Acute Chest Pain: When Is It Life-Threatening?

Emerg Med 38(10):20, 2006

Differentiating acute coronary syndrome from more benign causes of chest pain is a critical decision for the emergency physician. The authors sort through the differential diagnosis and present emergent interventions for life-threatening etiologies.

By Daniel S. Clark, MD, FACC, FAHA, Joseph Esherick, MD, FAAFP, and Robert Dachs, MD, FAAFP

Patients experiencing chest pain represent more than 5.3 million emergency department visits annually—or 2% to 8% of all visits. At least one third of these patients will have a non-lifethreatening etiology. Also, it appears that the percentage of patients with acute coronary ischemia who are mistakenly discharged from the emergency department is decreasing. Nevertheless, that risk is always present and is associated with significant morbidity and mortality and costly litigation.

The challenge to the emergency physician is to triage patients who have chest pain due to acute coronary syndrome (ACS) or other life-threatening causes from those patients with chest pain of more benign etiologies (see table below).

In this article, we will present an effective approach to the diagnosis and treatment of life-threatening chest pain in the emergency department.

DELAY IN SEEKING TREATMENT

Most patients with chest pain do not seek medical attention quickly after the onset of pain. The average delay is two hours. The causes for this include incorrect self-diagnosis, the presence of atypical symptoms, attempts to self-medicate, denial that the symptoms could be cardiac in origin, and lack of knowledge of the importance of rapid intervention.

Acute coronary syndrome is by far the most common life-threatening cause of chest pain. More than
1.4 million patients are hospitalized annually for ACS, and more than 1 million myocardial infarctions (MIs) occur each year.

Acute coronary syndrome includes unstable angina, non-ST-segment elevation MI (NSTEMI), and ST-segment-elevation MI (STEMI). The three conditions are usually the result of the sudden rupture of a soft, cholesterol-rich, atherosclerotic coronary artery plaque. They can be differentiated by ECG findings and the extent of myocardial damage.

KEY HISTORY FINDINGS

The common tools available to evaluate the patient with chest pain include the history, physical examination, 12-lead ECG, cardiac biochemical markers, chest x-ray, and treadmill stress testing. An echocardiogram and myocardial perfusion imaging can provide further information about the patient’s cardiovascular status, but these tests may not be readily available in all hospitals 24 hours a day.

The history, a limited physical examination, and an ECG should be performed within 10 minutes of the patient’s arrival. The chest pain history can be especially helpful. The presenting symptoms, characteristics of the pain, presence of associated symptoms or cardiovascular risk factors, and a history of cardiovascular disease should all be investigated.

Chest pain characteristics that suggest a cardiac etiology include: pain described as similar to prior angina or MI; associated nausea, vomiting, or diaphoresis; pain radiating to the neck or shoulder; and pain that worsens with exertion. Characteristics of chest pain that suggest a noncardiac etiology include: pain that is not exacerbated by effort; pain localized to a small area of the chest wall; pain that starts at maximum intensity; pain lasting only seconds or for hours to days; and pain that worsens with swallowing, deep breathing, coughing, palpation, or position changes (see table below).

The intensity of the chest pain is not particularly helpful. Neither can the response to a “GI cocktail” (viscous lidocaine plus antacid) reliably differentiate between gastrointestinal and cardiac causes of chest pain. Radiation of the chest pain to either the right or left shoulder has equal predictability. Elderly patients, diabetic patients, and patients with renal disease may present with atypical symptoms or may have no symptoms at all. Dyspnea may be the only symptom of cardiac ischemia in the elderly. Women may present with atypical symptoms related either to a true gender difference or due to the fact that women are typically older than men when coronary artery disease (CAD) develops.

Although the majority of patients with stable CAD will have more than one traditional risk factor, the absence of these factors does not exclude ACS. New independent risk factors (high sensitivity-C reactive protein levels and coronary calcium score, for example) are also poor predictors in the diagnosis of acute MI or ACS.

PHYSICAL EXAM, ECG,AND CHEST X-RAY RESULTS

Physical examination findings that suggest a cardiac etiology for chest pain include hypotension, a new murmur of mitral insufficiency secondary to papillary muscle dysfunction, an S3 gallop, malignant ventricular arrhythmias, and pulmonary rales or edema. Findings that suggest a noncardiac etiology are chest wall or epigastric tenderness, pulmonary egophony, dullness to chest percussion, tracheal shift from the midline, unilateral decreased breath sounds, significant blood pressure difference between arms, and loss of peripheral arterial pulses in a young individual.

The ECG is very helpful in the majority of patients with ACS. Localized ST-segment changes (elevation or depression) from baseline and new localized T-wave changes strongly support a cardiac etiology for chest pain. Approximately 50% of patients with acute MI will have ST-segment elevation; the remainder will have ST-segment depression, T-wave inversion, or no changes at all. Patients presenting with a T-wave inversion infarction have a better prognosis than those with an ST-depression infarction. Sometimes patients presenting with an NSTEMI may progress to an STEMI. If the ECG is not diagnostic but strong clinical suspicion remains, a repeat ECG every 5 to 10 minutes is recommended.

When ST-segment elevation is noted in the inferior leads (II, III, and avF), a concomitant right ventricular infarction (RVI) has been shown to be present in approximately 50% of cases. An ECG using right-sided precordial leads (V leads) will identify ST-T changes in leads RV3 and RV4 that arediagnostic of an RVI. Diagnosing an RVI is important because it is associated with increased mortality.

A 12-lead ECG may be normal in up to 20% of patients with chest pain who present to the emergency department with ACS. Up to 10% of patients with an acute MI will have a normal ECG. However, a normal ECG after 12 hours of chest pain has a high negative predictive value for ACS. Many ECG patterns interfere with the diagnosis of ACS, including left bundle branch block (LBBB), Wolff-Parkinson-White syndrome, ventricular pacemaker rhythm, myopericarditis, early repolarization ST changes, T-wave abnormality associated with an intracranial bleed, left ventricular hypertrophy, and hyperkalemia.

The chest X-ray is most helpful in identifying noncardiac etiologies of chest pain. Pulmonary infiltrates, a pleural effusion, a pneumothorax with or without midline tracheal shift, free intra-abdominal air, or a widened mediastinal shadow all suggest a noncardiac cause. Chest x-rays in an acute MI or unstable angina are nonspecific; a normal-sized or enlarged heart, findings of pulmonary venous congestion, or, rarely, coronary artery calcifications may be seen in patients with ACS.

BIOCHEMICAL MARKERS

If the etiology of the chest pain can be determined from the history, physical exam, ECG, and chest x-ray, then therapy should be initiated immediately without waiting for the results of biochemical marker testing. If the patient is stable and the etiology remains unclear, then analysis of biochemical markers is the next step in identifying ACS.

Because of their increased specificity, troponin I and T are the preferred markers of the American College of Cardiology (ACC), American Heart Association (AHA), and European Society of Cardiology. Elevated troponin levels in the setting of ischemic symptoms indicate myocardial damage (either STEMI or NSTEMI), and the degree of troponin elevation correlates with the patient’s prognosis. Troponin levels will remain normal in a patient with unstable angina. A normal troponin level measured after six hours from the onset of pain may exclude an acute MI; however, this is not always the case because the onset of chest pain does not always equate with the onset of myocardial damage. If the diagnosis remains unclear, serial troponin levels should be measured at three- to six-hour intervals.

It is important to remember that while normal serial troponin levels do rule out an acute MI, this biochemical marker does not exclude the presence of ongoing ischemia due to unstable angina. In the presence of a concerning ischemic history, physical exam, or ECG, normal cardiac troponin levels should not be used in the decision to admit or discharge a patient.

While there is improved specificity with troponin as compared to myoglobin or creatine kinase-MB, false positive elevations can occur in patients with a low likelihood of coronary disease. Elevated troponin levels may be seen in patients with nonischemic myocardial damage (from myocarditis, pericarditis, cardiac contusion, chemotherapy, or sustained tachycardia) or in other conditions such as heart failure, hypertension, hypothyroidism, pulmonary embolus, sepsis, burns, stroke, transplant vasculopathy, renal failure on dialysis, or physical exhaustion.

If the evaluation favors a noncardiac chest pain etiology, then therapy should be directed to the appropriate gastrointestinal, musculoskeletal, pulmonary, or psychiatric cause.

OTHER DIAGNOSTIC TESTS

If the patient remains stable and the etiology is still unclear, performing an echocardiogram, myocardial perfusion imaging study, or treadmill stress testing should be considered. A resting transthoracic echocardiogram is a sensitive tool in the diagnosis and exclusion of acute MI. Shortly after the onset of cardiac ischemia, regional left ventricular wall motion abnormalities (hypokinesis, akinesis, or dyskinesis) are noted. The absence of regional wall motion abnormalities with ongoing chest pain decreases the likelihood that the pain is ischemic in origin. An echocardiogram can also help identify right ventricular wall motion abnormalities consistent with an RVI. The sensitivity of an echocardiogram is very high, but its specificity is limited by the presence of pre-existing systolic cardiac dysfunction and the inability to obtain adequate images in patients with marked obesity or significant lung disease.

The recent addition of myocardial contrast studies to echocardiography may increase its sensitivity in the acute MI setting. The diagnosis of other life-threatening causes of chest pain, such as proximal aortic root dissection or pulmonary embolism, may be suggested by an echocardiogram.

A resting myocardial perfusion imaging study with thallium-201 in patients with chest pain of unknown origin may be helpful. This agent accumulates in myocardial tissue in direct proportion to myocardial blood flow. If it is injected into a peripheral vein, either during chest pain or within three hours after the onset of chest pain, a decreased nucleotide accumulation will be noted in ischemic or dead tissue. The limitations of this initial study are the inability to obtain acute images in the emergency department around the clock and the inability to distinguish between acute heart muscle damage and pre-existing damage. If clinically indicated, a repeat scan in 4 to 24 hours will help separate an acute process from a prior infarction.

Exercise or stress evaluation should never be performed in an unstable patient. However, if the evaluation favors a low risk of chest pain, an early exercise or stress evaluation should be considered to risk-stratify the patient. If the ECG is normal and the patient can exercise, a routine treadmill stress test can be helpful. If the ECG shows baseline abnormalities (for example, ST-T changes or bundle branch block) and the patient can exercise, a treadmill test with radionuclide imaging or exercise echocardiography is indicated. If the patient cannot exercise, a pharmacologic radionuclide imaging ECG test or echocardiography is indicated.

If stress evaluation does not show ischemia, the patient should be referred for appropriate noncardiac follow-up. If the evaluation reproduces the patient’s symptoms or demonstrates a drop in systolic blood pressure, malignant arrhythmias, or an ischemic response, a cardiology consult is indicated. If the treadmill test is nondiagnostic due to technical limitations or because the patient could not reach a required heart rate, a cardiology consult is also indicated.

MEDICAL THERAPY FOR ACS

We will now discuss therapies indicated for patients with unstable angina, STEMI, and NSTEMI. The ACC and AHA recommendations and levels of evidence are outlined in the table below.

Sublingual nitroglycerine is the initial drug of choice for ischemic chest pain. However, if a phosphodiesterase-5 inhibitor has been used in the last 24 hours (sildenafil or vardenafil) or last 36 hours (tadalafil), nitroglycerine is absolutely contraindicated. Caution is required with nitroglycerine use in the presence of significant diastolic dysfunction or RVI since both conditions are very volume-dependent states. Pain relief with nitroglycerine does not prove that chest pain has a cardiac origin; the drug also improves esophageal and gallbladder spasm.

Aspirin, beta blockers, and antithrombin agents (such as unfractionated heparin or enoxaparin) are indicated in all patients with ACS unless contraindicated. The enoxaparin dose would need to be adjusted for patients in renal failure; the drug should be avoided in patients who likely will need early bypass surgery (class IIaA). Clopidogrel benefits patients with unstable angina or NSTEMI for up to 9 to 12 months; it is also used in patients with STEMI but the data are less compelling for this indication. In patients considered for early heart catheterization, clopidogrel should be started only after the coronary artery anatomy has been defined.

Angiotension-converting enzyme inhibitors are indicated in ACS patients, but they should be administered in the emergency department only for persistent hypertension after therapy with nitrates and beta blockers. Statins should be initiated during hospitalization and titrated to a low-density lipoprotein (LDL) level below 100 mg/dl. If the patient has associated diabetes mellitus or the metabolic syndrome, an LDL level below 70 mg/dl is the long-term goal. Whether early initiation of statin therapy within 24 hours of the onset of cardiac ischemia may help to lower subsequent cardiac complications has yet to be determined.

Early invasive therapy with primary percutaneous coronary intervention (PCI) is recommended in ACS patients with STEMI, new or presumed new LBBB, and high-risk unstable angina or NSTEMI, if available within 90 minutes of patient presentation. If PCI is unavailable, patients with STEMI or a new or presumed new LBBB presenting within 12 hours of symptom onset should receive fibrinolytic therapy, unless contraindicated. If PCI is unavailable, patients with unstable angina or NSTEMI and continued ischemia should receive a glycoprotein IIb/IIIa agent, such as eptifibatide or tirofiban (class IIA). In ACS patients who do not meet the high-risk criteria, either early medical therapy alone or medical therapy plus early invasive therapy with primary PCI can be considered (class IB).

ACUTE AORTIC DISSECTION

In the presence of severe chest pain, a high degree of clinical suspicion of acute aortic dissection is required. Unfortunately, delays in diagnosis are common. The acute mortality rate is 1% to 2% per hour in the first 48 hours after presentation. Aortic dissection is most common in men over age 60, patients with hypertension, cystic medial necrosis, a bicuspid aortic valve, or coarctation of the aorta, and those using methamphetamines or cocaine.

The classic symptoms in aortic dissection are a tearing interscapular pain radiating into the abdomen, a heart murmur of aortic insufficiency, and a widened mediastinum, but this triad occurs in less than one third of cases. Pain is the most common presenting symptom, although the quality of the pain is not always helpful in the diagnosis. Sudden onset of pain is noted in the majority of patients. Anterior chest pain is more common in proximal aortic root dissection (Stanford type A), whereas back and abdominal pain are more common in distal aortic root dissections (Stanford type B). Symptoms of a focal neurologic deficit, heart failure related to acute severe aortic insufficiency, syncope, and leg pain have all been reported.

The combined history of chest pain and acute focal neurologic symptoms is strongly associated with acute proximal aortic root dissection. A few patients will have no symptoms, and the diagnosis is typically made as an incidental finding on further testing.

Physical examination is not diagnostic in the majority of patients. However, a missing peripheral arterial pulse, the presence of a new or presumed new murmur of aortic insufficiency, and a difference in systolic blood pressure of more than 20 mm Hg between arms may be suggestive of the diagnosis.

The ECG is usually normal or will show only nonspecific ST-T changes. Localized ST-segment elevation, sug-gesting acute STEMI, is unusual, occurring in less than 5% of patients with type A dissections. This ECG change reflects closure of the coronary ostium by the dissection. The right coronary artery is most often involved.

The classic chest X-ray finding of a widened mediastinum is present in 63% of aortic dissections. A pleural effusion is present in about 20%. A chest computed tomography scan, transeophageal echocardiogram, and magnetic resonance imaging are all excellent modalities in diagnosing acute aortic dissections. The sensitivity and specificity of these tests approach 100%. An aortogram, the traditional method of evaluation, is also very effective but is more invasive. The most appropriate diagnostic test depends on the availability of the various technologies and staff expertise.

Treatment of aortic dissection requires rapid lowering of systolic blood pressure to between 100 and 120 mm Hg. Beta blockers should be the first agents used when the diagnosis is considered or confirmed. These drugs are not only effective in lowering blood pressure but also in decreasing the risk of continued dissection. For refractory hypertension, combination drug therapy with a beta blocker and nitroprusside is often needed. If beta blocker therapy is contraindicated, intravenous diltiazem should be considered.

Early surgical consultation is suggested for all patients with type A aortic root dissection and in patients with type B dissection associated with acute vascular compromise.

PULMONARY EMBOLISM

Acute pulmonary embolism (PE) is a common and highly lethal disease. An estimated 600,000 patients are diagnosed each year with PE, and it is believed that that number represents only about 50% of the true incidence of the condition.

The diagnosis of PE is difficult because symptoms may be subtle, masked by distracting comorbid disease, or, in rare cases, totally absent. If the diagnosis is missed, the mortality rate approaches 30% in the untreated patient, but mortality falls to 2% to 8% with appropriate therapy.

Pulmonary emboli usually originate in the lower extremities, often without clinical symptoms of venous thrombosis. In addition, clinical venous thrombosis is frequently associated with asymptomatic pulmonary emboli.

The classic history of sudden-onset shortness of breath and pleuritic chest pain occurs in about two thirds of patients with PE. Cough with or without hemoptysis and chest wall tenderness are less frequently noted. Symptoms are usually more pronounced when the pulmonary embolus is large or associated with pre-existing cardiopulmonary disease. Risk factors for PE are well established and should be reviewed when the patient’s symptoms are suggestive of the condition. They include immobilization, surgery within the previous three months, thrombophilia, estrogen therapy, and a history of stroke, venous thromboembolism, or malignancy.

Physical examination may find unexplained tachypnea or tachycardia, a more intense second heart sound, pleural rub, and pulmonary wheezes or rales. Chest wall tenderness, which is most commonly associated with chest pain of musculoskeletal origin, was recently demonstrated to be present in 19.9% of patients with acute PE and therefore can not be used to exclude the diagnosis.

The most common ECG findings are sinus tachycardia with nonspecific ST-T changes. However, one-third of patients with submassive or massive PE have ECG evidence of right heart strain, including an abnormal right QRS axis, right atrial and ventricular hypertrophy, and ST-T changes (S₁Q₃T₃ syndrome).

A normal chest x-ray in a patient with acute dyspnea should raise suspicion for the presence of PE. However, chest x-rays in acute PE are normal in only 12% of patients. The most common chest x-ray abnormalities noted are atelectasis and pulmonary infiltrates. A pleural effusion, focal pulmonary oligemia (Westermark’s sign), and a peripheral wedged-shaped infiltrate (Hampton’s hump) are less common.

DETERMINING PRETEST PROBABILITY

The clinical pretest probability for the presence of PE, based on the history and physical exam, can be calculated using the Wells’ scoring system (see table below). Low clinical probability patients represent 25% to 65% of patients in whom PE is suspected; the actual PE prevalence in these patients is 10%. Intermediate clinical probability patients also represent 25% to 65% of suspected patients, with a PE prevalence of 25% to 45%. High clinical probability patients represent 10% to 30% of suspected patients, with a PE prevalence of 70% to 90%. Assigning a pretest probability is necessary to determine whether the patient should undergo D-dimer testing or proceed directly to imaging studies.

The high-sensitivity D-dimer assays commonly used in the diagnosis of PE are the ELISA and turbidimetric quantitative assays. However, with their increased sensitivity, they have the least specificity of the D-dimer assays. A negative high-sensitivity ELISA D-dimer assay, when combined with a low clinical pretest probability, adequately excludes the presence of PE. In a patient with a Wells’ intermediate or high pretest clinical probability, the D-dimer is not reliable and should not be ordered. In these cases, imaging studies should be obtained.

The two most commonly used imaging studies for diagnosing PE are the ventilation/perfusion (V/Q) lung scan and the multidetector computed tomography (MDCT) pulmonary angiogram. Until recently, the V/Q scan has been the standard of care. It is helpful when the results are normal or demonstrate a high probability for PE. However, most scans show an intermediate probability and need further confirmatory tests to make the diagnosis. As a result, the MDCT angiogram is quickly becoming the new standard of care. The negative predictive value for the MDCT angiogram is identical to that of a pulmonary angiogram, which remains the gold standard for diagnosing PE. The MDCT angiogram is superior to V/Q scans for diagnosing or excluding PE and can result in an alternate diagnosis in two thirds of the cases in which PE is not present. It also has the potential to allow for a simultaneous contrast venogram of the legs.

The MDCT is limited in the diagnosis of subsegmental pulmonary emboli and is often not interpretable in very obese patients. The limitation regarding subsegmental PE, however, appears to have little clinical significance.

A positive MDCT angiogram confirms a clinically significant PE. Initial studies suggest that a negative MDCT angiogram has a high negative predictive value for excluding an acute PE. However, pending further confirmatory studies, the clinician should combine the negative MDCT findings with clinical probability and D-dimer findings.

Troponin I levels are increased in 16% to 39% of patients with acute PE. Such an elevation reflects right ventricular dysfunction from either a PE with preexisting cardiopulmonary disease or a massive PE. This finding is associated with hemodynamic compromise and denotes a poor prognosis. Echocardiographic evidence of right ventricular wall motion abnormalities will also be noted.

Treatment for PE involves the rapid simultaneous administration of heparin and warfarin, unless contraindicated. It is imperative to achieve therapeutic drug levels within the first 24 hours, as measured by an activated partial thromboplastin time of at least 1.5 times control or a plasma heparin level of 0.3 to 0.7 IU/ml anti-Xa activity. Heparin therapy should be continued for at least five days and not stopped until a therapeutic INR of 2 to 3 is achieved for two consecutive days. The duration of warfarin therapy ranges from three months (reversible risk factors) to 6 to 12 months (idiopathic etiology) to indefinite (life-threatening or recurrent PE). Low-molecular-weight heparin has been noted to be as effective as heparin.

Thrombolytic agents are best reserved for patients with submassive or massive PE or patients with massive proximal venous (iliofemoral) thrombosis. Inferior vena cava filters should be considered when anticoagulant therapy is contraindicated, when emboli recur despite adequate anticoagulation, or when recurrent emboli are associated with pulmonary hypertension.

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