Of all the diagnostic tools clinically used in assessing chest pain, the electro-cardiogram (ECG) is the most reliable when used and interpreted correctly. Patients with acute infarctions may have ECG findings that range from acute ST-segment elevations to completely normal. This range means that the ECG is useful only when it has a positive, or diagnostic, finding. New ST-segment elevations, Q waves, bundle branch block, and T-wave inversions or normalizations are strongly suggestive of ischemia and warrant aggressive management in the emergency department (ED). The presence of a normal or unchanged ECG does not rule out the diagnosis of acute myocardial ischemia.
Serum markers, if positive, are highly specific for AMI. Creatinine kinase and its MB isoenzyme constitute the historical gold standard for diagnosing AMI, but have been replaced by troponin as the standard for the diagnosis of AMI. Cardiac-specific troponin I and T are not found in skeletal muscle, and have a much greater sensitivity and specificity for AMI. Other clinical conditions such as aortic dissection, acute CHF, aortic valve disease, and some arrhythmias can be associated with an elevated troponin in the absence of ischemic heart disease. However, the documentation of normal serum markers in the bloodstream does not exclude the diagnosis of AMI. These enzymes will not become elevated in serious disease conditions such as unstable angina. The use of these markers can aid the clinician in assessing risk for patients with chest pain, including disposition within the hospital. A serial enzyme evaluation can be used to appropriately risk stratify individual patients (Fig. 17-1).
Serum biomarker curve. Typical pattern of serum marker elevation after acute myocardial infarction (AMI).
Key: CK-MB = MB fraction of creatine kinase; cTnI = cardiac troponin I; cTnT = cardiac troponin T; LD1 = lactate dehydrogenase isoenzyme 1; MLC = myosin light chain.
Emergency 2-dimensional echocardiography may have value in the evaluation of chest pain when the ECG is nondiagnostic, eg, in patients with pacemakers, have a bundle branch block, or have an abnormal ECG at baseline. The finding of regional wall motion abnormalities in the acutely symptomatic patient is strongly suggestive of active ischemia. Wall motion abnormality also may represent previous myocardial injury. Two-dimensional echocardiography also may aid in the diagnosis of other conditions that may mimic ischemic disease, such as pericarditis, aortic dissection, or hypertrophic cardiomyopathy.
Many tests currently being performed in some EDs will unmask otherwise unrecognized but clinically significant ischemic disease. Patients with atypical chest pain and a normal stress thallium or technetium scan have a very low incidence of short- and long-term subsequent ischemic events. Thallium or sestamibi testing can be done in the ED to further risk stratify patients in the hospital and perhaps be used in consideration for patient discharge from the ED.
The priority must always be to exclude life-threatening conditions, and the ED physicians should organize their test-ordering strategies to screen for those conditions first. (Table 17-1 lists possible causes of nontraumatic chest pain.)
Table 17-1 Life-Threatening Causes of Chest Pain: Classic Symptoms Compared* ||Download (.pdf)
Table 17-1 Life-Threatening Causes of Chest Pain: Classic Symptoms Compared*
|Disorder||Character of Pain|
|Angina pectoris||Tightness, crushing, or squeezing pressure in the retrosternal or epigastric area, with radiation to R or L shoulder, arm, or jaw.|
|Massive pulmonary embolism||Heaviness, tightness involving the whole chest, in the setting of unstable vital signs, and/or syncope, with a sense of impending doom.|
|Segmental pulmonary embolism||Pleuritic chest pain in a focal area of the chest, with associated tachypnea or tachycardia and/or dyspnea.|
|Aortic dissection||Ripping or tearing substernal pain, radiating to the back (intrascapular), possibly with neurologic symptoms (focal hypoperfusion).|
|Pneumothorax||Sharp, sudden, lancinating, pleuritic pain on one side of the chest, associated with dyspnea.|
|Esophageal rupture||Sudden, sharp, substernal chest pain following forceful vomiting, with radiation to the back.|
|Pericarditis||Sharp, constant or pleuritic substernal chest pain, with radiation to the back or shoulder.|
|Pneumonia||Sharp, pleuritic focal chest pain associated with fever.|
|Perforated ulcer||Severe, sharp epigastric pain, radiating to the back, with acute distress.|
What follows is list of common etiologies of chest pain that should be considered by the emergency physician (Table 17-1).
The typical pain of chronic stable angina is episodic and lasts 5 to 15 min. It is precipitated by exertion and relieved with rest or sublingual nitroglycerin within 3 min. The pain is typically visceral in nature (aching, pressure, and squeezing), with radiation to the neck, jaw, arm, or hand. In individual patients the character of each attack varies little with recurrent episodes. Most patients can differentiate their usual angina from other causes of pain. Physicians evaluating patients with stable angina should screen carefully for changes in the pattern that would suggest a shift from stable to unstable angina or even suggest a different diagnosis.
Patients who complain of recent onset of angina, changes in the character of the angina, or angina at rest are thought to have an unstable pattern of their angina. They are at risk for an AMI or sudden cardiac death (see Chapter 18 for management).
Variant (Prinzmetal) Angina
This form of angina is thought to be due to spasm of the epicardial vessels in patients with normal coronary arteries (one-third of cases) or in patients with underlying atherosclerotic disease (two-thirds of cases). Pain typically occurs at rest and may be precipitated by the use of tobacco or cocaine. The ECG typically shows ST-segment elevations during an acute attack.
Acute Myocardial Infarction
Ischemic pain that lasts longer than 15 min, is not relieved by nitroglycerin, or is accompanied by diaphoresis, dyspnea, nausea, or vomiting suggests the diagnosis of AMI. The clinician must understand the limitations of the screening tools used in the ED and should have a high level of suspicion for AMI in patients with risk factors and prolonged or persistent symptoms for which there is no other clear diagnosis (see Chapter 18).
This diagnosis should be suspected in the patient who complains of sudden onset of severe, tearing pain in the retrosternal or midscapular area. High-risk patients are also those at risk for AMI, specifically the middle-age hypertensive male. The patient may be hypertensive or hypotensive in shock. There may be a diastolic murmur of aortic regurgitation, indicating a proximal dissection, or distal pulse deficits, indicating a distal dissection. The dissection may occlude coronary ostia, resulting in myocardial infarction, or the carotids, resulting in cerebral ischemia and stroke. Chest x-ray, computed tomography, transesophageal echocardiography (TEE), and angiography can aid in the diagnosis of this condition (see Chapter 27 for a complete discussion of aortic dissection).
The patient with pericarditis typically will complain of pain that is constant, retrosternal, and radiating to the back, neck, or jaw. Pain is classically worsened by lying supine and is relieved by sitting forward. The presence of a pericardial friction rub supports the diagnosis. ECG may show PR-segment depressions, diffuse ST-segment elevations, or T-wave inversions that are typically diffuse (see Chapter 24 for a complete discussion of pericarditis).
Acute Pericardial Tamponade
Patients with acute tamponade may complain of positional or pleuritic chest pain, dyspnea, and palpitations. Physical examination will show tachycardia, hypotension, jugular venous distention, and distant heart sounds. If cardiovascular collapse is imminent, emergent pericardiocentesis is indicated.
Patients typically complain of sudden onset of pleuritic chest pain associated with dyspnea, tachypnea, tachycardia, or hypoxemia. The absence of any of these findings does not preclude the diagnosis, and a high index of suspicion is essential (see Chapter 25 for a complete discussion of pulmonary embolism).
Chest pain due to irritation or inflammation of structures in the chest wall is commonly seen in the ED. Possible causes include costochondritis, intercostal strain due to severe coughing, and pectoralis muscle strain in the setting of recent physical exertion. Patients will complain of sharp pain that is worsened with movement of the chest wall (eg, coughing, and some pain that can be elicited by palpation of the chest wall). These findings in patients without any other symptoms and no history of significant cardiac disease support the diagnosis of musculoskeletal pain. This pain is generally responsive to nonsteroidal anti-inflammatory drugs. It is important to emphasize that the presence of chest wall tenderness does not rule out the possibility of myocardial ischemia.
Esophageal reflux, dyspepsia syndromes, and esophageal motility disorders can produce chest pain that is difficult to distinguish from ischemic pain. Patients may complain of burning, gnawing pain associated with an acid taste radiating into the throat. Pain may be exacerbated by meals, worsen when supine, and may be associated with belching. Clinicians should determine whether the symptoms are due to a GI disorder based on the clinical presentation and the absence of findings and/or risk factors suggesting an ischemic cause. Diagnostic decisions should not be made on the basis of a response to a therapeutic trial of antacids, GI cocktails, or nitroglycerin (see Chapters 35, 40, and 41 for more discussion on GI causes of chest pain).