Why are temperature, pulse, respirations, and BP called vital signs? These are the signs of life (L. vitalis, from vita: life); their presence confirms life and their absence confirms death. The more abnormal these parameters become, singly, but especially in combination, the greater the life is threatened. Since ancient times, practitioners have used the skin temperature, the pulse, and the respirations as prognostic signs. More recently, the BP has been found to have similar predictive strength.
These signs have played a major role in the history of medicine. In the nineteenth century, entire texts were written on the interpretation of pulse, fever, and respiratory patterns. It is now apparent that these signs are not sufficient to establish a specific diagnosis. On the other hand, they are sensitive indicators of disease and are useful in forming pathophysiologic hypotheses and a differential diagnosis. They remain strongly correlated with severity of illness and outcome.
Internal body temperature is tightly regulated to maintain vital organ function, particularly the brain. Temperature deviation of more than 4°C above or below normal can produce life-threatening cellular dysfunction. Internal temperature is regulated by the hypothalamus, which maintains a temperature set point. The autonomic nervous system maintains body temperature by regulating blood flow, conducting heat from the internal organs to the skin, and innervating sweat glands. Increasing flow and dilating cutaneous capillaries radiate heat away by conductive loss whereas sweat increases evaporative heat loss. Behavioral adaptations are also important; in hot conditions, people become less active and seek shade or a cooler environment. Decreased body temperature is countered by shivering (increasing heat generation in muscles) and by behavioral adaptations such as putting on clothes and seeking warmer environs. Deviations of body temperature indicate changes in the set point, increased heat production, decreased heat dissipation, failure of regulatory systems, or any combination of those.
The patient’s temperature is recorded at each visit to establish a baseline for future reference. Deviations from this baseline are either fever or hypothermia. Scales on clinical thermometers are either Fahrenheit or Celsius. Conveniently remembered clinical equivalents are 35°C = 95°F, 37°C = 98.6°F, and 40°C = 104°F.
Internal body temperature is maintained within a narrow range, ±0.6°C (1.0°F), in each individual. However, the population range of this set point varies from 36.0°C to 37.5°C (96.5–99.5°F) making it impossible to know an individual’s normal temperature without an established baseline. Without a baseline it is reasonable to regard an oral temperature above 37.5°C (99.5°F) and a rectal temperature over 38.0°C (100.5°F) as fever. The minimum normal temperature is more difficult to define; the oral temperature often dips to 35.0°C (95.0°F) during sleep.
Diurnal variation of body temperature
Daytime workers, who sleep at night, register their minimum temperature at 3 to 4 am, whence it rises slowly to a maximum between 8 and 10 pm. This pattern is reversed in nightshift workers. The transition from one pattern to the other requires several days.
Simultaneous temperatures in various regions
Heat is produced by the chemical reactions of cellular metabolism, so a temperature gradient extends from a maximum in the liver to a minimum on the skin surface. Customarily, the body temperature is measured in the rectum, the mouth, the ear, the axilla, or the groin. Among these sites, the rectal temperature is approximately 0.3°C (0.6°F) higher than that of the oral or groin reading; the axillary temperature is approximately 0.5°C (1.0°F) less than the oral value.
Increased body temperature results from excessive heat production or interference with heat dissipation. Each of these mechanisms may be physiologic (i.e., occurring as a normal response to a physiologic challenge) or pathologic (i.e., temperature elevation as a result of damage to the normal thermoregulatory pathways). Physiologic elevation of temperature results from an elevation of the hypothalamic physiologic set point for body temperature, a fever. Pathologic elevations of body temperature, hyperthermia, result from unregulated heat generation and/or impairment of the normal mechanisms of heat exchange with the environment.
Physiologic elevated temperature—fever
Release of endogenous pyrogens, particularly interleukin (IL-1), triggered by tissue necrosis, infection, inflammation, and some tumors, elevates the hypothalamic set point leading to increased body temperature. Onset of fever may be marked by a chill with shivering and cutaneous vasoconstriction as the body begins generating increased heat and decreasing heat loss; particularly severe chills are called rigors. When the new set point is reached, the skin is usually warm, moist, and flushed; but absence of these signs does not exclude fever. Occasionally, the skin temperature may be subnormal or normal, while the core temperature is markedly elevated. Tachycardia usually accompanies fever, the increase in pulse rate being proportionate to the temperature elevation. During the fever, the patient usually feels more comfortable in a warm environment. The new set point and the pattern of the fever reflect the dynamics of the particular pathophysiologic process. Return of the set point to normal, either temporarily or permanently, is marked by sweat and flushing as the body dissipates the accumulated heat. Night sweats occur in many chronic infections, inflammatory diseases, and some malignancies, particularly lymphomas. They represent an exaggeration of the normal diurnal variation in temperature, the sweat marking the decline of the temperature at night.
Fevers occurring in several specific patient populations require special consideration. These include fever in immunocompromised hosts, HIV-infected patients, and nosocomial fever. Discussion of these topics is beyond the scope of this text. Some patients cannot mount a fever in response to infection. This is particularly true for those with renal failure, on high doses of corticosteroids, and the elderly.
Congenital: Familial Mediterranean fever, other familial periodic fevers, porphyrias; Endocrine: Hyperthyroidism, pheochromocytoma; bacterial, viral, rickettsial, fungal, and parasitic infections either localized (e.g., SBE) or systemic (occult abscess is common); Inflammatory/Immune: Systemic lupus erythematosus (SLE), acute rheumatic fever, Still disease, vasculitis, serum sickness, any severe local or systemic inflammatory process (e.g., sarcoidosis, bullous dermatosis); Mechanical/Traumatic: Tissue necrosis (e.g., myocardial infarction, pulmonary infarction, stroke), exercise; Metabolic/Toxic: Drug reactions, gout; Neoplastic: Leukemia, lymphomas, and solid tumors; Neurologic: Seizures; Psychosocial: Factitious; Vascular: Thrombophlebitis, tissue ischemia and infarction, vasculitis, subarachnoid hemorrhage.
The pattern of temperature fluctuations may be a useful diagnostic clue. Many patterns have been described including:
The diurnal temperature fluctuation is 0.5°C to 1.0°C (1.0°F to 1.5°F).
The diurnal temperature fluctuation is more than 1.1°C (2.0°F) without any normal readings.
Episodes of fever are separated by days of normal temperature. Examples include tertian fever from Plasmodium vivax in which malaria paroxysms are separated by an intervening normal day; quartan fever in which paroxysms from Plasmodium malariae occur with two intervening normal days.
Fevers occur every 5 to 7 days in borreliosis and Colorado tick fever.
Fever lasts for days or longer followed by remission of fever and clinical illness for at least 2 weeks. This pattern is typical of the familial periodic fevers [Drenth PPH, van der Meer JWM. Hereditary periodic fever. N Engl J Med. 2001;345:1748–1757].
Several days of continuous or remittent fever are followed by afebrile remissions lasting an irregular number of days. This is characteristic of Hodgkin disease.
Three conditions define a fever of unknown origin (FUO): (1) the illness has lasted >3 weeks; (2) the temperature is repeatedly >38.3°C (100.9°F); and (3) ≥ three outpatient visits or ≥3 days in the hospital have not yielded a diagnosis. In the modern era the most common causes of FUO in immunocompetent patients are noninfectious inflammatory diseases, infections, and malignancies, especially hematologic malignancies. However, fever remains unexplained in almost 50% of patients, especially those with episodic fevers [Mourad O, Palda V, Detsky AS. A comprehensive evidence-based approach to fever of unknown origin. Arch Intern Med. 2003;163:545–551; Vanderschueren S, Knockaert D, Adriaenssens T, et al. From prolonged febrile illness to fever of unknown origin: the challenge continues. Arch Intern Med. 2003;163:1033–1041; Jha AK, Collard HR, Tierney LM. Diagnosis still in question. N Engl J Med. 2002;346:1813–1816]. CLINICAL OCCURRENCE: Noninfectious Inflammatory Diseases: Still disease, SLE, sarcoidosis, Crohn disease, polymyalgia rheumatica, vasculitis (giant cell arteritis, Wegener disease, polyarteritis nodosa); Infections: Endocarditis, tuberculosis, urinary tract infection, cytomegalovirus, Epstein–Barr virus, HIV, subphrenic abcess, cholangitis and cholecystitis; Neoplasms: Non-Hodgkin lymphoma, Hodgkin disease, leukemia, adenocarcinoma; Miscellaneous: Habitual hyperthermia, subacute thyroiditis, Addison disease, drug fever.
Pathologic overproduction and impaired dissipation of heat
Hyperthermia. Unregulated heat production or damage to the heat dissipation systems leads to rapid and severe uncompensated temperature elevations. Fever from the causes noted above rarely produces hyperthermia without primary failure of the normal control mechanisms. More commonly, the environment, impaired judgment, or toxin exposure is the direct cause. CLINICAL OCCURRENCE: Impaired Heat Loss: High environmental temperature and humidity, moderately hot weather for a person with congenital absence of sweat glands, congestive heart failure, heat stroke, anticholinergic drugs and toxins. Poverty, homelessness, and psychosis all inhibit the ability to adapt to environmental challenges. Increased Heat Generation: Malignant hyperthermia, neuroleptic malignant syndrome, heavy exertion in hot and humid environment.
Neuroleptic malignant syndrome. Medications disrupt central dopamine pathways leading to uncontrolled hyperthermia. One to two days after exposure to a neuroleptic (antipsychotic) drug, the patient develops hyperthermia, rigidity, altered mental status, labile BP, tachycardia, tachypnea, and progressive metabolic acidosis. Myoglobinuria and acute renal failure can occur. It can be confused with worsening of the psychotic state leading to delayed diagnosis and administration of more neuroleptics.
Malignant hyperthermia. An inherited disorder of muscle sarcoplasmic reticulum calcium release produces sustained muscle contraction on exposure to inhalational anesthetics or succinylcholine. The patient develops rigidity, hyperthermia, rhabdomyolysis, metabolic acidosis, and hemodynamic instability. Prompt recognition and treatment is lifesaving.
Heat stroke. Failure of the thermoregulatory system leads to decreased sweating and rapid increases in core body temperature. Cardiovascular disease increases risk by limiting increased cardiac output necessary for skin perfusion. Diuretics and anticholinergic drugs also increase the risk. The typical victim is a chronically ill adult confined in a hot, humid environment during heat waves. The patient is often delirious or comatose; the diagnostic clue is the hot dry skin [Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002;346:1978–1988].
Heat exhaustion (heat prostration)
Exertion in a hot, usually humid, environment leads to loss of fluid and electrolytes and decreased ability to dissipate body heat. This is classically seen in younger individuals participating in athletic events or working in hot, humid environments. Symptoms are palpitations, faintness, lassitude, headache, nausea, vomiting, and cramps. Patients have tachycardia, diminished BP, diaphoresis, ashen, cool, moist skin, and dilated pupils. The core body temperature is elevated, but <40°C (104°F). Untreated it can lead to heat stroke.
This is a common form of malingering and Munchausen syndrome. Clues are high temperatures with unusual fluctuation and fever not accompanied by other signs of acute illness.
Infections presenting as fever
Fever accompanies many infections and inflammatory diseases. The following are diseases that often present with fever and no localizing symptoms or signs.
Infection with Mycobacterium tuberculosis may be limited to the lung or spread via the lymph nodes or bloodstream to affect any organ. Primary infection is in the lung and may leave a calcified middle or lower lobe nodule and hilar lymph nodes (Ghon complex). Progressive primary tuberculosis is seen commonly in HIV-infected patients but may occur in otherwise healthy people. It presents as progressive lung infection (usually in the lower lung zones), pleural effusion, and lymphadenopathy. In immunosuppressed hosts or dark-skinned races, there is an increased risk for early hematogenous dissemination to multiple organs. Miliary tuberculosis presents with fever, anorexia, and weight loss and may have hepatomegaly, splenomegaly, or lymphadenopathy. Reactivation tuberculosis may be miliary or localized to one organ system, most commonly the apices of the lungs. Patients present with fever, malaise, night sweats, cough with sputum production, and lung consolidation and/or cavity formation. Reactivation can also occur in bones, especially the spine (Pott disease), the peritoneum, meninges, kidneys and urinary tract, lymph nodes, intestine, and pericardium [Tanoue LT, Mark EJ. Case records of the Massachusetts General Hospital. Case 1–2003. N Engl J Med. 2003;348:151–161].
Endemic North American fever syndromes
Several infectious diseases that present as undifferentiated febrile illnesses are found exclusively or with increased frequency in specific regions of the United States. In the first days of illness they cannot be clinically differentiated so travel history is essential for timely recognition and treatment. CLINICAL OCCURRENCE: Rocky mountain spotted fever (RMSF), other rickettsial infections, babesiosis, ehrlichiosis and anaplasmosis, Lyme disease, Q fever, leptospirosis, relapsing fever, Colorado tick fever, and other viral exanthems.
Rickettsial spotted fever syndromes
Rickettsia are transmitted by arthropod bites and usually present as systemic disease with headache and rash without localizing symptoms or signs. Travel and exposure history are essential for an accurate differential and evaluation. Early treatment can be lifesaving. DDX: RMSF is described below; it produces the archetypical syndrome. The other rickettsial diseases present in a similar fashion with severe headache, fever, myalgias, and malaise. Confusion with babesiosis, Lyme disease, and Ehrlichiosis/anaplasmosis can be reduced by careful history and examination.
Rocky mountain spotted fever
Rickettsia rickettsii are transmitted by the bite of an infected tick. The obligate intracellular parasites infect endothelial cells producing acute systemic illness. The disease is highly endemic to the Atlantic coastal states where it may be acquired by vacationers. It can be acquired in any state and many foreign countries. The onset is nonspecific with headache, fever, chills, myalgias, and asthenia frequently accompanied by nausea, vomiting, and abdominal pain. An erythematous macular rash spreading centrally from the wrists and ankles may be seen after the third day; the palms and soles may be affected and dorsal edema of the hands and feet is characteristic. The lesions are initially blanching but progress to papules which become nonblanching purpura. Systemic involvement leads to widespread organ damage and death in 25% of untreated patients [Cunha BA. Rocky mountain spotted fever revisited. Arch Intern Med. 2004;164:221].
Louse borne typhus (epidemic typhus, trench fever), endemic typhus (murine typhus), and rickettsialpox
All are endemic to the United States but are also imported. Rickettsialpox, seen in the Northeastern United States, has a papular erythematous rash at the mite bite site that becomes a necrotic eschar with regional lymphadenopathy. Nausea and vomiting are highly characteristic of murine typhus.
Babesia are intracellular protozoa transmitted by infected Ixodes ticks. They parasitize red blood cells where they can be identified on blood smears. Babesiosis is a worldwide zoonotic infection in which humans are infected incidentally. It is highly endemic in the Atlantic coastal regions of New York, Connecticut, Rhode Island, and Massachusetts. It has been reported from many other locales, however, and imported cases are seen. There is gradual onset of fever, headache, myalgias, and fatigue. There may be hepatosplenomegaly and hemolysis. A rash does not occur. Coincident infection with other tick borne diseases (Lyme, ehrlichiosis, and anaplasmosis) is not rare.
Ehrlichiosis and anaplasmosis
Ehrlichia and anaplasma are intracellular parasites that reproduce in either mononuclear phagocytic cells in the blood and tissues (Ehrlichia chaffeensis) or granulocytes (Ehrlichia ewingii and Anaplasma phagocytophilia) forming vacuolar inclusions (morula) visible on light microscopy. Human monocytotropic ehrlichiosis and ehrlichiosis ewingii are transmitted by the Lone Star tick (Amblyomma americanum) and are most prevalent in the south-central, southeastern and Mid-Atlantic States. Onset of both diseases is nonspecific with fever, headache, malaise, and myalgia often accompanied by nausea, vomiting, and diarrhea. Rash, cough, and confusion may be seen. A. phagocytophilia is transmitted by bites of the Ixodes ticks with high concentrations in the northeastern and upper Midwestern states. A high index of suspicion is required to make these diagnoses promptly.
Infection with Borrelia burgdorferi is transmitted by bites of Ixodes ticks. Initially infection is in the skin with a characteristic rash, but it disseminates within days to involve virtually all organs and tissues. The characteristic rash of erythema migrans may be missed or ignored. If so, the patient presents with symptoms of systemic disease with fever, headache, myalgias, neck stiffness, arthralgias, and striking fatigue and malaise. These symptoms may persist for several weeks, gradually resolving or being replaced with neurologic symptoms and signs (peripheral neuropathy, mononeuritis multiplex, cranial neuropathy, aseptic meningitis, or chorea); Bell palsy is quite common at this stage. Cardiac conduction block with symptomatic bradycardia may be seen. The most common late manifestation is an inflammatory oligoarthritis of the large joints, especially the knee.
Gram-negative bacilli (Bartonella henselae) are inoculated by the scratch, lick, or bite of a healthy cat. The organisms travel to the regional lymph nodes and then disseminate. Symptoms are nonspecific with malaise and headache. Signs include fever, a papule or pustule at the inoculation site, followed by painful fluctuant regional lymphadenopathy with overlying reddened skin. Dissemination in immunocompromised hosts can lead to hepatitis (peliosis hepatitis), osteomyelitis, or meningoencephalitis. Conjunctival infection produces preauricular lymphadenopathy (Parinaud oculoglandular syndrome) [Koehler JE, Duncan LM. Case 30–2005: a 56-year-old man with fever and axillary lymphadenopathy. N Engl J Med. 2005;353:1387–1394; Pael UD, Hollander H, Saint S. Index of suspicion. N Engl J Med. 2004;350:1990–1995].
Leptospirosis is a world-wide zoonosis transmitted by ingestion of contaminated water or contact with urine or tissues of infected animals. The onset is abrupt with fever, headache, myalgias, and malaise often accompanied by conjunctival suffusion. There may be muscle tenderness, lymphadenopathy, hepatosplenomegaly, or rashes. History of contact with contaminated water in the summer or fall is a key to making the diagnosis. Men are more often exposed than women. If not recognized and treated initially, symptoms may subside or disappear for a week only to recur. Severe disease causes multiorgan failure, that is, Weil syndrome with jaundice, renal insufficiency, and hemorrhage.
Borrellia spp. infects humans after louse or tick bites. The organisms can change their antigenic coating of variable major proteins causing escape from an initially effective immune response leading to relapsing illness. Tick borne relapsing fever is a zoonotic infection with Borrelia spp. transmitted by infected argasid ticks feeding on humans. The patient presents with fever, myalgias, chills, nausea, vomiting, and arthralgias. Abdominal pain, cough, photophobia, neck stiffness, and rash are less common. Delirium can accompany the high fever making sleep difficult. The illness reaches a crisis in 3 to 5 days when the fever peaks with chills followed by lysis of fever, diaphoresis and hypotension. Relapse occurs with the next antigenic variant after 7 to 9 days. Each crisis is equivalent to a Jarisch–Herxheimer reaction. DDX: Louse borne relapsing fever is transmitted by the human body louse. The symptoms are similar. It is endemic to portions of Ethiopia but has caused major epidemics in wartime Europe.
This is a zoonotic infection with Coxiella burnetii transmitted by infected cattle, goats, and sheep, especially via products of conception during delivery and infected milk. Both inhalation of organisms and ingestion produce infection. The illness has protean manifestations. Common symptoms are fever, severe fatigue and headache, cough, nausea, vomiting, diarrhea, and rash may be present. Presentations include an influenza-like illness, pneumonia, hepatitis, meningoencephalitis, and culture negative endocarditis. Chronic disease with hepatosplenomegaly implies persistent endocardial infection. Diagnosis is difficult.
Colorado tick fever virus is transmitted by infected wood ticks (Dermacentor andersoni) in the northern Rocky mountain states from late spring to fall. It causes a biphasic illness that manifest as fever, myalgia, headache, and occasionally meningoencephalitis and rash. It is self-limited.
Fever in returning travelers. This is a common problem with rapid global travel. Patients present with fever and a travel history to exotic, usually tropical, locations. In addition to common illnesses, a host of unusual infections are possible. A clinically useful approach is presented in the references [Ryan ET, Wilson ME, Kain KC. Illness after international travel. N Engl J Med. 2002;347:505–516; Spira AM. Assessment of travellers who return home ill. Lancet. 2003;361:1459–1469].
The four dengue viruses are transmitted by mosquitoes well adapted to tropical and subtropical urban environments worldwide. The most common febrile illness in travelers returning from the Caribbean presents with fever, headache, back pain, and severe myalgias (break-bone fever). Dengue hemorrhagic fever is potentially fatal.
P. vivax, Plasmodium ovale, P. malariae, and Plasmodium falciparum are transmitted by anopheles mosquitoes. Initial hepatocyte infection is followed by invasion of erythrocytes. Cyclical release of mature merozoites from ruptured erythrocytes produces cyclical fever. Plasmodium falciparum infection can produce severe hemolysis, hypoglycemia, and obstruction of cerebral capillaries (cerebral malaria). P. vivax and P. ovale can persist in the liver causing relapsing infections. Patients present with fever, headache, malaise, and myalgias. Nausea, vomiting, and abdominal pain may be present, and progression to delirium and coma can occur. Prompt diagnosis relies on obtaining the travel history and examination of blood smears by trained personnel. DDX: Dengue fever may present a similar clinical picture but blood smears are negative.
Disseminated Salmonella typhi or Salmonella paratyphi infection follows ingestion of contaminated food or water. The incubation period is 3 days to as much as 60 days. Symptoms are chills and prolonged, persistent fever, prostration, cough, epistaxis, and constipation or diarrhea. There is slowly progressing lassitude, abdominal distention and tenderness, splenomegaly, and rose spots on the trunk and chest. Delirium may occur. Complications include localized infections (gallbladder, bone, liver, spleen, endocarditis, pneumonia, meningitis, and orchitis), gastrointestinal bleeding and bowel perforation with peritonitis.
Systemic infection with Brucella abortus (cattle), suis (pigs), melitensis (goats), or canis (dogs) is acquired by exposure to unpasteurized milk, contaminated meat or other animal tissues. Lassitude and weight loss accompany recurrent (undulant) fever and sweating. Back and joint pains are common. Physical findings include splenomegaly, lymphadenopathy, and tender bones or joints. The disease may be acute or chronic [Drapkin MS, Kamath RS, Kim JY. Case 26–2012: a 70-year-old woman with fever and back pain. NEJM. 2012;367:754; Vogt T, Hasler P. A woman with panic attacks and double vision who liked cheese. Lancet. 1999;354:300].
Rickettsial infections endemic to other countries, as well as those endemic to North America, may be imported. Fever, headache, myalgias, and rash are characteristic of the spotted fever syndromes (e.g., Boutonneuse fever). Scrub typhus is imported from Australia, the southern Pacific region and southern and southeast Asia. In addition to fever, headache, myalgias, and malaise, cough is a prominent symptom. An inoculation eschar from the mite bite and regional lymphadenopathy typical of ulceroglandular syndromes may be present (Chapter 6).
Decreased hypothalamic set point, insufficient heat generation, and excessive heat loss due to behaviors and environmental conditions all lead to a sustained decline in core temperature. Low body temperature impairs cellular metabolism and brain function, particularly judgment, and the combination prevents protection from continued exposure leading to fatal hypothermia. Hypothermia also protects the tissues from ischemic injury, so complete recovery is possible from rapid and sustained cooling even when the patient appears clinically dead. This is especially true for cold water immersion (drowning). Relative or absolute hypothermia in situations where fever would be expected (e.g., severe infection) is a poor prognostic sign. Core temperature is usually lower in older adults making them particularly susceptible to decreased environmental temperatures. CLINICAL OCCURRENCE: Endocrine: Hypothyroidism; Idiopathic: Advanced age; Infectious: Sepsis; Mechanical/Traumatic: Exposure and immersion, hypothalamic injury from trauma or hemorrhage, burns; Metabolic/Toxic: Antipyretics, hypoglycemia, drug overdoses; Neoplastic: Brain tumors; Neurologic: stroke; Psychosocial: Poverty, homelessness, and psychosis all inhibit the ability to adapt to environmental challenges; Vascular: Stroke.
The Pulse: Rate, Volume, and Rhythm
The sinoatrial (SA) node is the heart’s normal pacemaker. It lies in the right atrial wall near the entrance of the superior vena cava (Fig. 4-1) generating regular excitation waves that spread quickly through the wall of both atria. In the atrioventricular (AV) node near the posterior margin of the interatrial septum, the excitation wave is delayed (during atrial systole) before excitation passes into the His bundle. The main His bundle divides into a right and a left branch which pass down the either side of the interventricular septum to excite the right and left ventricular myocardium more or less simultaneously. Changes in atrial or ventricular excitation or AV conduction alter the cardiac rate and rhythm. Left ventricular systolic contraction ejects blood into the aorta producing a pulse wave that travels along the arteries at a rate dependent upon the ejection force and the elastic properties of the arterial wall. The rate and regularity of the pulse is determined by the rhythm of cardiac electrical depolarization and muscular contraction.
Disturbances of Cardiac Rate and Rhythm I
A. Diagram illustrating the spread of excitation over the heart. The stimulus starts in the SA node and spreads throughout the walls of the atria, finally reaching the AV node, where there is a short delay. The stimulus then proceeds down the His bundle by its two branches along the right and left wall of the interventricular septum to the apex, spreading from there to the muscle of the right and left ventricles. The atria contract before the impulse has left the AV node; ventricular systole occurs when the impulse has spread over the walls of the lower chambers. Note that the heart sounds that result from ventricular systole are the only perceptible physical signs of this process. B. Atrial premature beat is represented as originating outside the SA node, an ectopic beat. This is followed by a short compensatory pause that cannot ordinarily be detected. C. An ectopic ventricular beat with a detectable compensatory pause. D. Respiratory or sinus arrhythmia. There is acceleration of the heart rate near the height of inspiration; this acceleration originates in the SA node. In any dysrhythmia, the heart sounds of a beat following a shortened interval are often fainter than normal; beats following an abnormally long pause are louder than normal. E. Ventricular rates.
Palpation of the arterial pulse
The pulse is palpable in any accessible artery (Fig. 4-2). The carotid, radial, femoral, posterior tibial, and dorsalis pedis pulses should be examined. Radial artery palpation is commonly used to assess the pulse rate and regularity. The pulse contour and volume are discussed under heart action (Chapter 8, and Fig. 8-42).
Sites of Palpable Arteries
A. The temporal artery is anterior to the ear and overlies the temporal bone, one of the few normally tortuous arteries. The common carotid is deep in the neck near the anterior border of the sternocleidomastoid muscle. The bifurcation of this artery is opposite the superior border of the thyroid cartilage. The carotid sinus is at the bifurcation. B. Elongation or dilation of the ascending aorta and arch makes this vessel accessible to palpation in the suprasternal notch. With slight shifting to the right or left, the innominate or left carotid arteries may also be felt in the notch. C. The brachial artery lies deep in the biceps-triceps furrow on the medial side of the arm near the elbow. It courses toward the midline of the antecubital fossa, where it is usually just medial to the biceps tendon. D. The radial artery is just medial to the outer border of the radius and lateral to the tendon of the flexor carpi radialis, where the finger can press it against the bone. The ulnar artery is in a similar position to the ulna, but it is buried deeper, so it often cannot be felt. E. The abdominal aorta and parts of the iliac arteries can usually be felt as generalized pulsations through the abdominal wall. The femoral artery is palpable at the inguinal ligament midway between the anterior superior iliac spine and the pubic tubercle. F. The posterior tibial artery is palpable as it curves forward below and around the medial malleolus of the tibia. The dorsalis pedis artery is felt usually in the groove between the first two tendons on the medial side of the dorsum of the foot.
Normal pulse rate and rhythm: sinus rhythm
Normal sinus rhythm is regular at a rate between 55 and 100 beats per minute (bpm). Normal infants and children have higher rates; consult pediatric references for the normal ranges. Well-conditioned athletes may have resting rates into the low forties, while deconditioned adults may have rates approaching 100. At heart rates <100 bpm, ventricular diastole is longer than systole; the two intervals become equal at approximately 100 bpm; above 100 bpm, systole is longer. Heart rates lower than 55 bpm are bradycardias and those above 100 bpm, tachycardias. Exertion may cause acceleration to almost 200 bpm in young, healthy adults; the maximum achievable heart rate declines predictably with age. The pulse rhythm is normally regular with slight respiratory variation. Vagus stimulation by breath holding, Valsalva or carotid sinus massage slows the rate.
Variations in the Rate and Rhythm of Ventricular Contraction
The emphasis is on ventricular phenomena since the signs of heart action are practically all ventricular (Fig. 4-1E). The atria usually function silently, contributing no important diagnostic signs except for the atrial components of the neck vein pulsations, generation of the fourth heart sound, the variations in loudness of the first heart sound that accompany AV dissociation, and the ventricular filling sounds associated with atrial contraction sometimes heard in AV block.
While a rhythm abnormality may be suspected on physical examination, none can be diagnosed with the certainty required in good clinical practice without an ECG
Nevertheless, a general grouping of rhythm disorders is possible from the heart rate (slow, normal, fast) and whether it is regular, irregular in a reproducible manner (regularly irregular), or irregular without pattern (irregularly irregular). [Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med. 2000;342:705–709].
Rates below approximately 55 bpm suggest sinus bradycardia, second-degree AV block (Fig. 4-3A), and third-degree AV block with junctional or ventricular escape rhythms (Fig. 4-3B).
Disturbances of Cardiac Rate and Rhythm II
In all diagrams, the audible heart sounds are the only physical signs to indicate the presence and operation of the mechanisms. A. Second-degree AV block is depicted with a 2:1 ratio. Alternate stimuli from the atria are blocked in the AV node, so the ventricles beat only half as fast as the atria. The only physical sign is a slow regular heartbeat with first sounds of equal intensity. B. Complete AV block is depicted, in which the ventricles beat independently of the atria and usually assume a slow rate, below 50/min, that accelerates little with exertion. A louder-than-common first sound occurs when ventricular filling is augmented by an atrial contraction occurring by chance at the optimal time, this is called by the French—the “bruit de canon.” C and D. When ventricular beats are regular with rates between 160 and 220/min, two conditions must be distinguished. C. Paroxysmal atrial tachycardia. D. Atrial flutter. Vagal stimulation may convert paroxysmal atrial tachycardia to normal rhythm, but there is no temporary slowing. In contrast, the only response of flutter to vagus stimulus is slowing for a few beats.
Regular rhythms with rates greater than 120 bpm
Rhythms include sinus tachycardia, atrial flutter with 2:1 AV block, paroxysmal supraventricular tachycardia (Fig. 4-3C), and ventricular tachycardia (VT). DDX: The response to vagus stimulation may give an indication of which rhythm is present. In flutter, the rate slows stepwise. Paroxysmal atrial tachycardia does not slow but may convert to a normal rate. Sinus rhythm may gradually slow and VT does not change.
Regular rhythms with rates of 60 to 120 bpm
These include sinus rhythm, accelerated junctional rhythm (nonparoxysmal junctional tachycardia), atrial tachycardia with block, idioventricular tachycardia (accelerated ventricular rhythm and slow or benign VT), and atrial flutter (Fig. 4-3D) with 3:1 or 4:1 AV block.
Rhythms that are irregular in no repetitive manner
Atrial flutter with variable AV block, atrial fibrillation, multifocal atrial tachycardia, and frequent atrial or ventricular premature beats that occur with no consistent pattern all need to be considered. The overall rates of such rhythms may vary from as slow as 50 up to 200 bpm. However, atrial flutter with variable AV block rarely exceeds 150 bpm and the range for multifocal atrial tachycardia is usually between 100 and 150 bpm.
Irregular rhythms with “regular irregularity”
This rhythm pattern suggests either atrial or ventricular premature beats occurring at regular intervals (i.e., bigeminal, trigeminal, and quadrigeminal premature beats) or Mobitz I (Wenckebach) AV block producing grouped beats. It is necessary to obtain an ECG to reach a definitive diagnosis.
Common dysrhythmias and their physical signs
Examination of the pulse is important, but only an electrocardiogram can diagnose specific rhythms.
Respiratory (sinus) arrhythmia
Depolarization originates in the SA node and are conducted normally. The ventricular rate normally accelerates as inspiration approaches its maximum and decelerates during expiration (Fig. 4-1D). When the ventricular rate is slow it is less evident.
Exertion and increased sympathetic tone increase the rate of SA node depolarizations to between 100 and 160 bpm with a regular rhythm; conduction is normal. Vagus stimulation produces smooth deceleration. This is normal and expected with exercise, anxiety, hyperthyroidism, anemia, fever, pregnancy, b-adrenergic medications, and deconditioning from any cause. Absence of tachycardia in these situations requires an explanation. DDX: Especially with rates higher than 140, sinus tachycardia must be distinguished from atrial flutter with 2:1 block. In flutter, vagus stimulation slows the rate in stepwise fashion; paroxysmal atrial tachycardia does not slow but may convert to normal rate.
See Orthostatic (postural) hypotension, Orthostatic Hypotension. A pulse rise of more than 15 bpm on sitting from the supine position, or at 2 minutes after standing from the sitting position, suggests intravascular volume depletion.
Postural orthostatic tachycardia syndrome (POTS)
The cause is unknown. It usually affects women between 15 and 50 years of age, following a minor illness. Standing from a sitting or lying position is associated with an increase in the heart rate to >120 bpm or >30 bpm above the baseline rate. Tachycardia is often associated with symptoms and signs of autonomic hyperactivity (tremor, palpitations, nausea) or presyncope (light headedness, weakness, visual change). [Benarroch, EE. Postural tachycardia syndrome: a heterogeneous and multifactorial disorder. Mayo Clin Proc. 2012;87(12):1214]
The rate is slow due to vagal stimulation or diseased SA pacemaker cells; the rhythm is regular and conduction is normal. Rates are rarely <40 bpm. This is expected in well-conditioned athletes. Severe hypothyroidism and sick sinus syndrome are other causes. DDX: The rate accelerates smoothly with exertion.
Sinus rhythm with second-degree block
In Mobitz I (Wenckebach) AV block, there is decremental conduction in the AV node so that, after a series of conducted beats, one beat is dropped. This produces grouped beats with a P to QRS ratio of n:n–1 (e.g., 3:2, 5:4). In Mobitz II block, SA impulses are regularly blocked in the His bundle or below; complete heart block may occur. The atrial rate is a multiple of the ventricular rate, 2:1, 3:1, 4:1, or higher; e.g., when every third atrial impulse is transmitted through the AV node it is 3:1 block. Mobitz I block is the most common type of AV block. The ventricular complexes appear in groups followed by a pause. The interval between beats shortens until a beat is dropped with a longer pause and the cycle recurs. The shortening of the R-R interval is only apparent on the ECG. In Mobitz II block, ventricular systoles occur at regular intervals with rates dependent upon the sinus rate and degree of block (Fig. 4-3A). Each beat has the same intensity. In 2:1 block, two A-waves may be seen in the jugular vein for each ventricular contraction. Although 2:1 block is relatively common, 3:1 block is rare. DDX: In both sinus bradycardia and second-degree heart block, the rate is accelerated with exertion; complete heart block exhibits little response. CLINICAL OCCURRENCE: Acute infections (especially rheumatic fever, Lyme disease, and diphtheria), valvular heart disease, digitalis intoxication, hyperkalemia, drugs (diltiazem, verapamil, b-blockers), coronary artery disease.
Third-degree (complete) AV block. The atria beat regularly driven by the SA node, but there is no conduction from the atria to the ventricles. Block may occur in the AV node or ventricular conduction system (His bundle or both bundle branches). Escape pacemakers in junctional tissue near the AV node or the ventricular conduction system establish an escape rhythm with rates of 25 to 60 bpm; the higher the pacemaker, the faster the escape rate. Ventricular contractions are regular; when an atrial systole happens to precede ventricular contraction the intensity of the heart sounds is increased (Fig. 4-3B). When ventricular contraction and atrial contraction nearly coincide, there is a booming sound, bruit de canon; it may come infrequently, so auscultate for >60 seconds. The causes are the same as second-degree AV block with the addition of degenerative and granulomatous diseases such as sarcoidosis. DDX: This is the only bradycardia in which exertion does not accelerate the ventricular rate. The variation in intensity of the first sounds is distinctive.
Premature beats. A depolarization arises from an ectopic focus in the atrium or ventricle producing a premature beat. An atrial premature beat occurs before its expected time (Fig. 4-1B) with a compensatory pause that is shorter than with ventricular premature beats. If the premature beat occurs shortly after a normal ventricular systole, ventricular filling is minimal, the heart sounds are less intense, and the stroke volume may be insufficient to produce a palpable arterial pulse. When premature beats are very frequent, they present a diagnostic problem (Fig. 4-4A) [Wang K, Hodges M. The premature ventricular complex as a diagnostic aid. Ann Intern Med. 1992;117:766–770].
Disturbance of Cardiac Rate and Rhythm III
As in previous diagrams, only the audible heart sounds are the physical signs of these disorders. A. Normal rhythm is interspersed with two random premature beats: if such beats are very frequent, the ear may not be able to distinguish them from atrial fibrillation unless some maneuvers are employed. The rhythm becomes regular as the rate accelerates to approximately 120 bpm. B. Atrial fibrillation: the ventricular rhythm is grossly irregular and continues to be irregular when the rate is accelerated by exercise to more than 120/min. C. Bigeminy: a normal beat is followed by a premature beat and this pattern repeats many times. The premature beats tend to fall out when exercise accelerates the rate to more than 120/min. D. Dropped beats in second-degree AV block: each successive impulse going through the AV node produces a longer interval until one fails to induce ventricular contraction. In contrast to premature beats, exercise tends to increase the number of dropped beats.
Coupled rhythm: bigeminy, trigeminy
One or two normal beats are followed regularly by a premature beat arising from reentry or an ectopic focus in the atrium or ventricle. The ventricular beats are grouped in pairs (bigeminy) or triplets (trigeminy), the last a premature beat; the compensatory pause after the premature beat separates one group from its successor (Fig. 4-4C). Bigeminy has a regular rhythm. Since the premature beat may not be palpable, a regular rhythm at half the true ventricular rate may be suspected if only the peripheral pulse is examined; heart auscultation reveals the bigeminy. As with other premature beats, exercise may restore the normal rhythm. Coupled premature ventricular contractions (PVCs) occur in normal hearts, all forms of organic heart disease and digitalis intoxication. DDX: A similar pulse pattern is produced by Mobitz type I second-degree AV block (Wenckebach) with 3:2 Wenckebach simulating bigeminy and 4:3 simulating trigeminy.
Grouped beats and dropped beats
The mechanism is sinus pauses or SA exit block, second-degree AV block (Mobitz type I or II), or regularly occurring premature atrial beats in a trigeminal or quadrigeminal pattern that are blocked in the AV node. A series of two, three, four, or more beats is followed by a pause. The pattern may recur regularly. The rhythm is unchanged by acceleration of the heart rate. Electrocardiography is essential to distinguish between these rhythms.
The risk for atrial fibrillation correlates with increased atrial volume seen with AV valve incompetence. The atria do not contract synchronously. Stimuli arrive in complete disorder at the AV node, and some are transmitted to the ventricles at irregular intervals (Fig. 4-B). The pulse is ‘irregularly irregular’ without a pattern. Rapid irregular ventricular responses are difficult to identify by palpation. At ventricular rate >70 bpm, the rhythm may seem regular with premature beats. At rates <60 or >120 bpm, the irregularity may be difficult to detect. Because ventricular contractions occur at all stages of chamber filling, the heart sounds and pulse volume vary in intensity. The pulse volume is greater after longer R–R intervals. The ventricular rate is accelerated by exertion. Atrial fibrillation can only be diagnosed by ECG with accurate measuring of the intervals [Falk RD. Atrial fibrillation. N Engl J Med. 2001;344:1067–1078]. DDX: In flutter with variable AV block, exercise increases the rate by large increments. CLINICAL OCCURRENCE: Organic heart disease (especially mitral and tricuspid valve disease and congestive heart failure), hyperthyroidism, acute infections including rheumatic fever, postoperative (especially chest surgery), electrolyte imbalances, hypoxia, and hypercarbia. “Lone atrial fibrillation” may occur in the absence of any structural heart disease or metabolic abnormalities.
Atrial reentry circuits produce atrial contractions from 220 to 360 times per minute (Fig. 4-3D). The AV node cannot transmit such rapid stimuli, so block develops, at 2:1, 3:1, 4:1, or higher; the block may be highly variable. Digitalis, verapamil, diltiazem, and b-adrenergic blocking drugs increase the AV block. Vagal maneuvers may suddenly increase the block, while the atrial rate remains unchanged. Ventricular contractions are regular, with consistent intensity of heart sounds from beat to beat. Variable block produces irregular ventricular contractions, which mimics atrial fibrillation. Flutter may be seen with almost any form of organic heart disease and is especially common after heart surgery. DDX: In sinus tachycardia, vagus stimulation causes smooth slowing; PSVT will not slow but may convert.
Paroxysmal supraventricular (atrial) tachycardia (PSVT, PAT, SVT)
PSVT is most often a reentrant or reciprocating tachycardia involving the AV node. True ectopic atrial tachycardia does occur. Attacks last for minutes to days; they begin and end suddenly. The rhythm is regular at a ventricular rate of 150 to 225 bpm. All pulse beats have the same intensity. PSVT occurs in normal hearts and with AV bypass pathways (Wolf–Parkinson–White syndrome). DDX: Vagus stimulation or intravenous adenosine does not slow the rate; either there is no response, or the attack is abruptly terminated (Fig. 4-3C). Sinus tachycardia slows smoothly; atrial flutter slows with varying AV block.
Ventricular tachycardia. VT is usually a reentry dysrhythmia triggered by a PVC and sustained by the dispersion of conduction and repolarization in damaged ventricular muscle. Urgent diagnosis is needed since ventricular fibrillation (VF) may supervene leading to sudden death. There is usually complete AV dissociation, with the ventricles beating faster than the atria. The onset and, when self-limited, the ending are abrupt. The ventricular rate usually is between 150 and 250 bpm; occasionally, the ventricular rate <150 bpm. The rhythm is regular, and is not influenced by vagal stimulation; it must be distinguished from atrial flutter and PSVT. The variable relationship of atrial to ventricular systole produces variation in the intensity of the first sound. Some sounds are especially loud cannon sounds resulting from superimposition of atrial systole with ventricular systole. The cannon sounds are absent when the atria are fibrillating. Only the first heart sound may be audible. CLINICAL OCCURRENCE: Acquired heart diseases acute myocardial ischemia and infarction, coronary artery disease, drugs (digitalis, quinidine, procaine amide), heart trauma from surgery or catheterization. Congenital heart diseases right ventricular dysplasia, long QT syndrome, hypertrophic cardiomyopathies and Brugada syndrome.
Ventricular fibrillation (VF). Chaotic depolarization of ventricular muscle fibers cannot produce effective ventricular contraction. No ventricular emptying occurs, so no heart sounds are produced. The diagnosis is made by ECG. Unless terminated by prompt electrical defibrillation, death follows rapidly. Abnormal pulse contour and volume. See Chapter 8.
Breathing: Respiratory Rate and Pattern
The normal respiratory rate of a newborn is about 44 breaths per minute (bpm); it decreases gradually to the adult rate of between 14 and 18 bpm. Women have slightly higher rates than men. People tend to breathe faster when their breathing is being observed, so the respiratory rate should be counted unobtrusively.
Increased respiratory rate—tachypnea
Increased respiratory rate occurs with central nervous system (CNS) stimulation and as compensation for metabolic acidosis. Hypoxia, increased oxygen demand, and increased CO2 generation and/or increased PaCO2 each lead to an increase in respiratory rate and tidal volume. Minute ventilation is maintained in restrictive lung or chest wall disease by increasing the respiratory rate to compensate for the reduced tidal volume. Tachypnea occurs with exertion, fear, fever, cardiac insufficiency, pain, pulmonary embolism, acute respiratory distress from infections, pleurisy, anemia, and hyperthyroidism. Breathing is faster when restricted by weakness of the respiratory muscles, emphysema, pneumothorax, or obesity. An arterial blood gas is required to distinguish pathological from compensatory tachypnea.
Decreased respiratory rate—bradypnea
Minute ventilation is preserved when slow rates are accompanied by an increased tidal volume (hyperpnea). Slow rates without an increase in tidal volume produce alveolar hypoventilation indicating an abnormality of the medullary respiratory center. A slower than usual respiratory rate is not abnormal if gas exchange is preserved as demonstrated by an arterial blood gas. Alveolar hypoventilation (PaCO2 > 45 mm Hg) often is caused by CNS-depressant drugs (e.g., opiates, benzodiazepines, barbiturates, alcohol), uremia, or structural intracranial lesions, especially with increased intracranial pressure.
Deep breathing—hyperpnea (Kussmaul breathing)
Increased tidal volume increases alveolar ventilation (hyperventilation), which increases CO2 excretion, an appropriate compensatory response to metabolic acidosis of any cause. It is also seen with hypoxia and is a direct toxic effect of salicylates. Deep, regular respirations are seen with common metabolic acidoses such as diabetic ketoacidosis and uremia. Hypoxemia and decreased oxygen delivery as a result of severe anemia or hemorrhage also lead to hyperpnea.
Decreased depth of breathing is the result of decreased medullary respiratory center drive, weakness of the respiratory muscles, obstruction of the airways, or restrictive disease. Muscular weakness can result from myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré, drugs (e.g., paralyzing agents, rarely amino-glycosides), and exhaustion from prolonged increase in the work of breathing due to decreased chest wall and/or lung compliance. Decreased effective lung volume can result from alveolar filling disorders (pulmonary edema, acute lung injury, alveolar hemorrhage, pneumonia, etc.), severe restrictive lung or chest wall disease, or severe airways obstruction (asthma, emphysema). Hypopnea associated with obstructive sleep apnea is particularly common.
Periodic breathing—Cheyne–Stokes respiration
Cyclic hyperventilation followed by compensatory apnea is caused by phase delay in the feedback controls attempting to maintain a constant PaCO2. This is the most common periodic breathing pattern. In each cycle, the rate and amplitude of successive breaths increase to a maximum, then progressively diminish into the next apneic period. Pallor may accompany the apnea. The patient is frequently unaware of the irregular breathing. Patients may be somnolent during the apneic periods and then arouse and become restless during the hyperpneic phase. CLINICAL OCCURRENCE: It may be seen during the sleep of normal children and the aged. Disorders of the Cerebral Circulation: Stroke, atherosclerosis; Heart Failure: Low cardiac output of any cause [McGee S. Cheyne-Stokes breathing and reduced ejection fraction. Am J Med. 2013;126:536–540]; Increased Intracranial Pressure: Meningitis, hydrocephalus, brain tumor, subarachnoid hemorrhage, intracerebral hemorrhage; Brain Injury: Stroke, head injury; Drugs: Opiates, barbiturates, alcohol; High Altitude: During sleep, before acclimatization.
Irregular breathing—Biot breathing
An uncommon variant of Cheyne-Stokes respiration, periods of apnea alternate irregularly with a series of breaths of equal depth that terminates abruptly. It is most often seen in meningitis.
Irregular breathing—painful respiration
Normal breathing is interrupted by pain caused by movements of the chest. Causes are pleurisy, injured or inflamed muscles, fractured ribs or cartilage, or subphrenic inflammation, such as liver or subdiaphragmatic abscess, acute cholecystitis, or peritonitis.
Irregular breathing—sleep apnea
Obstructive sleep apnea results from extra-thoracic airway obstruction caused by pharyngeal muscle and/or tongue relaxation. Ineffective inspiratory efforts often are terminated by a loud snort or snore. Central apnea occurs when respiratory effort ceases because of absence of medullary respiratory drive. The periods of apnea are accompanied by hypoxia, acidosis, and cardiac dysrhythmias (bradycardia, tachycardia, especially ventricular) that can cause sudden death. Daytime somnolence is caused by deep sleep deprivation resulting from the multiple arousals associated with apneas lasting more than 10 seconds. The classic patient with advanced disease is a morbidly obese male with daytime somnolence, polycythemia, alveolar hypoventilation, and pulmonary hypertension producing right ventricular failure. Symptoms of early disease include early morning headaches, depression or irritability from chronic sleep deprivation, and systemic hypertension. Physical examination findings predictive of obstructive sleep apnea are increased Mallampati grade of oropharyngeal narrowing (Chapter 7), tonsil size, neck circumference, and BMI [Netzer MC, Stoohs RA, Netzer CM, et al. Using the Berlin questionnaire to identify patients at risk for the sleep apnea syndrome. Ann Intern Med. 1999;131:485–491].
Irregular breathing—sighing respirations
The normal respiratory rhythm at rest is occasionally interrupted by a long, deep sigh. The patient briefly senses shortness of breath without limitations of exertion when active. This is commonly encountered in anxious individuals.
Blood pressure and pulse pressure
Every patient’s BP should be checked at each visit to establish a benchmark for future comparison and to detect hypertension. The BP should be taken in both arms at the first visit and again in both arms when the patient has new cardiovascular or neurologic complaints. When elevated arm pressures are found in young persons, the pressures in both legs should be checked. Many circumstances temporarily raise BP in the absence of disease, for example, anxiety, the ‘white-coat syndrome’, rushing to make the appointment on time, bladder distention, chronic alcoholism, amphetamines, cocaine, recent caffeine intake, and cigarette smoking. Frequent BP checks are encouraged [Bailey RH, Bauer JH. A review of common errors in the direct measurement of blood pressure: sphygmomanometry. Arch Intern Med. 1993;153:2741–2748].
Measurement of arterial BP
The intraarterial BP is measured directly in intensive care units. Elsewhere, the indirect method is used. External pressure is applied to the overlying tissues and the pressure (measured in millimeters of mercury) necessary to occlude the artery is assumed to be the intraarterial pressure. The arm cuff should be at least 10 cm wide; for the thigh, a width of 18 cm is preferable. A thick arm will yield readings 10 to 15 mm Hg higher than the actual pressure unless a wide cuff is used [Reeves RA. The rational clinical examination. Does this patient have hypertension? How to measure blood pressure. JAMA. 1995;273:1211–1218].
In some situations, the BP measured by the arm cuff may be higher than the actual intraaortic pressure; this can lead to further efforts to lower an already low BP with tragic consequences. It is important for the clinician caring for critically ill patients to understand this possibility [O’Rourke MF, Seward JB. Central arterial pressure and arterial pressure pulse: new views entering the second century after Korotkov. Mayo Clin Proc. 2006;81:1057–1068; Moser M, Setaro JF. Resistant or difficult-to-control hypertension. N Engl J Med. 2006;355:385–392]. If the radial artery remains palpable after the BP cuff is inflated above systolic pressure (the Osler maneuver), calcified arteries are present [Messerli FH, Ventura, HO. Amodeo C. Osler’s maneuver and pseudo-hypertension. N Engl J Med. 1985;312:1548–1551].
In hypotensive states with coincident intense peripheral vasoconstriction, the sphygmomanometric method may seriously underestimate the true intraarterial pressure. This often occurs in shock. With smaller degrees of vasoconstriction the Korotkoff sounds underestimate the systolic pressure and overestimate diastolic values.
Measurement of the brachial artery pressure
The BP is measured either sitting or lying supine after a 5 to 10 minute rest. If sitting, the back and feet should be supported. The cuff is applied snugly to the bare arm with the distal cuff margin at least 3 cm above the antecubital fossa, which should be at the heart level. Palpate the brachial artery; inflate the cuff to about 30 mm Hg beyond where the palpable pulse disappears. Open the valve so the pressure drops gradually (no more than 2 mm Hg per second) while auscultating over the brachial artery.
Arterial vibrations, called Korotkoff sounds, detected by the stethoscope bell pressed lightly over the brachial artery, are used to determine the BP. The pressure at which sounds first appear is the systolic pressure. As deflation proceeds, the sounds become louder, maintain a maximum, then become muffled, and finally disappear. Note the pressures at the point of muffling and where the sounds disappear. Record the readings, for example, 130/80/75. The highest value is the systolic pressure, but disagreement exists as to whether the second or third value represents the closest approximation to the intraarterial diastolic pressure. With all three values recorded, readers can draw their own conclusions. The American Heart Association recommends the point of disappearance for the diastolic pressure in most instances. Occasionally, as in hyperthyroidism and aortic regurgitation, the sounds persist to zero pressure. In such cases, accept the second value, since a diastolic pressure of zero is impossible. Palpation can check the results by auscultation or when Korotkoff sounds are imperceptible. Palpate the brachial or radial artery distal to the cuff, and record as the pressure at which pulse first appears. A Doppler ultrasound device can be used to identify the pulse and the systolic pressure.
In some patients the Korotkoff sounds appear then disappear before reappearing again as the cuff pressure is lowered, producing an auscultatory gap. This is observed more commonly in older individuals with hypertension and may indicate increased arterial stiffness. It is important to inflate the cuff to well above the putative systolic pressure in order avoid recording a falsely low systolic pressure.
The pulse pressure is the difference between the arterial systolic and diastolic pressures. The normal mean value is 50 mm Hg in men and women.
It is often difficult to get an accurate BP in a short fat arm, in which case the wrist BP should be recorded. The cuff is wrapped around the forearm and the stethoscope bell is placed over the radial artery.
Have the patient lie prone, wrap an wide cuff around the thigh, with the lower margin several centimeters above the popliteal fossa. Inflate the cuff and auscultate the popliteal artery. Even compression is difficult on a conical thigh.
With the patient supine, apply the cuff just above the malleolus. Place the stethoscope bell distal behind the medial malleolus on the posterior tibial artery or on the dorsal extensor retinaculum of the ankle over the dorsalis pedis artery. In patients with unobstructed arteries, BP by this method is comparable to brachial artery BP.
Manometric detection of pulse wave disturbances
During measurement of the BP, changes in the volume of individual pulse waves may be detected that are too subtle to be detected by palpation. This can be seen in atrial fibrillation, pulsus paradoxus (tamponade, COPD), and pulsus alternans.
The precise bounds of the normal BP are difficult to define and definitions of normal and hypertension continue to evolve (Table 4-1). The risk for cardiovascular disease begins to increase with pressures >115/75 and doubles for each 20/10 mm Hg thereafter. Statistical data show an increase in the average systolic pressure with age. Normal adults exhibit a circadian variation in the BP; it is highest at midmorning, falls progressively during the day, and reaches its lowest point at approximately 3 am. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-7) has defined the ranges for the description of BP [Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. JAMA. 2003;289:2560–2572]. The evidence-based JNC-8 recommendations published in late 2013 remain controversial at this writing.
Table 4-1JNC-7 BP Classification |Favorite Table|Download (.pdf) Table 4-1 JNC-7 BP Classification
|Classification ||Systolic Pressure mm Hg ||Diastolic Pressure mm Hg |
|Normal ||<120 ||<80 |
|Prehypertension ||120–139 ||80–89 |
|Hypertension || || |
| Stage 1 ||140–159 ||90–99 |
| Stage 2 ||>159 ||>100 |
BPs normally differ by < 10 mm Hg between the arms; the right arm is usually greater than the left. Inequality is frequent and sometimes cannot be explained. Conditions to be considered are obstruction in the subclavian artery, thoracic outlet syndrome, and aortic dissection [Eguchi K, Yacoub M, Jhalani J, et al. Consistency of blood pressure differences between the left and right arms. Arch Intern Med. 2007;167:388–393].
Most hypertension is of unknown cause, essential hypertension. The primary lesion is suspected to be in the kidney. Increased systolic pressure can result from increased stroke volume or decreased compliance of the aorta. Increased diastolic pressure results from increased peripheral resistance, either by vasoconstriction or intimal thickening. The systolic pressure may be elevated with a normal diastolic pressure: isolated systolic hypertension. More commonly, both the systolic and diastolic pressures are elevated. If only the diastolic pressure is elevated, the pulse pressure is narrowed suggesting reduced cardiac output. The diastolic pressure represents the minimal continuous load on the vascular tree and makes the greatest contribution to the mean arterial pressure. Both isolated systolic and systolic combined with diastolic hypertension are strongly correlated with stroke, heart failure, left ventricular hypertrophy, and chronic kidney failure. In patients older than 50 years of age, elevated systolic BP is more important than diastolic BP as a risk factor for cardiovascular disease. Discovery of sustained hypertension should lead to a search for hypertensive retinopathy, left ventricular hypertrophy, and renal insufficiency. CLINICAL OCCURRENCE: Essential hypertension is a diagnosis of exclusion, so alternative explanations need to always be considered. Congenital: Coarctation of the aorta, congenital adrenal hyperplasia (early or late onset), polycystic kidney disease; Endocrine: Pheochromocytoma, aldosteronoma, adrenal hyperplasia, hypercortisolism (Cushing disease and syndrome), hyperthyroidism, hypothyroidism, hyperparathyroidism, acromegaly; Idiopathic: Essential hypertension, toxemia of pregnancy; Inflammatory/Immune: Atherosclerosis, vasculitis; Metabolic/Toxic: Renal insufficiency, medications (NSAIDs, estrogens, oral contraceptives, cyclosporine), drug abuse (cocaine, amphetamines, etc.), porphyria, lead poisoning, hypercalcemia; Mechanical/Trauma: Obstructive sleep apnea; Neoplastic: Adrenal adenoma, pheochromocytoma, pituitary adenoma, brain tumors; Neurologic: Stroke, diencephalic syndrome, increased intracranial pressure, acute spinal cord injury; Psychosocial: Substance abuse (cocaine, amphetamines, alcohol); Vascular: Renal artery stenosis (atherosclerosis, fibromuscular dysplasia).
Isolated systolic hypertension
The increased systolic pressure is the result of either increased stroke volume or increased rigidity of the aorta its branches. Systolic hypertension is seen with increased cardiac output (hyperthyroidism, anemia, arteriovenous fistulas, aortic regurgitation, anxiety), a rigid aorta as a result of atherosclerosis, and is particularly common in the older adults. It is associated with an increased risk for stroke, left ventricular hypertrophy, and heart failure.
Some patients have an elevated BP only when it is taken in the office by a physician or nurse. Ambulatory and home readings are normal. The risk of cardiovascular complications is intermediate for this syndrome.
Malignant hypertension. Severely elevated BP leads to end-organ dysfunction with positive feedback loops as a result of ischemia, further elevating the pressure. Patients present with headache, confusion, dyspnea, seizures, angina or rapidly progressive renal insufficiency; diastolic pressures are >120 mm Hg and systolic pressures usually >200 mm Hg. Rapid moderation of pressures is required to prevent irreversible damage to the brain, heart, eyes, and kidneys.
Paroxysmal hypertension: pheochromocytoma. A benign tumor of the adrenal or sympathetic chain secretes epinephrine or norepinephrine. In one-third of the patients, the tumor secretes intermittently. The patient’s BP may be normal except for episodes of hypertension associated with pallor, anxiety, sweating, palpitation, nausea, and vomiting. However, most patients have sustained hypertension. Orthostatic hypotension is common, due to intravascular volume depletion. Pheochromocytoma must be distinguished from panic attacks and the white-coat syndrome.
Hypotension results from a loss of blood volume, loss of vascular tone, or decreased cardiac output. Both the systolic and diastolic pressures are below normal. Normal BP is hypotension in a patient whose baseline is sustained hypertension. Signs of hypoperfusion (cool skin, decreased urine output, decreased mental alertness) and compensatory cardiovascular responses (peripheral vasoconstriction, tachycardia) indicate that low BP is pathologic. CLINICAL OCCURRENCE: Loss of Blood Volume: Bleeding, capillary leak syndrome (anaphylaxis, sepsis, IL-2, idiopathic), third-spacing (ascites, burns, secretory diarrheas), polyuria (diabetes mellitus, diabetes insipidus, diuretics), inadequate fluid intake, excessive sweating (heat prostration and heat stroke), adrenal insufficiency; Loss of Vascular Tone: Sepsis, drugs (vasodilators, tricyclic antidepressants, ganglionic blockers), fever, autonomic insufficiency (multisystem atrophy), acute spinal cord injury (spinal shock), arteriovenous malformations; Decreased Cardiac Output: Acute myocardial infarction, ischemic cardiomyopathy, idiopathic dilated cardiomyopathy, aortic stenosis, saddle pulmonary embolism, pericardial tamponade, and severe mitral insufficiency.
Orthostatic (postural) hypotension
The patient is hypovolemic, sympathetic drive to the heart and blood vessels is diminished, or venous return to the heart is deficient. The BP is normal in the recumbent position, but when the patient stands there is a fall, within 3 minutes, of 20 mm Hg in the systolic or 10 mm Hg in the diastolic BP and/or the heart rate rises by ≥15 bpm. This is an early sign of intravascular volume loss [McGee S, Abernethy WB III, Simel DL. The rational clinical examination. Is this patient hypovolemic? JAMA. 1999;281:1022–1028]. When the drop in BP is not accompanied by a rise in pulse rate, autonomic insufficiency is suggested. Patients with chronic orthostatic hypotension frequently have postprandial hypotension and reversal of the normal circadian BP pattern (i.e., higher BP at night than during the day) [Ejaz AA, Haley WE, Wasiluk A, Meschia JF, Fitzpatrick PM. Characteristics of 100 consecutive patients presenting with orthostatic hypotension. Mayo Clin Proc. 2004;79:890–894]. CLINICAL OCCURRENCE: Loss of Blood Volume: See Hypotension above; Loss of Vascular Tone: Deconditioning after long illnesses, autonomic insufficiency (multisystem atrophy), peripheral neuropathies (diabetes, tabes dorsalis, alcoholism), drugs (vasodilators, tricyclic antidepressants, ganglionic blockers); Impaired Venous Return: Ascites, pregnancy, venous insufficiency, inferior vena cava obstruction or hemangiomas of the legs.
In some individuals, especially older adults on vasoactive medications, the BP drops following meals by 20 mm Hg or more. The exact mechanisms are unclear, but the result is an increased risk for falls, syncope, dizziness and fatigue. Careful questioning about the relationship of symptoms to meals will help identify this syndrome [Jansen RWMM, Lipsitz LA. Postprandial hypotension: epidemiology, pathophysiology, and clinical management. Ann Intern Med. 1995;122:286–295].
Anaphylactic shock. IgE-mediated mast cell degranulation leads to release of histamine and other vasoactive substances, producing vasodilatation and opening of endothelial tight junctions with loss of plasma volume. This is a fulminant and life-threatening hypersensitivity reaction occurring on exposure to a specific allergen. Sudden vascular collapse is preceded or accompanied by malaise, pruritus, pallor, stridor, cyanosis, syncope, vomiting, diarrhea, tachypnea, tachycardia, and distant heart sounds. Angioedema and urticaria may be present, but are often absent. CLINICAL OCCURRENCE: Hymenoptera stings, drugs (e.g., penicillin and other antibiotics), peanut ingestion, and many others. Anaphylaxis may occur with exercise, cold exposure, heat exposure or without evident cause (idiopathic anaphylaxis). Clinically identical anaphylactoid reactions occur when mast cell release is stimulated by non-IgE-mediated mechanisms such as radiographic contrast agents.
Septic shock. This is a complex physiologic reaction to endotoxin release into the systemic circulation with activation of inflammatory and thrombotic pathways. Patients present with hypotension, often, but not always, accompanied by fever and prostration. Initially, the skin is warm and flushed, despite the low BP. As the condition worsens, peripheral vasoconstriction, decreased urine output, confusion, progressive hypotension and acidosis ensue. Prompt recognition and treatment of infection are essential.
Toxic shock syndrome. A toxin produced by certain strains of Staphylococcus aureus produces hypotension with high cardiac output and generalized erythroderma. Originally described in association with highly absorbent vaginal tampons, infected surgical wounds containing foreign bodies (sutures) and sinusitis are now the most common identified sites of infection. The patient suddenly develops high fever, myalgia, nausea, vomiting, and diarrhea. Diffuse erythroderma is followed by confusion, acute lung injury, hypotension, and shock. Exfoliation of the palms and soles may occur in convalescence.
Pulse pressure increases when the peak systolic pressure is increased (increased stroke volume, increased rate of ventricular contraction, decreased aortic elasticity) and/or there is a decreased diastolic pressure (decreased peripheral resistance, arteriovenous shunts, aortic insufficiency). A pulse pressure of ≥65 mm Hg is abnormal. With a large stroke volume, the pulse is often described as bounding or, in the case of aortic regurgitation, collapsing. The head may bob with each heart beat. Thrills may be palpable and murmurs audible over AV shunts, either congenital, traumatic, or iatrogenic. With decreased peripheral resistance from vasodilation, the skin is usually warm and flushed. Widened pulse pressure is associated with increased cardiovascular morbidity and mortality, including atrial fibrillation [Asmar R, Vol S, Vrisac A-M, Tichet J, Topouchian J. Reference values for clinical pulse pressure in a nonselected population. Am J Hyperens. 2001;14:415–418; Mitchell GF, Vasan RS, Keyes MJ, et al. Pulse pressure and risk of new-onset atrial fibrillation. JAMA. 2007;297:709–715]. CLINICAL OCCURRENCE: Increased Systolic Pressure: Systolic hypertension, atherosclerosis, increased stroke volume (aortic regurgitation, hyperthyroidism, anxiety, bradycardia, heart block, post-PVC, after a long pause in atrial fibrillation, pregnancy, fever, systemic arteriovenous fistulas); Increased Diastolic Runoff: Aortic regurgitation, sepsis, vasodilators, patent ductus arteriosus, hyperthyroidism, arteriovenous fistulas, beriberi.
Pulse pressure narrows with decreased stroke volume and decreased rate of ventricular ejection. Pulse pressures less than 30 mm Hg may occur with tachycardia and conditions associated with a low stroke volume. CLINICAL OCCURRENCE: Decreased Stroke Volume: Severe aortic stenosis, dilated cardiomyopathy, restrictive heart disease, constrictive pericarditis, pericardial tamponade, intravascular volume depletion, venous vasodilatation; Decreased Rate of Ventricular Contraction: Ischemic and dilated cardiomyopathy, aortic stenosis, myocarditis.