ventricular emptying, increasing the normal split and accentuating P2. Pulmonic stenosis also delays P2, but decreases its intensity. In left bundle-branch block and aortic stenosis, LV ejection is delayed so A2 coincides with P2 and the normal expiratory movement of P2 causes paradoxic splitting during expiration.
Widened inspiratory splitting of S2
This indicates either delayed PV tensing or early AV tensing. P2 delay occurs with right bundle-branch block, ASD, and pulmonic stenosis. Early AV closure valve occurs with severe MR (Fig. 8-38).
Reversed or paradoxic splitting of S2
A delay of LV ejection causes A2 to occur with or after P2. There is a single sound, or more closely approximated sounds, during inspiration; expiration increases splitting of S2. It is seen in hypertrophic cardiomyopathy with dynamic LV outflow obstruction, valvular aortic stenosis, left bundle-branch block, and RV pacing (Fig. 8-38).
Triple rhythms and gallops
These are low-pitched sounds best heard in a quiet room. Listen specifically for triple heart sounds (couplets alternating with single sounds) resembling a horse’s gallop. The couplet may be either a normal S2 followed closely by an audible S3 or an audible S4 preceding a normal S1. Differentiating S3 from S4 requires accurate identification of S1 and S2. The galloping rhythm is most evident at rates > 100 bpm and some reserve “gallop” for the presence of an S3 and/or S4 and a rate >100 bpm. At very fast rates S3 and S4 fuse creating a mid-diastolic summation gallop.
S3, ventricular or protodiastolic gallop
S3 occurs at the transition from the rapid to the slow-filling phase ventricular filling. The reverberations caused by deceleration of ventricular muscle and blood mass cause the S3 (Fig. 8-20 and Fig. 8-38). An audible S3 closely follows S2 in early diastole. It has the cadence of Kentucky: ken. . TUCK..eh. By whispering “ken . . TUCK..eh” to yourself as you listen, timing “ken” to S1 and “TUCK” to S2 you can train your ear to listen for the low-pitched S3 coincident with “eh.” A left ventricular S3 is best heard at the apex with the patient lying 45 degrees to the left side; a right ventricular S3 is best heard near the lower left sternal border. S3 is best heard in expiration and is accentuated by increasing venous return by exercise, abdominal pressure, or flexing the knees on the abdomen. An S3 is normal in children, young adults, and in pregnancy. After the third decade it may indicate myocardial systolic dysfunction with increased LV end-diastolic pressure and elevated left atrial pressure. It is also seen, although of less concern, in hyperkinetic circulatory states (such as fever, anemia, and hyperthyroidism) or by very rapid ventricular filling from MR or a large left to right shunt with a VSD.
S4, presystolic or atrial gallop
S4 is caused by vibrations of the LV muscle, mitral valve apparatus, and LV outflow tract subsequent to atrial contraction (Fig. 8-20 and Fig. 8-38). S4 occurs after atrial contraction but before S1. The cadence is Tennessee: “te..NUH … ..see.” This is the most difficult to hear of all heart sounds; listening at apex with patient in left lateral decubitus position is mandatory. As you listen, whisper to yourself “te..NUH … .see,” timing “NUH” to S1 and “see” to S2; train your ear for the S4 coincident with “te.” S4 is low pitched, identical to S3. The S4 always indicates a high pressure, powerful atrial contraction, most often associated with decreased ventricular compliance. S4 is heard with a thickened, noncompliant left ventricle, as occurs with LVH, aortic stenosis, subaortic stenosis, hypertension, and acute ischemia or infarction from coronary artery disease (CAD).
Diastolic sound—summation gallop, mesodiastolic gallop
High heart rates compress diastole moving S3 and S4 together giving the impression of a single sound or a rumbling murmur. Vagus stimulation may slow the rate enough reveal the four sounds.
Auscultation of extracardiac sounds
These relatively uncommon precordial sounds are often mistaken for murmurs. The key is that the extracardiac sounds may move about within a specific part of the cardiac cycle.
Early systolic ejection sound—ejection click, aortic ejection sound
Sudden tensing of the aortic root occurs at the onset of LV ejection. Alternatively, sudden doming of a stenotic yet flexible noncalcified aortic valve may be the cause (Fig. 8-20). A click is heard in early systole, at the onset of LV ejection, at the base and apex. It is usually louder at the base and unaffected by respirations. Ejection clicks occur with dilation of the aortic root because of ascending aortic aneurysm, coarctation, hypertension, valvular aortic stenosis, a bicuspid aortic valve, or aortic regurgitation.
Early systolic ejection sound—ejection click, pulmonic ejection sound
See Aortic ejection sound above and Fig. 8-20. This is a click at the onset of right ventricular ejection, occurring with pulmonary valve stenosis or dilatation. It is best heard at the left second interspace in early systole. In some cases, a loud click fuses with S1 making S1 sound louder. The closer the sound is to S1, the more severe the stenosis. Pulmonic clicks may decrease or disappear with inspiration.
Mid or late systolic click—mitral valve prolapse
This click is heard at the apex in mid or late systole; it may be intermittent (Fig. 8-20). It is unchanged by respiration but can be delayed or abolished with increased LV volume following a squat from standing or raising the legs of a supine patient. The click may first become apparent or, if already audible, will move toward the S1 as the LV cavity dimension decreases with standing or Valsalva. It is sometimes associated with a late systolic murmur of mitral insufficiency. Most individuals are otherwise normal, although mitral prolapse occurs with increased frequency in Marfan syndrome and myxomatous mitral valve changes.
Diastolic snap—mitral opening snap
When LV pressure drops below LA pressure, stenotic but still flexible (noncalcified) mitral valve leaflets that are tethered at their commissures buckle or bow into the left ventricle producing a snap. The diastolic rumble begins a few hundredths of a second later (Fig. 8-20). The snap is best heard at the apex but may radiate to base and left sternal border, simulating a widely split S2. This sign is characteristic of rheumatic mitral stenosis.
Diastolic snap—tricuspid opening snap
See mitral opening snap above. Usually associated with other rheumatic valvular abnormalities, this snap is difficult to identify.
Diastolic sound—pericardial knock
With constrictive pericarditis ventricular filling is stopped abruptly in early diastole producing vibrations known as a pericardial knock. Knocks are higher pitched than S3 and are heard widely over the precordium. They can be earlier than S3 and increase with inspiration (Fig. 8-20).
Two inflamed pericardial surfaces rub together creating the sound which seems closer to the ear than murmurs. Pericardial effusions often do not cover the entire pericardium, so rub and effusion can coexist. Listen during full expiration with the patient prone or sitting and leaning forward. Rubs are scratchy, grating, rasping, or squeaky. In about 50% of cases, the rub is triphasic, in systole and early and late diastole. In one-third it is systolic and late diastolic. The rest are heard only in systole. Rubs are often intermittent.
Mediastinal crunch (Hamman sign)
High-velocity flow in the internal jugular veins, especially the right, produces a humming sound. Hums are usually heard in both supraclavicular fossae and often in the second and third interspaces near the sternum. They are low pitched, persist throughout the cardiac cycle, and frequently increase during diastole. Hums are intensified by sitting or standing; they do not vary with respirations. The hum is readily abolished by light pressure on the jugular veins beside the trachea. It is frequently mistaken for an intracardiac murmur. Venous hums can be normal. They are more common with hyperthyroidism and anemia.
Auscultation of Heart Murmurs
In normal vessels and heart chambers, blood flow at rest is laminar and silent. Murmurs result from turbulence (vortices) developing near the vessel wall–bloodstream interface as the blood passes an obstruction or dilatation (vortex-shedding theory). Imagine 60 cm of pliable rubber tubing attached to a water faucet. When the faucet is turned on, a flow velocity can be attained that will not vibrate the tubing, because the flow is laminar and smooth. At this flow, slightly constricting the tubing will cause vibrations distally. Similarly, increasing the flow without constriction will induce turbulence. In a normal heart, murmurs may be induced when the velocity of normal blood is increased by high output states such as exercise, anemia, pregnancy, or hyperthyroidism, that is, a flow murmur. Normal blood flowing over obstructions or through unusual openings in the circulation creates turbulence and collision currents that result in murmurs. Murmurs should be described by their location, pitch, and position in the cardiac cycle. Accurate observation can lead to remarkably accurate diagnoses. The quality of a murmur is of some diagnostic value. Ventricular filling murmurs involving diastolic flow across the AV valves are relatively low pitched because of the low pressure gradients; blood flowing through narrow orifices with higher pressure gradients cause high-pitched murmurs. Figures 8-39 to 8-41 show the murmur and anatomy of each major condition.
Common Pathologic Heart Murmurs
The diagrams are drawn to represent intensity of the heart sounds and murmurs on the vertical axis and duration on the horizontal axis. Pitch is depicted by the spacing of the shading: wider spacing lower pitch. “A” and “P” refer to the aortic and pulmonic components of the S2. “OS” indicates the opening snap of the mitral valve in mitral stenosis. Note that the systolic ejection murmurs are inaudible at either end of systole and attain maximum intensity at mid-systole (in this diagram they form the upper halves of “diamond-shaped” figures of the phonocardiogram). Systolic regurgitant murmurs are pansystolic. The configuration of the diastolic ejection murmur of mitral stenosis terminates in a crescendo caused by superimposition of atrial contraction. Although the diastolic regurgitant murmurs are pandiastolic, in aortic and pulmonic regurgitation, the late diastolic part is seldom heard.
Systolic murmurs are described when they occur in systole, early, mid, or late. Murmurs heard throughout systole are pansystolic or holosystolic. Blood moving across a rising then falling pressure gradient produces a crescendo–decrescendo murmur as flow accelerates then slows. Aortic stenosis is an example; the murmur starts soon after S1, intensifies to a maximum at mid-systole, and tapers off disappearing before S2. When blood flows continuously from a high-pressure region to one of low pressure, a pansystolic murmur of almost uniform intensity is produced; this is typical of atrioventricular valve regurgitation. It is usually possible to distinguish the systolic murmurs of organic disease from those occurring only in early systole or mid-systole that are of little significance [McGee S. Etiology and diagnosis of systolic murmurs in adults. Am J Med. 2010;123:913--921; Etchells E, Bell C, Robb K. The rational clinical examination. Does this patient have an abnormal systolic murmur? JAMA. 1997;277:564–571]. Since some lesions can be missed even by experienced observers, echocardiography is an important adjunct in evaluation of pathological systolic murmurs. Common errors are underestimating the severity of aortic stenosis caused by decreased LV function, failing to identify combined mitral and aortic murmurs, and missing aortic insufficiency in association with aortic systolic murmurs [Jost CHA, Turina J, et al. Echocardiography in the evaluation of systolic murmurs of unknown cause. Am J Med. 2000;108:614–620].
Basal systolic murmurs—benign, innocent, physiologic, functional, nonpathologic murmurs
Some authors believe these murmurs are produced by increased velocity or decreased viscosity of the blood. Most commonly located in the second left interspace, they are medium pitched and usually grade I or II. They are best heard in the supine position and tend to disappear with sitting or standing. They are infrequently transmitted to the neck. Functional murmurs occur in normal adults with anemia, fever, anxiety, exercise, hyperthyroidism, or pregnancy. Approximately 50% of normal children have functional systolic murmurs.
Progressive commissural fusion and leaflet fibrosis result in a narrow valve orifice with impedance to LV ejection (Fig. 8-40C). The Murmur: Classically the murmur is heard in the second right interspace, but almost as often it is audible along the left sternal border in the third and fourth interspaces and at the apex. In approximately 15% of cases, it is loudest at the apex. Regardless of the area of maximal intensity, it is transmitted to the carotid arteries. Loud murmurs can be accompanied by systolic thrills at the base and in the carotids. Onset is very shortly after S1, when intraventricular pressure first exceeds aortic pressure. It ceases at or before S2. It is diamond shaped, initially rising (crescendo) then falling (decrescendo) in intensity (Fig. 8-39). The murmur is usually harsh, medium pitched, and audible with the bell and diaphragm. Occasionally it sounds like the call of a gull or a dove cooing. With decreased LV contractility, it may decrease in intensity and duration. Heart Sounds: In moderate or severe stenosis accompanied by significant valvular calcification, A2 is diminished or absent at the apex. If the valve is stenotic but not calcified (as in congenital aortic stenosis), S2 may split during expiration (paradoxically) from delayed closure of the aortic valve (Fig. 8-38). Normal inspiratory splitting of S2 suggests mild stenosis. When the valve remains flexible although stenotic, the murmur is preceded by an ejection or early systolic sound caused by doming of the valve in early systole; this disappears when the valve becomes calcified. An apical S4 is frequently audible. Precordial Thrust: Left ventricular hypertrophy accentuates the precordial apical thrust. In the left lateral decubitus position, a double (bifid) apical thrust is sometimes felt; the first impact comes from atrial contraction, the second from LV systole. Arterial Pulse: Severe aortic stenosis produces a slowly rising carotid pulse contour (tardus or anacrotic pulse, Fig. 8-42D) felt as a sustained push on the finger rather than the normal brief tap. Decreased pulse amplitude is often palpable; it is best assessed by the pulse pressure. Physical findings do not reliably assess the severity of aortic stenosis [Munt B, O’Legget ME, Draft CD, et al. Physical examination in valvular aortic stenosis: correlation with stenosis severity and prediction of outcome. Am Heart J. 1999;137:298–306]. Symptoms: Aortic stenosis may be asymptomatic until severe, when exercise induces dyspnea, angina, or syncope. The most common etiologies are rheumatic valvulitis, valve sclerosis, and congenital bicuspid valve. X-ray Findings: Calcification of the aortic valve may be seen on the films. DDX: The systolic murmur of aortic sclerosis is briefer and accompanied by normal heart sounds at the base. The apical systolic murmur of MR has a blowing quality and is often holosystolic. A systolic diamond-shaped murmur may occur with either valvular or subaortic stenosis [Carabello BA. Aortic stenosis. N Engl J Med. 2002;346:677–682].
Anatomic Bases for Cardiac Murmurs I.
Hypertrophic obstructive cardiomyopathy (IHSS)
Asymmetric LV hypertrophy with prominent hypertrophy of the basal interventricular septum is associated with dynamic outflow obstruction starting shortly after the onset of systole. Obstruction is caused by apposition of the anterior mitral leaflet to the hypertrophied septum; this may cause mitral insufficiency as well. A family history with autosomal dominant inheritance is often present; unexplained sudden deaths in the family should suggest hypertrophic cardiomyopathy, with or without obstruction. The apical impulse is often double. The Murmur: A systolic ejection murmur begins well after S1 and is best heard at the apex and left sternal border. It is less intense in the right second interspace and usually does not radiate to the carotids. At the apex, the murmur may have a blowing holosystolic quality like MR. The murmur varies with ventricular volume changes, peripheral resistance, and contractility. The outflow obstruction and murmur are intensified by reduced LV filling (standing and/or the Valsalva maneuver), whereas the valvular aortic stenosis murmur diminishes. Raising diastolic blood pressure by handgrip reduces the dynamic obstruction and murmur. Squatting or lifting the legs increases venous return and LV end-diastolic volume, reducing the obstruction and murmur. Arterial Pulse: The arterial pulse wave has a sharp upstroke in contrast to the diminished and delayed pulse of valvular stenosis. A double peaking or bisferiens pulse may be present. Heart Sounds: As in valvular stenosis, an S4 is frequent. There is no systolic ejection click with subaortic stenosis. Symptoms: The symptoms are identical to those of severe valvular stenosis. The diagnosis is confirmed by echocardiography.
Supravalvular aortic stenosis
A rare congenital anomaly; this is the result of a narrowing of the ascending aorta or a small-holed diaphragm distal to the valve. It produces most of the signs of valvular stenosis, but A2 is accentuated and the carotid murmurs are unusually loud. The finding of a systolic blood pressure that is more than 10 mm Hg greater in the right arm than the left is typical of supravalvular aortic stenosis.
Aortic sclerosis is caused by leaflet thickening and calcification (sclerosis) without significant obstruction (stenosis). A medium-pitched murmur of moderate intensity is heard in the aortic region and may be heard at the apex. It is often brief and confined to early systole and usually softer than an aortic stenosis murmur. The murmur may be faintly heard in the carotids. A2 is usually present at the apex. DDX: Aortic stenosis is easily excluded, because the murmur is seldom loud or long, or accompanied by abnormality of the carotid pulse. Preservation of A2 at the apex speaks against severe calcific aortic valvular stenosis.
Valvular pulmonic stenosis
The Murmur: An ejection murmur with diamond shape is loudest in the second left interspace (Figs. 8-40E and 8-39C). Its intensity, configuration, and pitch are similar to an aortic stenosis murmur, but its intensity increases with inspiration. Carotid transmission may occur (left > right). Heart Sounds: Slow ejection delays P2 so S2 is widely split; P2 is less intense because of the reduced pulmonary artery pressure (Figs. 8-20 and 8-39C). An early ejection sound indicates valvular rather than infundibular stenosis. Palpation: An accentuated precordial thrust or sternal lift indicates RVH. DDX: The murmur is similar to the pulmonary flow murmur with ASD. In ASD P2 is undiminished. Pulmonary stenosis is usually congenital, alone or in the tetralogy of Fallot. It can be acquired with carcinoid tumors.
Infundibular pulmonic stenosis
The infundibulum is the funnel-shaped portion of the right ventricular chamber leading to the pulmonary artery. Congenital narrowing produces a form of pulmonic stenosis. The Murmur: In contrast to valvular stenosis, the ejection murmur and the systolic thrill are usually in the third left interspace and there is no ejection click. Although this lesion may be isolated, it is usually accompanied by a VSD, as in the tetralogy of Fallot.
The systolic murmur is produced by high-volume, high-velocity flow across the pulmonic valve because of right ventricle overfilling from the congenital left-to-right interatrial shunt (Fig. 8-41A). The Murmur: A medium-pitched murmur is heard in the second or third left interspace with maximum intensity a little before mid-systole (Fig. 8-39E). This murmur is sometimes accompanied by a low-pitched diastolic flow murmur along the lower left sternal border resulting from increased flow through the tricuspid valve. Heart Sounds: S2 is widely split, and usually fixed in its splitting. P2 is not diminished. DDX: The murmur may be indistinguishable from pulmonic stenosis. It is usually lower pitched, peaks earlier in systole, and rarely becomes as loud as that of pulmonic stenosis.
Anatomic Basis for Cardiac Murmurs II
Same symbols as in Fig. 8-40.
This is a congenital opening in septum near the AV valves, often associated with a cleft mitral valve leaflet. The Murmur: There is a harsh systolic murmur at left sternal border and an apical systolic murmur transmitted to axilla if MR is present. Sometimes a mid-diastolic murmur is heard at the lower left sternal border. Heart Sounds: S2 is accentuated with fixed splitting during inspiration and expiration. The right ventricular impulse is prominent; the LV apical impulse may be accentuated and laterally displaced because of MR.
See also Coarctation of the aorta. The constriction is in the descending aorta so the murmur is faintly heard, if at all, on the anterior chest. The murmur of the coarctation is heard best in the posterior interscapular area. A continuous bruit can sometimes be heard over the sternum from the dilated internal mammary arteries.
Ventricular septal defect
Blood flows from the left ventricle into the much lower pressure right ventricle through an opening in the interventricular septum (Fig. 8-41B). VSD is more common in the membranous than muscular septum. The Murmur: The high-pitched murmur is typically pansystolic with peak intensity in the fourth and fifth left interspace. It may be transmitted over the entire precordium and to the interscapular region. With muscular septal defects, the murmur may not persist throughout systole. The intensity and harshness diminish and the midsystolic accentuation is lost when pulmonary hypertension supervenes. Palpation: Loud murmurs may be accompanied by a thrill. Heart Sounds: When the defect is large S2 may be accentuated. DDX: With pulmonary hypertension, imaging may be needed to distinguish VSD from persistent ductus arteriosus. Faint murmurs must be distinguished from benign systolic murmurs [Ammash NM, Warnes CA. Ventricular septal defects in adults. Ann Intern Med. 2001;135:812–824]. CLINICAL OCCURRENCE: Congenital septal defects occur alone and in Eisenmenger and Fallot syndromes. VSD may complicate MI, typically at the cardiac apex; large acquired defects are rapidly fatal.
Tricuspid regurgitation (TR)
Right ventricular contraction produces backflow of blood into the right atrium and major veins, with a pulsatile increase in CVP (Fig. 8-41H). The Murmur: Faint murmurs are early systolic; loud murmurs are heard throughout systole; both are augmented by inspiration. They are high pitched and blowing, best heard with the diaphragm. The point of maximum intensity is along the lower left sternal border and may be sharply localized or transmitted to the apex. Palpation: Right ventricular hypertrophy may be present with a palpable right ventricular precordial thrust. When severe, tricuspid insufficiency produces prominent jugular “v” waves, neck vein engorgement, and hepatic pulsations. Heart Sounds: There are no characteristic changes in the heart sounds. DDX: The location of maximum intensity, large “v” waves and the effect of inspiration are diagnostic. CLINICAL OCCURRENCE: Congenital TR occurs with Ebstein anomaly. It is acquired in rheumatic heart disease, right ventricular failure of any cause, endocarditis, carcinoid tumor, and PE.
Blood is forced back through the mitral orifice with almost constant velocity during the entire systolic interval (Fig. 8-41F). With severe MR, the left ventricle empties prematurely, so A2 is early, causing wide splitting of S2. The Murmur: Classically, this loud high-pitched murmur with maximum intensity at the apex begins with S1, continues throughout systole, and ends at or near S2 (Fig. 8-39H). However, many variations occur: the murmur may mask S1, begin with S1 and decrescendo to end in early-to-mid systole or begin in mid-to-late systole and crescendo to end with, or even after, S2. Faint murmurs are well localized; loud murmurs are transmitted to the axilla. Eccentric jets may produce murmurs with radiation to the base and carotids, or to the lung bases and spine. There is little variation with phases of respiration or rhythm irregularities. A rumbling diastolic murmur may be heard from the increased flow volume across the mitral valve. Many variations in the murmur of MR occur. It may begin in mid to late systole and crescendo up to and end with S2. Heart Sounds: S1 is often diminished or difficult to appreciate being embedded in the onset of the murmur. S2 is widely split with severe regurgitation. A2 may be difficult to appreciate at the apex being lost in the terminal portion of the murmur. An S3 is sometimes heard with moderate or severe MR. Palpation: Accentuation and lateral displacement of the apical thrust suggest LVH hypertrophy and dilatation, respectively. An increased left parasternal thrust or lift may indicate left atrial systolic expansion rather than right ventricular disease. DDX: The murmur must be distinguished from aortic stenosis which is often loud at the apex as well as at the base. Comparison of the duration and quality at the apex and base can differentiate the two [Otto CM. Evaluation and management of chronic mitral regurgitation. N Engl J Med. 2001;345:740–746]. CLINICAL OCCURRENCE: MR results from myxomatous change in the valve, endocarditis, rheumatic valvulitis, ruptured chordae, papillary muscle ischemia or rupture, MI, and dilatation of the mitral valve ring by any condition producing LV dilatation.
Mitral valve prolapse—midsystolic click and apical late systolic murmur
The valve undergoes myxomatous degeneration, producing redundant valve tissue (especially the posterior leaflet), enlargement of the valve annulus, and elongation of the chordae tendineae. During systole, as the ventricular volume is reduced, one or more scallops of the valve leaflets billow and prolapse backward into the atrium losing coaptation and producing MR. This occurs in 2% to 5% of the population, more frequent in women. It can be inherited, probably as an autosomal dominant with reduced male expressivity. The Murmur: The systolic crescendo murmur is heard best at the apex and classically occurs late in systole. It is usually short, relatively high pitched and blowing, persisting into S2. It may be transmitted to the back, left of the spine. In unusual cases, it is described as cooing, honking, or whooping. It may be inaudible or so loud as to be heard without a stethoscope. It typically moves closer to S1 with standing (decreased venous return, smaller LV volume) and becomes shorter and later in systole with the patient squatting or recumbent (increased venous return, larger LV volume). Auscultation in the erect position during a Valsalva maneuver may elicit a murmur inaudible at rest with the patient supine. Heart Sounds: A clicking sound is sometimes heard during mid-systole, coincident with the onset of the murmur; the click may occur without a murmur. Associated Dysrhythmias: Ventricular premature beats, paroxysmal atrial tachycardia, atrial fibrillation, sinus bradycardia, periods of sinus arrest, and positional atrial flutter can all occur in association. Noncardiac Signs: There is an increased incidence of chest wall abnormalities, particularly pectus excavatum. Mitral valve prolapse is common in Marfan syndrome. Symptoms: Most persons are asymptomatic. A minority develop easy fatigue, shortness of breath, nonanginal chest pain, palpitation, or syncope. Complications: There is an increased relative risk for cerebral transient ischemic attacks, rupture of chordae tendineae, congestive cardiac failure, endocarditis, and sudden death, but these are rare.
Rupture of interventricular septum, papillary muscle, or chordae tendineae. Sudden appearance of a loud pansystolic murmur suggests rupture of the interventricular septum, a chordae, or papillary muscle, or severe papillary muscle dysfunction. There may be a precordial thrill; severe pulmonary edema occurs with chordae or papillary muscle injury. The murmur is usually grade IIto IV/VI; however, severe mitral insufficiency may be associated with a surprisingly soft murmur. With a ruptured septum, there are signs of right-sided failure, low cardiac output, and poor peripheral perfusion. Prompt recognition and treatment may be life saving.
Diastolic murmurs are almost always pathologic. They are classified as early, mid, and late diastolic. Diastolic regurgitant murmurs caused by flow from the aorta or pulmonary artery back into a ventricle begin with S2 and may be prolonged since the arterial pressure exceeds ventricular pressure throughout diastole. The diastolic murmur of mitral stenosis does not start with S2 because pressure in the ventricle must continue to fall before becoming less than atrial pressure (the period of isovolumic relaxation).
Aortic regurgitation (aortic insufficiency)
The decreasing transvalvular pressure gradient from early to late diastole produces the decrescendo murmur. The high pitch is caused by blood being forced through a relatively small orifice at high pressure (Fig. 8-40D). The Murmur: The high-pitched blowing decrescendo murmur immediately follows S2; it may not last throughout diastole (Fig. 8-39B). The murmur is best heard with the diaphragm held firmly against the chest while the patient is leaning forward in full expiration. The point of maximum intensity is in either the right second or left third interspace. There is often an accompanying aortic systolic murmur. Transmission down the right rather than the left sternal border suggests aortic root aneurysm. Heart Sounds: S1 is usually normal; A2 may be accentuated. Palpation: Accentuation and lateral displacement of the apical thrust suggest LV hypertrophy and dilatation. Arterial Pulses: The pulse has a collapsing quality. Vasodilatation, high pulse pressure, and pistol-shot sounds may be found. Nailbed pulsation is easily seen. DDX: The quality and location do not distinguish AI from pulmonic regurgitation, but maximal intensity in the aortic area, an accentuated and displaced apical thrust, increased pulse pressure, brisk carotid upstrokes, pulsus bisferiens, and Duroziez sign all favor AI [Choudhry NK, Etchells EE. The rational clinical examination. Does this patient have aortic regurgitation? JAMA. 1999;281:2231–2238]. CLINICAL OCCURRENCE: Common causes are rheumatic valvulitis, congenitally bicuspid aortic valve, and endocarditis. Marfan syndrome, aortic dissection, aneurysm of the sinus of Valsalva, and annular ectasia of the aorta are less common. Syphilitic aortitis is increasingly uncommon.
This most commonly results from dilation of the pulmonic valve ring in pulmonary hypertension leading to backflow of blood from the pulmonary artery into the right ventricle resulting in RV volume and pressure overload (Fig. 8-40F). The Murmur (Graham Steell): It is indistinguishable in quality and timing from aortic regurgitation, though it is usually softer and transmitted less widely (Fig. 8-39D). The point of maximum intensity is in the second or third left interspace. In the absence of pulmonary hypertension the murmur is medium to low pitched. Heart: P2 may be accentuated. Palpation: A right ventricular precordial thrust may be palpated. CLINICAL OCCURRENCE: Pulmonary valve regurgitation occurs with pulmonary hypertension from any cause (mitral stenosis, left-sided heart failure, pulmonary emphysema, idiopathic pulmonary hypertension, congenital heart lesions, obstructive sleep apnea, chronic pulmonary emboli) or after pulmonary valvotomy.
Right atrial contraction against the stenotic valve orifice causes presystolic accentuation of the murmur and giant “a” waves. Impedance to right ventricular filling leads to elevated CVP (Fig. 8-41G). The Murmur: The diastolic murmur is low pitched and rumbling with a presystolic crescendo when atrial fibrillation is absent. It is best heard with the bell lightly placed. When mild, the murmur is late diastolic; with increasing severity, it occupies mid and even early diastole. The murmur becomes louder during inspiration because of increased venous return. Venous Pulse: Giant “a” waves are present; the CVP will progressively elevate as stenosis worsens. Heart Sounds: S1 is accentuated. Sometimes an opening snap of the tricuspid valve can be identified. Palpation: The point of maximum intensity is quite sharply localized at the lower-left sternal border in the fourth or fifth interspace. In severe stenosis, signs of central venous congestion (elevated CVP, hepatomegaly, ascites, edema) are found, mimicking right ventricular failure. DDX: The murmur can usually be distinguished from that of mitral stenosis by its location and accentuation during inspiration. A murmur identical to the mid-diastolic rumble of tricuspid stenosis is the diastolic flow rumble that accompanies severe TR or a large ASD. CLINICAL OCCURRENCE: Rheumatic valvulitis, congenital heart disease, and carcinoid tumor produce this lesion.
In mild mitral stenosis ventricular filling is only slightly delayed and the period of rapid filling is shortened, so a mid-diastolic murmur is produced. With moderate or severe stenosis, ventricular filling is prolonged, so atrial systole increases the pressure gradient across the valve, producing a presystolic crescendo murmur. The accentuated S1 is caused by thickened but flexible leaflets. Pulmonary hypertension produces the accentuated P2. The opening snap is attributed to the thickened but flexible leaflets, tethered at their commissures, bulging forward into the left ventricle when the elevated atrial pressure exceeds LV pressure; the snap is absent with immobile leaflets (Fig. 8-41E). The Murmur: This low-pitched and rumbling murmur is heard best in the left lateral position near the apex. It is usually sharply localized, so the bell must be placed lightly directly on the apex. Sometimes, only by carefully inching the bell over the entire apex will a loud murmur be discovered. In mild stenosis the murmur occurs in mid-diastole. As the orifice narrows, the murmur starts earlier and ends later, until it almost covers the diastolic interval. There is always a pause after S2 before the murmur begins. A long murmur often has a presystolic crescendo (Fig. 8-39G). Heart Sounds: S1 at the apex is accentuated if the thickened leaflets are mobile. If there is pulmonary hypertension, P2 is accentuated and occurs early but is normally delayed by inspiration. When the murmur is loud, there is usually a mitral opening snap shortly after A2, heard best at the left sternal border between the second and fourth interspaces. This is commonly mistaken for a split second sound. The opening snap disappears when the mitral cusps become rigid because of calcification. Palpation: The murmur is often accompanied by a thrill at the apex when the patient is in the left decubitus position. Often there is a palpable right ventricular thrust indicating right ventricular hypertrophy. DDX: Tricuspid stenosis produces a similar murmur, but it is localized nearer the sternum. A similar diastolic apical rumble may be heard with increased mitral diastolic flow caused by severe MR. The diastolic murmurs of aortic and pulmonic regurgitation also occur at the apex but have a blowing, not rumbling quality [Thibault GE. Studying the classics. N Engl J Med. 1995;333:648–653]. CLINICAL OCCURRENCE: Congenital stenosis is rare. Mitral stenosis nearly always results from rheumatic heart disease.
Aortic insufficiency is often associated with fluttering of the anterior mitral valve leaflet. However, neither this phenomenon nor others accompanying chronic aortic regurgitation seem consistently to correlate with this apical diastolic murmur. Authors vary on the criteria for diagnosis; the methods of Levine and Harvey are cited here. Some patients with severe AI and normal mitral valves have a murmur at the cardiac apex similar in pitch and timing to mitral stenosis. The examiner confronted with a combination of aortic and mitral murmurs must decide if the mitral valve is normal. DDX: Accentuation of S1 or P2 favors organic mitral stenosis. The opening snap of the mitral valve is absent in the Flint murmur. CLINICAL OCCURRENCE: AI from rheumatic valvulitis, syphilis, or acute endocarditis.
Murmurs heard throughout the cardiac cycle indicate that turbulent flow is occurring without interruption. Therefore, the flow must be from a continuous high-pressure source to a low-pressure sump, e.g., from the aorta to the pulmonary artery or a vein, or across a fixed obstruction in the aorta.
A persistent ductus arteriosus is an arteriovenous fistula between the aorta and the pulmonary artery (Fig. 8-41C) that produces a continuous murmur throughout the heart cycle. The higher aortic pressure during ventricular systole increases murmur’s pitch. Uncorrected, the increased PA pressure leads to RVH and eventually right-to-left shunting with peripheral cyanosis confined to the lower extremities (Eisenmenger physiology). The Murmur: A murmur heard in the first and second left interspace throughout systole and diastole is usually caused by a persistent ductus. The murmur is medium pitched and rough, heard with either bell or diaphragm. Louder murmurs are harsh. There is typically a crescendo late in systole and a decrescendo after S2, producing a machinery murmur (Fig. 8-39F). Most frequently, transmission is to the interscapular region; occasionally it is transmitted down the left sternal border, sometimes to the apex. As pulmonary artery pressures approach aortic pressures, the diastolic portion of the murmur may disappear. TR may develop from the pulmonary hypertension. Increased flow through the mitral orifice may produce a diastolic rumble simulating mitral stenosis. Heart Sounds: S2 may be buried in the crescendo portion of the murmur. Frequently there is a short pause between S1 and the murmur. Palpation: The precordial thrust of both ventricles may be accentuated. Arterial Pulses: With large shunts the peripheral pulse may have a collapsing quality, similar to AI. DDX: Clubbing in the toes but sparing the fingers is seen with persistent right to left shunt in Eisenmenger physiology. The continuous murmur must be distinguished from a venous hum.
Coronary arteriovenous fistula and ruptured sinus of Valsalva aneurysm
These conditions present similarly with a continuous mid-precordial murmur; imaging is needed for differentiation. The Murmur: A continuous murmur with late systolic accentuation (machinery or to-and-fro) is audible on either or both sides of the lower sternum, often accompanied by a systolic or continuous thrill. DDX: Although the to-and-fro murmur has the same quality as that in ductus arteriosus, the location is sufficiently different to be distinctive. A mid-precordial to-and-fro murmur can occur with the combination of VSD and aortic regurgitation, but the quality of the systolic and diastolic components are distinct and there is no late systolic accentuation. Although a venous hum may be audible behind the upper sternum, its accentuation is diastolic and it is abolished by pressure on the internal jugular vein.
Vascular Signs of Cardiac Activity
LV contraction maintains arterial blood pressure and produces palpable pulsations in all accessible arteries. Right atrial and ventricular contractions generate venous pulsations in the upper body. Because arterial pressure is normally approximately 16 times higher than CVP, arterial pulsations are palpable whereas venous pulsations are not. This is useful in determining the origin of visible pulsations.
The systolic arterial pressure contour is determined by aortic compliance, LV stroke volume, and the rate of flow from LV to aorta. These, in turn, are influenced by LV contractility and the size of the aortic valve orifice and LV outflow tract. The diastolic pressure contour reflects the volume of run off per cardiac cycle. The carotid pulse most accurately reflects the contour of the aortic pulse wave. Alterations of the normal pulse contour and volume are diagnostically significant.
The palpable primary wave is a swift upstroke to the peak systolic pressure, followed by a more gradual decline. A smaller upstroke caused by blood rebounding off the closed aortic valve, the dicrotic wave, occurs near the end of ventricular systole but is not usually palpable (Fig. 8-42A).
Arterial Pulse Contour
A. Normal pulse contour. B. Dicrotic pulse. C. Bounding or collapsing pulse. D. Tardus or Plateau pulse. E. Pulsus alternans. F. Bigeminal pulse. G. Pulsus paradoxus.
Twice peaking (dicrotic) pulses
There are two types of twice peaking arterial pulses (Fig. 8-42B). Most common is pulsus bisferiens with two palpable waves during systole. Less common is the dicrotic pulse, which has one wave palpable in systole and a second in diastole. CLINICAL OCCURRENCE: Pulsus Bisferiens: Severe aortic regurgitation especially when associated with moderate aortic stenosis, hypertrophic subaortic stenosis, and hyperkinetic circulatory states such as hyperthyroidism; Dicrotic Pulse: Very low cardiac output as with dilated cardiomyopathy or cardiac tamponade, especially in patients with normal aortic compliance.
Bounding or collapsing pulse (Corrigan pulse, water-hammer pulse)
A large stroke volume and/or vigorous LV contraction generates a rapid upstroke followed by rapid runoff of blood from the aorta. With high pulse pressure the upstroke may be very sharp, whereas the down slope is precipitous (Fig. 8-42C). It may be accompanied by the pistol-shot sound. CLINICAL OCCURRENCE: This is encountered in hyperthyroidism, anxiety, aortic regurgitation, persistent ductus arteriosus, and arteriovenous fistula.
Plateau pulse (pulsus tardus)
The upstroke is gradual and the peak delayed toward late systole (Fig. 8-42D). Carotid palpation reveals a gentle, sustained lifting movement in contrast to the normal brief pulsatile tap. This occurs in severe aortic stenosis.
Absent pulses, pulseless disease
Bigeminy (coupled rhythm)
A normal beat is followed by a premature beat and a pause (Fig. 8-42F). If the premature beat occurs with a very short coupling interval so that ventricular filling is incomplete, it has a smaller stroke volume than the preceding normal beat and may not produce a palpable arterial pulsation; the radial pulse rate appears to be half the ventricular rate. This is detected by auscultating the rhythm over the precordium.
The pulse waves alternate between greater and lesser volume, despite a normal rhythm and a constant rate (Fig. 8-42E), a sign of LV dysfunction. This may not be palpable but is detected while auscultating the blood pressure: as the cuff is slowly deflated every other beat becomes audible first, then, with further deflation, the rate appears to double as all the beats are heard. DDX: This must be distinguished from bigeminal rhythm, in which a normal beat is followed by a premature beat.
Normally, inspiration decreases intrathoracic pressure, increases blood flow into the chest and right ventricle, and decreases LV filling resulting in a small decrease in LV stroke volume and systolic blood pressure. In pericardial tamponade total heart volume (pericardial sac and chambers) is fixed. With inspiration the right heart volumes expand, bulging the septum leftward, resulting in further compromise of left heart volumes, leading to an exaggerated fall in LV stroke volume and systolic arterial pressure. Labored breathing associated with exacerbations of obstructive airway disease also produces a paradoxical pulse. Under normal resting conditions the inspiratory fall in arterial systolic pressure is less than 10 mm Hg. A paradoxical pulse exists when inspiration creates more than a 10-mm-Hg drop in systolic arterial pressure. This can be detected by auscultating the blood pressure; sometimes the exaggerated waxing and waning in the pulse volume can be detected by palpation (Fig. 8-42G). DDX: In AV asynchrony pulse volume is variable so pulsus paradoxus cannot be accurately assessed. CLINICAL OCCURRENCE: Pericardial tamponade, pulmonary emphysema, severe asthma.
Disparity between the right and left arterial pulse volumes is detected by simultaneous palpation and confirmed by taking the blood pressure at both sites. Arterial pressure differences between the arms must be interpreted cautiously: pressures not measured precisely simultaneously are >10 mm Hg different in up to 20% of normal individuals, whereas, when measured simultaneously by cuff, 5% or less show the same difference. Nonsimultaneously measured systolic pressure differences of >10 mm Hg occur in almost 30% of hypertensive patients [Harrison EG Jr, Roth GM, Hines EA. Bilateral indirect and direct arterial pressures. Circulation. 1960;22:419–436]. Asymmetry suggests atherosclerosis, dissecting aneurysm or another arterial disease.
See Chapter 4. Many dysrhythmias produce arterial beats of greater or lesser volume and disordered timing. It is preferable to evaluate the disturbance from the precordial findings rather than the peripheral pulse. Any ventricular contraction before the ventricle has had time to fill will produce a peripheral pulse wave of diminished volume, or none at all. The ECG, not palpation or auscultation, is the only way to accurately diagnose rhythm disturbances.
Arteries are normally silent when auscultated. Turbulence is heard as a murmur and palpated as a thrill. Although murmur and bruit are literally synonymous, there is a tendency to reserve bruit for arterial sounds. The presence of a bruit does not necessarily indicate limitation of flow. CLINICAL OCCURRENCE: Arteries become tortuous from arteriosclerosis or other circumstances or dilate with aneurysm. They may be constricted congenitally by intimal proliferation or by an atherosclerotic plaque. Dilatation of the thyroid arteries with increased blood flow occurs in Graves disease (here, the word bruit is often used). Blood flow through an arteriovenous fistula or large arterial collaterals, as in aortic coarctation, is often accompanied by bruits. A continuous murmur is produced by an arteriovenous fistula or a partially obstructed artery when the collateral circulation is poor and the diastolic pressure is quite low distal to the obstruction.
Most of the blood flow to the brain and virtually all to the cerebral cortex comes via the internal carotid arteries. Despite collateral flow through the circle of Willis from the contralateral carotid and vertebrobasilar system, high-grade obstruction of one common and/or internal carotid artery is associated with a high risk for disabling stroke. The neck should always be auscultated for bruits, and any bruit should be evaluated by imaging. The degree of stenosis cannot be estimated by physical examination. Symptoms of cerebral ischemia in the distribution of the affected artery are associated with a high risk for stroke within hours to days.
Arterial sound—pistol-shot sound
This is produced by the wave front of an arterial pulse wave of higher than normal pulse pressure striking the arterial wall in the region of auscultation. When the stethoscope bell is placed lightly over an artery, particularly the femoral, a sharp sound like a gunshot may be heard. CLINICAL OCCURRENCE: Although commonly associated with aortic regurgitation, it also occurs in other conditions with high pulse pressure, such as hyperthyroidism, and anemia.
Incorrectly attributed to retrograde flow of blood in the vessel, the second murmur is actually associated with a second exaggerated forward acceleration of blood flow. Compressing the femoral artery with the stethoscope bell produces eddies and a systolic bruit. Listen while pressure on the bell is gradually increased. First, the normal systolic murmur appears, but with further pressure a critical point is reached when the second murmur becomes audible; this is Duroziez sign. Most commonly encountered in severe aortic regurgitation, it occurs in other conditions with a high pulse pressure (Chapter 4).
Venous Signs of Cardiac Action
Cardiac action produces signs in the venous system by altering peripheral venous pressure and pulse contour and by producing venous congestion in the viscera.
Elevated CVP indicates overfilling of the intravascular space, exceeding venous capacitance, and/or impedance to filling of the right atrium or right ventricle. Impedance to right ventricular filling often occurs as a result of impaired outflow from the right ventricle causing elevated right ventricular end-diastolic pressure. When the venous pressure exceeds 10 or 12 cm of water under resting conditions, it should be considered elevated. DDX: A generalized increase in venous pressure must be distinguished from SVC and/or IVC obstruction. Always assess whether the venous pressure appears uniformly elevated above and below the diaphragm; it must be if the CVP is elevated. Absence of signs below the diaphragm suggests SVC obstruction [Cook DJ, Simel DL. The rational clinical examination. Does this patient have abnormal central venous pressure? JAMA. 1996;275:630–634; Vinayak AG, Levitt J, Gehlbach B, et al. Usefulness of the external jugular vein examination in detecting abnormal central venous pressure in critically ill patients. Arch Intern Med. 2006;166:2132–2137]. CLINICAL OCCURRENCE: Overfilling of the Vascular Space: Kidney failure, rapid infusion of fluids and blood products, chronic CHF with edema; Impedance to Right Heart Filling: Tricuspid stenosis or regurgitation, pericardial tamponade, constrictive pericarditis; Impaired Right Ventricular Outflow: Pulmonary hypertension, pulmonary embolus, pulmonic stenosis, right ventricular infarction.
Diminished venous pressure
This occurs in peripheral circulatory failure that is part of the shock syndrome, usually associated with intravascular hypovolemia, diminished venous tone and/or peripheral pooling. The peripheral veins are collapsed when the patient is supine. See the discussion of Hypotension, Chapter 4.
Giant “a” waves—tricuspid stenosis
Atrial contraction against a closed tricuspid valve produces retrograde ejection of atrial blood into the central venous channels. Intermittent prominent venous pulsations are visible in the neck veins, cannon “a” waves. They are identified as “a” waves, since they are asynchronous with the apical impulse and carotid upstroke. They are easily obliterated by gentle pressure at the base of the neck insufficient to diminish the carotid pulse. DDX: Irregular cannon “a” waves suggest that at least some atrial contractions are occurring simultaneously with ventricular contraction. A regular pattern of cannon “a” waves suggests a fixed pattern of AV block, for example, atrial flutter with 2:1 block. An irregular pattern with variable “a” wave volume suggests AV dissociation, for example, complete heart block. An ECG is required to diagnose the rhythm. Regular giant “a” waves occurring consistently in synchrony with the heart sounds and arterial pulse suggests impedance to right atrial outflow, for example, a noncompliant right ventricle or tricuspid stenosis.
Large “v” waves in the venous pulse—TR
Tricuspid insufficiency allows the right ventricle to eject blood retrograde into the central venous channels. Large “v” waves are visible in the jugular veins and there may be palpable liver pulsation. The waves are identified as “v” waves since they are synchronous with the apical impulse and carotid upstroke.
Hepatojugular reflux and Kussmaul sign
These phenomena are caused by inability of the right heart to accommodate increased venous return. Position the patient so the blood column is just visible in the jugular veins above the clavicle. With the patient breathing normally, place the right hand on the right upper abdominal quadrant and press firmly upward under the costal margin for at least 10 to 15 seconds. The hepatojugular reflux sign is present if the top of the jugular venous column in the neck rises and persists as long as the abdominal pressure is continued. Kussmaul sign is present when the jugular venous column fails to collapse during inspiration. CLINICAL OCCURRENCE: The hepatojugular reflux sign is most commonly seen with early right heart failure. Both signs may be seen with severe right heart failure, constrictive pericarditis, and right ventricular infarction [Bilchick KD, Wise RA. Paradoxical physical findings described by Kussmaul: Pulsus paradoxus and Kussmaul’s sign. Lancet. 2002;359:1940–1942; Wiese J. The abdominojugular reflux sign. Am J Med. 2000;109:59–61].
Arterial Circulation Signs
Decreased arterial blood flow causes dermal pallor, coldness, and tissue atrophy. Small-vessel disturbances are often recognizable as by their cutaneous manifestations (Examination of the Arterial Circulation in the Extremities and Chapter 6). Diseases of the larger vessels cause regional hypoperfusion syndromes; diseases affecting smaller vessels, such vasculitis, tend to be more diffuse.
Normal skin temperature indicates adequate arterial flow. The normal nailbed color is red or pink.
See Chapter 6. Embolization of cholesterol-rich atheroma to the small arteries produces hemorrhagic cutaneous infarcts and livedo.
Skin pallor and coldness—chronic arterial obstruction
Chronic progressive arterial obstruction promotes development of collateral circulation and tissue accommodation to ischemia. Pallid cool skin strongly suggests regional hypoperfusion. It is normal in a cold environment but should rapidly resolve on exposure to warm air or water. Failure to do so suggests that the problem is not limited to the skin vessels but involves a major trunk artery. Pain may be present with exertion (claudication). The distribution of the arterial deficit will depend upon the site of the obstruction and the presence and extent of collateral circulation. Other useful signs are prolonged venous filling time; abnormal pedal pulses and a femoral bruit [McGee SR, Boyko EJ. Physical examination and chronic lower-extremity ischemia: a critical review. Arch Intern Med. 1998;158:1357–1364]. CLINICAL OCCURRENCE: Atherosclerosis is most common; less common causes are large vessel vasculitis (Takayasu aortitis, giant cell arteritis (GCA)), Buerger disease, vasospastic disorders, and ergotism.
Dependent rubor and coldness—chronic arterial obstruction
Acute pain with skin pallor and coolness—arterial embolus or thrombosis
Acute occlusion of a major peripheral artery causes cutaneous and muscular ischemia producing skin and nailbed pallor, decreased temperature, and ischemic pain. The pain is severe and unremitting with changes in position. Embolic arterial occlusion is most common in native vessels, whereas thrombus is more common in prosthetic vascular channels. Urgent relief of the obstruction is necessary to preserve the part. See Acute extremity artery obstruction—embolism and arterial thrombosis. CLINICAL OCCURRENCE: The heart is the most common source for emboli (endocarditis, prosthetic valve, atrial fibrillation); less commonly, it arises from thrombus within an aortic aneurysm or paradoxical embolism via a patent foramen ovale.
Nodular vessels—polyarteritis nodosa
Chest, Cardiovascular, and Respiratory Syndromes
Chest pain intensified by respiratory motion
Pain accentuated by breathing, coughing, laughing, or sneezing usually indicates inflammation or injury to the ribs, cartilages, muscles, nerves, and pleurae of the chest wall. The specific area may also be tender, so see Chest Wall Pain with Tenderness, as there is significant overlap between these categories.
The parietal pleura has sensory fibers from the intercostal nerves that also give off twigs to the skin. The visceral pleura is anesthetic. Pleural pain is caused either by stretching of the inflamed parietal pleura or by separation of fibrous adhesions between two pleural surfaces. It is difficult to accept that pain is produced by rubbing the two pleural surfaces together: pain often occurs without a friction rub, and a rub is often present without pain. Pleural inflammation (pleuritis) produces knife-like shooting pains in the chest wall, intensified by breathing, coughing, and laughing. Listen and palpate for a friction rub; rubs are not constantly present, so repeat the examination. Pleural effusion may develop. The diagnosis of pleurisy is made from the typical pain history or the presence of a friction rub after excluding other causes of pleuritis, rib fractures, myositis, and neuritis. Pleurisy and a rub may precede radiographic evidence of pneumonia. CLINICAL OCCURRENCE: Bacterial and viral pneumonia, tuberculosis, empyema, viral pleuritis, pulmonary infarction from embolus, mesothelioma, primary and metastatic lung neoplasm, and connective tissue diseases.
Diaphragmatic pleuritis and pleurisy
The periphery of the diaphragmatic pleura is supplied by the fifth and sixth intercostal nerves, which give pain near the costal margins. The central diaphragm (thoracic and peritoneal) is innervated by the phrenic nerve (C3–4), which also innervates the neck and supraclavicular fossae. Thus, pain in the neck may result from irritation of the diaphragmatic pleura (Fig. 8-43). There is sharp shooting pain intensified by deep breathing, coughing, or laughing. Pain may be localized along the costal margins, epigastrium, lumbar region, or neck at the superior border of the trapezius or the supraclavicular fossa, always on the same side. A pleural or pericardial friction rub may be present. DDX: The diagnosis of pleurisy is suggested when pain is accompanied by fever and a friction rub; later, pleural effusion may appear. A history of dysphagia or intraabdominal disease should suggest disorders of the esophagus, subphrenic abscess, peptic ulcer, splenic infarction, splenic rupture or pancreatitis. Hiatal hernia may produce similar pain. Pericarditis with pleuritic pain (pleuropericarditis) should be considered.
Referral of Left Diaphragmatic Pain.
Epidemic pleurodynia (Bornholm disease, devil’s grip)
Infection with group B coxsackievirus is the common cause. After a nondescript prodrome, the patient is suddenly seized with sharp, knife-like thoracic or abdominal pain, intensified by breathing and movement, and accompanied by fever. The chest may be splinted and the thighs flexed on the belly. Paroxysms of intense pain are separated by intervals of complete comfort. Cases may be sporadic or epidemic. Mild pharyngitis and myalgias with tenderness of the neck, trunk, and limbs may be noted. A friction rub is detected in 25% of cases. The sudden retrosternal pain suggests MI or dissecting aneurysm. Close observation until symptoms subside is the usual method of diagnosis.
Chest wall twinge syndrome (precordial catch)
The patient experiences brief episodes of nonexertional sharp pain or “catches” in the anterior chest, usually on the left side. Some patients report onset while bending over. The pains last from seconds to minutes and are aggravated by deep breathing and relieved by shallow respirations. The cause is unknown. The condition is common and harmless.
Rib fracture, periosteal hematoma, periostitis, intercostal myositis
Rupture of a subpleural bleb or penetrating chest trauma allows air to enter the pleural space separating the lung from the chest wall leading to failure of respiratory mechanics and lung collapse. There is usually sudden severe chest pain, often unilateral and rarely localized, followed immediately by increasing dyspnea. With a large pneumothorax, the physical signs are distinctive: hyperresonant percussion, decreased fremitus, voice transmission and breath sounds on the affected side, and tracheal deviation away from the affected side (Dullness with accentuated vibration—pneumonia with lobar consolidation). Respiratory rib movements are decreased with persistent expiratory distention of the hemithorax. When tension pneumothorax develops, urgent diagnosis and treatment are necessary to prevent suffocation. With a small pneumothorax, the only sign may be decreased breath sounds. On chest X-ray, lung markings are absent and often the visceral pleura can be seen as a line. CLINICAL OCCURRENCE: Pneumothorax results from rupture of a pleural bleb in pulmonary emphysema, and, occasionally, from nonsuppurative lung disease, such as sarcoidosis, fibrosis, or silicosis. Puncture of the lung by a fractured rib is the most common traumatic cause. It is not rare in slender, healthy young persons with no discernible pulmonary lesion. The sudden pain must be distinguished from PE, MI, and acute pericarditis.
Acute infection is usually viral; less commonly, it is an atypical organism. Airway inflammation produces persistent cough and often retrosternal burning pain. Fever is absent. Secretions in the bronchi and trachea produce rhonchi and, occasionally, wheezing. Secretions high in the trachea produce rhonchi that are heard throughout the thorax. The cough may be unproductive or tenacious; mucoid sputum may be raised. Usually, there is no airway impairment, so breath sounds are normal. DDX: Influenza, parainfluenza, and RSV are common. Chest X-ray is normal.
Infection or inflammation of the lung is called pneumonitis or pneumonia. The process may be limited to the airways and alveolar airspaces or involve the pulmonary interstitium and vascular channels. The diagnostic challenges are to separate infectious from noninfectious forms of pneumonia and then to identify the specific etiology. Onset may be sudden or gradual, depending upon the etiology. Patients present with cough, dyspnea, fatigue, and, especially with infection, high fever, often with rigors. Physical findings range from minimal signs of airspace disease (bronchophony, whispered pectoriloquy) to respiratory failure with multilobar consolidation. Infectious pneumonia is separated into community-acquired or hospital-healthcare-associated categories. An approach to the diagnosis of specific etiologies of pneumonia is beyond the scope of this text [Metlay JP, Kapoor WN, Fine MJ. The rational clinical examination. Does this patient have community-acquired pneumonia? Diagnosing pneumonia by history and physical examination. JAMA. 1997;278:1440–1445; File TM. Community-acquired pneumonia. Lancet. 2003;362:1991–2001]. CLINICAL OCCURRENCE: Congenital: pulmonary sequestration (may be confused with pneumonia on chest X-ray); Idiopathic: idiopathic interstitial pneumonia, eosinophilic pneumonia (acute and chronic primary alveolar proteinosis); Inflammatory/Immune: hypersensitivity pneumonitis, vasculitis, lymphomatoid granulomatosis, Goodpasture syndrome, lipoid pneumonia, collagen vascular diseases; Infectious bacterial, viral, tuberculosis, nontuberculous mycobacteria, rickettsia, fungi, Nocardia, pneumocystis, parasites; Metabolic/Toxic: inhalational injury, drug reactions, pneumoconioses; Mechanical/Trauma: aspiration, lung contusion; Neoplastic: endobronchial neoplasm with post-obstructive infection, bronchioloalveolar cell carcinoma; Vascular: vasculitis (Churg-Strauss, Wegener).
Severe acute respiratory syndrome (SARS) and middle east respiratory syndrome (MARS). Infection with novel coronaviruses cause severe lung inflammation leading to hypoxia and respiratory failure. The SARS outbreak in 2003 originated in China and spread rapidly but was controlled. In 2012 a different coronavirus causing the same syndrome was identified in Saudi Arabia and the Near East and entered the US in 2014. The initial symptoms are those of a flu-like illness, followed by rapidly progressive pneumonia. The case fatality rate is high. Spread is by droplets. To make the diagnosis, a high index of suspicion is necessary with careful questioning about contact with infected or potentially infected people and travel to known areas of ongoing transmission. Current information is available at the Centers for Disease Control web site, www.cdc.gov.
Aspiration of oral secretions, food, or regurgitated stomach contents causes mechanical airway obstruction with secondary inflammation (especially with low pH gastric contents) and secondary infection often with anaerobic oral flora. The right middle and apical segment of the right lower lobe are commonly affected. Aspiration is common in association with impaired consciousness or swallowing. Coughing with meals and nocturnal regurgitation with cough and dyspnea are suggestive of chronic aspiration. Necrotizing anaerobic infections may lead to lung abscess with fetid sputum. Aspiration should be suspected in any patient with a history of impaired consciousness or oropharyngeal neurologic dysfunction who presents with pneumonia [Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med. 2001;344:665–671].
Infection with necrotizing organisms destroys lung tissue creating cavities with low oxygen tension, ideal for growth of microaerophilic or anaerobic organisms. A history compatible with aspiration is often present. The sputum is scant to intermittently copious, purulent, and foul smelling. Signs of consolidation may be present; amphoric breath sounds may be heard if the cavity communicates with a bronchus and is only partially filled (see Fig. 8-34). Old abscess cavities may become colonized with Aspergillus producing a fungus ball.
Bronchopleural fistula with empyema
A communication between a bronchus and the pleural cavity is usually caused by an empyema draining through a bronchus or a lung abscess invading the pleural cavity. Patients present with chronic cough producing a large volume of purulent sputum. The sudden drainage of pus into the pleural cavity produces severe prostration, chills, fever, or shock. Dullness and absent of breath sounds in lower hemithorax, with a resonant region above—the whole devoid of breath sounds—suggest the diagnosis. A succussion splash may be heard.
Pulmonary embolism. A deep vein thrombus (DVT) becomes dislodged and passes through the RA and RV into the pulmonary circulation. Large emboli obstruct the main pulmonary artery at its bifurcation or one of its branches producing acute pulmonary hypertension, right ventricular pressure overload, and failure with circulatory collapse. Infarction of lung tissue results in local inflammation. Hypoxia occurs from ventilation–perfusion mismatching and intrapulmonary shunts. DVT develops after surgery (particularly total hip and knee replacement), prolonged bed rest and air travel, immobilization, and venous stasis. Thrombophilia (factor V Leiden, prothrombin gene mutations, antiphospholipid syndrome, protein C or S deficiency, mucinous adenocarcinomas, estrogens, pregnancy, etc.) increases the risk of DVT. Less-commonly embolized material are fat (from the marrow of fractured bones), air, amniotic fluid (when the fluid contains meconium, it is especially dangerous), and tumor tissue. Patients may be minimally symptomatic or present with sudden dyspnea, chest pain, and circulatory failure. Symptoms: Sudden dyspnea, with or without pain or tachypnea, is the key symptom. The pain is either pleuritic or a deep, crushing sensation in the six-dermatome band. Sometimes painless dyspnea resembles asthma because of the release of serotonin from platelets in the blood clot. Massive pulmonary embolus may present with syncope and no other symptoms [Goldhaber SZ, Nadel ES, King ME, et al. Case 17–2004. NEJM. 2004;350:2281–2290]. Signs: Systemic effects may predominate, with weakness, prostration, sweating, nausea, and vomiting. Tachycardia is constant and fever occurs with infarction. Dyspnea, tachypnea, and cyanosis may be extreme. When present, hemoptysis, a pleural friction rub, and bloody pleural effusion strongly support the diagnosis. Massive infarction is indicated by the onset of shock, jaundice, or right-sided heart failure. Pulmonary hypertension is marked by the louder P2 and the appearance of a palpable precordial RV thrust. Sudden death is not uncommon. Occasionally, PE may be accompanied by abdominal rigidity because of the splinting of the diaphragm adjacent to infarcted lung. The clinician must have a high index of suspicion for PE and pursue the diagnosis aggressively; recurrent emboli may be fatal. Chronic recurrent pulmonary emboli lead to pulmonary hypertension [Fedullo PF, Auger WR, Kerr KM, Rubin LJ. Chronic thromboembolic pulmonary hypertension. N Engl J Med. 2001;345:1465–1472]. DDX: Sudden onset of pain in the chest or dyspnea, tachypnea, or unexplained sinus tachycardia in a patient with a predisposing condition should raise the question of PE with or without infarction. The symptoms and signs may suggest asthma, bronchopneumonia, pleurisy, pericarditis, spontaneous pneumothorax, MI, acute pancreatitis, or perforated peptic ulcer [Chunilal SD, Eikelboom JW, Attia J, et al. Does this patient have pulmonary embolism? JAMA. 2003;290:2849–2858; Douma RA, Mos ICM, Erkens, PMG, et al. Performance of 4 clinical decision rules in the diagnostic management of acute pulmonary embolism: a prospective cohort study. Ann Intern Med. 2011;154:709–718; Lucassen W, Geersing G-J, Erkens PMG, et al. Clinical decision rules for excluding pulmonary embolism: a meta-analysis. Ann Intern Med. 2011;155:448–460].
Sleep-disordered breathing—obstructive and central sleep apnea
Sleep-disordered breathing results from either mechanical obstruction by redundant, lax oropharyngeal soft tissues (obstructive sleep apnea) or from decreased medullary respiratory drive (central sleep apnea). Hypoventilation and hypoxia at night produce frequent arousals, disrupting effective sleep. Patients are often, but not always, obese. They have daytime hypersomnolence and irritability and frequently have morning headaches and hypertension; snoring is prominent but may not have been noted by the patient. History from the bed partner is critical. In severe disease, severe hypoxia leads to pulmonary hypertension and signs of right heart failure. Increased risk for obstructive sleep apnea is associated with enlarged tongue, oropharyngeal soft tissue thickening (Mallampati score of 3 or 4, Chapter 7) or neck circumference >43 cm (17 inches) in men or >40.5 cm (16 inches) in women.
Patients present with chronic irritating cough and normal physical findings. Ninety percent of cases are caused by chronic postnasal drip, unsuspected asthma, and gastroesophageal reflux; evaluation for each is required. Angiotensin-converting enzyme inhibitors also cause chronic cough, which may begin months after starting the medication.
Most primary lung cancers result from cigarette smoking or exposure to ionizing radiation. Patients present with symptoms and signs related to the chest (cough, hemoptysis, dyspnea, pneumonia, pleural effusion), regional symptoms (lymphadenopathy, SVC syndrome, brain mass) or systemic symptoms (weight loss, weakness, hypercalcemia, hyponatremia). Endobronchial lesions may present as recurrent or slowly resolving pneumonia or atelectasis. Bronchioloalveolar cell carcinoma presents with cough, hypoxia, and diffuse infiltrates, often mistaken for an infection. Early detection strategies are controversial. Superior sulcus tumors (neoplasms in the pulmonary apex, the upper mediastinum, or the superior thoracic aperture) produce Pancoast syndrome with severe pain in the neck, shoulder or down the arm [Arcasoy SM, Jett JR. Superior pulmonary sulcus tumors and Pancoast’s syndrome. N Engl J Med. 1997;337:1370–1376].
Interstitial pulmonary edema leading to alveolar flooding is caused by LV failure, MR, or acute lung injury. An acute increase in LV end-diastolic pressure is transmitted across the mitral valve to the left atrium and pulmonary veins. The increased hydrostatic pressure in the pulmonary capillaries causes transudation of fluid into the pulmonary interstitium and subsequently the alveoli. Increased fluid in the lung leads to decreased pulmonary compliance, shortness of breath, and cough. As the alveoli are flooded, hypoxia and extreme respiratory distress ensue. Intense dyspnea is accompanied by crackles, rhonchi, and gurgles throughout the lungs. Breathing is labored, with cyanosis and frothy sputum, often pink, occasionally bloody. Percussion is resonant and auscultation reveals bubbling crackles and sometimes wheezes. DDX: In chronic heart failure pulmonary edema is often relapsing making the diagnosis fairly obvious. It may occur suddenly with acute MI, especially with papillary muscle rupture and flail mitral valve leaflet. Occasionally, paroxysmal nocturnal dyspnea in cardiac patients may closely resemble asthma with a prolonged expiratory phase and wheezing. CLINICAL OCCURRENCE: Idiopathic: High altitude; Inflammatory/Immune: Mismatched blood transfusion, hypertransfusion syndrome, SLE; Metabolic/Toxic: Acute lung injury (inhalation of noxious gases, aspiration, radiation, hemorrhagic pancreatitis, sepsis, drugs, fresh water drowning, etc.), intravenous heroin, snakebite; Mechanical/Trauma: LV failure-systolic and diastolic dysfunction (MI, cardiomyopathies, tachy- and bradyarrhythmias), mitral stenosis, mitral and aortic insufficiency (especially acute), PE; Neoplastic: Bronchioloalveolar cell carcinoma (not pulmonary edema, but may appear similar radiographically), lymphangitic carcinoma or lymphoma; Neurologic: Postictal, head trauma, subarachnoid hemorrhage; Vascular: Severe hypertension, intravascular volume overload (crystalloid, colloid, transfusions, kidney failure).
Interstitial lung disease
Inflammation with cellular infiltration, interstitial edema, and/or collagen deposition leads to thickening of the alveolar walls and septa, decreased lung compliance, reduced lung volume, and impaired gas exchange. Inflammation may involve the entire alveolus; granuloma formation is characteristic of some diseases and is diagnostically important. Patients usually present with chronic nonproductive cough and dyspnea. A thorough occupational and avocational exposure history is critical in order to identify respiratory irritants, toxins, and allergens. Physical examination shows resonant percussion, decreased breath sounds, and crackles of varying intensity, often at end inspiration and usually most prominent at the bases. Chest X-ray shows increased interstitial markings, with or without alveolar signs [Gong MN, Mark EJ. Case records of the Massachusetts General Hospital. Case 40--2002. N Engl J Med. 2002;347:2149–2157]. High-resolution CT may be diagnostic with characteristic patterns for specific entities [Gross TJ, Hunninghake GW. Idiopathic pulmonary fibrosis. N Engl J Med. 2001;345:517–525; Collard HR, King TE Jr. Demystifying idiopathic interstitial pneumonia. Arch Intern Med. 2003;163:17–29]. CLINICAL OCCURRENCE: Inhaled Toxic Substances: Asbestosis, fumes and gases, aspiration pneumonia; with granulomas—hypersensitivity pneumonitis (organic dusts, e.g., farmer’s lung), inorganic dusts (beryllium, silica); Lung Injury: After acute respiratory distress syndrome, radiation; Connective Tissue Diseases: SLE, RA, ankylosing spondylitis, systemic sclerosis, CREST (calcinosis cutis, Raynaud phenomenon, esophageal motility disorder, sclerodactyly, and telangiectasia) syndrome, Sjögren syndrome, polymyositis–dermatomyositis; Pulmonary Hemorrhage Syndromes: Antibasement membrane disease (Goodpasture), idiopathic pulmonary hemosiderosis; Congenital Diseases: tuberous sclerosis, neurofibromatosis, Niemann–Pick disease, Gaucher disease; Miscellaneous: Drugs (antibiotics, amiodarone, gold, bleomycin, and other chemotherapy agents), eosinophilic pneumonia, lymphangioleiomyomatosis, amyloidosis, graft-versus-host disease, with gastrointestinal or liver disease (Crohn disease, ulcerative colitis, primary biliary cirrhosis, chronic active hepatitis); Idiopathic Interstitial Pneumonia: Idiopathic interstitial pneumonia (usual interstitial pneumonia), desquamative interstitial pneumonia, respiratory bronchiolitis-associated interstitial lung disease, acute interstitial pneumonia, cryptogenic organizing pneumonia, nonspecific interstitial pneumonia.
Exposure to organic dusts at work or home elicits a chronic inflammatory response which may progress to irreversible fibrosis. Careful history is the key to diagnosis. Patients present with cough, shortness of breath, and increasing dyspnea, often with airflow obstruction on exposure to the agent. Examination may be normal or show crackles and wheezes.
Pulmonary renal syndromes
There are antibodies to basement membrane in the glomerulus and pulmonary capillaries (Goodpasture), or vasculitis involving the lung and glomeruli (granulomatous vasculitis–Wegener). This causes pulmonary inflammation and/or hemorrhage and acute kidney injury. Goodpasture syndrome often presents acutely with dyspnea, hemoptysis, and cough. Wegener may be either acute or subacute. Limited forms of both occur. Prompt diagnosis and treatment is required to preserve kidney function.
Noncaseating granulomatous inflammation involves many organs singly or in combination. The cause is unknown. The lungs and hilar and mediastinal lymph nodes are most commonly affected. Patients may be asymptomatic or present with nonproductive cough and dyspnea accompanied by fever, malaise, weight loss, and night sweats. Lung examination may be normal or show crackles; hepatosplenomegaly, lymphadenopathy, uveitis, cutaneous plaques and salivary gland occur.
Pulmonary arteriovenous shunts enlarge with standing leading to decreased oxygen saturation (orthodeoxia) and shortness of breath. The cause appears to be circulating vasodilators usually metabolized by the liver. Patients all have advanced liver disease with portal hypertension and portosystemic shunting, with or without cirrhosis. They complain of shortness of breath and weakness with standing and may become visibly cyanotic in the upright position. Symptoms are often relieved by sitting and always by lying down; patients may become unable to sit or stand for any length of time. Physical examination shows stigmata of chronic liver disease including spider angiomata and ascites; cyanosis may be present in the upright position. Diagnosis is by bubble contrast echocardiography which shows appearance of contrast in the left atrium in more than three and less than seven cardiac cycles [Lange PA, Stoller JK. The hepatopulmonary syndrome. Ann Intern Med. 1995;122:521–529].
Tracheal or bronchial obstruction
Complete obstruction of the trachea is incompatible with life. Partial tracheal obstruction by a foreign body, neoplasm, or other plug produces forceful prolonged inspiratory effort with retraction of the intercostal spaces, suprasternal notch, supraclavicular fossae, and epigastrium. A low-pitched rhonchus, or stridor, may be heard over the chest and at the opened mouth during inspiration and expiration. In a ball-valve obstruction the rhonchus occurs only during inspiration or expiration. An isolated wheeze suggests a localized bronchial obstruction by bronchial adenoma, carcinoma, or foreign body. Bagpipe sign is another indication of partialbronchial obstruction. While listening to the chest, have the patient cut short a forced expiration; an expiratory sound continues after the patient’s effort has ceased. If the obstructive rhonchus is heard on both sides of the chest, the affected side is the one with the palpable rhonchus. In obstruction of a large bronchus, there is a pendular movement of the trachea toward the affected side during inspiration and away from it with expiration. Movement of a foreign body may cause an audible slap with coughing or breathing. Slow development of bronchial obstruction may be asymptomatic; sudden obstruction causes severe dyspnea. Higher-pitched rhonchi arise from smaller bronchi. CLINICAL OCCURRENCE: Aspirated foreign bodies, intraluminal benign neoplasms (bronchial adenoma, amyloidoma), malignant neoplasm, relapsing polychondritis, extrinsic compression from mediastinal masses (retrosternal goiter, neoplasms, teratoma), laryngeal mass or paralysis, tracheomalacia following prolonged endotracheal intubation.
Chronic obstructive pulmonary diseases
Airflow obstruction in expiration is the hallmark of asthma and chronic obstructive lung disease (COPD). The obstruction is fully reversible, at least initially, in asthma and may be either fixed or partially reversible in COPD. Expiratory airflow obstruction leads to air trapping (increased residual volume) and a sustained inspiratory position of the chest (flat diaphragm, horizontal ribs, increased anterior–posterior diameter, hyperresonance) which increases the work of breathing and decreases the inspiratory capacity. The combination of history, physical signs, chest radiographic features, and pulmonary function testing allow differentiation [Straus SE, McAlister FA, Sackett DL, et al. The accuracy of patient history, wheezing, and laryngeal measurements in diagnosing obstructive airway disease. JAMA. 2000;283:1853–1857; Holleman DR Jr, Simel DL. The rational clinical examination. Does the clinical examination predict airflow limitation? JAMA. 1995;273:313–319].
Asthma is an acquired syndrome of increased airway responsiveness to allergic and nonallergic stimuli, airway inflammation, bronchospasm, hyperplasia of mucous-producing cells, and bronchial smooth muscle hypertrophy. Airway obstruction leads to air trapping and lung hyperinflation. Asymptomatic patients may have active airway inflammation. Between attacks, the patient is well and the chest is normal. Asthma flairs begin with nonproductive cough and progressive dyspnea. Nocturnal awaking with coughing and chest tightness is common. Sitting and leaning over a table or chair back improves the dyspnea. The respiratory rate does not increase, but inspiration is short whereas expiration is prolonged and labored; the patient is often anxious. As air trapping increases, the chest becomes hyperresonant, the diaphragm flattens, and the thorax maintains the inspiratory position. The costal margins only diverge slightly, or they may actually converge during inspiration. In severe asthma attacks, the sternocleidomastoid and platysma muscles tense and the alae nasi flare with each inspiratory effort. Wheezing becomes less prominent as the attack worsens. Auscultation discloses decreased air movement, wheezes, and coarse crackles. Localized absence of breath sounds suggests bronchial plugging. As the attack subsides, clear tenacious sputum is raised, and breathing gradually becomes less labored. Asthma can occur without wheezing. The only sign that consistently identifies severe asthma is use of the accessory muscles of respiration. Clinical history and bedside or home airflow measurements are useful for assessing severity (Table 8-1) and planning management. DDX: Wheezing occurs in acute bronchitis, without the labored respiration. When wheezing is limited to a single region, bronchial obstruction from foreign body or neoplasm should be considered. The sudden occurrence of LV failure or MR may closely simulate asthma: there are wheezes and crackles, and labored breathing may limit heart auscultation. Vocal cord dysfunction (i.e., paradoxical closure of the cords during inspiration) is identified by examination of the glottis during an attack; it is suggested when the wheezes are loudest over the neck. The symptoms and signs of asthma are often relieved in a few minutes by inhaled bronchodilators; reversible airway obstruction can be demonstrated with spirometry.
TABLE 8-1Asthma Clinical Severity Classification |Favorite Table|Download (.pdf) TABLE 8-1 Asthma Clinical Severity Classification
| ||Symptoms || |
|Asthma Severity ||Day ||Night ||FEV1; Peak Expiratory Flow Variability |
|Mild intermittent ||2 or less d/wk ||2 or less nights/mo ||≥80; <20% |
|Mild persistent ||>2 d/wk ||>2 nights/mo ||≥80; 20–30% |
|Moderate persistent ||Daily ||>1 night/wk ||60–79%; >30% |
|Severe persistent ||Continual ||Frequent ||<60%; >30% |
Smoking or, rarely, alpha-1 antitrypsin deficiency leads to the destruction of alveolar walls with loss of alveolar surface area and decreased elastic recoil produces collapse with expiration. Patients present with progressive dyspnea, often accompanied by gradual weight loss. They often exhale with pursed lips, especially with exertion. The chest is hyperresonant with decreased breath sounds and prolonged expiration (Dullness with accentuated vibration—pneumonia with lobar consolidation). Wheezes and crackles are uncommon unless infection supervenes. Physical findings are poorly correlated with the severity of airflow obstruction or abnormalities of gas exchange. Early detection of obstructive airways disease in patients with symptoms or risk factors is best accomplished by spirometry. The Gold clinical staging system is now used to classify patients, see Table 8-2. Alpha-1 antitrypsin deficiency also produces liver disease that may dominate the clinical picture.
TABLE 8-2Gold Criteria for COPD Severity |Favorite Table|Download (.pdf) TABLE 8-2 Gold Criteria for COPD Severity
|Stage ||Severity ||FEV1 (% Predicted) ||FEV1/FVC |
|I ||Mild ||≥80 ||<0.7 |
|II ||Moderate ||<80 ||<0.7 |
|III ||Severe ||<50 ||<0.7 |
|IV ||Very severe ||<30 or <50 with respiratory failure or right heart failure ||<0.7 |
Chronic inflammation and secondary infection of the airways results from chronic exposure to tobacco smoke. Airways obstruction is prominent and hypoxia is common. Patients present with chronic cough with >60 mL/d of sputum (chronic bronchitis with or without bronchiectasis) and progressive dyspnea. Lung examination shows diminished breath sounds and prolongation of expiration; wheezing and inspiratory crackles may be present. Physical finding are poorly correlated with the severity of airflow obstruction or abnormalities of gas exchange.
Severe acute or chronic pulmonary infections result in multiple chronically infected dilatations of the smaller bronchi. Cough with purulent sputum and occasionally hemoptysis or recurrent pneumonia are presenting symptoms. Sputum is copious and purulent. A resonant chest with coarse basilar crackles suggests bronchiectasis. Clubbing may be present. Chronic infection with nontuberculous mycobacteria is common. High-resolution CT imaging is diagnostic [Barker AF. Bronchiectasis. N Engl J Med. 2002;346:1383–1393].
A variegated array of lymphatic cells, atypical lymphocytoid, plasmacytoid, and reticuloendothelial cells invade various tissues and vessels. Nodules of various sizes occur in the lungs, skin, kidneys, and central nervous system; the spleen, lymph nodes, and bone marrow are usually spared. In contrast with Wegener granulomatosis, the lung is always involved but the upper respiratory tract is seldom involved. Transition to malignant lymphoma is common.
Fourfold diagnosis of heart disease
Proper assessment of patients with heart disease requires a fourfold description: the etiology, anatomic abnormalities, physiologic disorders, and functional capacity. A formal statement of the diagnosis is as follows: “rheumatic heart disease, inactive; mitral stenosis, right ventricular hypertrophy and dilatation, pulmonary congestion; atrial fibrillation; functional class II.”
Common etiologies are congenital (genetic and developmental), infectious, rheumatic, hypertensive, and ischemic.
Abnormalities of the aorta and pulmonary arteries, coronary arteries, endocardium and valves, myocardium, and pericardium are listed. Congenital anatomic abnormalities are listed as either cyanotic or noncyanotic (i.e., with or without significant right-to-left shunt).
Disturbances in cardiac rhythm and conduction, myocardial, systolic or diastolic dysfunction, and clinical syndrome (e.g., anginal syndrome, CHF, cardiac tamponade) are listed.
Two commonly used functional classification systems are:
New York Heart Association (for classification of angina or dyspnea)
Class I (No Incapacity). Although the patient has heart disease, the functional capacity is not sufficiently impaired to produce symptoms.
Class II (Slight Limitation). The patient is comfortable at rest and with mild exertion. Symptoms occur only with more strenuous activity.
Class III (Incapacity With Slight Exertion). The patient is comfortable at rest but dyspnea, fatigue, palpitation, or angina appears with slight exertion.
Class IV (Incapacity With Rest). The slightest exertion invariably produces symptoms, and symptoms frequently occur at rest.
Canadian Cardiovascular Society (use restricted to patients with angina)
Class I. No angina with ordinary activity but angina occurs with strenuous or rapid or prolonged exertion.
Class II. Slight limitation of ordinary activity (e.g., walking more than two level blocks or climbing more than one flight of stairs at a normal pace).
Class III. Marked limitation of ordinary activity (walking one to two blocks on the level and climbing one flight of stairs).
Class IV. Inability to carry on any physical activity without angina; angina may also be present at rest.
Six-dermatome pain syndromes
Myocardial Ischemia Six-Dermatome Pain Syndromes
Angina is caused by a reversible increase in local myocardial oxygen demand exceeding supply. Angina may result from inadequate oxygen supply, excessive demand, or a combination of both. Abnormalities of oxygen delivery can be best remembered by rearrangement of the Fick equation: MVO2 = (coronary blood flow) × (myocardial arteriovenous oxygen difference). Because the arteriovenous oxygen difference is nearly maximal at rest, inadequate oxygen delivery is most likely caused by inadequate coronary flow. Flow is directly proportional to the pressure gradient across the coronary bed (aortic diastolic minus coronary sinus pressure) and inversely proportional to resistance in the coronary arteries. The most common cause of impaired oxygen delivery is coronary artery obstruction caused by atherosclerotic narrowing. Cold or exertion induced vasospasm may be superimposed. Increased myocardial oxygen demand is caused by increases in heart rate, myocardial contractility, ventricular systolic pressure, and/or ventricular cavity radius. The increase in oxygen demand occurs whether or not there is a change in cardiac output or stroke volume. Angina pectoris is a deep, steady pain or discomfort lasting 1 to 10 minutes in the six-dermatome region and often accompanied by shortness of breath, anxiety, and diaphoresis. It is classically precipitated by exercise or anxiety and relieved by rest. Other precipitants are related to the cause of increased myocardial oxygen demand: clinically important examples of increased rate work are sinus tachycardia and atrial or ventricular tachycardias; digitalis, other inotropic agents and anxiety increased contractility; hypertension and aortic stenosis increase systolic LV pressure; and aortic regurgitation and systolic heart failure increase LV radius. Stable angina is reproducible, does not awaken the patient at night, or occur at rest without significant provocation [Chun AA, McGee SR. Bedside diagnosis of CAD: a systematic review. Am J Med. 2004;117:334–343]. PQRST: Provocation Stable angina has several classic provocations. (1) Exertion. An important characteristic of exertional angina is the lag period before the pain begins, and again, before it subsides with rest. Exertional pain without a lag period suggests another etiology; (2) Postprandial. Exertion after a heavy meal is especially an issue; (3) Intense emotion. Fear, anxiety, and sexual desire increase heart rate, blood pressure, and contractility; (4) Cold. Peripheral vasoconstriction and increased blood pressure and heart rate may play a role; (5) Positive inotropic or chronotropic drug effects. Caffeine, amphetamines, and cocaine increase the heart rate and blood pressure; (6) Anemia. Oxygen delivery is reduced when the hemoglobin is less than 10 g/dL. Palliation: Rest, a warm environment, and nitroglycerin may each relieve an angina attack. Complete relief of pain or other discomfort in the six-dermatome band after the administration of nitroglycerin is strongly suggestive of angina pectoris but it is not diagnostic. The pain of esophageal spasm may also respond to nitroglycerin. If headache or flushing occurs without pain relief, stable angina is unlikely. Quality: Angina is usually described as crushing, aching, or a sense of tightness or pressure, frequently illustrated by clenching the fist over the sternum, the Levine sign. Region–Radiation: The pain may occur anywhere in the six-dermatome band. Often it is most intense behind the sternum or in the precordium, radiating upward into the neck or throat, or down the medial aspect of either arm. Ischemia in the right coronary artery distribution may radiate to the interscapular region of the back. Less frequently, the pain is felt in the spine or right shoulder and arm. The rare patient complains of pain in the limbs or neck exclusively, denying chest pain. Severity: Pain may be mild, moderate, or severe and sometimes causing a sense of impending death. Timing: The pain is continuous, not fleeting or lancinating usually lasting from 1 to 10 minutes. Physical Signs: No physical findings may be present. S4 frequently occurs during angina because of decreased compliance of the ischemic ventricle. Less commonly, an S3 may appear. If papillary muscle ischemia occurs, an apical systolic mitral insufficiency murmur may be heard. A precordial bulge or apical thrust because of LV dyskinesia may be palpated. DDX: Anginal attacks are brief (<10 minutes), which usually excludes MI, dissecting aneurysm, PE, and neoplasm. Atherosclerotic CAD is the most common cause, but less common causes of reduced coronary flow include vasculitis, aortic regurgitation, LV hypertrophy, anemia, and hypoxemia. Pain with swallowing and a sensation of food sticking suggest an esophageal source. The supine position often initiates gastroesophageal reflux pain. Pain from cholecystitis often occurs after meals but without concurrent exertion; epigastric and/or right upper quadrant tenderness support gallbladder disease. When walking induces pains in the shoulder girdle or spine, as well as the chest, and there is no lag period, musculoskeletal pain is favored. Angina is clinically classified as follows:
Typical, or definite, angina
(1) Substernal chest discomfort with the characteristic quality and duration that is (2) provoked by exertion or emotional stress and (3) relieved by rest or nitroglycerin.
Atypical, or probable, angina
It meets two of the three characteristics listed above.
It meets one or none of the typical angina characteristics.
Variant angina pectoris (Prinzmetal angina)
Coronary artery spasm with ST-segment elevations occurs with or without angiographically detectable coronary narrowing. The pain quality and location resemble classic angina, but it occurs at rest. The pain recurs in cycles, often at the same time each day. ST segments on ECG are transiently elevated during pain suggesting myocardial injury. Pain is relieved promptly by nitroglycerin. Migraine and Raynaud phenomenon occur more commonly in patients with variant angina.
Acute coronary syndromes: unstable angina and MI
There is almost always disruption of the endothelium overlying an atherosclerotic coronary plaque, exposing the plaque contents to platelets and procoagulants, initiating formation of a platelet plug, a fibrin clot, and release of vasoconstrictor substances resulting in intermittent or fixed arterial obstruction. Myocardial necrosis occurs with prolonged severe ischemia. Lesser degrees of ischemia result in unstable angina syndromes and myocardial hibernation (decreased contractile function without pain or necrosis). Less-common causes of acute coronary syndromes are coronary artery embolism and vasculitis. The transition from severe ischemia to infarction is gradual and depends upon the collateral coronary flow to the ischemic area, the contractile state of the myocardium, and the previous history of that myocardium. Myocardium subjected to repeated episodes of ischemia (stable angina) is relatively less susceptible to infarction.
Unstable angina. Patients present with classic anginal pain that is new in onset, worsening in severity (more easily provoked and/or more difficult to relieve, lasting >15 minutes), occurring at rest or awakening the patient from sleep but is not associated with evidence of myocardial necrosis. These syndromes are best described as unstable angina with a detailed description of the unstable pattern, for example, prolonged pain, occurring at rest, and increasing frequency. A substantial number of patients, although a minority, will develop an acute MI if untreated.
The TIMI Risk Score is used to estimate risk for rapid evolution to acute ST-elevation MI in patients with unstable angina and non-ST-elevation acute MI. Give 1 point each for age ≥65 years, ≥3 traditional risk factors (CAD family history, hypertension, hypercholesterolemia, diabetes, current smoker), known ≥50% coronary stenosis, ST-segment changes, ≥2 anginal episodes in the preceding 24 hours, aspirin use in the last 7 days and elevated CK or troponin. Scores of 0 to 2 are low risk, 3 to 4 intermediate risk, and ≥5 are high risk.
Acute MI. MI occurs most commonly from the early morning hours to midday. The pain is usually not induced by exertion, nor does it remit with rest. The discomfort is identical to angina pectoris in its quality, location, intensity, and constancy, but it lasts from 20 minutes to several hours. In some cases, the pain quickly increases to an intensity seldom experienced with angina; this may be sustained for hours, after which the pain subsides to a dull ache that can last for days. The patient often complains of shortness of breath that may be related to increased LV end-diastolic pressure, depressed systolic function, or mitral insufficiency caused by papillary muscle dysfunction. Nausea and vomiting are common, particularly with inferior wall infarction. A sympathetic response is triggered with sweating, pallor, and cold moist skin. The heart rate may be slow, normal, or accelerated; similarly, blood pressure may be low, normal, or quite elevated. An S4 may be heard; the heart sounds often become muted. Crackles may appear at the lung bases. Cardiac rhythms requiring immediate therapy may occur at any time. A pericardial friction rub appears in approximately 15% > 24 hours after onset of the MI. Occasionally, MI is painless and the diagnosis is suggested by the associated symptoms and signs. Large infarcts produce rapid progression to shock, cardiac failure, and death. DDX: Simple angina is excluded by the longer pain duration and unresponsiveness to nitroglycerin. Three potentially life-threatening disorders may closely mimic the pain and presentation of MI: massive, central PE (Post-cardiotomy syndrome), acute dissection of the thoracic aorta (Post-cardiotomy syndrome), and acute pericarditis (Post-cardiotomy syndrome). The clear lung fields by physical examination and chest X-ray in the setting of marked dyspnea and hypotension suggest PE rather than MI. Pain from dissection may be more excruciating and reach peak intensity more rapidly than MI. Prominent pain in the back makes dissection more likely, however, pain radiation to the back occurs with MI and may be absent with dissection. Development of an aortic diastolic murmur transmitted, down the right sternal border, and/or asymmetrical pulses or blood pressures between extremities, suggests dissection as does a widened superior mediastinum on chest X-ray. The pain of acute pericarditis may be severe and resemble MI; the pain may be intensified by reclining, breathing or swallowing. Adding potential confusion is the fact that pericarditis can be a sequel of MI [Panju AA, Hemmelgarn BR, Guyatt GH, Simel DL. The rational clinical examination. Is this patient having a myocardial infarction? JAMA. 1998;280:1256–1263; Goldman L, Kirtane AJ. Triage of patients with acute chest pain and possible cardiac ischemia: the elusive search for diagnostic perfection. Ann Intern Med. 2003;139:987–995].
Current recommended terminology for MI (necrosis documented by elevated cardiac biomarkers such as troponin) is based on the EKG interpretation. Those presenting with ST elevations are termed ST elevation infarctions (STEMI). Most of these will go on to form Q waves, so that the infarction is then also called a Q-wave MI. If no Q forms, the term non-Q-wave MI is then applied. If no ST elevation occurs, the term non-ST elevation MI (NSTEMI) is applied. Most of these do not form Q waves, and the term non-Q-wave MI is then also applied. If a Q wave does appear, then the infarction is also labeled as a Q-wave infarction.
Inflammatory Six-Dermatome Pain Syndromes
The visceral pericardium and the inner surface of the parietal pericardium are anesthetic (Fig. 8-44), but the outer surface of the lower parietal pericardium is pain sensitive. The parietal pleura surrounds the anterior and lateral pericardium, accounting for pleural involvement from pericarditis. Inflammation of the esophagus and phrenic nerves, because of their close proximity, causes dysphagia and phrenic pain. All these structures are innervated by fibers from the vagus and six-dermatome band. Phrenic nerve sensory fibers from the central diaphragm can be irritated in the lower pericardium causing neck pain at the superior border of the trapezius. Symptoms: Deep constant or pleuritic pain occurs in the six-dermatome band or the phrenic distribution. The location and quality of pain often resembles that of MI, but it is usually accentuated by breathing or coughing, worse in recumbency, and lessened while sitting and leaning forward. It may be intensified by swallowing. Pleuritic pain referred to the shoulder, particularly the left trapezius ridge, is quite suggestive of pericarditis (Fig. 8-43). The pain may last for hours; it is not relieved by nitroglycerin. Rarely, the pain is throbbing and synchronous with the heart beat. Signs: Fever may follow the onset of pain. A transient pericardial friction rub is often heard. ECG: Widespread ST elevation followed by T wave inversion is diagnostic. The ST-T findings of pericarditis must be differentiated from the injury currents of infarction and normal early repolarization. DDX: Pericarditis can result from almost any infectious agent, malignancy, rheumatic fever, collagen vascular diseases, trauma, uremia, or following MI or chest radiation. Until a pericardial friction rub appears or ECG signs develop, the steady pain suggests MI, dissecting aneurysm, pulmonary infarction, cholecystitis, or peptic ulcer. Pain on swallowing may suggest an esophageal lesion. The pleural pain must be distinguished from that of pleurisy, subphrenic abscess, and splenic infarction [Spodick DH. Acute pericarditis: current concepts and practice. JAMA. 2003;289:1150–1153].
A transverse section of the lower thorax with anesthetic serosal surfaces represented by heavy beaded lines and pain-sensitive surfaces by lighter beaded lines. Note the proximity of the phrenic nerves and esophagus to the parietal pericardium, so pericarditis can produce pain in the phrenic nerve distribution or pain on swallowing.
A hypersensitivity reaction to antigen derived from injured myocardium occurs several weeks after MI, cardiac surgery, or other heart injury. Findings are fever, pericarditis, pleuritis, pericardial and/or pleural effusions, and pneumonitis. Recurrences are common, usually with decreasing severity. The symptoms often respond dramatically to NSAIDs. Recurrent MI should be considered in patients with ischemic heart disease. The appearance of a pericardial friction rub and absence of new Q waves or ST-segment depressions on ECG help distinguish post-cardiotomy (Dressler) syndrome from recurrent MI.
Mediastinal and Vascular Six-Dermatome Pain Syndromes
Cystic medial necrosis and intramural hemorrhage lead to intimal rupture; intimal tears may be the primary event. The intimal tear occurs most commonly in the lateral wall of the proximal ascending aorta, or, less commonly, just distal to the ligamentum arteriosum in the descending aorta.Luminal blood penetrates the weakened media producing a hematoma that splits the vessel wall. Distal progression sequentially occludes aortic branches causing distal ischemia. A second intimal tear may occur distally providing egress from the false lumen; thus the aorta may consist of two concentric tubes, a double-barreled aorta. There is progressive diminution of pulses in the aortic branches and loss of specific nerve functions. Symptoms: In 80% of cases, the onset is sudden, with excruciating pain in the precordium and/or the interscapular region that may move successively to the lower back, abdomen, hips, and thighs. The pain often suggests MI. Sometimes the onset is gradual and without chest pain. Signs: Blood pressure is usually unaffected. Hypotension and collapse occur with rupture into the pericardium or left pleural space. Proximal Progression: When the hematoma extends proximally from a tear in the aortic arch, it may: (1) distort the aortic valve ring separating the commissures and causing aortic regurgitation, the murmur often transmits down the right sternal border; (2) occlude the coronary ostia and cause an MI; (3) produce hemopericardium with a pericardial rub and cardiac tamponade; or (4) swell the base of the aorta, causing a pulsating sternoclavicular joint. Distal Progression: When the hematoma extends away from the heart there is sequential asymmetrical decrease or loss of pulses in aortic branches and signs of nervous system injury. Carotid occlusion causes cerebral ischemia with localizing neurologic signs. Obstruction of the spinal arteries is indicated by paraplegia and anesthesia. Renal artery occlusion with infarction causes pain simulating renal colic. Aortic dissection may be rapidly fatal [Klompas M. The rational clinical examination. Does this patient have an acute thoracic aortic dissection? JAMA. 2002;287:2262–2272]. Chest X-ray: Widening of the aorta, an enlarged aortic knob or separation of calcified intimal plaques from the outer border of the aortic wall all suggest dissection. Imaging studies should be performed urgently when dissection is suspected. DDX: Most commonly, dissection occurs in association with cystic medial necrosis of the aorta, especially in patients with Marfan and Ehlers–Danlos syndromes. It occurs with less frequency in patients with hypertension, advancing age, during labor, and after penetrating or blunt trauma. Dissection may occur in a thoracic aortic aneurysm afflicted with aortitis from bacteria, syphilis, or GCA.
Leakage and rupture of aortic aneurysm. Expansion of aneurysms is usually painless, but breach of the wall with leakage of blood into the surrounding tissue is accompanied by the sudden onset of severe pain at the site of leakage or radiating into the body wall at that spinal segment. The pain is often accompanied by restlessness, diaphoresis, and tachycardia. The specific pain pattern reflects the site of leakage. Urgent evaluation and surgery is life saving. Complete rupture presents as sudden severe pain followed shortly by refractory hypotension and death.
Mediastinal masses rarely cause chest pain. Most attract attention by compression of normal structures or are found incidentally on chest X-ray. Signs suggesting mediastinal tumors are dyspnea from retrosternal goiter, hoarseness, and brassy cough from compression of the recurrent laryngeal nerve, Horner syndrome (unilateral ptosis, miosis, and anhidrosis) from involvement of the superior cervical ganglion, edema of the arms and neck with cyanosis from obstruction of the SVC, and chylous pleural effusion. Lymph nodes are enlarged in Hodgkin disease, non-Hodgkin lymphoma, carcinoma, germ cell tumors, or tuberculosis. Other locations of neoplastic tissue are retrosternal goiter, thymoma, and teratoma (dermoid cyst). When a dermoid forms a tracheal fistula, it may produce trichoptysis, coughing up of hair.
Gastrointestinal Six-Dermatome Pain Syndromes
Spontaneous esophageal rupture—Boerhaave syndrome. Forceful vomiting is suddenly accompanied by chest or upper abdominal pain and severe dyspnea. Subcutaneous emphysema may appear in the supraclavicular fossae along with a precordial crunching sound indicating mediastinal emphysema (Hamman sign). DDX: The symptoms are common to MI, perforated peptic ulcer, cholecystitis, pancreatitis, esophagitis, hepatitis, nonperforating ulcer, and pneumonia. Demonstration of mediastinal emphysema excludes all the foregoing in favor of ruptured esophagus.
Six-dermatome pain with dysphagia
Although lesions below the diaphragm usually produce abdominal pain, frequent exceptions make it imperative to consider subphrenic disorders with six-dermatome band pain. It is dangerous to the patient and embarrassing to the physician to overlook this possibility. Subphrenic abscess, acute cholecystitis, peptic ulcer, acute pancreatitis, and splenic infarction need to be considered.
Pulmonary Six-Dermatome Pain Syndromes
Pulmonary artery embolism and pulmonary infarction
Other Cardiovascular Syndromes
Dilatation of heart chambers is caused by either poor systolic function or chronic volume overload. The dilated heart of trained athletes accommodates a larger stroke volume maintaining a high cardiac output at relatively low heart rates, thereby minimizing myocardial oxygen demand. Heart enlargement detectable by physical examination (apical impulse and borders of cardiac dullness) or chest radiograph implies dilatation of a cardiac chamber. The elongated fibers of the dilated heart with depressed contractility produce a weak apical impulse, which may be more diffuse than normal. Displacement of the apical impulse to the left with a normal right heart border suggests LV dilation. DDX: Pericardial effusions will enlarge the heart silhouette and borders of dullness, but the apical impulse is usually undetectable and the heart sounds are diminished. CLINICAL OCCURRENCE: Left Ventricular Dilation: Aortic insufficiency, mitral insufficiency, ischemic cardiomyopathy, after MI, dilated cardiomyopathy, viral myocarditis; Right Ventricular Dilation: Pulmonic insufficiency, tricuspid insufficiency, ASD with left-to-right shunt, right ventricular infarction, pulmonary hypertension with right ventricular failure.
Hypertrophy occurs with or without dilation because of pressure and/or volume overload or hypertrophic cardiomyopathy. Hypertrophied LV myocardium produces a more powerful apical impulse than normal. Physical examination findings of heart enlargement are not present without concomitant dilation (Fig. 8-45). A palpable thrust along the left sternal edge, over the right ventricle, may be produced by right ventricular hypertrophy. CLINICAL OCCURRENCE: LV Hypertrophy: Valvular aortic stenosis, mitral or aortic insufficiency, hypertension, hypertrophic cardiomyopathy; Right Ventricular Hypertrophy: Pulmonic stenosis, ASD, pulmonary hypertension, hypertrophic cardiomyopathy.
Contribution of Myocardial Hypertrophy to the Area of Cardiac Dullness
Without dilatation of the chambers, concentric hypertrophy of the cardiac muscle to twice its normal thickness and weight cannot cause enough increase in an area of cardiac dullness to exceed the width of the percussing finger. Therefore, increase in the area of dullness must be attributed to dilatation when pericardial effusion is excluded.
Congestive heart failure (CHF)
Classically, decreased LV contractility leads to increased left ventricular end-diastolic pressure and LV dilation, maintaining higher stroke volume at the expense of left atrial hypertension and dilation and distention of the pulmonary veins. Decreased cardiac output with renal hypoperfusion leads to retention of salt and water, weight gain, and edema. The ventricular ejection fraction is low when systolic function is impaired but not when congestion is principally caused by diastolic dysfunction, that is, decreased diastolic compliance. Symptoms and signs are attributable to decreased cardiac output and volume expansion with pulmonary and peripheral vascular congestion. Early symptoms of LV failure are pulmonary congestion with dyspnea, orthopnea, nocturia, and cough. Crackles are heard in the lung bases. Retrograde congestion causes right-ventricular failure with elevated CVP, indicated by engorged jugular veins [Butman SM, Ewy GA, Standen JR, et al. Bedside cardiovascular examination in patients with severe chronic heart failure: importance of rest or inducible jugular venous distension. J Am Coll Cardiol. 1993;22:968–974; Dosh SA. Diagnosis of heart failure in adults. Am Fam Physician. 2004;70:2145–2152]. Even before the increase in CVP, a hepatojugular reflux sign can be demonstrated. Frequently an S3 develops [Drazner MH, Rame JE, Stevenson LW, Dries DL. Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure. N Engl J Med. 2001;345:574–581; Marcus GM, Gerber IL, et al. Association between phonocardiographic third and fourth heart sounds and objective measures of left ventricular function. JAMA. 2005;293:2238–2244; Badgett RG, Lucey CR, Mulrow CD. The rational clinical examination. Can the clinical examination diagnose left-sided heart failure in adults? JAMA. 1997;277:1712–1719; Wang CS, Fitz Gerald JM, Schulzer M, et al. Does this dyspneic patient in the emergency department have congestive heart failure? JAMA. 2005;294:1944–1956]. Arterial pressure response to the Valsalva maneuver correlates inversely with the left ventricular filling pressure; absence of the normal “overshoot” of systolic pressure following release the Valsalva and failure of the BP to drop during the breath hold suggest increasing LV filling pressure [Felker GM, Cuculich PS, Gheorghiade M. The Valsalva maneuver: a bedside “biomarker” for heart failure. Am J Med. 2006;119:117–122]. With biventricular failure, the liver becomes large, tender, and painful. Chronic congestive hepatomegaly may produce capsular and parenchymal fibrosis without tenderness. Edema accumulates as right-sided or bilateral hydrothorax, ascites, and pitting edema of the ankles, legs, genitals, and abdomen. The lips, ears, and nail beds may be cyanotic. Impaired cerebral circulation may result in confusion and periodic breathing. Physical examination findings have independent prognostic value [Marantz PR, Tobin JN, Wassertheil Smoller S, et al. Prognosis in ischemic heart disease. Can you tell as much at the bedside as in the nuclear laboratory? Arch Intern Med. 1992;152:2433–2437]. DDX: Portal hypertension may present similarly except that the patient does not have orthopnea or elevated jugular venous pressure. Metastasis from carcinoma may produce fluid in the abdominal and thoracic cavities with a distribution similar to that in cardiac failure [Jessup M, Brozena S. Heart failure. N Engl J Med. 2003;348:2007–2018]. CLINICAL OCCURRENCE: The most common cause is chronic ischemic heart disease. Dilated cardiomyopathy (pregnancy and postpartum, alcohol, hemochromatosis, idiopathic, secondary to viral infections) is also common, especially in younger patients. Diastolic heart failure is common in longstanding hypertension with LVH and hypertrophic cardiomyopathies. Restrictive cardiomyopathy may result from amyloidosis, hemochromatosis, sarcoidosis, and other infiltrative diseases.
The American College of Cardiology and the American Heart Association developed a heart failure staging system in 2006 [ACC/AHA guideline update for the diagnosis and management of chronic heart failure in the adult. J Am Coll Cardiol. 2005;46:1116–1143 or Circulation. 2005;112:1825–1852].
Stage A: Patients at high risk for heart failure but without structural heart disease or symptoms of heart failure.
Stage B: Patients with structural heart disease but without signs or symptoms of heart failure.
Stage C: Patients with structural heart disease with prior or current symptoms of heart disease.
Stage D: Patients with refractory heart failure (symptoms at rest despite maximal medical therapy) requiring specialized intervention.
Patients once assigned to a given heart failure stage cannot be reclassified to an earlier stage, for example, reverting back from Stage C to Stage B. This is in contrast to the New York Heart Association and Canadian Cardiovascular Society classifications where patients may move from any class to another as symptoms change.
Right ventricular failure and cor pulmonale
Right ventricular failure occurs because of damage to the myocardium, volume overload, and/or pressure overload of the right ventricle. The right and left ventricles function so primary LV failure may be accompanied by some degree of RV failure. When the CVP exceeds 22 cm, the liver enlarges; above 25 cm, there are ascites, edema, and orthopnea. The venous pressure is always high with RV failure, but it falls before other signs of failure resolve. The most frequent cause of right ventricular failure is advanced ischemic heart disease. Right ventricular failure caused by primary pulmonary disease is called cor pulmonale. It occurs as a consequence of pulmonary hypertension resulting from hypoxia induced vasoconstriction or obliteration of the pulmonary vascular bed. CLINICAL OCCURRENCE: Impaired Myocardial Function: Ischemic heart disease (especially right ventricular infarction), hypertrophic and dilated cardiomyopathies, endomyocardial fibrosis (e.g., drugs, carcinoid syndrome), restrictive myocardial disease (e.g., amyloidosis); Volume Overload: TR, ASD with left-to-right shunt, pulmonic insufficiency; Pressure Overload: Primary pulmonary hypertension, secondary pulmonary hypertension—cor pulmonale (hypoxia caused by emphysema, cystic fibrosis, interstitial pulmonary diseases, pneumoconioses, hypersensitivity pneumonitis, pulmonary fibrosis, etc.), pulmonary embolus, pulmonic stenosis, Eisenmenger complex, mitral stenosis, pulmonary veno-occlusive disease.
Cardiac output is limited by impedance to ventricular filling as a result of decreased diastolic compliance leading to elevated ventricular end-diastolic pressure. Systolic function is preserved. Patients present with dyspnea exacerbated by exertion and intermittent pulmonary congestion. Signs of right ventricular failure with edema, elevated CVP, and ascites may predominate. The heart is not enlarged. S4 gallops are common. Causes are ventricular diastolic dysfunction, infiltrative disease of the heart (amyloid, sarcoid, hemochromatosis), and endomyocardial fibroelastosis. DDX: This must be distinguished from hypertrophic cardiomyopathy and constrictive pericarditis.
Inherited defects of myocardial contractile proteins lead to progressive hypertrophy, disorganization of myocardial architecture, impaired diastolic relaxation, ventricular conduction abnormalities, and dysrhythmias. Asymmetric septal hypertrophy may produce dynamic obstruction to LV outflow during early systole. A family history of sudden death is common. Patients present with dyspnea, angina, and presyncope. Carotid upstrokes are brisk and may show a bisferiens pattern. An S4 is common. A characteristic murmur, augmented with Valsalva, is heard with outflow obstruction (Hypertrophic obstructive cardiomyopathy (IHSS)). Echocardiography is diagnostic.
Heart valve infection leads to fibrin-platelet vegetations harboring the organism. Low virulence organisms (e.g., viridans streptococci, HACEK organisms) present with subacute disease; high virulence organisms (e.g., Staphylococcus aureus, fungi) present with acute symptoms and rapid valvular destruction with or without systemic emboli. Subacute Bacterial Endocarditis: Patients present with subacute or chronic fever, weight loss, arthralgia, myalgias, and signs of immune complex disease. Acute Endocarditis: Patients, often with a history of injection drug use, have fever and rigors. Peripheral emboli with organ infarction and metastatic infection are common. Systemic illness, especially with a new insufficiency murmur, should always trigger an endocarditis evaluation. The Duke criteria are sensitive and specific for diagnosis [Durack DT, Lukas AS, Bright DK. New criteria for diagnosis of infective endocarditis. Am J Med. 1994;96:200–209].
Nonbacterial thrombotic endocarditis (NBTE)
Nonbacterial thrombotic endocarditis (NBTE) results from endocardial inflammation with sterile vegetations. Multiple large emboli suggest marantic endocarditis associated with occult neoplasms, most often a mucin-secreting adenocarcinoma. Libman–Sacks lesions occur on the valves and endocardium of patients with SLE and antiphospholipid syndrome. Patients may be asymptomatic, have peripheral emboli, or present with progressive valvular stenosis or regurgitation.
These clinical conditions are discussed with their physical findings under the sections Cardiovascular Signs and Auscultation of Heart Murmurs.
Many patients with congenital heart disease are surviving well into adult life. All clinicians should be familiar with the more common syndromes. ASDs and small VSDs may be asymptomatic for decades and elude diagnosis well into adult life.
Ventricular septal defect
Persistent ductus arteriosus
An intra or extra-cardiac left-to-right shunt between the pulmonary and arterial circulation creates chronic volume and/or pressure overload of the right ventricle and pulmonary arteries leading to severe pulmonary hypertension and, left untreated, reversal of flow into a right-to-left shunt with peripheral hypoxemia and cyanosis. The RV and PA respond with hypertrophy and fibromuscular hyperplasia, respectively. This should be suspected when valvular signs are coupled with cyanosis, decreased oxygen saturation not relieved with 100% oxygen, right-to-left shunt, clubbing of the fingers and/or toes, and polycythemia.
The components of the tetralogy are a VSD, obstruction to right ventricular outflow (usually infundibular pulmonic stenosis), an overriding aorta, and right ventricular hypertrophy (Fig. 8-41D).
There is congenital tricuspid deformity with small thin cusps; a portion of the valve originates below the AV ring, producing an “atrialized” portion of the right ventricle. Tricuspid insufficiency is not prominent; dysrhythmias are common.
Sudden cardiac death—cardiac arrest. Cardiac arrest demands immediate treatment for any chance of survival. For 25% of patients, sudden cardiac death is the first symptom of severe CAD. Less-common causes are hypertrophic cardiomyopathy (especially in young male athletes), coronary artery emboli, right ventricular dysplasia, Brugada syndrome, long QT syndrome, and anomalous coronary artery anatomy. Public education seeks to teach all adults in basic cardiopulmonary resuscitation. Increasingly, automated defibrillators are present in public places to reverse fatal ventricular arrhythmias. All health care personnel should be trained in basic cardiopulmonary resuscitation; nurses and physicians should be trained in advanced cardiac life support.
Fluid accumulates within the pericardial sac because of infection, inflammation, malignancy, or transudation. Slowly accumulating fluid distends the pericardium compressing surrounding lung; rapidly accumulating fluid is more likely to compress the heart chambers producing tamponade. Symptoms may be absent or will reflect the etiology (e.g., pain and fever with pericarditis; weakness, nausea and anorexia with uremia) or the hemodynamic consequences (e.g., shortness of breath and fatigue with tamponade). Signs include absent precordial impulse, decreased intensity and/or muffling of heart sounds, and low voltage ECG; a rub may be present. Ewart sign is dullness at the left scapular tip because of left lower lobe atelectasis from large effusions. CLINICAL OCCURRENCE: Congenital: Familial Mediterranean fever, familial pericarditis; Endocrine: Hypothyroidism; Idiopathic: Sarcoidosis; Inflammatory/Immune: Rheumatic fever, SLE, RA, anky-losing spondylitis, scleroderma, Wegner, drug reactions; Infectious: Bacterial, viral, tuberculosis, fungal, Whipple; Metabolic/Toxic: Drug-induced, uremia; Mechanical/Trauma: Trauma, post-pericardiotomy, post-irradiation; Neoplastic: Metastatic carcinoma, especially lung and breast, lymphoma; Vascular: MI, aortic dissection with rupture into the pericardium, chylopericardium, vasculitis.
Progressive pericardial fibrosis leads to restricted diastolic filling and decreased cardiac output. Symptoms are shortness of breath and fatigue. Signs are those of right heart failure: jugular venous distention, edema, ascites, and hepatic congestion. The initial pericardial injury is caused by pericarditis (viral, tuberculous, neoplasm), cardiac surgery, mediastinal irradiation, and uremia [Wang A, Bashore TM. Undercover and overlooked. N Engl J Med. 2004;351:1014–1019]. DDX: It must be distinguished from restrictive cardiomyopathies and right ventricular failure.
Rapid or massive pericardial fluid accumulation leads to compression of the heart impairing diastolic atrial and ventricular filling. Cardiac output falls and CVP is elevated. Patients complain of shortness of breath and fatigue that may rapidly progress to hypotension and circulatory collapse. The key physical signs are an elevated CVP with clear lung fields, no stigmata of chronic right ventricular failure, and a drop in systolic blood pressure during inspiration of >10 mm Hg (paradoxical pulse and Fig. 8-42). Pulsus paradoxus may not be found in the presence of aortic insufficiency, left or right ventricular hypertrophy, or pulmonary hypertension. The heart size is usually normal by examination and chest X-ray. Suspected tamponade must be urgently evaluated by echocardiography. DDX: Easily confused with tamponade are acute PE, right ventricular infarction, constrictive pericarditis, and restrictive cardiomyopathy.
Disorders of the Arterial and Venous Circulations
Large vessel vasculitides are of unknown etiology. Vasculitis of medium-sized arteries may be associated with infection (polyarteritis nodosa with hepatitis B and C) or specific immunologic markers (granulomatosis with polyangiitis with c-ANCA). Small-vessel vasculitides are associated with immune complex deposition in the vessel walls. In some cases the association with a specific infection is strong (e.g., mixed cryoglobulinemia and chronic hepatitis C infection), whereas in others there is a strong association with serologic markers (e.g., microscopic polyangiitis and p-ANCA). Each involves vessel wall inflammation leading to vascular obstruction and end-organ damage. The current working classification for vasculitis syndromes has proven helpful for selecting appropriate treatment. Vasculitides are classified by the size of the involved vessel, Table 8-3 [Jennette JC, Falk RJ, Andrassay K, et al. Nomenclature of systemic vasculitides: proposal of an international consensus conference. Arthritis Rheum. 1994;37:187–192]. The clinical manifestations depend upon the size and distribution of the vessels involved. Symptoms and signs are related to local ischemia and systemic inflammation. Skin involvement is usually manifested as palpable purpura with or without skin infarction. Involvement of arteries to other organs is manifested as signs of specific organ dysfunction, for example, renal failure, transient ischemic attacks, stroke, and pneumonitis. The pattern of involvement suggests the size of the vessel and the specific vasculitis syndrome [Weyand CM, Goronzy JJ. Medium-and large-vessel vasculitis. N Engl J Med. 2003;349:160–169; Jennette JC, Falk RJ. Small-vessel vasculitis. N Engl J Med. 1997;337:1512–1523; McCluskey P, Powell R. The eye in systemic inflammatory diseases. Lancet. 2004;364:2125–2133; Kathiresan S, Kelsey PB, Steere AC, et al. Case 14--2005: a 38-year-old man with fever and blurred vision. N Engl J Med. 2005;352:2003–2012].
TABLE 8-3Systemic Vasculitis Syndromes |Favorite Table|Download (.pdf) TABLE 8-3 Systemic Vasculitis Syndromes
|Size of the Vessel ||Specific Diseases |
|Large arteries ||GCA |
Primary central nervous system vasculitis
|Medium arteriesa ||Polyarteritis nodosa |
|Small vessels ||Leukocytoclastic vasculitis (e.g., Henoch–Schonlein purpura, cryoglobulinemia, infections, drugs) |
Systemic rheumatic syndromes
|Pseudovasculitisb ||Antiphospholipid syndrome |
Embolic phenomena (atrial myxomas, cholesterol, NBTE/ Libman–Sacks endocarditis)
Giant cell arteritis (temporal arteritis)
The cause is unknown. Histologic examination shows patchy medial necrosis of temporal artery segments, with diffuse mononuclear infiltration and giant cells throughout the vessel walls (GCA). Thromboses are frequent. GCA affects major branches of the proximal aorta, especially the external carotid. Patients over age 50 present with fever and weight loss and may have headache, jaw claudication, or scalp tenderness. Visual symptoms forebode irreversible visual loss from retinal and ophthalmic artery occlusion. The headache is severe, persistent, and throbbing. Polymyalgia rheumatica (see Polymyalgia rheumatica) may antedate other manifestations or occur simultaneously. Systemic symptoms (fever, profound weakness, weight loss, malaise, and prostration) are common and may be the only manifestations of disease. Physical signs are few, but scalp tenderness and tortuous, tender, or nodular temporal arteries may be identified. The overlying skin is often red and swollen. Vision is often impaired and ophthalmoplegia may occur, temporarily or permanently. The retina may be normal or show evidence of retinal ischemia. Prompt diagnosis and treatment may prevent loss of vision. The typical ophthalmic finding is anterior ischemic optic neuropathy (AION). The disk appears pale and swollen because of closure of the posterior ciliary arteries that supply the nerve head. Aortic aneurysms (thoracic and abdominal) and dissection occur with increased frequency [Salvarani C, Cantini F, Boiardi L, Hunder GG. Polymyalgia rheumatica and giant cell arteritis. N Engl J Med. 2002;347:261–271].
There is inflammation of the aorta and its major branches producing markedly reduced flow and thrombosis in the involved vessels. Patients are usually young women presenting with arterial ischemic symptoms. A characteristic triad of signs is (1) absent pulses in upper extremity or neck vessels (pulseless disease), (2) carotid sinus sensitivity with head movement inducing syncope, and (3) ocular disorders, such as cataract and retinal defects.
Small and intermediate muscular arteries have transmural inflammation and necrosis, sometimes extending to adjacent veins and arterioles. Involvement is segmental with a predilection for arterial bifurcations and branch points. Vascular occlusion leads to tissue ischemia and necrosis. Aneurysms up to 1 cm in diameter are frequent. Symptoms include fever, weight loss, malaise, and pain in viscera and muscles. Skin lesions are common, especially on the legs, and subcutaneous nodules may be palpable along the course of vessels or nerves. Frequently involved organs are the kidneys (renal failure, hypertension), gastrointestinal tract (visceral infarction), heart (MI, pericarditis), liver (acute to chronic hepatitis), peripheral nerves (mononeuritis multiplex), skin (subcutaneous nodules on superficial vessels, palpable purpura, livedo reticularis), joints, and muscles (myalgias, arthralgias, arthritis). The lungs are rarely involved [Stone JH. Polyartertitis nodosa. JAMA. 2002;288:1632–1639; Coblyn JS, McCluskey RT. Case records of the Massachusetts General Hospital. Case 3--2003. A 36-year-old man with renal failure, hypertension, and neurologic abnormalities. N Engl J Med. 2003;348:333–342].
Granulomatosis with polyangiitis (Wegener)
The cause is unknown. Inflammation of small arteries and veins is associated with granuloma formation; neutrophil anticytoplasmic antibody (c-ANCA) to proteinase 3 is highly specific. Patients present with fever, malaise and signs of upper airway disease (sinusitis, obstructive, and/or destructive symptoms and signs), pulmonary involvement, and/or progressive renal failure. Other organ systems, including the skin, may be involved. Disease may be limited to the upper airway. It is most common in the fourth and fifth decades. Facial pain and epistaxis are caused by erosion of the nose (resulting in saddle deformity), sinuses, palate, or nasopharynx. The lungs may have infiltrates, nodules, and cavitations; the kidney lesion is a rapidly progressive glomerulonephritis.
Eosinophilic granulomatosis with polyangiitis (Churg–Strauss syndrome)
The cause is unknown. Eosinophilia is associated with nodular lung infiltrates and asthma. Patients present with signs and symptoms of asthma in association with eosinophilia and persistent slowly evolving abnormalities on the chest radiographs. Systemic symptoms and signs mimic polyarteritis nodosa. It may appear during tapering of corticosteroid treatment or introduction of leukotriene inhibitor therapy for asthma [Wolf M, Rose H, Smith RN. Case 28–2005: a 42-year-old man with weight loss, weakness, and a rash. N Engl J Med. 2005;353:1148–1157].
The cause is unknown, but immune complexes and complement are not present in the vessel walls (pauci-immune vasculitis). There is a high prevalence of anticytoplasmic antibodies to myeloperoxidase, (p-ANCA); granuloma formation does not occur. Patients are systemically ill with fever, malaise, dyspnea, nonproductive cough, arthralgias, and myalgias. Acute rapidly progressive glomerulonephritis is very common and pulmonary hemorrhage may be fatal. It is clinically indistinguishable from granulomatosis with polyangiitis, except for the absence of airway involvement.
Immune complexes lodge in the walls of the terminal arteriole and venules inciting an inflammatory response that may lead to vessel occlusion with local tissue infarction. This common vasculitis most frequently affects the skin, particularly on the lower legs. The physical finding is purpura which is often palpable. The lesions come in crops that clear over days without scarring. Systemic symptoms (fever, malaise) and involvement of visceral organs including the kidneys (glomerulonephritis), lungs, gut, and rarely the heart and central nervous system can occur. Precipitating events include infection, drugs, malignancies, and primary inflammatory disorders. Several distinct syndromes are identified, but overlap is frequent. DDX: This vasculitis must be distinguished from other causes of vasculopathy including disseminated fungal (e.g., histoplasmosis), viral (e.g., Rocky Mountain spotted fever) and bacterial infections (e.g., meningococcemia, gonococcemia), atheroembolism, scurvy, and thrombocytopenia.
This is a hypersensitivity vasculitis caused by antibody formation against a widely disseminated exogenous antigen, most often penicillin. Deposition of antigen–antibody complexes in the subendothelial space elicits a local inflammatory reaction. Headache and pruritus are accompanied by wheal formation at the site of subcutaneous or intramuscular injection. The urticaria spreads, and large areas of skin may become edematous. An erythematous rash is often present. Myalgias and arthralgias may be severe; nausea and vomiting may occur. Generalized lymphadenopathy is frequent.
This describes leukocytoclastic vasculitis occurring in association with another primary disease or condition that incites formation of immune complexes. Commonly encountered causes are infections (endocarditis, HIV, EBV, etc.), primary inflammatory diseases (e.g., SLE, RA, Sjögren syndrome and polymyositis-dermatomyositis), serum sickness, and drugs (see below).
Idiopathic cutaneous vasculitis
This applies to immune complex vasculitis limited to the skin and without any identifiable inciting event or exposure. It may be recurrent and the crops of purpura may be preceded by a burning sensation. Other skin signs that may accompany the purpura include urticaria, bullae, and erythematous macules. The lesions may itch.
Many drugs, especially the penicillins and sulfonamides, are associated with immune complex-mediated, typically cutaneous and/or urticarial, vasculitis. A p-ANCA positive small vessel vasculitis clinically identical to microscopic polyangiitis has been described with use of propylthiouracil and hydralazine. Drug-induced TTP-HUS (Tuberous sclerosis) is a vasculopathy that may be confused with vasculitis.
Henoch–Schönlein purpura (anaphylactoid purpura)
This is thought to represent a postinfectious condition. There is IgA deposition and inflammation in the small vessels of the skin, gastrointestinal tract, and kidneys. Patients, usually children or young adults, present with palpable purpura on the abdomen, buttocks and lower extremities, abdominal pain, fever, and heme-positive stools. Proteinuria and hematuria indicate glomerulitis. Nausea, vomiting, arthralgias, and myalgias are common. Urticaria may be present. The condition resolves spontaneously within a few days.
This is a vasculitis of unknown cause characterized by the triad of relapsing iridocyclitis, oral aphthous ulcerations, and genital ulcers. The great majority of cases have come from Greece, Cyprus, Turkey, the Middle East, and Japan, but an increasing number of cases are reported in the United States. There is a high incidence of erythema nodosum and arthritis. A characteristic sign is pathergy, formation of sterile pustules at skin puncture sites. Many patients have thrombophlebitis, neurologic disorders, or intestinal involvement. The disease is chronic with relapses and remissions [Sakane T, Takeno M, Suzuki N, et al. Behçet’s disease. N Engl J Med. 1999;341:1284–1291].
Arteriovenous fistula: acquired
Communication between an artery and adjacent vein may be induced surgically to facilitate venous access or be caused by a stab or gunshot wound, diagnostic catheterization, or erosion from neoplasm or infectious arteritis. Hemorrhage after the inciting trauma is profuse but easily controlled. A thrill and bruit may develop some hours later. After the wound has healed, signs of chronic circulatory disturbance develop. Although fistulas may occur in any body part, signs are most evident when an extremity is involved (Fig. 8-46). Venous congestion is manifested by dilated veins and changes of stasis dermatitis. Arterial hypoperfusion can produce distal gangrene. If injury occurs before the epiphyses have closed, hypertrophy of the extremity may occur. A thrill and bruit are present throughout the cardiac cycle, with systolic accentuation. The skin temperature is increased distal to the fistula. Paradoxically, these signs assure that an arteriovenous shunt established surgically to facilitate venous access has remained patent.When the shunt is large, the dilated superficial veins become tense, venous pressure approaches arterial diastolic pressure, venous flow velocity increases, the RV dilates, arterial diastolic pressure falls, and cardiac failure may result. External compression, temporarily closing the fistula, produces a sharp slowing of the heart rate, called the Branham bradycardiac sign. Signs of shunts abdominal or thoracic shunts are a bruit and changes in venous and arterial pressure.
Signs of Arteriovenous Fistula
A fistula between the popliteal artery and vein is represented. A. It shows the communication between artery and vein behind the knee joint. B. The lesion is in the left leg. The superficial veins are greatly dilated from blood under arterial pressure; they are tense to the touch and sometimes pulsatile. Distal to the fistula, the skin is warm from the arterial blood in the veins, cyanotic, and pigmented from hemostasis. Distal gangrene may occur. At the site of the leak a thrill and bruit may be felt. These are continuous throughout the cardiac cycle, with systolic accentuation. The arterial pulse pressure is greater than normal if the orifice of the fistula is large enough. C. Closure of the fistula by digital compression produces slowing of the heart rate (Branham bradycardiac sign) and augmentation of both systolic and diastolic arterial pressures in the general circulation.
Congenital arteriovenous fistula
Cutaneous birthmarks are found in one-half of cases, so arteriovenous fistula should be considered when port-wine spots, blue-red cavernous hemangiomas, or diffuse hemangiomas are present. Frequently, congenital fistulas are quite small, so the signs associated with the acquired type are not evident: thrills and bruits may be absent and the bradycardiac sign of Branham is less pronounced. The affected limb may be hypertrophied, and it may exhibit increased sweating and hypertrichosis. There is no history of trauma.
Disorders of Circulation in the Head, Neck, and Trunk
The large arteries and veins in the head, neck, and trunk are less accessible to inspection and palpation than those in the extremities (Figs. 8-47 and 8-48A). Vascular disorders in these regions frequently must be inferred from combinations of physical signs.
Large Superficial Arteries of the Head and Neck
The accessible arterial segments are diagrammed in solid black; inaccessible parts are stippled. The temporal artery courses anterior to the ear and upward to the temporal bone. The carotid arteries are deep to the anterior margin of the sternocleidomastoid muscle. The carotid sinus, at the bifurcation of the common carotid, is located by being level with the upper margin of the thyroid cartilage. A short segment of the subclavian artery is often palpable in the supraclavicular fossa.
The Aortic Arch
A. Aortic arch variations. The normal pattern 1 is only slightly more common than the other two; it has a right innominate artery, branching into the subclavian and common carotid. There is no left innominate artery; the left subclavian and common carotid originate from the aorta itself. There may be both a right and left innominate 2 or the right innominate may give off the left common carotid 3 in addition to the right carotid and subclavian. B. Anatomic relations of a dilated aortic arch. Aneurysm of the aortic arch or dilatation of the left atrium may compress the left recurrent laryngeal nerve against the vertebrae or the left main bronchus to produce paralysis of the left vocal cord, resulting in hoarseness or a brassy cough. Expansion of the arch downward impinges upon the left main bronchus so the trachea is depressed with each pulse wave, giving a physical sign called the tracheal tug.
The carotid arteries supply blood to the head and brain. The external carotid system supplies the extracranial tissues; vascular symptoms and signs in its territory are unusual except for frequent involvement in giant cell (temporal) arteritis producing jaw claudication and scalp tenderness. The internal carotid system supplies the brain and eye and is frequently involved with atherosclerotic occlusive disease and atheroembolic events such as amaurosis fugax. The most common sites for atherosclerotic obstruction are the carotid bifurcation, the carotid siphon, and the middle cerebral artery. Disease of the carotid bifurcation is frequently accompanied by a bruit audible in the neck. Carotid bruits with ipsilateral cerebral symptoms carry a high risk for stroke within hours or days; bruits without symptoms must also be evaluated to assess the severity of obstruction.
The vertebral arteries are not accessible to direct examination. They join to form the basilar artery in the posterior fossa and collateralize the cerebral circulation via the posterior cerebral and posterior communicating arteries. Vertebral occlusive disease occurs because of atherosclerosis or dissection giving symptoms of brainstem ischemia (e.g., vertigo, dysarthria, dysequilibrium).
Aneurysmal arterial dilatation may be congenital or result from cystic medial necrosis, atherosclerosis, hypertension, vasculitis, or infection. The forms of aneurysms are fusiform, saccular, and dissecting. Aneurysms may consume platelets and clotting factors. Similar physical signs are produced by fusiform and saccular dilatations, but the arterial dissection presents an entirely different clinical picture (Post-cardiotomy syndrome). If pain accompanies an aneurysm, consider a penetrating aortic ulcer, leakage of the aneurysm, or dissection of the arterial wall.
The cause of thoracic aneurysms is multifactorial. Breakdown of structural proteins in the aortic media and adventitia plays a central role. The process also leads to smooth muscle necrosis and development of cystic spaces filled with mucoid material (cystic medial necrosis). Predisposing factors include genetic abnormalities (e.g., Marfan syndrome), hypertension, pregnancy, inflammation (e.g., GCA, syphilis), and possibly atherosclerosis. Thoracic aneurysms are classified by their proximal extent, regardless of distal extension, into those involving the ascending aorta and those only involving the aorta distal to the left subclavian artery. The signs and symptoms are related to compression or distortion of adjacent structures and pain related to medial dissection or sudden dilation without dissection. Dissection may occur prior to aneurysmal dilatation.
Ascending aortic aneurysms
These can produce aortic regurgitation from either dilation of the ascending aorta or dissection extending proximally to the valve ring and leaflets. The murmur characteristically transmits down the right sternal border rather than the left. A palpable thrust may develop in the right second or third intercostal spaces. The width of retromanubrial dullness is increased. Erosion of ribs and protrusion of a pulsatile mass may occur. Compression signs include hoarseness (recurrent laryngeal nerve traction), cough, wheezing, or hemoptysis (compression and/or erosion of bronchi). Acute “six-dermatome” chest pain may result from dissection or myocardial ischemia from dissection of coronary ostia (usually the right). Proximal dissection can rupture into the pericardium, producing acute tamponade.
Retrosternal pain is frequent, radiating to the left scapula, left shoulder, or left neck. Dilatation of the arch can compress the left recurrent laryngeal nerve against the trachea or the left main bronchus causing hoarseness and a brassy cough (Fig. 8-48B). Obstruction or dissection of the left subclavian artery causes delay and diminution of pulse volume and reduces left arm blood pressure by more than 20 mm. The dilated aortic arch can depress the left main bronchus producing a tracheal tug with each beat: grasp the cricoid cartilage lightly with the thumb and forefinger to feel the trachea dip with each pulse (Fig. 8-48B).
Aneurysms of the descending aorta
These are frequently silent and discovered incidentally. They may erode vertebral bodies causing back pain radiating around the chest via the intercostal nerves. With dissection, the spinal arteries may be occluded producing paraplegia. Pain from dissection of descending thoracic aneurysms is similar to pain from acute MI or ascending aorta dissection, except that the vast majority has pain in the back with or without anterior chest pain.
Abdominal aortic aneurysm
These are the most common aortic aneurysms. AAA involves all three layers of the aorta; the risk of rupture is directly related to its diameter. Aortic atherosclerosis is uniformly present and often widespread. AAA is uncommon in individuals younger than age 60, but prevalence increases with each decade. Major risk factors are atherosclerosis, cigarette smoking, and male sex. Family clustering has been noted. Estimate the width by placing the fingers on the lateral walls of the pulsatile mass just cephalad to the umbilicus. Pulsatile expansion is demonstrated by lateral as well as anteroposterior movement; this does not occur with a solid mass anterior to the aorta transmitting pulsations. Imaging is required for reliable measurement of size and changes over time. The presence or absence of abdominal or femoral bruits has no predictive value for the presence or absence of AAA. Pain in the mid to lower abdomen and appearance of a pulsatile epigastric mass suggest recent expansion or leaking of the aneurysm; rapid enlargement in size may, however, be asymptomatic. Rupture is associated with severe pain in the abdomen, back, and/or inguinal areas, accompanied by hypotension. The sensitivity of abdominal palpation for the detection of AAA depends upon the size of the aneurysm and the patient’s body habitus. Aneurysms >5 cm in diameter have a high risk of rupture and should be considered for elective surgery; physical examination is only 75% sensitive for detecting aneurysms of this size. Diagnostic imaging is the preferred method of detection, and male smokers between 65 and 73 years of age should be considered for screening [Arnell TD, de Virgilio C, Donayre C, et al. Abdominal aortic aneurysm screening in elderly males with atherosclerosis: the value of physical exam. Am Surg. 1996;62:861–864; Rink HA, Lederle FA, Roth CS, et al. The accuracy of physical examination to detect abdominal aortic aneurysm. Arch Intern Med. 2000;160:833–836; Lederle FA, Simel DL. The rational clinical examination. Does this patient have abdominal aortic aneurysm? JAMA. 1997;281:77–82; Lin PH, Lumsden AB. Small aortic aneurysms. N Engl J Med. 2003;348:19; Ashton HA, Buxton MJ, Day NE, et al. The multicentre aneurysm screening study (MASS) into the effect of abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial. Lancet. 2002;360:1531–1539]. Aneurysms of the iliac arteries are not rare and may rupture. They are identified as pulsatile masses in the lower abdominal quadrants on deep palpation [van der Wliet JA, Boll APM. Abdominal aortic aneurysm. Lancet. 1997;349:863–866].
Dissecting aortic aneurysm
These are saccular aneurysms caused by weakening of the arterial walls from infectious processes other than syphilis. These may develop as extensions of localized suppuration, actinomycosis, or tuberculosis. More frequently, an embolic arteritis occurs from subacute bacterial endocarditis or septicemia. Mycotic aneurysms usually involve vessels subject to bending and lightly protected by overlying muscles, for example, the axillary, brachial, femoral, and popliteal arteries.
A congenital aortic arch stricture occurs just proximal or distal to the aortic insertion of the ductus arteriosus (preductal or postductal). The most common constriction is distal to the left subclavian artery takeoff. Almost invariably, the adult type has a closed ductus. Perfusion of tissues distal to the coarctation is maintained via high resistance chest wall collaterals perfused at the cost of sustained central arterial hypertension. The collateral arterial circulation is via the left internal mammary artery and other branches of the left subclavian to the left intercostal arteries (excepting the first two), the musculophrenic, and the superior epigastric arteries (Fig. 8-49). In most cases the collateral circulation is sufficient for the patient to remain asymptomatic into adulthood. Hypertension develops in the upper limbs with slight hypotension and a dampened pulse wave in the legs. A coincident bicuspid aortic valve is common so aortic systolic (often with an early systolic ejection sound) and/or diastolic murmurs may be heard. The Murmur: The murmur of the coarctation is heard best in the posterior interscapular area. The site of constriction is remote from the precordium, so the murmur is faint, if heard at all, on the anterior chest. When a murmur is audible anteriorly, it is usually a brief early systolic ejection murmur caused by an associated bicuspid aortic valve. A continuous bruit can sometimes be heard over the sternum from the dilated internal mammary arteries. Arterial Pulses: The pulse waves in the distal aorta and its branches are dampened; this is most easily detected by palpating the femoral arteries. If the femoral pulses have good volume, coarctation is suggested when there is a peak pulse lag between the femoral and radial arteries. The collateral circulation through the dilated intercostal arteries may be palpated in the posterior intercostal spaces (which is diagnostic). Notching in the inferior rib margins posteriorly is visible on chest X-ray. Hypertension in young adults should suggest the possibility of coarctation; it is common in patients with the gonadal dysgenesis (Turner syndrome).
Coarctation of the Aorta: Collateral Circulation
The diagram shows the collateral channels causing dilatation of the intercostal arteries from the costocervical trunk and the internal mammary artery. The circulation around the scapula is augmented by blood through the transverse cervical artery. The pulse volume in the arms is normal; in the femoral arteries it is diminished. The dilated scapular and intercostal arteries may be palpated in the back.
Aberrant right subclavian artery (dysphagia lusoria)
Subclavian steal syndrome
Patients have atherosclerotic subclavian artery stenosis proximal to the vertebral artery origin. Retrograde flow occurs in the ipsilateral vertebral artery inducing brainstem ischemia with neurologic signs (Fig. 8-50). A bruit can be heard in the supraclavicular fossa, occasionally with a thrill. The arterial pulse volume and blood pressure are diminished in the affected arm. Symptoms and signs of cerebral ischemia are intermittent or continuous, ranging from vague dizziness to vertigo, slurring of speech, and hemiparesis. The neurologic signs and symptoms can be induced by exercising the affected arm.
Two Syndromes of Large Artery Obstruction
A. Obstruction at the aortic bifurcation (Leriche syndrome): a short thrombus closes the lower part of the abdominal aorta and extends a variable distance down the common iliac arteries. The accessible segments of the femoral, popliteal, dorsalis pedis, and posterior tibial arteries are pulseless. Pain in the legs and intermittent claudication are the common symptoms. B. Subclavian steal syndrome: the most common site of narrowing is the left subclavian artery, although other sites have also been reported.
Thoracic outlet syndromes—subclavian and brachial plexus compression
The roots of C5-T1 form the brachial plexus in the lateral neck, between the scalenus medius and the scalenus anticus. The subclavian artery exits the rib cage over the first rib. Artery and nerves run together over the first and second ribs and under the clavicle and pectoralis minor into the upper arm. These syndromes result from the compression of nerves and vessels as they course between muscles and bones while making their exit from the neck and chest respectively (Fig. 8-51A). The symptoms arise from brachial plexus compression and are largely sensory (paresthesias); the signs are those of positional arterial obstruction. Therefore, the patient presents with subjective neurologic symptoms and the clinician evaluates for signs of arterial compression.
Compression Syndromes of the Superior Thoracic Aperture
A. Scalenus anticus syndrome: the scalenus anticus muscle has attachments to the transverse processes of the cervical vertebrae above and below to the first rib. Posteriorly and behind the subclavian artery, the scalenus medius attaches to the same bones. Hypertrophy of the bellies of the two muscles causes compression of the artery between them, with motions such as turning the head to the ipsilateral side. This is tested by the Adson maneuver (a), where the patient sits with chin raised, head rotated to the left, and chest held in the inspiratory position. A positive test is marked by diminution or disappearance of the left radial pulse. The other side is tested similarly. B. Cervical rib syndrome: the diagram shows a cervical rib compressing the left scalenus anticus muscle and indirectly the subclavian artery. This may produce diminution in the radial pulse or a peripheral neuritis of parts of the brachial plexus. C. Costoclavicular syndrome: the geometry of the aperture may be such that rotation of the clavicles downward and backward compresses the subclavian arteries against the first rib. This is tested (c) by having the patient seated in a chair and the examiner standing behind him. The physician pushes the shoulders downward and backward while an assistant feels for diminution of the radial pulses. D. Hyperelevation of the arm: the geometry of the thorax in some persons is such that hyperelevation of the arm causes the coracoid process of the scapula to impinge and compress the subclavian artery. This is tested by (d) demonstrating that the radial pulse is lost with hyperelevation.
Scalenus anticus syndrome
There is intermittent or constant pain and/or paresthesia in the ulnar aspect of the arm and hand, sometimes associated with weakness and wasting. Adson Test: Have the patient sit with the palms on the knees, chin high, and turned to the side being examined. Examine the radial pulse with breath holding in deep inspiration. A positive test is dampening or obliteration of the radial pulse that resolves when the chin turns forward, still holding the breath. CLINICAL OCCURRENCE: Muscular hypertrophy or edema may occur after unusually vigorous arm use or in those with unusual occupations, such as weight lifters. Muscle spasm may result from poor posture, anomalous first rib, or cervical rib.
In addition to producing spasm of the scalenus anticus muscle (scalenus anticus syndrome, above), a cervical rib may directly compress the subclavian artery dampening the radial pulse in any position (Fig. 8-51B). Occasionally, the extra rib is palpable in the supraclavicular fossa. The rib may also compress the brachial plexus to produce pain or paresthesias in the hand.
There is intermittent or constant pain and/or paresthesia in the ulnar aspect of the arm and hand. Have the patient stand with elbows flexed at 90 degrees; then elevate the elbows, maintaining 90 degrees of abduction, to 45 degrees, 90 degrees, and 135 degrees (the last position places the hands on the head). Palpate the radial pulse and auscultate beneath the midportion of the clavicle at each position. Patients with costoclavicular syndrome have pulse obliteration in at least one position; a palpable pulse with a subclavicular systolic bruit indicates partial obstruction. The Costoclavicular Maneuver tests for clavicular compression of the subclavian artery on the first rib. The patient sits while his radial pulses are palpated by an assistant. Stand behind the patient forcing his shoulders down and back narrowing the thoracic outlet (Fig. 8-51C). The pulse volumes are diminished if compression is sufficient to cause symptoms. This test is specific but not sensitive. CLINICAL OCCURRENCE: Situations in which the shoulders are forced downward and backward, such as walking with a heavy backpack carried on the shoulders.
Ischemia from arm elevation
In some persons, elevation of the arm causes compression of the subclavian artery by the coracoid process (Fig. 8-51D). The patient complains of intermittent or constant numbness and tingling in one or both hands or arms. Patients often sleep on their backs with the hands behind or over the head. Another precipitant is working with the arms elevated, such as painting ceilings. Hyperabduction Test: Have the patient lift the hand to the top of the head then open and close his hand several times noting whether the radial pulse is diminished or abolished.
Superior vena cava obstruction—SVC syndrome
The principal signs are edema and cyanosis of the head, neck, and both arms, edema of the face, both arms, and the upper third of the thoracic wall, with venous engorgement without the pulsations normally transmitted from the right atrium (Fig. 8-52). The neck is enlarged by nonpitting edema (Stokes collar) and collateral veins may be visible on the chest and abdominal wall. CLINICAL OCCURRENCE: Mediastinal neoplasm; cervical or retrosternal goiter; thoracic aortic aneurysm; chronic mediastinitis; thrombosis from an indwelling intravenous catheter.
Superior and Inferior Venae Cavae.
IVC occlusion retards venous drainage from the lower extremities and pelvis leading to development of collateral veins in the hemorrhoidal complex and abdominal wall. Renal vein thrombosis causes acute renal failure. Acute IVC Obstruction: It may be asymptomatic until lower extremity edema develops. Symmetrical rapidly progressive edema of both legs without evidence of heart or kidney disease suggests mechanical IVC obstruction. Chronic IVC Obstruction: It is suggested by dilated superficial collateral veins with cephalad flow on the abdomen. Visible collaterals may appear within a week of obstruction, the veins attaining maximal size in 3 months. To localize the obstruction, consider the vena cava in three segments (Fig. 8-52). Lower Segment (below the renal veins): The collaterals are distributed over thighs, groins, lower abdomen, and flanks. Leg edema, initially pitting, develops fibrosis with chronic venous stasis dermatitis. Pelvic congestion produces low back pain and genital edema. Middle Segment (above the renal veins and below the hepatic vein): The venous collaterals are large intra-abdominal veins without abdominal wall collaterals. Occlusion of the renal veins produces nephrotic syndrome. Gastrointestinal manifestations include nausea, vomiting, diarrhea, and abdominal pain; malabsorption may develop. Upper Segment (above the hepatic veins): Venous collaterals form a prominent periumbilical plexus and large veins appear over the anterior abdomen. Budd–Chiari syndrome develops with hepatosplenomegaly, ascites, jaundice, and elevated transaminases. CLINICAL OCCURRENCE: Intraluminal: Thrombosis, embolism, neoplastic invasion, or extension from renal cell carcinoma; Intramural: Rare benign or malignant neoplasms; External Pressure: Hepatomegaly, lymphadenopathy, aortic aneurysm, surgical ligation, pregnancy.
Disorders of Large Limb Arteries
Arterial disorders are either nonocclusive or occlusive, and occlusion may be partial or complete. Four mechanisms cause arterial circulatory deficit: (1) extrinsic compression; (2) vasospasm; (3) luminal obstruction (intimal thickening, thrombus, embolus); or (4) arteriopathy (vasculitis, fibromuscular dysplasia). Temporary arterial compression is often related to extremity positioning. Vasospasm is recognized by the sharp border between ischemic and normal tissue. Intimal proliferation is inferred when the blood flow is diminished but still present. Complete occlusion is usually caused by embolism or thrombosis. Thrombosis is often the result of gradual, usually atherosclerotic, narrowing allowing development of collaterals; symptoms are gradual in onset and relatively mild. Sudden embolic or thrombotic occlusion causes severe pain and a cold white part. Arteriopathy such as vasculitis is usually inferred from the total clinical picture.
When an acute arterial occlusion is suspected, first determine the most distal site with adequate flow by noting the presence or absence of pulses along the vessel; the vessel walls are palpated for signs of intrinsic disease. Urgent vascular imaging is required by Doppler ultrasound, and/or CT, MR, or contrast angiography.
Atherosclerosis is characterized by medial degeneration and fibrosis, together with occlusive intimal proliferation. Arterial narrowing results from progressive intimal thickening, plaque formation with accumulation of cholesterol-rich lipid deposits, foam cells, and smooth muscle proliferation. Rupture of intimal plaques leads to thrombus formation. Arterial segments lengthen and, when the ends of a segment are anchored, the elongated vessel buckles producing visible and palpable tortuosity. The disease may be diffuse or focal, often occurring at arterial bifurcations. In patients age >45, atherosclerosis is the most likely cause of major arterial obstruction. Patients with diabetes mellitus have an increased risk inversely related to glycemic control. Hyperhomocysteinemia, congenital or acquired (folic acid and B12 deficiency), also increases risk for atherosclerosis and thromboembolic events. Atheromatous plaques may be felt in the walls of accessible arteries; the vessels may be noncompressible and feel thick. Noninvasive vascular examination with Doppler ultrasonography and plethysmography are required for accurate diagnosis; angiography with contrast or MRA is anatomically definitive.
Acute arterial obstruction
Occlusion of arteries to the organs of the head, thorax, and abdomen presents with symptoms referable to those organs: stroke, acute MI, PE, mesenteric, renal, or splenic infarction.
Acute extremity artery obstruction—embolism and arterial thrombosis
This is most common in the legs but can occur in the arms. The patient experiences sudden excruciating pain followed by numbness and weakness. Occasionally, anesthesia and weakness precede the pain which appears more gradually. The distal extremity is pulseless and becomes pallid, the skin becoming cool. Venous pooling causes the skin distally to gradually become cyanotic while mottling occurs proximally; the cyanosis diminishes with limb elevation. Occasionally, the pain may be quite mild. Thrombosis is more likely when there are signs of diffuse vascular disease or a history of claudication. Embolism is likely with atrial fibrillation. CLINICAL OCCURRENCE: Thrombosis: Atherosclerosis; thromboangiitis obliterans; vasculitis; sludging from polycythemia, hemoconcentration, cryoglobulinemia, and hyperglobulinemia; infection; trauma; antiphospholipid syndrome; Embolism: Atrial fibrillation, mitral stenosis, endocarditis (infectious, NBTE) left atrial myxoma, LV mural thrombus following MI, atheroembolism.
Chronic extremity peripheral vascular disease
This is most common in the legs but may involve the arms. The patient complains of claudication and coldness progressing to continuous and/or night pain. Assess the ABI; see Doppler ultrasound examination. Arterial insufficiency can cause skin pigmentation, pallor, purplish discoloration that fades with elevation, coldness, warm areas of collateral circulation, local hair loss, malnutrition of toenails, ulceration, and gangrene (Fig. 8-24 and 8-53). Pulses are weak or absent. Muscular wasting may be present. Popliteal artery occlusion leads to collateral circulation via geniculate artery branches producing cold feet with especially warm knees or anteromedial lower thigh. ABI of <0.9 is associated with an increased risk of cardiovascular morbidity and mortality. ABI <0.5 is more strongly associated with decreased physical activity and absence of sustained walking than are symptoms of claudication [McDermott MM, Greenland P, et al. The ankle brachial index is associated with leg function and physical activity: the walking and leg circulation study. Ann Intern Med. 2002;136:873–883].
Signs of Arterial Insufficiency
A. Poor wound healing. B. Nail dystrophy. C. Digital gangrene.
(Fig. 8-50A). After examining the abdomen, always palpate the femoral arteries. When a femoral pulse is diminished or absent, palpate the iliac pulses up to and including the aortic bifurcation, 2 cm below and slightly to the left of the umbilicus. The iliac arteries run in a line between the bifurcation and the midpoint of the inguinal ligament; the upper third represents the common iliac, the lower two-thirds the external iliacs. These vessels may not be palpable in normal persons, but asymmetric findings are significant. Bilateral decreased or absent femoral pulses suggest coarctation of the aorta, distal aortic thrombosis (Leriche syndrome), or dissecting aortic aneurysm; unilateral absence suggests common iliac artery thrombosis. The significance of an absent or diminished femoral pulse is determined by the status of the distal pulses.
Thromboangiitis obliterans (Buerger disease)
Beginning as an acute segmental panarteritis involving all three layers of medium-sized arteries, intimal granulation tissue ultimately causes arterial obstruction, producing tissue ischemia and necrosis. Thromboangiitis is a condition of young male smokers, usually between 20 and 40, an earlier appearance than atherosclerosis. It is often associated with superficial migrating thrombophlebitis. DDX: No physical signs distinguish Buerger disease from atherosclerosis. The distribution of affected vessels may differ from atherosclerosis: thromboangiitis has a predilection for the radial, ulnar, and digital arteries, in addition to affecting the lower extremities [Olin JW. Thromboangiitis obliterans (Buerger disease). N Engl J Med. 2000;343:864–869]. Approximately 7% of Japanese patients are nonsmokers [Naito AT, Minamino T, Tateno K, et al. Steroid-responsive thromboangiitis obliterans. Lancet. 2004;364:1098].
Raynaud disease and phenomenon
Intense spasm of the digital arteries and dermal vessels produces initial pallor, followed over minutes by capillary dilatation and filling with deoxygenated venous blood, producing a phase of cyanosis. Relaxation of arterial spasm flushes the capillaries with arterial blood producing the warm red phase of vasodilation. Approximately 80% of patients are young women. Attacks are induced by cold exposure or emotional stress. The onset is sudden, either unilateral or bilateral, most commonly affecting the fingers and involving the toes in half the cases. One to four fingers may be affected, rarely the thumbs. Episodes last up to 60 minutes; the terminal digits become chalk-white, numb and sweaty; the pallor is succeeded by intense cyanosis and pain. Sometimes either pallor or cyanosis is absent. During spontaneous recovery, or after warm water immersion, projections of hyperemia replace cyanosis until the digit becomes brilliant red. Hyperemia is accompanied by tingling, throbbing, and edema. After many attacks, trophic changes may appear in the nails and adjacent skin and small areas of gangrene may develop on the fingertips and toes. The term Raynaud disease is used when there is no associated condition and Raynaud phenomenon when it is associated with scleroderma, vibratory trauma, SLE, polyarteritis, peripheral neuropathy, thromboangiitis obliterans, or atherosclerosis. Raynaud phenomenon occurs more frequently in patients with migraine (26%) than in those without (6%). There is also an increased prevalence of chest pain and migraine in patients with Raynaud disease [O’Keeffe SJ, Taspatsaris NP, Beethan WP Jr. Increased prevalence of migraine and chest pain in patients with primary Raynaud disease. Ann Intern Med. 1992;116(12) (pt 1):985–989]. DDX: Always inspect the nailbed capillaries (Examination of the Skin and Nails); abnormal capillaries are highly suggestive of scleroderma. The sequence of pallor, cyanosis, and redness is diagnostic when induced by exposure to cold. It should not be confused with the vascular changes of complex regional pain syndromes [Wigley FM. Raynaud’s phenomenon. N Engl J Med. 2002;347:1001–1008].
Excessive arteriolar constriction is ascribed to increased sympathetic tone, although humoral factors may contribute. This is a benign painless condition in which the skin of the hands and feet is persistently cold, cyanotic, and moist. It is most common in young women. The skin is uniformly cyanotic, which worsens on cold exposure. The cyanosis is abolished with elevation and sleep.
Gangrene of the finger and toe tips can be caused by any disease or condition impairing peripheral perfusion. CLINICAL OCCURRENCE: Scleroderma, pneumatic hammer disease, atherosclerosis, thromboangiitis obliterans, cold agglutination disease, cryoglobulinemia, atheroemboli, sepsis, meningococcemia, vasopressor medications, antiphospholipid syndrome, warfarin skin necrosis (protein C deficiency), ergotism, chronic renal failure.
An intense constriction of the peripheral blood vessels is caused by the ingestion of ergot; some individuals are particularly sensitive. Ergot may be taken as a drug or eaten with dietary grain contaminated by a fungus. The first symptom is often burning pain in the extremities (St. Anthony fire) with loss of arterial pulses in the hands or feet; headache, weakness, nausea, vomiting, visual disturbances, and angina pectoris may occur. Cold skin and mottled cyanosis of the extremities follows. Finally, symmetrical gangrene involves the fingers and toes, sometimes extending proximally.
Congenital cavernous hemangiomas may occur anywhere in the body. The limb is circumferentially enlarged and dilated, purplish, blood-filled, readily compressible sinuses raise the skin surface. This is distinguished from varicosities by the distribution, which does not correspond to the large limb veins. With leg involvement standing may pool enough blood to cause orthostatic hypotension. Massive cavernous hemangiomas (Kasabach–Merritt syndrome) trap platelets producing thrombocytopenia, purpura, and bleeding.
Aneurysms in the arms and neck
The subclavian, axillary, and brachial arteries are most commonly affected; the carotids are rarely involved. Trauma to the vessel wall is the most common cause; rarely, the vessels are involved by mycotic, necrotizing, or atherosclerotic aneurysms. The dilatations are readily palpated.
The most common sites are the femoral artery in the Scarpa triangle and the popliteal artery in its fossa. Atherosclerosis is the most common cause. The aneurysms are readily palpable.
Disorders of the Major Extremity Veins
See Pulmonary Embolism. Intraluminal thrombus forms with or without an inciting event, usually in association with a lower extremity venous valve. The thrombus may propagate proximally or distally; it may partially or completely occlude flow. Absence of inflammation facilitates dislodgment of the thrombus. Leg veins are the most common identified source of PE. Hip and knee surgery have particularly high incidence of associated DVT. This term is usually applied to thrombosis of the deep veins of the legs. Deep venous thrombosis requires timely diagnosis to initiate appropriate therapy, the goals of which are to prevent pulmonary embolus and diminish damage to the venous valves that predisposes to future thrombosis and stasis damage to the skin. The history and physical examination can separate patients into low-, intermediate-, and high-risk categories (Table 8-4); all patients in whom DVT is suspected should undergo further testing [Anand SS, Wells PS, Hunt S, et al. The rational clinical examination. Does this patient have deep vein thrombosis? JAMA. 1998;279:1094–1099]. Diagnostic algorithms are constantly changing, so consult current protocols. Early diagnosis can be lifesaving. Symptoms: Often, tightness or a sense of fullness is noted in the leg which is aggravated by standing and walking. Signs: DVT may be accompanied by cutaneous cyanosis of the dependent foot and lower leg. Pitting edema of the foot, ankle, or leg that does not resolve overnight and venous engorgement on the feet persisting with the legs elevated to 45 degrees, suggest venous obstruction. Leg pain following the course of the thrombosed vein may be induced by sneezing or coughing; the pain disappears when the vein is compressed proximal to the obstruction (Louvel sign). Palpation may detect tenderness of vein segments. Homan Sign: With the knee in flexion, the examiner forcefully dorsiflexes the ankle; calf or popliteal pain occurs in approximately 35% of the patients with DVT. Homan sign is neither sensitive nor specific for DVT.
TABLE 8-4Wells Criteria for Deep Venous Thrombosis Risk Stratification |Favorite Table|Download (.pdf) TABLE 8-4 Wells Criteria for Deep Venous Thrombosis Risk Stratification
|Clinical Feature ||Score |
|Current cancer or within the last 6 mo ||1 |
|Paralysis, significant limb weakness or immobilization of one or both legs ||1 |
|Bedridden for >3 d or surgery within 4 wk ||1 |
|Localized tenderness along the deep veins ||1 |
|Entire leg swollen ||1 |
|Calf circumference >3 cm compared to the asymptomatic leg, 10 cm below the tibial tuberosity ||1 |
|Pitting edema greater in the symptomatic leg ||1 |
|Collateral (nonvaricose) superficial veins in the symptomatic leg ||1 |
|Alternative diagnosis as likely or more likely the dvt ||2 |
|Summary pretest risk estimation score observed prevalence of DVT: || |
|Low ||0 or less ||3% || |
|Moderate ||1–2 ||17% || |
|High ||3 or more ||75% || |
As the name implies, thrombosis and inflammation of the venous walls are associated; inflammation may either precede or follow clot formation. In addition to the signs and symptoms described above, pain and inflammation are prominent features. When acute, the veins are painful and tender and the overlying skin is red and hot. Adjacent muscles may cramp. Fever and leukocytosis are common. Acute femoral vein thrombophlebitis may present with excruciating pain, massive leg edema, and pallor from arterial spasm (phlegmasia alba dolens). The signs can suggest arterial embolism, but the pallor is less intense, there is more cyanosis, the femoral vein is tender, and anesthesia is absent; arterial pulses can usually be demonstrated by ultrasound. When the entire venous drainage of an extremity is obstructed, there is extreme pain, massive edema, and deep cyanosis of the entire limb (phlegmasia cerulea dolens). Arterial and venous imaging are indicated.
This is a squeal to proximal leg vein DVT in up to 50% of patients. Pain and tenderness are slight and the skin is normal to cool. The leg is swollen, initially with edema, but, if untreated, progresses to nonpitting fibrosis of the subcutaneous tissues and skin. Varicose veins may or may not be prominent. Venous stasis dermatitis is common. Severe cases can be disabling [Prandoni P, Lensing AWA, Prins MH, et al. Below-Knee elastic compression stockings to prevent the post-thrombotic syndrome. Ann Intern Med. 2004;141:249–256]. CLINICAL OCCURRENCE: Congenital: Congenital thrombophilia is suggested by DVT at a young age, at unusual sites (upper extremity, mesenteric vessels, etc.), a history of recurrent thromboses or emboli, a family history of DVT, or DVT with minimal trauma or minor surgery. Identified etiologies include resistance to activated protein C, factor V Leiden mutation, protein C deficiency, protein S deficiency, dysfibrinogenemia, homocystinuria, antithrombin III deficiency, and sickle cell disease. Acquired: Antiphospholipid syndrome (lupus-like anticoagulant, anticardiolipin antibodies), heparin-induced thrombocytopenia and thrombosis (HITT syndrome), leg fractures, limb surgery, trauma, prolonged inactivity (bed rest, international air travel, automobile travel), infection, cancer (especially mucin-producing adenocarcinomas), hyperhomocysteinemia, estrogen-containing medications, pregnancy, obesity, venous stasis and insufficiency, diabetes mellitus, polycythemia vera, idiopathic thrombocythemia, and paroxysmal nocturnal hemoglobinuria. Recurrent deep venous thrombosis may precede the diagnosis of cancer.
Thrombosis and inflammation of superficial veins occurs either alone, or extending from the deep veins. The patient complains of tender red nodules or cords under the skin. Often there is a history of recent trauma. Superficial thrombophlebitis may mask the coincidental occurrence of deep vein disease. Superficial thrombophlebitis is a very rare cause of life-threatening pulmonary embolus. Underlying DVT should be investigated. DDX: Lymphangitis and other skin and soft-tissue infections can be confused with superficial thrombophlebitis, but the firm palpable venous cords are diagnostic.
Migratory superficial thrombophlebitis
Successive episodes of thrombophlebitis involve different veins in widely separated parts of the body. In a single episode, a segment of vein becomes tender, reddened, and indurated. Involution begins in a few days and the adjacent tissues become successively blue and yellow, often resolving with some skin pigmentation. Arm and leg veins are most commonly involved, but the subcutaneous veins of the abdomen and thorax may be affected. Although the lesions do not cause serious discomfort, this complex should prompt a search for an underlying disease. CLINICAL OCCURRENCE: Antiphospholipid syndrome, thromboangiitis obliterans, Behçet syndrome, pancreatic carcinoma, and thrombophilic hematologic disorders, especially paroxysmal nocturnal hemoglobinuria.
See Stasis Dermatitis. Venous stasis results from vein occlusion or incompetence of the valves. Occlusion is caused by external compression or from plugging of the lumina by fibrosis, thrombi, or neoplasms growing in the vessel lumen. Dilation of vessels exacerbates stasis. Dilated superficial veins drain poorly into smaller communicating veins. Dilatation of deeper veins leads to incompetence of their valves. Decreased capillary flow produces poor skin nutrition, inflammation, and fibrosis. Signs of venous stasis are pitting edema, stasis pigmentation (hemosiderin), erythema, fibrosis, decreased skin elasticity, and ulceration. The pumping action of voluntary muscles is inhibited by bed rest and by immobilizing an extremity [Bergan JJ, Schmid-Schonbein GW, Smith PD, et al. Chronic venous disease. N Engl J Med. 2006;355:488–498].
Varicose veins are grossly dilated subcutaneous veins, often filling by retrograde flow from the deep veins because of incompetent valves in the perforating and deep veins; they are most common in legs (Fig. 8-54). Primary varicosities develop spontaneously; secondary varicosities result from proximal obstruction, e.g., pregnancy, trauma, thrombophlebitis. When unilateral, extrinsic compression or an arteriovenous fistula should be considered. An AVM produces pulsation in the dilated veins.
Large Superficial Veins of the Lower Limb
The great saphenous vein begins on the medial aspect of the foot, courses backward under the medial malleolus, up the medial aspect of the calf, behind the medial epicondyle, and then obliquely across the anterior thigh to the femoral vein as it enters the femoral canal beneath the inguinal ligament. The small saphenous vein begins on the lateral side of the foot, curves backward beneath the lateral malleolus, and then upward on the posterior surface of the calf to enter the popliteal fossa and join with the popliteal vein. The middle figure diagrams the communications between the superficial veins (heavy solid lines) and the deep veins (broken lines) and the communicating vessels (dotted lines).
Thrombosis of the axillary vein
This usually follows trauma or intensive use of the arm in hyperabduction, such as throwing. The entire arm swells and aches. The tissues are firm and there is no pitting edema. The superficial veins at the superior thoracic aperture may be dilated. Poor collateral circulation produces cyanosis of the skin. Axillary vein thromboses are less likely to lead to lethal pulmonary emboli than deep venous thromboses in the legs, but it does occur. DDX: In chronic cases, it must be distinguished from lymphedema. Both conditions produce solid, nonpitting swelling, but venous obstruction causes some cyanosis of the skin; the skin is pallid in lymphedema. Lymphedema of the arm is common after radical mastectomy.