EZRA A. AMSTERDAM, MD Professor of Medicine (Cardiology); Associate Chief, Division of Cardiovascular Medicine, University of California, Davis,
School of Medicine, Sacramento; and a member of the Patient Care Subspecialist Advisory Board.
Chest pain causes several million visits to emergency departments (EDs) across the country each year.1 Since most of these patients are considered to be at low risk for cardiac ischemic events, knowing how to proceed in a cost-effective
manner can be difficult. Less than 30% of the 2 million patients admitted for suspected acute MI each year in the United States
ultimately receive a diagnosis related to a coronary condition.2 On the other hand, 2% to 4% of patients with acute MI are released from the ED because the event goes unrecognized, and failure
to diagnose MI is a leading cause of malpractice suits among ED physicians. Safe navigation of this clinical situation requires
that physicians know how to make an accurate and cost-effective risk assessment.
As stated in the 31st Bethesda Conference on Emergency Cardiac Care, the goals of the initial clinical assessment of any patient
presenting with acute chest pain include
- Differentiating patients with ischemia or infarction from those with other potentially lethal conditions, such as pulmonary
embolism or aortic dissection.
- Determining whether the patient with ischemia or infarction is at risk for an early bad outcome.
- Initiating appropriate therapy promptly.
1
Categorizing patients with chest pain
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Since we now understand that many patients who present with chest pain are at low risk for an acute coronary syndrome (ACS),
new protocols for their evaluation have been developed. Depending on the institution, patients who are identified as low risk
on presentation may be admitted to a short-stay unit, telemetry unit, or chest pain center. Accelerated diagnostic protocols
(ADPs) for patients initially identified as being at low risk have increased the accuracy and efficiency of the workup for
chest pain. ADPs include observation with serial ECGs and cardiac markers for 6 to 12 hours and, if results are negative,
a stress test prior to discharge. If the evaluation results are positive at any point, the patient is admitted for further
management.
SPOTTING THE "LOW-RISK" PATIENT Over the past 20 years, cardiologists have grown more confident in identifying clinically stable patients with nontraumatic
chest pain as low-risk based on the nature of the chest pain, the cardiac history, and initial ECG findings.3
The risk of MI in a low-risk patient is less than 5%, and the risk of cardiac complications is less than 1%.4 These estimates are based on the results of a 1996 study in which a derivation set of more than 10,000 patients with chest
pain was used to identify predictors of major complications. The predictors were then validated in a second set of more than
4600 patients with chest pain evaluated at one hospital between 1990 and 1994 (see "Categorizing patients with chest pain").5
Nature of the chest pain Not reliably diagnostic by itself, the nature of chest pain can point the clinical investigation in one direction or another
depending on other findings, such as the ECG results, history, and physical examination. In the absence of other clues (such
as ECG evidence of injury/ischemia), erratic, inconsistent chest symptoms are strikes against an ischemic source. More detailed
information about chest pain is presented in the next main section.
Cardiac history Chest discomfort suggestive of angina is more ominous in a 70-year-old man with a history of hyperlipidemia, smoking, and
previous angina than in a 25-year-old woman with no known cardiac risk factors. Although the history may be less clear-cut
in many patients, it nonetheless holds important clues. The likelihood of coronary artery disease (CAD) in a symptomatic patient
according to age and sex was presented in a recent guideline published by the American College of Cardiology and the American
Heart Association (ACC/AHA) (see Table 1).6
TABLE 1 : Pretest likelihood of coronary artery disease by age and sex
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Initial ECG findings In the 1996 study mentioned above, investigators found that the following findings were associated with an increased risk
of complications: ST-segment elevation or Q waves on the ECG that were indicative of acute MI, other ECG changes indicative
of ischemia, low systolic BP, pulmonary rales above the bases, and exacerbation of known ischemic heart disease.4 In practice, any of the following ECG findings are considered abnormal and indicative of possible ACS:
- Pathologic Q waves
- ST-segment elevation
- ST-segment depression
- T-wave inversion consistent with ischemia/injury or strain
- Left ventricular hypertrophy
- Left bundle branch block
- Paced rhythm.7
Evaluating and managing patients with possible acute coronary syndrome
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In contrast, normal or near-normal ECG findings on admission are associated with a low risk of complications or bad outcomes.
In a landmark study, the serious complication rate was 0.6% among patients with normal ECG results, compared with 14% among
patients with abnormal findings.8 It is often easier to determine which patients with chest pain are unlikely to have a bad outcome than it is to determine
the source of the chest pain itself.
Immediate steps Low-risk patients with chest pain can expect to undergo
- 6 to 12 hours of observation with serial 12-lead ECGs
- Continuous ECG monitoring
- Serial measurements of cardiac markers.
If ACS is confirmed at any time during the evaluation, definitive treatment begins in earnest (see "Evaluating and managing
patients with possible acute coronary syndrome,") 9
Aspirin, yes or no? It is usually safe to delay administering aspirin to low-risk patients with chest pain. If another etiology, notably aortic
dissection or peptic ulcer is confirmed, aspirin will complicate treatment. Aspirin can be administered at any point at which
the evaluation becomes positive for ACS.
TABLE 2 : Diagnostic features of chest pain
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HISTORY, PHYSICAL EXAMINATION, RISK ASSESSMENT ACS in its several forms (ST-elevation MI, non-ST-elevation MI, unstable angina) is only one of the multiple causes of chest
pains (see Table 2). When a patient seeks medical help because of chest pain, primary concerns include determining the likelihood
that acute MI, aortic dissection, or pulmonary embolism may be involved so that the appropriate treatment steps are taken
quickly. Cardiologists note that a very large percentage of patients whose chest pain does not have a cardiac etiology are
found to have panic disorder. This underscores the need to determine the cause of the chest pain, even if a life-threatening
condition is ruled out, to ensure that the patient receives effective treatment and unnecessary ED utilization is minimized.
Conversely, it is important to understand that 25% of acute MIs are silent or occur without chest discomfort, and that dyspnea,
not angina, may be the predominant symptom. These atypical presentations are more common in women and the elderly but are
not limited to them.
Pain characteristics and history Typical, stable angina has the following characteristics:
- Chest discomfort that is substernal
- Pain that is provoked by exertion or emotional stress
- Pain that is relieved by rest or nitroglycerin in less than 5 minutes. (In unstable angina or MI, symptoms tend to be more
prolonged, or there may be minimal response to nitroglycerin.)
Atypical angina meets 2 of these 3 criteria. Noncardiac chest pain meets 1 or none of these criteria. Although response to
nitroglycerin has been traditionally utilized for diagnostic purposes in patients presenting with chest pain, several studies
have recently shown that its utility for this purpose is very limited.
Because the word pain means different things to different people and the chest sensations associated with acute MI can assume different forms,
we prefer to ask patients about the nature of their chest discomfort. Patients typically use these or similar words to describe the sensations in their chest during ACS: pressure, heaviness,
squeezing, tightness, burning, sharp, sticking, and throbbing.
Other important characteristics of the pain include its location, duration, frequency ("Does this happen to you very often?"),
and precipitants. If the patient has had similar episodes, ask what measures relieve the pain and whether the pain is stable,
better, or worse than it has been in the past.
Suspect a possible psychogenic disorder when a patient reports severe pain but appears to be relatively comfortable. Conversely,
do not overlook the possibility that a person with a history of panic disorder might also have new-onset CAD. Gastroesophageal
reflux disease can make evaluation of chest symptoms very difficult, since it frequently coexists with CAD, and stress may
exacerbate both conditions.
Physical examination The thorax and abdomen are the focus of the physical examination. A thorough examination that includes inspection, palpation,
and auscultation may help avoid more expensive diagnostic modalities. For example, a physician who is skilled in physical
examination can accurately estimate left ventricular size (by palpation) and right-heart filling pressure (by inspection of
jugular venous pulse and detection of a positive hepatojugular reflux).
When taking the patient's vital signs, it is crucial to obtain BP measurements in both arms. Discrepant measurements (more
than 10 mm Hg) suggest an aortic aneurysm. Is facial pallor or flushing present? Are the lips cyanotic, suggesting pulmonary
insufficiency? Signs of circulatory insufficiency (pallor, poor capillary refill, and peripheral cyanosis) should be sought
in the hands and feet. Check the neck veins for distention and abnormal wave forms.
Does the chest wall have sore spots that suggest fractured ribs? Is there sternal tenderness that is consistent with costochondritis?
An area of hyperresonance in a patient with chest pain and dyspnea suggests pneumothorax, while dullness to percussion may
be a clue to pulmonary consolidation. A pulsatile mass in the abdomen is strongly suggestive of an aneurysm. Consider pancreatitis
if there is epigastric tenderness or biliary tract disease if right upper quadrant tenderness is present with Murphy's sign.
A rectal examination and stool guaiac test are essential if thrombolytic therapy may be necessary.
In a patient with CAD who has no history of MI, the results of cardiac auscultation may be normal. During periods of ischemia,
however, BP and heart rate may increase, and S3 or S4 gallops, pulmonary crackles, and murmurs suggestive of mitral regurgitation may be audible. These signs remit when the ischemia
resolves because they are the result of transient left ventricular dysfunction.10 Other points to keep in mind during cardiac auscultation include the following:
- Aortic stenosis is possible if a harsh systolic ejection murmur is present over the aortic valve.
- Acute MI may cause a mitral regurgitation murmur or gallop rhythm.
- Pericarditis is present if you hear a precordial rub. A similar sound over the lungs suggests a pleuritic process.
EXERCISE TESTING Stress testing follows a 6- to 12-hour observation period with negative findings. The test may be treadmill exercise or stress
imaging (nuclear or echocardiographic), which can be performed either with exercise or, if the patient is unable to exercise,
pharmacologic stress. At our institution, exercise treadmill testing (ETT) is the preferred method in patients who can exercise
and have a normal baseline ECG. While the relative insensitivity of the ETT for identifying CAD is acknowledged, a negative
ETT indicates absence of inducible ischemia, and this finding is a strong indicator that the patient does not have ACS and can be safely discharged to further outpatient
evaluation.
This represents a marked shift from the thinking of several years ago, when exercise testing in a patient with chest pain
was generally proscribed. As a result of several studies demonstrating the safety and efficacy of ETT in selected patients,
the ACC/AHA now approves its use in patients who have undergone the requisite hours of observation and in whom other test
results have not indicated ischemia or MI. In ETT, the speed and grade of a treadmill are increased in an attempt to induce
myocardial ischemia detectable on an ECG. Patients who are candidates for ETT meet the following criteria:
- Chest pain suggestive of ACS
- Ability to exercise
- Normal ECG results, minor ST-T changes, or no change from a previous abnormal result
- Normal cardiovascular examination, including bilateral BP
- Hemodynamic stability
- No arrhythmia
- Normal serial serum cardiac markers
- No acute process apparent on chest x-ray film.11
TABLE 3 : Contraindications to exercise testing
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Contraindications to exercise testing are listed in Table 3. In conventional ETT, the test is limited by symptoms, but in
this situation, the onset of any abnormality is a signal to stop the test. In addition to symptom onset, other test end points
include
- Ischemic ST-segment depression
- A decrease in systolic BP of 10 mm Hg or more
- A sustained arrhythmia
- Two or more sustained ventricular ectopic complexes.
Chest pain that develops during the test is a less reliable indicator of ischemia than a 1-mm or greater horizontal or downsloping
ST-segment depression that occurs during exercise or in the recovery period. Severe CAD and a serious prognosis are more likely
when the ST-segment depression is greater than 2 mm or develops while the patient's heart rate is less than 130 beats per
minute.
Results are considered nondiagnostic when there is no evidence of ischemia but the maximum attained heart rate is less than
85% of the age-predicted rate. Patients with positive test results are admitted, and those with negative results are discharged
and typically have a cardiac event rate of less than 1% over the subsequent 30 days.11 Selected patients with nondiagnostic test results can be discharged with prompt outpatient follow-up.
A recent study that included more than 3000 patients who were members of the Framingham Heart Study cohort confirmed the usefulness
of ETT in coronary heart disease (CHD) prediction.12 (These patients were stable and undergoing elective, outpatient evaluations and not experiencing chest pain at the time of
the test, however.) Among men with a 10-year predicted CHD risk of at least 20% based on the cardiac risk-factor profile,
failure to reach the target heart rate and ST-segment depression were associated with more than a doubling of the risk of
a cardiac event during follow-up. Each metabolic equivalent increment in exercise capacity reduced the risk of a cardiac event
by 13%. Because so few events occurred among women in this cohort, it was not possible to assess the relationship between
ETT results and CHD risk in this subpopulation.
Either myocardial stress scintigraphy or echocardiography is an option for patients who are unable to exercise, but each is
more expensive than ETT. The sensitivity and specificity of these methods are 80% to 90%. Note that exercise testing with
myocardial perfusion scintigraphy, echocardiography, and coronary angiography are recommended to rule out coronary anomalies
in athletes, especially young ones, who present with chest pain, exertional syncope, or serious arrhythmias.
There have been several studies with electron-beam computed tomography in low-risk patients presenting to the ED with chest
pain. Although the accuracy of a negative test result is excellent in predicting the absence of cardiac events in the short
term, there is a high rate of false positive tests (positive coronary calcium score without obstructive CAD) that result in
unnecessary admissions. This method requires further investigation in the ED setting.
FOLLOW-UP CARE Although it is sometimes easier to rule out a cardiac event as the cause of a patient's chest pain than it is to identify
the actual cause of the pain, follow-up is essential, both as a means of relieving the patient's discomfort and to reduce
unnecessary future use of the ED. After any further indicated cardiac tests, the focus should be on the GI, musculoskeletal,
and pulmonary systems. The possibility of psychogenic causes should be explored as well, since as many as 40% of low-risk
patients with chest pain have panic disorder, somatization disorder, or a so-called sensitive heart.
This viewpoint article was written by Mary Desmond Pinkowish, MPH, in consultation with Dr Amsterdam.
Dr Amsterdam discloses that he has no financial involvements with any companies doing business in this field.
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