Do not use the 3 or 5 Lead ECG Monitor as a 12-lead Electrocardiogram
Tuhin K. Roy MD, PHD
Continuous electrocardiogram (ECG) monitoring is a standard monitor utilized for the detection of arrhythmias and ischemia. Many common monitoring systems utilize 3 or 5 leads instead of the 12 leads captured by the standard ECG. Even though both systems can potentially be used for detection of arrhythmias as well as ischemia, the limitations of the 3- or 5-lead system monitors should be understood so that the care of the patient may be optimized by obtaining further studies as necessary. The standard 12-lead ECG provides a 10-second snapshot of three bipolar leads (I, II, III), three augmented unipolar leads (a VR, a VL, a VF), and six precordial leads (V1 to V6); the standard 5-lead system allows the monitoring of seven different leads (I, II, III; a VR, a VL, a VF; and V5). It is important to remember that the ECG reflects only electrical activity and not heart function (e.g., pulseless electrical activity) and can be altered by physiologic factors, pathophysiological factors (e.g., electrolyte imbalances, pacemakers, pericarditis, hypothermia, subarachnoid hemorrhage), and technical factors (e.g., calibration, lead position, and body position).
Arrhythmia Detection
Accurate detection and identification of arrhythmias is crucial since inadequate or inappropriate treatment can be harmful or fatal. Although lead II is commonly used for the detection of cardiac dysrhythmias since its direction parallels atrial depolarization and results in the maximum P-wave amplitude, lead V1 is more useful for diagnosing bundle branch blocks and discriminating between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrant conduction. Both of these leads should be monitored if possible so that the relationship between atrial and ventricular depolarizations can be determined.
Premature atrial contractions typically result in abnormal P waves from an ectopic atrial focus with a variable PR interval and no compensatory pause. If part of the ventricular conduction system is refractory, the resulting aberrant conduction leads to an abnormal QRS complex and can be confused with a premature ventricular contraction. Look for a preceding (likely abnormal) P wave, a QRS complex suggestive
of a right bundle branch block, an rSR’ in V1, and concordance of the initial deflection with the preceding beat to distinguish these from premature ventricular contractions.
of a right bundle branch block, an rSR’ in V1, and concordance of the initial deflection with the preceding beat to distinguish these from premature ventricular contractions.
Paroxysmal SVT results from transient activity of an ectopic atrial pacemaker and is seen as a rapid regular rhythm with abnormal P waves and normal QRS complexes. SVT with aberrant conduction (as mentioned earlier) can be confused with ventricular tachycardia. Atrial flutter is characterized by sawtooth flutter (F) waves best seen in leads II and V1 with normal QRS complexes typically conducted at 2:1, 3:1, or 4:1. In atrial fibrillation, P waves cannot be identified and the QRS complexes are narrow with irregular interval.
Junctional rhythms such as atrioventricular (AV) nodal re-entry tachycardia can result from ectopic activity near the AV node that is conducted retrograde as well as anterograde, leading to inverted P waves in leads II, III, and a VF and positive P waves in a VR. High nodal rhythms produce shortened PR intervals, whereas low nodal rhythms produce P waves that follow a normal QRS. If the rhythm is midnodal, the P wave can distort the QRS complex, causing a pseudo S wave in the inferior leads and a pseudo R wave in V1.
AV re-entrant tachycardias are due to accessory conduction pathways that permit ventricular pre-excitation. Wolff-Parkinson-White syndrome (WPW) generates a regular rhythm with a delta wave and a slurred QRS complex resulting from early ventricular depolarization. Type A WPW is characterized by an upright delta wave and QRS complex in the precordial leads with an upright dominant R wave in V1; this can be confused with a right bundle branch block (RBBB). Type B WPW has a downward delta wave and QRS complex in leads V1 and V2 with upward deflections in the other precordial leads similar to a left bundle branch block (LBBB). The majority of tachycardias in WPW are classified as orthodromic and result from antegrade conduction of impulses through the AV node that return to the atria via the accessory pathway; P waves follow the normal-width QRS complexes and no delta waves are seen. Antidromic AV re-entrant tachycardia results from antegrade conduction via the accessory pathway (causing wide QRS complexes) with retrograde conduction via the AV node. Atrial fibrillation in WPW results in an irregular wide complex tachycardia.
Premature ventricular contractions result in a prolonged abnormal QRS complex since the ectopic ventricular pacemaker impulses are conducted via ventricular muscle rather than the Purkinje fibers; typically, the QRS voltage is increased and the T wave appears inverted. Retrograde or blocked atrial depolarization may lead to the
presence of P waves on the tracing. A compensatory pause occurs since a subsequent depolarization from the sinoatrial (S-A) node is blocked. An R-on-T phenomenon may happen if this occurs near the vulnerable period of the preceding depolarization, leading to ventricular fibrillation. The QRS complex may be of the RBBB variant with a prominent R wave in V1 or may be of the LBBB variant with notching of the S wave with less acute downsloping.
presence of P waves on the tracing. A compensatory pause occurs since a subsequent depolarization from the sinoatrial (S-A) node is blocked. An R-on-T phenomenon may happen if this occurs near the vulnerable period of the preceding depolarization, leading to ventricular fibrillation. The QRS complex may be of the RBBB variant with a prominent R wave in V1 or may be of the LBBB variant with notching of the S wave with less acute downsloping.
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