Electrocardiography artifact: what you do not know, you do not recognize.

“Wat je niet kent, herken je niet” (1). (“What you do not know, you do not recognize.”) Reminder to students of electrocardiography inscribed in the lecture hall of Professor Hein J.J. Wellens, MD. Measurement of the heart’s electrical activity by the surface electrocardiogram (ECG) was a breakthrough in the evaluation of cardiac arrhythmias. The ECG is critical to the safety and care of hospitalized patients with heart disease. Accurate and timely recognition of life-threatening cardiac arrhythmias is required of all physicians who work in acute care settings. Of equal importance is the distinction of arrhythmias from artifact due to disconnected leads, motion, electromagnetic interference, or equipment failure. The ECG records electrical activity from cardiac depolarization and repolarization detected by electrodes on the skin. The resulting electrical potentials are small (several millivolts, at most) and occur over a frequency range of 0.05 to 100 Hz (cycles per second) (2,3). Signals of similar frequency and of similar or larger amplitude generated by noncardiac sources cause ECG artifact. These signals can be classified as nonphysiologic or physiologic (2). Nonphysiologic artifact is usually caused by poor electrode contact, electromagnetic interference, or defective ECG equipment. Physiologic artifact can be produced by muscle activitity (electromyographic potentials) or skin. Because muscle electrical signals are high frequency and dissimilar from cardiac electrical activity, they can usually be filtered from the ECG. Skin electrical signals are produced by movement and stretching of the skin and are the primary source of ECG motion artifact. Because the potential for ECG artifact is widely recognized, the results of the survey conducted by Knight and coworkers (4) published in this issue of the American Journal of Medicine are surprising. Of 766 physicians who reviewed an ECG rhythm strip of artifact that mimicked a wide QRS tachycardia, only 6% of internists, 42% of cardiologists, and 62% of cardiac electrophysiologists recognized the ECG abnormality. These concerning misdiagnoses occurred despite visible sinus rhythm QRS complexes that marched independently through the tracing and were clearly dissociated from the artifact. The clinical implications of such a misdiagnosis are important. Electrophysiologic testing is appropriate for patients with nonsustained ventricular tachycardia and depressed left ventricular function after myocardial infarction because implantable defibrillators (ICD) improve survival for those patients found to have inducible ventricular tachycardia. Thus a misdiagnosis of nonsustained ventricular tachycardia may extend the hospital stay or lead to unnecessary cardiac testing. In fact, a retrospective review of patients referred for arrhythmia management documented these misdiagnoses (5). The distinction of artifact from fact is not always easy. Artifact may mimic tachycardia, bradyarrhythmia, or pacemaker malfunction. The reliable hallmarks of either undisturbed true QRS complexes marching unimpeded through the tracing or nonphysiologic rapid or “premature” electrical activity may be absent. When simultaneous recordings of blood pressure or pulmonary artery pressure are available, as is common in intensive care units, dissociation of systolic pressure waveforms from the surface electrocardiogram may provide clues to the diagnosis of artifact. Occasionally artifact cannot be unequivocally distinguished from an arrhythmia, and further assessment guided by concern for the patient’s safety is appropriate. Although the findings of this study are concerning, the incidence of clinically relevant misdiagnoses is unknown and may be less than implied by the present study. Surveys have important limitations and, by nature, invite bias. The response rate was low; only 16% of internists and fewer than half of the cardiologists and electrophysiologists responded. Perhaps the nonrespondents did not answer because they felt the ECG was obviously artifact. The inability of the respondents to interview the patient to clarify the clinical context may result in an overestimation of the incidence of the problem. Finding that an alleged 19-beat run of rapid heart action was asymptomatic would hopefully prompt a more careful review of the tracing with attention to the possibility that artifact is the cause. Despite these limitations, the findings are provocative. Even if the rate of misdiagnosis were reduced by Am J Med. 2001;110:402– 403. From the Cardiovascular Division, Brigham and Women’s Hospital, Boston, Massachusetts. Requests for reprints should be addressed to William G. Stevenson, MD, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis Street, Boston, Massachusetts 02115.