Clinical application of the electrocardiogram.

fundamental observations about cardiac pathophysiology. The purpose of this editorial comment is to expand the findings covered in that review to demonstrate how clinical investigators have applied those advances in electrocardiography toward an understanding of the physiology of cardiac arrhythmias (2–4). This knowledge has enabled the practicing cardiologist, armed with no more than a pair of calipers and deductive reasoning, to use the 12-lead electrocardiogram (ECG) to diagnose arrhythmias in ways that rival the clinical electrophysiologist. In fact, the early electrocardiographers did just that, and the advent of invasive clinical electrophysiology has proven their insight correct in many instances, ranging from observations about concealed conduction, accessory pathway (Wolff-Parkinson-White) tachycardias, aberration, focal causes of atrial fibrillation, ventricular tachycardias, and others. Let us consider a few of the lessons that they learned. Interpretation of supraventricular tachycardias. Based on their ECG presentation, paroxysmal supraventricular tachycardias (SVTs) can be classified into two major groups: short RP and long RP tachycardias, that is, the P wave during the SVT occurs either in the first or second half of the tachycardia cycle. Because the PR interval is inversely related to the RP interval, short RP tachycardias have a long PR interval, and long RP tachycardias have a short PR interval. Although exceptions to any classification are to be expected, this grouping includes the vast majority of SVTs and enables the clinician to deduce the SVT mechanism with relative ease and accuracy. From that information, appropriate therapeutic decisions follow. SHORT RP SVTs. These SVTs are defined by having atrial activity 1) obscured by the QRS complex because of the simultaneous inscription of both, 2) occurring in the terminal portion of the QRS complex and often giving the appearance of an R9 in lead V1, or 3) present in the ST segment. Hence, the interval from the onset of the QRS complex to the onset of the P wave is short—“short RP SVT”—and in fact can be a negative value when the retrograde P wave is buried in the beginning portion of the QRS complex. Invasive electrophysiologic studies have shown that the most likely SVT for the first and second examples is atrioventricular nodal reentrant tachycardia (AVNRT), using the slow AV nodal pathway anterogradely and the fast AV nodal pathway retrogradely. An SVT traveling to the ventricle over the AV node and back to the atrium over an accessory pathway, called “atrioventricular reentrant tachycardia” (AVRT; Wolff-Parkinson-White syndrome), is the most likely cause of the third example, and less commonly the second. Thus, careful study of the ECG can explain these very common SVTs. One can become even more sophisticated in diagnosing the SVT if an episode of functional bundle branch block (FBBB) also occurs. Prolongation of the SVT cycle length during FBBB is most consistent with an AVRT and the location of the accessory in the same ventricle that gave rise to the FBBB. Thus, prolongation of the SVT cycle length during a period of a functional left bundle branch block (LBBB) would be found during AVRT due to retrograde conduction over a left-sided accessory pathway; the same reasoning applies to functional right BBB (RBBB) and a right-sided accessory pathway. The cycle length of the SVT prolongs because, during the FBBB, the anterograde impulse must first activate the ventricle contralateral to the site of FBBB and then travel across the interventricular septum to reach the opposite ventricle, gain access to the accessory pathway, and activate the atrium retrogradely. Failure of the FBBB to prolong the cycle length of the AVRT occurs when the accessory pathway is located contralateral to the ventricle with the FBBB, in many AVRTs due to septal accessory pathways, and during non-WPW forms of SVT. The ECG algorithms based on the morphology of the delta wave of the WPW complex can also be used to determine the location of the accessory pathway.