Standard EKG bats .500 in detecting AMI
Changes may not appear for hours or days
Even though electrocardiograms (EKG) and creatine kinase (CK-MB) tests can’t offer a differential diagnosis of acute myocardial infarction (AMI), they are a starting point. AMI is unlikely in patients with a normal EKG, but a normal tracing, or one showing only nonspecific changes, is inadequate to rule out AMI. Admit to the ICU or CCU when in doubt.
"An EKG may show no acute injury or ischemia and is diagnostic in only 30% to 50% of patients with AMI," says Catherine Hamilton, RN, MPH, clinical coordinator for the Heart ER program at the University of Cincinnati Medical Center. "And patients with AMI are in the minority of those who present with chest pain."
Some small infarctions involving the lateral or posterior walls of the left ventricle may not produce changes on the EKG, and serum enzymes are necessary for diagnosis. A single determination of a serum marker for myocardial injury such as the isoenzyme CK-MB, obtained upon presentation to the ED, has a sensitivity of 35% for detecting AMI.1
Nevertheless, order a 12-lead EKG for all incoming chest pain, except where it is clearly pleuritic and reproduced by chest wall palpation or position change. Only 10% of ED patients fall into that exception, so virtually everyone should have the diagnostic procedure.
When you suspect AMI, but the EKG results are not diagnostic, obtain another after 30 minutes. Whether diagnostic or not, the EKG should be repeated if symptoms change or if chest pain increases. Male patients with classic presentations that include chest pressure, radiating discomfort, and diaphoresis are more likely to have AMI or unstable angina despite an initially normal or nondiagnostic EKG. Conversely, an atypical history and nondiagnostic EKG put the patient at lower risk.
The criteria for AMI include ST segment elevation of at least 0.1 mV 0.08 second after the J-point in at least two contiguous leads describing one myocardial region, such as:
• Any two of three inferior leads II, III, and a VF implies inferior AMI.
• Two of six precordial leads V1- V6 implies anterior AMI.
• Leads I and a VL implies anterolateral AMI.
Posterior infarction may be indicated by the following:
• ST segment depression in leads V1- V4;
• ST elevation in the inferior wall leads;
• a tall R wave in V1 , V2, or both, with an R/S ratio of 1¼1 or greater;
• an upright T wave.
The initial tracing on presentation of a patient with myocardial necrosis may show no ST segment elevation or depression and no Q wave formation. Changes may not appear for hours or days after AMI. They may remain subtle and consist of nonspecific ST-T wave abnormalities, loss of R wave amplitude, or the formation of minor Q waves. EKG changes that accompany AMI may be obscured by concomitant bundle-branch block, paced ventricular rhythms, left or right ventricular hypertrophy, early repolarization, electrolyte disorders, or a previous infarction which may have occurred in an electrically silent area of the heart, such as the apex, the right ventricle, or the posterobasal portion of the left ventricle.
Patients with infarction but normal EKGs (or those with nonspecific ST-T wave changes only) are at low risk of developing life-threatening complications such as ventricular arrhythmias. It is these patients those with normal or nonspecific EKGs who can be sent to intermediate rather than coronary care units.
Because life-threatening ventricular arrhythmias may develop during the first few hours of infarction and because therapeutic interventions can limit infarct size when begun early enough, the patient should be admitted to an ICU or CCU if doubt exists.
Most studies have found that ST segment elevation of 1 mm or more in two contiguous leads indicates AMI in 80% or more of patients. This criterion is most reliable in those with no prior AMI but decreases to about 50% in patients with a past infarction.
Reference
1. Gibler WB, Runyon JP, Levy RC, et al. A rapid diagnostic and treatment center for patients with chest pain in the emergency department. Ann Emerg Med 1995; 25:1-8.
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