Patients usually appear anxious and are often sweating profusely. The heart rate may range from marked bradycardia (most commonly in inferior infarction) to tachycardia resulting from increased sympathetic nervous system activity, low cardiac output, or arrhythmia. The blood pressure may be high, especially in former hypertensives, or low in patients with shock. Respiratory distress usually indicates heart failure. Fever, usually low-grade, may appear after 12 hours and persist for several days.
Clear lung fields are a good prognostic sign, but basilar rales are common and do not necessarily indicate heart failure. More extensive rales or diffuse wheezing suggests pulmonary edema.
The cardiac examination may be unimpressive or very abnormal. An abnormally located ventricular impulse often represents the dyskinetic infarcted region. Jugular venous distention reflects right atrial hypertension, which may indicate right ventricular infarction or elevated left ventricular filling pressures. The absence of elevated central venous pressure, however, does not indicate normal left atrial or left ventricular diastolic pressures. Soft heart sounds may indicate left ventricular dysfunction. Atrial gallops (S4) are the rule, whereas ventricular gallops (S3) are less common and indicate significant left ventricular dysfunction. Mitral regurgitation murmurs are not uncommon and usually indicate papillary muscle dysfunction or, rarely, rupture. Pericardial friction rubs are uncommon in the first 24 hours but may appear later.
Edema is usually not present. Cyanosis and cold temperature indicate low output. The peripheral pulses should be noted, since later shock or emboli may alter the examination.
The most valuable laboratory tests are cardiac-specific markers of myocardial damage, including quantitative determinations of CK-MB, troponin I, and troponin T. All are relatively specific for necrosis (the troponins somewhat more so), though they may be elevated following severe ischemic episodes. Each of these tests may become positive as early as 4-6 hours after the onset of a myocardial infarction and should be abnormal by 8-12 hours. Circulating levels of troponins may remain elevated for 5-7 days or longer and should obviate the use of less specific LDH isoenzyme assays.
Most patients with acute infarction have ECG changes, and a normal tracing is rare. The extent of the electrocardiographic abnormalities provides only a crude estimate of the magnitude of infarction. The classic evolution of changes is from peaked (“hyperacute”) T waves, to ST segment elevation, to Q wave development, to T wave inversion. This may occur over a few hours to several days. The evolution of new Q waves (> 30 ms in duration and 25% of the R wave amplitude) is diagnostic, but Q waves do not occur in 30-50% of acute infarctions (subendocardial or non-Q wave infarctions). If these patients have an appropriate clinical presentation, characteristic cardiac enzymes, and ST segment changes (usually depression) or T wave inversion lasting at least 48 hours, they are classified as having non-Q wave infarctions.
The chest x-ray may demonstrate signs of congestive heart failure, but these changes often lag behind the clinical findings. Signs of aortic dissection should be sought as a possible alternative diagnosis.
Echocardiography provides convenient bedside assessment of left ventricular global and regional function. This can help with the diagnosis and management of infarction; echocardiography has been used successfully to make judgments about admission and management of patients with suspected infarction, since normal wall motion makes an infarction unlikely. Doppler echocardiography is probably the most convenient procedure for diagnosing postinfarction mitral regurgitation or Ventricular septal defect.
Technetium-99m pyrophosphate scintigraphy can be used to diagnose acute myocardial infarction. When injected at least 18 hours postinfarction, the radiotracer complexes with calcium in necrotic myocardium to provide a “hot spot” image of the infarction. This test is insensitive to small infarctions, and false-positive studies occur, so its use is limited to patients in whom the diagnosis by electrocardiography and enzymes is not possible-principally those who present several days after the event or have intraoperative infarctions. Radiolabeled antimyosin antibody fragments are more sensitive and specific imaging agents, but scintigraphy must be performed 24 and 48 hours postinjection, so this test has limited clinical utility in the diagnosis of acute myocardial infarction.
Scintigraphy with thallium-201 or the newer technetium-based perfusion tracers will demonstrate “cold spots” in regions of diminished perfusion, which usually represent infarction when the radio-tracer is administered at rest, but abnormalities do not distinguish recent from old damage.
Radionuclide angiography demonstrates akinesis or dyskinesis in areas of infarction and also measures ejection fraction, which can be valuable. Right ventricular dysfunction may indicate infarction of this chamber.
These can be invaluable in managing the complicated patient. Their use is described below and in below.
Hemodynamic subsets in acute myocardial infarction.
|Category||CI or SWI||PCWP||Treatment||Comment|
|Normal||> 2.2, < 30||< 15||None||Mortality rate < 5%.|
|Hyperdynamic||> 3.0, > 40||< 15||Beta-blockers||Characterized by tachycardia; mortality rate < 5%.|
|Hypovolemic||< 2.5, < 30||< 10||Volume expansion||Hypotension, tachycardia, but preserved left ventricular function by echocardiography; mortality rate 4-8%.|
|Left ventricular failure||< 2.2, < 30||> 15||Diuretics||Mild dyspnea, rales, normal blood pressure; mortality rate 10-20%.|
|Severe failure||< 2.0, < 20||> 18||Diuretics, vasodilators||Pulmonary edema, mild hypotension; inotropic agents, IABC may be required; mortality rate 20-40%.|
|Shock||< 1.8, < 30||> 20||Inotropic agents, IABC||IABC early unless rapid reversal occurs; mortality rate > 60%.|
CI = cardiac index (L/min/m2); SWI = stroke work index (g-m/m2, calculated as [mean arterial pressure - PCWP] � stroke volume index � 0.0136); PCWP = pulmonary capillary wedge pressure (in mm Hg; pulmonary artery diastolic pressure may be used instead); IABC = intra-aortic balloon counterpulsation.
Ammann P et al: Characteristics and prognosis of myocardial infarction in patients with normal coronary arteries. Chest 2000;117:333.
Myocardial infarction redefined-a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol 2000;36:959.
Serum marker analysis in acute myocardial infarction. American College of Emergency Physicians. Ann Emerg Med 2000; 35:534.
Zimetbaum PJ et al: Current concepts. Use of the electrocardiogram in acute myocardial infarction. N Engl J Med 2003; 348:933.
Essentials of Diagnosis
C. Laboratory Findings
E. Chest X-Ray
G. Scintigraphic Studies
H. Hemodynamic Measurements
B. Thrombolytic Therapy
C. Acute PTCA and Stenting for ST Segment Elevation Myocardial Infarction
D. Initial Management of Non-ST-Segment Elevation Myocardial Infarction
E. General Measures
G. Beta-Adrenergic Blocking Agents
I. Angiotensin-Converting Enzyme (ACE) Inhibitors
J. Antiarrhythmic Prophylaxis
K. Calcium Channel Blockers
A. Postinfarction Ischemia
C. Myocardial Dysfunction
D. Right Ventricular Infarction
E. Mechanical Defects
F. Myocardial Rupture
G. Left Ventricular Aneurysm
I. Mural Thrombus
A. Risk Stratification
B. Secondary Prevention
C. ACE Inhibitors in Patients With Left Ventricular Dysfunction
Revision date: June 20, 2011
Last revised: by Andrew G. Epstein, M.D.