Causes of Chest Discomfort
Myocardial Ischemia and Injury
Myocardial ischemia occurs when the oxygen supply to the heart is insufficient to meet metabolic needs. This mismatch can result from a decrease in oxygen supply, a rise in demand, or both. The most common underlying cause of myocardial ischemia is obstruction of coronary arteries by atherosclerosis; in the presence of such obstruction, transient ischemic episodes are usually precipitated by an increase in oxygen demand as a result of physical exertion. However, ischemia can also result from psychological stress, fever, or large meals or from compromised oxygen delivery due to anemia, hypoxia, or hypotension. Ventricular hypertrophy due to valvular heart disease, hypertrophic cardiomyopathy, or hypertension can predispose the myocardium to ischemia because of impaired penetration of blood flow from epicardial coronary arteries to the endocardium.
(See also Chap. 243) The chest discomfort of myocardial ischemia is a visceral discomfort that is usually described as a heaviness, pressure, or squeezing (Table 12-2). Other common adjectives for anginal pain are burning and aching. Some patients deny any “pain” but may admit to dyspnea or a vague sense of anxiety. The word “sharp” is sometimes used by patients to describe intensity rather than quality.
Table 12-2 Typical Clinical Features of Major Causes of Acute Chest Discomfort |Favorite Table|Download (.pdf)
Table 12-2 Typical Clinical Features of Major Causes of Acute Chest Discomfort
|Angina||More than 2 and less than 10 min||Pressure, tightness, squeezing, heaviness, burning||Retrosternal, often with radiation to or isolated discomfort in neck, jaw, shoulders, or arms—frequently on left|
Precipitated by exertion, exposure to cold, psychologic stress
S4 gallop or mitral regurgitationmurmur during pain
|Unstable angina||10–20 min||Similar to angina but often more severe||Similar to angina||Similar to angina, but occurs with low levels of exertion or even at rest|
|Acute myocardial infarction||Variable; often more than 30 min||Similar to angina but often more severe||Similar to angina|
Unrelieved by nitroglycerin
May be associated with evidence of heart failure or arrhythmia
|Aortic stenosis||Recurrent episodes as described for angina||As described for angina||As described for angina||Late-peaking systolic murmurradiating to carotid arteries|
|Pericarditis||Hours to days; may be episodic||Sharp||Retrosternal or toward cardiac apex; may radiate to left shoulder|
May be relieved by sitting up andleaning forward
Pericardial friction rub
|Aortic dissection||Abrupt onset of unrelenting pain||Tearing or rippingsensation; knifelike||Anterior chest, often radiating to back, between shoulder blades|
Associated with hypertension and/or underlying connective tissue disorder, e.g., Marfan syndrome
Murmur of aortic insufficiency, pericardial rub, pericardial tamponade, or loss of peripheral pulses
|Pulmonary embolism||Abrupt onset; several minutes to a few hours||Pleuritic||Often lateral, on the side of the embolism||Dyspnea, tachypnea, tachycardia, and hypotension|
|Pulmonary hypertension||Variable||Pressure||Substernal||Dyspnea, signs of increased venous pressure including edema and jugular venous distention|
|Pneumonia or pleuritis||Variable||Pleuritic||Unilateral, often localized||Dyspnea, cough, fever, rales, occasional rub|
|Spontaneous pneumothorax||Sudden onset; several hours||Pleuritic||Lateral to side of pneumothorax||Dyspnea, decreased breath sounds on side of pneumothorax|
|Esophageal reflux||10–60 min||Burning||Substernal, epigastric|
Worsened by postprandial recumbency
Relieved by antacids
|Esophageal spasm||2–30 min||Pressure, tightness, burning||Retrosternal||Can closely mimic angina|
|Peptic ulcer||Prolonged||Burning||Epigastric, substernal||Relieved with food or antacids|
|Gallbladder disease||Prolonged||Burning, pressure||Epigastric, right upper quadrant, substernal||May follow meal|
Aggravated by movement
May be reproduced by localized pressure on examination
|Herpes zoster||Variable||Sharp or burning||Dermatomal distribution||Vesicular rash in area of discomfort|
|Emotional and psychiatricconditions||Variable; may be fleeting||Variable||Variable; may be retrosternal|
Situational factors may precipitate symptoms
Anxiety or depression often detectable with careful history
The location of angina pectoris is usually retrosternal; most patients do not localize the pain to any small area. The discomfort may radiate to the neck, jaw, teeth, arms, or shoulders, reflecting the common origin in the posterior horn of the spinal cord of sensory neurons supplying the heart and these areas. Some patients present with aching in sites of radiated pain as their only symptoms of ischemia. Occasional patients report epigastric distress with ischemic episodes. Less common is radiation to below the umbilicus or to the back.
Stable angina pectoris usually develops gradually with exertion, emotional excitement, or after heavy meals. Rest or treatment with sublingual nitroglycerin typically leads to relief within several minutes. In contrast, pain that is fleeting (lasting only a few seconds) is rarely ischemic in origin. Similarly, pain that lasts for several hours is unlikely to represent angina, particularly if the patient's electrocardiogram (ECG) does not show evidence of ischemia.
Anginal episodes can be precipitated by any physiologic or psychological stress that induces tachycardia. Most myocardial perfusion occurs during diastole, when there is minimal pressure opposing coronary artery flow from within the left ventricle. Since tachycardia decreases the percentage of the time in which the heart is in diastole, it decreases myocardial perfusion.
Unstable Angina and Myocardial Infarction
(See also Chaps. 244 and 245) Patients with these acute ischemic syndromes usually complain of symptoms similar in quality to angina pectoris, but more prolonged and severe. The onset of these syndromes may occur with the patient at rest, or awakened from sleep, and sublingual nitroglycerin may lead to transient or no relief. Accompanying symptoms may include diaphoresis, dyspnea, nausea, and light-headedness.
The physical examination may be completely normal in patients with chest discomfort due to ischemic heart disease. Careful auscultation during ischemic episodes may reveal a third or fourth heart sound, reflecting myocardial systolic or diastolic dysfunction. A transient murmur of mitral regurgitation suggests ischemic papillary muscle dysfunction. Severe episodes of ischemia can lead to pulmonary congestion and even pulmonary edema.
Myocardial ischemia caused by hypertrophic cardiomyopathy or aortic stenosis leads to angina pectoris similar to that caused by coronary atherosclerosis. In such cases, a loud systolic murmur or other findings usually suggest that abnormalities other than coronary atherosclerosis may be contributing to the patient's symptoms. Some patients with chest pain and normal coronary angiograms have functional abnormalities of the coronary circulation, ranging from coronary spasm visible on coronary angiography to abnormal vasodilator responses and heightened vasoconstrictor responses. The term “cardiac syndrome X” is used to describe patients with angina-like chest pain and ischemic-appearing ST-segment depression during stress despite normal coronary arteriograms. Some data indicate that many such patients have limited changes in coronary flow in response to pacing stress or coronary vasodilators.
(See also Chap. 239) The pain in pericarditis is believed to be due to inflammation of the adjacent parietal pleura, since most of the pericardium is believed to be insensitive to pain. Thus, infectious pericarditis, which usually involves adjoining pleural surfaces, tends to be associated with pain, while conditions that cause only local inflammation (e.g., myocardial infarction or uremia) and cardiac tamponade tend to result in mild or no chest pain.
The adjacent parietal pleura receives its sensory supply from several sources, so the pain of pericarditis can be experienced in areas ranging from the shoulder and neck to the abdomen and back. Most typically, the pain is retrosternal and is aggravated by coughing, deep breaths, or changes in position—all of which lead to movements of pleural surfaces. The pain is often worse in the supine position and relieved by sitting upright and leaning forward. Less common is a steady aching discomfort that mimics acute myocardial infarction.
(See also Chap. 248) Aortic dissection is a potentially catastrophic condition that is due to spread of a subintimal hematoma within the wall of the aorta. The hematoma may begin with a tear in the intima of the aorta or with rupture of the vasa vasorum within the aortic media. This syndrome can occur with trauma to the aorta, including motor vehicle accidents or medical procedures in which catheters or intraaortic balloon pumps damage the intima of the aorta. Nontraumatic aortic dissections are rare in the absence of hypertension and/or conditions associated with deterioration of the elastic or muscular components of the media within the aorta's wall. Cystic medial degeneration is a feature of several inherited connective tissue diseases, including Marfan and Ehlers-Danlos syndromes. About half of all aortic dissections in women under 40 years of age occur during pregnancy.
Almost all patients with acute dissections present with severe chest pain, although some patients with chronic dissections are identified without associated symptoms. Unlike the pain of ischemic heart disease, symptoms of aortic dissection tend to reach peak severity immediately, often causing the patient to collapse from its intensity. The classic teaching is that the adjectives used to describe the pain reflect the process occurring within the wall of the aorta—”ripping” and “tearing”—but more recent data suggest that the most common presenting complaint is sudden onset of severe, sharp pain. The location often correlates with the site and extent of the dissection. Thus, dissections that begin in the ascending aorta and extend to the descending aorta tend to cause pain in the front of the chest that extends into the back, between the shoulder blades.
Physical findings may also reflect extension of the aortic dissection that compromises flow into arteries branching off the aorta. Thus, loss of a pulse in one or both arms, cerebrovascular accident, or paraplegia can all be catastrophic consequences of aortic dissection. Hematomas that extend proximally and undermine the coronary arteries or aortic valve apparatus may lead to acute myocardial infarction or acute aortic insufficiency. Rupture of the hematoma into the pericardial space leads to pericardial tamponade.
Another abnormality of the aorta that can cause chest pain is a thoracic aortic aneurysm. Aortic aneurysms are frequently asymptomatic but can cause chest pain and other symptoms by compressing adjacent structures. This pain tends to be steady, deep, and sometimes severe.
(See also Chap. 262) Chest pain due to pulmonary embolism is believed to be due to distention of the pulmonary artery or infarction of a segment of the lung adjacent to the pleura. Massive pulmonary emboli may lead to substernal pain that is suggestive of acute myocardial infarction. More commonly, smaller emboli lead to focal pulmonary infarctions that cause pain that is lateral and pleuritic. Associated symptoms include dyspnea and, occasionally, hemoptysis. Tachycardia is usually present. Although not always present, certain characteristic ECG changes can support the diagnosis.
(See also Chap. 263) Sudden onset of pleuritic chest pain and respiratory distress should lead to consideration of spontaneous pneumothorax, as well as pulmonary embolism. Such events may occur without a precipitating event in persons without lung disease, or as a consequence of underlying lung disorders.
(See also 9128129 and 263) Lung diseases that damage and cause inflammation of the pleura of the lung usually cause a sharp, knifelike pain that is aggravated by inspiration or coughing.
(See also Chap. 292) Esophageal pain from acid reflux from the stomach, spasm, obstruction, or injury can be difficult to differentiate from myocardial syndromes. Acid reflux typically causes a deep burning discomfort that may be exacerbated by alcohol, aspirin, or some foods; this discomfort is often relieved by antacid or other acid-reducing therapies. Acid reflux tends to be exacerbated by lying down and may be worse in early morning when the stomach is empty of food that might otherwise absorb gastric acid.
Esophageal spasm may occur in the presence or absence of acid reflux and leads to a squeezing pain indistinguishable from angina. Prompt relief of esophageal spasm is often provided by antianginal therapies such as sublingual nifedipine, further promoting confusion between these syndromes. Chest pain can also result from injury to the esophagus, such as a Mallory-Weiss tear caused by severe vomiting.
Chest pain can result from diseases of the gastrointestinal tract below the diaphragm, including peptic ulcer disease, biliary disease, and pancreatitis. These conditions usually cause abdominal pain as well as chest discomfort; symptoms are not likely to be associated with exertion. The pain of ulcer disease typically occurs 60 to 90 min after meals, when postprandial acid production is no longer neutralized by food in the stomach. Cholecystitis usually causes a pain that is described as aching, occurring an hour or more after meals.
Cervical disk disease can cause chest pain by compression of nerve roots. Pain in a dermatomal distribution can also be caused by intercostal muscle cramps or by herpes zoster. Chest pain symptoms due to herpes zoster may occur before skin lesions are apparent.
Costochondral and chondrosternal syndromes are the most common causes of anterior chest musculoskeletal pain. Only occasionally are physical signs of costochondritis such as swelling, redness, and warmth (Tietze's syndrome) present. The pain of such syndromes is usually fleeting and sharp, but some patients experience a dull ache that lasts for hours. Direct pressure on the chondrosternal and costochondral junctions may reproduce the pain from these and other musculoskeletal syndromes. Arthritis of the shoulder and spine and bursitis may also cause chest pain. Some patients who have these conditions and myocardial ischemia blur and confuse symptoms of these syndromes.
Emotional and Psychiatric Conditions
As many as 10% of patients who present to emergency departments with acute chest discomfort have panic disorder or other emotional conditions. The symptoms in these populations are highly variable, but frequently the discomfort is described as visceral tightness or aching that lasts more than 30 min. Some patients offer other atypical descriptions, such as pain that is fleeting, sharp, and/or localized to a small region. The ECG in patients with emotional conditions may be difficult to interpret if hyperventilation causes ST-T-wave abnormalities. A careful history may elicit clues of depression, prior panic attacks, somatization, agoraphobia, or other phobias.
Approach to the Patient: Chest Discomfort
The evaluation of the patient with chest discomfort must accommodate two goals—determining the diagnosis and assessing the safety of the immediate management plan. The latter issue is often dominant when the patient has acute chest discomfort, such as patients seen in the emergency department. In such settings, the clinician must focus first on identifying patients who require aggressive interventions to diagnose or manage potentially life-threatening conditions, including acute ischemic heart disease, acute aortic dissection, pulmonary embolism, and tension pneumothorax. If such conditions are unlikely, the clinician must address questions such as the safety of discharge to home, admission to a non-coronary care unit facility, or immediate exercise testing. Table 12-3 displays a sequence of questions that can be used in the evaluation of the patient with chest discomfort, with the diagnostic entities that are most important for consideration at each stage of the evaluation.
Table 12-3 Considerations in the Assessmentof the Patient with Chest Discomfort |Favorite Table|Download (.pdf)
Table 12-3 Considerations in the Assessmentof the Patient with Chest Discomfort
|1. Could the chest discomfort be due to an acute, potentially life-threatening condition that warrants immediate hospitalization and aggressive evaluation?|
|Acute ischemic heart disease||Pulmonary embolism|
|Aortic dissection||Spontaneous pneumothorax|
|2. If not, could the discomfort be due to a chronic condition likely to lead to serious complications?|
|3. If not, could the discomfort be due to an acute condition that warrants specific treatment?|
|4. If not, could the discomfort be due to another treatable chronic condition?|
|Esophageal reflux||Cervical disk disease|
|Esophageal spasm||Arthritis of the shoulderor spine|
|Peptic ulcer disease||Costochondritis|
|Gallbladder disease||Other musculoskeletal disorders|
|Other gastrointestinal conditions||Anxiety state|
In patients with acute chest discomfort, the clinician must first assess the patient's respiratory and hemodynamic status. If either is compromised, initial management should focus on stabilizing the patient before the diagnostic evaluation is pursued. If, however, the patient does not require emergent interventions, then a focused history, physical examination, and laboratory evaluation should be performed to assess the patient's risk of life-threatening conditions.
Clinicians who are seeing patients in the office setting should not assume that they do not have acute ischemic heart disease, even if the prevalence may be lower. Malpractice litigation related to myocardial infarctions that were missed during office evaluations is becoming increasingly common, and ECGs were not performed in many such cases. The prevalence of high-risk patients seen in office settings may be increasing due to congestion in emergency departments.
In either setting, the history should include questions about the quality and location of the chest discomfort (Table 12-2). The patient should also be asked about the nature of onset of the pain and its duration. Myocardial ischemia is usually associated with a gradual intensification of symptoms over a period of minutes. Pain that is fleeting or that lasts hours without being associated with electrocardiographic changes is not likely to be ischemic in origin. Although the presence of risk factors for coronary artery disease may heighten concern for this diagnosis, the absence of such risk factors does not lower the risk for myocardial ischemia enough to be used to justify a decision to discharge a patient.
Wide radiation of chest pain increases probability that pain is due to myocardial infarction. Radiation of chest pain to the left arm is common with acute ischemic heart disease, but radiation to the right arm is also highly consistent with this diagnosis. Figure 12-1 shows estimates derived from several studies of the impact of various clinical features from the history on the probability that a patient has an acute myocardial infarction.
Impact of chest pain characteristics on odds of acute myocardial infarction (AMI). (Figure prepared from data in Swap and Nagurney.)
Right shoulder pain is also common with acute cholecystitis, but this syndrome is usually accompanied by pain that is located in the abdomen rather than chest. Chest pain that radiates between the scapulae raises the question of aortic dissection.
The physical examination should include evaluation of blood pressure in both arms and of pulses in both legs. Poor perfusion of a limb may be due to an aortic dissection that has compromised flow to an artery branching from the aorta. Chest auscultation may reveal diminished breath sounds; a pleural rub; or evidence of pneumothorax, pulmonary embolism, pneumonia, or pleurisy. Tension pneumothorax may lead to a shift in the trachea from the midline, away from the side of the pneumothorax. The cardiac examination should seek pericardial rubs, systolic and diastolic murmurs, and third or fourth heart sounds. Pressure on the chest wall may reproduce symptoms in patients with musculoskeletal causes of chest pain; it is important that the clinician ask the patient if the chest pain syndrome is being completely reproduced before drawing too much reassurance that more serious underlying conditions are not present.
An ECG is an essential test for adults with chest discomfort that is not due to an obvious traumatic cause. In such patients, the presence of electrocardiographic changes consistent with ischemia or infarction (Chap. 228) is associated with high risks of acute myocardial infarction or unstable angina (Table 12-4); such patients should be admitted to a unit with electrocardiographic monitoring and the capacity to respond to a cardiac arrest. The absence of such changes does not exclude acute ischemic heart disease, but the risk of life-threatening complications is low for patients with normal electrocardiograms or only nonspecific ST-T-wave changes. If these patients are not considered appropriate for immediate discharge, they are often candidates for early or immediate exercise testing.
Table 12-4 Prevalence of Acute Ischemic Heart Disease Syndromes among Subsets of Emergency Department Patients with Chest Pain |Favorite Table|Download (.pdf)
Table 12-4 Prevalence of Acute Ischemic Heart Disease Syndromes among Subsets of Emergency Department Patients with Chest Pain
|Finding||PrevalenceMyocardial Infarction, %||Unstable Angina, %|
|ST elevation (≥1 mm) or Q waves on ECG not known to be old||79||12|
|Ischemia or strain on ECG not known to be old (ST depression ≥1 mm or ischemic T waves)||20||41|
|None of the preceding ECG changes but a prior history of angina or myocardial infarction (history of heart attack or nitroglycerin use)||4||51|
|None of the preceding ECG changes and no prior history of angina or myocardial infarction (history of heart attack or nitroglycerin use)||2||14|
Markers of myocardial injury are often obtained in the emergency department evaluation of acute chest discomfort. In recent years, the cardiac troponins (I and T) have superceded creatine kinase (CK) and CK-MB as the markers of choice for detecting myocardial injury. Some data support the use of other markers, such as myeloperoxidase and B-type natriuretic peptide (BNP), but their roles in routine care have not been established. Single values of any of these markers do not have high sensitivity for acute myocardial infarction or for prediction of complications. Hence, decisions to discharge patients home should not be made on the basis of single negative values of these tests, including the cardiac troponins.
Provocative tests for coronary artery disease are not appropriate for patients with ongoing chest pain. In such patients, rest myocardial perfusion scans can be considered; a normal scan reduces the likelihood of coronary artery disease and can help avoid admission of low-risk patients to the hospital. Computerized tomographic angiography (CTA) is emerging as an alternative diagnostic strategy for patients in whom the likelihood of coronary disease is not clear.
Clinicians frequently employ therapeutic trials with sublingual nitroglycerin or antacids or, in the stable patient seen in the office setting, a proton pump inhibitor. A common error is to assume that a response to any of these interventions clarifies the diagnosis. While such information is often helpful, the patient's response may be due to the placebo effect. Hence, myocardial ischemia should never be considered excluded solely because of a response to antacid therapy. Similarly, failure of nitroglycerin to relieve pain does not exclude the diagnosis of coronary disease.
If the patient's history or examination is consistent with aortic dissection, imaging studies to evaluate the aorta must be pursued promptly because of the high risk of catastrophic complications with this condition. Appropriate tests include a chest CT scan with contrast, MRI, or transesophageal echocardiography. Current data indicate that elevated d-dimer levels should raise clinicians' suspicion of aortic dissection.
Acute pulmonary embolism should be considered in patients with respiratory symptoms, pleuritic chest pain, hemoptysis, or a history of venous thromboembolism or coagulation abnormalities. Initial tests usually include CT angiography or a lung scan, which are sometimes combined with lower extremity venous ultrasound or d-dimer testing.
If patients with acute chest discomfort show no evidence of life-threatening conditions, the clinician should then focus on serious chronic conditions with the potential to cause major complications, the most common of which is stable angina. Early use of exercise electrocardiography, stress echocardiography, or stress perfusion imaging for such patients, whether in the office or the emergency department, is now an accepted management strategy for low-risk patients. Exercise testing is not appropriate, however, for patients who (1) report pain that is believed to be ischemic occurring at rest or (2) have electrocardiographic changes not known to be old that are consistent with ischemia.
Patients with sustained chest discomfort who do not have evidence for life-threatening conditions should be evaluated for evidence of conditions likely to benefit from acute treatment (Table 12-3). Pericarditis may be suggested by the history, physical examination, and ECG (Table 12-2). Clinicians should carefully assess blood pressure patterns and consider echocardiography in such patients to detect evidence of impending pericardial tamponade. Chest x-rays can be used to evaluate the possibility of pulmonary disease.
Guidelines and Critical Pathwaysfor Acute Chest Discomfort
Guidelines for the initial evaluation for patients with acute chest pain have been developed by the American College of Cardiology, American Heart Association, and other organizations. These guidelines recommend performance of an ECG for virtually all patients with chest pain who do not have an obvious noncardiac cause of their pain, and performance of a chest x-ray for patients with signs or symptoms consistent with congestive heart failure, valvular heart disease, pericardial disease, or aortic dissection or aneurysm.
The American College of Cardiology/American Heart Association guidelines on exercise testing support its use in low-risk patients presenting to the emergency department, as well as in selected intermediate-risk patients. However, these guidelines emphasize that exercise tests should be performed only after patients have been screened for high-risk features or other indicators for hospital admission.
Many medical centers have adopted critical pathways and other forms of guidelines to increase efficiency and to expedite the treatment of patients with high-risk acute ischemic heart disease syndromes. These guidelines emphasize the following strategies:
- Rapid identification and treatment of patients for whom emergent reperfusion therapy, either via percutaneous coronary interventions or thrombolytic agents, is likely to lead to improved outcomes.
- Triage to non-coronary care unit monitored facilities such as intermediate-care units or chest pain units of patients with a low risk for complications, such as patients without new ischemic changes on their ECGs and without ongoing chest pain. Such patients can usually be safely observed in non-coronary care unit settings, undergo early exercise testing, or be discharged home. Risk stratification can be assisted through use of prospectively validated multivariate algorithms that have been published for acute ischemic heart disease and its complications.
- Shortening lengths of stay in the coronary care unit and hospital. Recommendations regarding the minimum length of stay in a monitored bed for a patient who has no further symptoms have decreased in recent years to 12 h or less if exercise testing or other risk stratification technologies are available.
Nonacute Chest Discomfort
The management of patients who do not require admission to the hospital or who no longer require inpatient observation should seek to identify the cause of the symptoms and the likelihood of major complications. Noninvasive tests for coronary disease serve both to diagnose this condition and to identify patients with high-risk forms of coronary disease who may benefit from revascularization. Gastrointestinal causes of chest pain can be evaluated via endoscopy or radiology studies, or with trials of medical therapy. Emotional and psychiatric conditions warrant appropriate evaluation and treatment; randomized trial data indicate that cognitive therapy and group interventions lead to decreases in symptoms for such patients.