Inpatients reporting chest pain should have an ECG, and comparison with prior ECGs should be made to assess for dynamic changes.
ST-segment elevation: The ESC/ACCF/AHA/WHF committee for the definition of myocardial infarction established specific ECG criteria for ST-segment elevation myocardial infarction including 2 mm of ST segment elevation in the precordial leads for men (1.5 mm for women) and greater than 1 mm in other leads. The elevations must be present in at least two contiguous leads, corresponding to a specific arterial territory. A new left bundle branch block should be treated similarly to ST-segment elevation in the appropriate patient, with immediate reperfusion therapy.
Many patients will have alternate causes of ST-segment elevation (benign early repolarization, left ventricular aneurysm, pericarditis, hyperkalemia, bundle branch block, Prinzmetals angina) so experience interpreting ECGs and comparison with old ECGs is critical.
Bundle branch block and paced rhythms make ECG interpretation challenging. The Sgarbossa criteria assign points to significant ECG findings in the presence of an old left bundle branch block: concordant ST-segment elevation of 1 mm or more in any lead (5 points), ST segment depression of 1mm or more in leads V1, V2, or V3 (3 points), discordant ST-segment elevation of 5 mm or more (2 points). A score of at least 3 is associated with high specificity for myocardial infarction but low sensitivity. In patients with LBBB or paced rhythms, the finding of ST-segment elevation ≥5 mm in leads with a negative QRS complex is highly specific for myocardial infarction.
Identification of inferior wall myocardial infarction should be followed by careful examination for evidence of posterior wall involvement (V1 ST depression), conduction disturbance (Wenckebach, bradycardia, or complete heart block) and right ventricular infarction (right-sided ECG, lead rV4).
ST-segment depression (0.5 mm or greater) predicts increased risk of myocardial ischemia. The greater the extent of depression, the higher the risk of MI and death. Posterior leads may help differentiate the patient with anterior ST-segment depression who has ischemia from the patient who has an acute posterior wall MI.
These indicate lower risk than ST depressions. Likewise, the presence of Q-waves is less predictive of adverse cardiac events than ST-segment depression or elevation.
The findings of right ventricular strain, S1Q3T3, and new incomplete right bundle branch block may suggest pulmonary embolism but are not sensitive. Sinus tachycardia is the most common rhythm disturbance. Atrial fibrillation is seen in a small percentage of patients with pulmonary embolism but is rarely the only sign pointing to that diagnosis.
Although often abnormal in small- to medium-sized pulmonary emboli, the ECG is nonspecific and is normal in 23% of patients with submassive PE and 6% of patients with massive PE. For this reason, a normal ECG by itself cannot guide decision making relating to further diagnostic workup.
Characteristic findings include diffuse ST-segment elevation that may be confused with acute MI or early repolarization. The lack of regional ischemic changes (ie, diffuse rather than localized ST elevations), as well as a suggestive history and cardiac examination will help distinguish this entity from acute MI.
Classic stages of ECG changes in pericarditis are:
Stage I (first few weeks of pericardial inflammation)
- Diffuse concave-upward ST-segment elevation with concordance of T waves
- ST-segment depression in aVR or V1
- PR-segment depression in all leads except aVR and V1
- Low voltage
- Absence of ST-segment changes
Stage II (days to several weeks)
- ST segments returning to baseline
- T-wave flattening
Stage III (end of second or third week)
Stage IV (lasts up to three months)
- Gradual resolution of T-wave inversion
The classic four stages of ECG changes occur in only 50% of patients, and the ECG may be normal in 10% of patients. Some of the changes are nonspecific and may be confused with myocardial infarction or early repolarization.
The findings of electrical alternans or low voltage in an ECG for a patient with chest pain should prompt consideration of pericardial effusion or hemorrhage. ECG abnormalities are common after stroke. Cerebral T waves (deep, symmetric T-wave inversions) are classically seen with subarachnoid hemorrhage. ST-segment deviations may occur in stroke patients as well, sometimes making differentiation between stroke and myocardial infarction difficult in difficult-to-assess patients.
Patients admitted to the hospital with chest pain or who develop chest pain while hospitalized should have basic laboratory tests performed, including a metabolic panel and complete blood count. Additional laboratory tests may be sent based upon clinical suspicion. Cardiac biomarkers and D-dimer assays are discussed below. Patients with possible intra-abdominal pathology should also have liver enzymes and a lipase ordered. Cardiac biomarkers should be drawn as a baseline but should not deter admission as they may initially be negative despite ischemia.
Cardiac biomarkers: A current definition of myocardial infarction involves typical rise and/or fall of cardiac biomarkers, along with ischemic symptoms, ischemic EKG findings (ST-segment deviation, Q waves), and/or coronary artery intervention.Thus, cardiac biomarkers are essential in the work-up of patients suspected of having cardiac etiology of their chest pain.
Creatine kinase (CK) and the CK-MB isoform (unique to the myocardium) have similar temporal patterns in cases of myocardial injury, rising within 4 to 8 hours and peaking between 12 and 24 hours (slightly earlier for CK-MB). CK-MB is cleared within 36 to 48 hours, and CK is cleared within 3 to 4 days. Troponin levels rise within 6 hours, peak after 12 hours, and are cleared after 7 to 14 days.
Troponins exhibit superior sensitivity and specificity when compared with CK and CK-MB for the diagnosis of myocardial infarction and help identify those patients at increased short- and long-term risk. Elevations identify patients who would benefit from aggressive treatment such as antithrombotic, antiplatelet, and coronary intervention. Cardiac troponin I has a higher specificity than cardiac troponin T, as it is not found in skeletal muscle. Some advisory groups argue for use of CK-MB to diagnose reinfarction, but others prefer troponin for this purpose as well.
Cutoff values for troponins, CK, and CK-MB vary by institutions. CK-MB in healthy patients generally ranges up to 5 microg/L or <3% of the total CK. Higher values are abnormal and may be due to myocardial injury or several other conditions generally easily differentiated based upon clinical grounds. There is ongoing debate regarding whether rises in serum biomarkers represent only irreversible or both reversible and irreversible injury, but rising cardiac biomarkers should be assumed to indicate at-risk myocardium. Likewise, the “normal range” of cardiac troponin is a troublesome concept, as any detectable troponin level has been shown to have prognostic significance and may be a marker of chronic as well as acute disease.
Troponins may be elevated in patients with renal failure who do not have evidence of myocardial damage. This is possibly due to decreased clearance as well as increased incidence of comorbid pathology (including pathology seen at the cellular level). These patients also have a high rate of coronary disease. Therefore, an appropriate serial rise in troponin is more helpful than an elevated, stable value for the diagnosis of myocardial infarction. Other conditions associated with increased troponin values include massive pulmonary embolism, myocarditis, cardiopulmonary resuscitation, cardioversion, heart failure, stroke, stress cardiomyopathy, and demand ischemia (Table 77-5).
Table 77-5 Differential Diagnosis of Elevated Troponin in the Absence of Acute Myocardial Infarction or Congestive Heart Failure ||Download (.pdf)
Table 77-5 Differential Diagnosis of Elevated Troponin in the Absence of Acute Myocardial Infarction or Congestive Heart Failure
|Cardiac and Vascular Disease||Aortic Dissection, CVA|
|Respiratory disease||Acute PE, ARDS|
|Cardiac inflammation||Pericarditis, endocarditis, myocarditis|
|Infections||Sepsis, viral disease|
|Acute complications of inherited disorders||Neurofibromatosis, Duchenne muscular dystrophy, Klippel-Feil syndrome|
|Environmental exposure||Carbon monoxide, hydrogen sulfide, colchicine, evenomations (snake, jellyfish, spider, centipede, scorpion)|
|Chronic diseases||ESRD, cardiac infiltrative disorders (amyloidosis, sarcoidosis, hemochromatosis, scleroderma), HBP, diabetes, hypothyroidism|
|Iatrogenic disease||Invasive procedures (heart transplant, congenital defect repair, radiofrequency ablation, lung resection, ERCP), noninvasive procedures (cardioversion, lithotripsy), pharmacologic (chemotherapy)|
|Myocardial injury||Blunt chest trauma, endurance athletes|
|Miscellaneous||Kawasaki disease, stress cardiomyopathy, TTP, birth complications in infants, GI bleeding|
A typical “rule-out” protocol after negative initial troponin often includes additional troponins at regular intervals (sometimes as frequently as every three hours) and a final troponin at the end of six to nine hours. Limitations: Although troponin is not detected in the blood of healthy people and is the standard criterion for the diagnosis of MI, the biomarker lacks sensitivity for USA.
D-dimer: The D-dimer is formed during breakdown of thrombi, occurring in cases of venous thromboembolism (VTE) but also as an integral part of the body's repair mechanism in other conditions (Table 77-6). The use of D-dimer in the appropriate patient can exclude pulmonary embolism as a cause of chest pain. The test demonstrates high sensitivity with poor specificity overall, but assays differ significantly in their sensitivities. ELISA assays are more sensitive than latex or erythrocyte agglutination assays for diagnosis of pulmonary embolism and are thus preferred. The Wells score defines low, moderate, and high risk patients. Evidence suggests that a low Wells score combined with a negative D-dimer result (less than 500 ng/mL) is sufficient to exclude pulmonary embolism (Table 77-7).
Table 77-6 Differential Diagnosis of Elevated D-Dimer ||Download (.pdf)
Table 77-6 Differential Diagnosis of Elevated D-Dimer
|Ischemic heart disease||Advanced age|
Table 77-7 Wells Score for Pulmonary Embolism ||Download (.pdf)
Table 77-7 Wells Score for Pulmonary Embolism
|Clinical signs and symptoms of deep vein thrombosis||3|
|Alternative diagnosis less likely than PE||3|
|Pulse greater than 100||1.5|
|Immobilization more than 3 days or surgery within prior 4 weeks||1.5|
|Previous PE or DVT||1.5|
|Malignancy (receiving treatment, treated within last 6 months or palliative)||1|
|Moderate||2 to 6|
The use of D-dimer testing may be of limited to no value in patients who are already hospitalized at the time of suspected pulmonary embolism, in contrast to those whose initial presentation is consistent with this diagnosis. Although the D-dimer has a very high negative predictive value, the test is not useful in cases of high pretest clinical probability. The usefulness of the test in patients with concomitant diseases is also limited. In pregnancy, not only are D-dimer levels typically elevated, but a negative D-dimer does not rule out VTE. The specificity of the D-dimer also decreases with increasing age. In 1 study, D-dimer allowed exclusion of VTE in roughly 52% of patients 40 years of age or less as compared to only 5% of those 80 years old. Hence, it should only be ordered in patients with a low clinical pretest probability of PE. It does not add any additional diagnostic value in those patients who need to proceed directly to imaging.
Patients reporting chest pain should have a chest radiograph taken. Lateral decubitus imaging is most sensitive for diagnosing pneumothorax (with the affected side positioned higher than the unaffected side), but pneumothoraces of at least 100 mL should be visible on upright films. Supine films may miss much larger pneumothoraces. Mediastinal air should raise concern for ruptured esophagus or airway. A widened mediastinum may be seen simply due to technique, but it is also associated with aortic dissection, seen in 61.6% of dissections in one study.
Computed tomography with contrast is commonly used to detect pulmonary embolism, and the historical gold standard, pulmonary angiography, is rarely needed. Studies have suggested a negative CT scan is sufficient in ruling out the diagnosis for patients with a low or moderate pretest probability, but high suspicion combined with a negative scan should prompt consideration of further workup. Further workup for high risk patients may include pulmonary angiography or lower-extremity venous ultrasound. Some institutions perform CT venography immediately after CT pulmonary angiography in order to increase sensitivity for thromboembolic disease but this requires an increased exposure to contrast.
Computed tomography is often the initial test for evaluation of aortic dissection, but transesophageal echocardiography is an excellent alternative and can be performed at the bedside. Magnetic resonance imaging is useful for imaging chronic dissections to determine whether an interval change has occurred.
Bedside echocardiography is a noninvasive imaging modality that can be rapidly performed to assist diagnosis and management of several conditions associated with chest pain. Specifically, its use should be considered for patients with suspected acute valvular disease, aortic dissection, pericardial effusion, or unexplained hemodynamic instability. It may also be helpful for distinguishing acute MI from pericarditis, with important treatment implications.
Hospitalists are increasingly asked to manage the workup of chest pain patients who are at low but not negligible risk for coronary disease. The admission status of these patients will vary by institution. Chest pain “observation units” are becoming more popular and may be staffed by emergency physicians, hospitalists, cardiologists, or midlevel providers. The general goal of these units is to expedite the workup of patients at low risk for an acute coronary syndrome. After a negative evaluation with serial biomarkers and ECGs, further risk stratification with stress testing is often performed to identify patients with missed acute coronary syndrome and those at high risk for early adverse events.
Choosing which type of stress test to use will depend on the characteristics of the patient, resources available, and the policies of the institution, as well as the information desired. Exercise ECG testing without imaging is the preferred test in most patients with interpretable ECGs and adequate exercise capacity. Exercise testing with echocardiography or radionuclide myocardial perfusion imaging will allow localization of abnormalities. Patients who are unable to exercise can undergo pharmacologic stress testing with dipyridamole, adenosine, or dobutamine. Dobutamine echocardiography, however, should be avoided in patients who may be suffering from active or unstable ischemia.
In general, patients with ongoing chest pain should be managed as if they have unstable angina. However, low-risk patients with no prior history of myocardial infarction may have rest imaging performed with myocardial perfusion imaging or echocardiography. Coronary computed tomographic angiography shows promise in single-center studies for excluding acute coronary syndromes in patients with no history of myocardial infarction or known coronary disease, but this alternative to stress testing requires further validation of efficacy, cost effectiveness, and safety before widespread use can be endorsed.
Stress testing is useful both for diagnostic and prognostic purposes in patients suspected of having coronary heart disease, but due to the test characteristics, diagnostic testing should not be performed in patients with a very low pretest probability (based upon any of several validated decision aids) of having disease, as most positive tests in this setting represent false positives. Women have been noted to exhibit more false positives on stress testing, though current recommendations do not differ for men and women.
Some patients assessed to be at low risk for acute coronary syndrome may be safely discharged for outpatient stress testing within 72 hours in accordance with the 2007 ACC/AHA guidelines. Prior to discharge, these patients should have undergone at least a 6–12 hour observation period with two or three sets of negative cardiac enzymes and have normal or unchanged ECGs. One observational study found this to be a safe and feasible approach associated with a low risk of short-term adverse outcomes. Of 871 low risk patients undergoing outpatient stress testing, 2% had coronary artery disease requiring intervention and 0.3% had a myocardial infarction within six months. Importantly, the stress test appointment was made for the patient at the time of evaluation, and 92.2% of patients completed the outpatient stress test. Seventy-six did not have the test completed due to cancellation of the test or failure to keep the appointment. Available follow-up on 67 of these 76 patients showed no adverse cardiac events. This strategy is not appropriate for patients with questionable compliance with follow-up appointments. Direct scheduling and/or verbal communication with the primary care physician is advisable. Patients with a positive (and possibly indeterminate) stress test result should have a cardiology consultation while in the hospital. Those with negative results may be discharged.