Prolonged A-V conduction a factor in atrial fibrillation
Commonplace bedside observations frequently provide profound clinical insights. They may seem trivial, but searching for them hones diagnostic skills. At times, one gains information otherwise not forthcoming and above all they may improve intelligent patient management.
After introducing cardioversion, I noted a high frequency of first-degree A-V block among patients just reverted from atrial fibrillation. This was true whatever the etiology of the fibrillation. It was observed equally among patients with rheumatic, ischemic, or hypertensive heart disease as well as among so-called lone fibrillators.
I related this finding to my teacher and mentor, Dr. Levine. To my disappointment, he was totally unimpressed. "Why shouldn't this be so?" he asked, "After all, the ventricular rate in atrial fibrillation is controlled by lengthening A-V conduction duration with digitalis glycosides which would manifest in those with sinus rhythm by a greater P-R duration. Stop digitalis and the heart block will disappear."
Dr. Levine, in this case, was wrong. In numerous patients, the P-R remained long after cardioversion, even after stopping digitalis. When an electrocardiogram was available before the onset of the arrhythmia, the P-R duration had already been of long duration. This also negated the possibility that the electrical discharge during the cardioversion lengthened A-V conduction.
Of 125 consecutive patients with atrial fibrillation who were studied immediately after cardioversion, 47 exhibited first-degree atrioventricular block. Thus, nearly 38% of patients who developed atrial fibrillation had a P-R of 0.21 seconds or greater (1). In earlier studies we noted a skewed distribution in P-R duration (2).
A short P-R interval of less than 0.14 seconds was rarely encountered among patients prior to the onset of atrial fibrillation or after its reversion. In prospective studies we learned that progressive prolongation of the P-R interval might precede the onset of atrial fibrillation among patients with rheumatic mitral valvular disease. We also found that in the presence of marked degrees of A-V block, cardioversion required more energy and normal rhythm was unlikely to be sustained even with the use of antiarrhythmic drugs.
The association of A-V block with atrial fibrillation was not our discovery. It had been reported some years before the introduction of cardioversion by a brilliant Boston cardiologist, Dr. Mark D. Altschule (3,4). He noted, as we later confirmed, that this relation also held in atrial fibrillation due to thyrotoxicosis.
No electrophysiological explanation has been hypothesized for this phenomenon. It may relate to the fact that the substrate for fibrillation requires an atrial region having a long refractory period; as a result the circulating wave front may not extinguish at the very onset of the arrhythmia. This may be only momentary, since the wave front rapidly fractionates into numerous circulating chaotic re-entrant wavelets of activation.
Now for the several clinical pearls:
- When one finds a short P-R interval of 0.13, or less in someone who has had atrial fibrillation, the arrhythmia is probably due to an accessory pathway.
- In patients with mitral valvular disease and first-degree A-V block the advent of frequent atrial premature ectopics is an augury for atrial fibrillation. One can then initiate antiarrhythmic therapy and delay the onset of atrial fibrillation for many years.
- Prior to the onset of atrial fibrillation, if patients had markedly prolonged P-R duration (0.28 seconds or greater) antiarrhythmic drugs will usually prove unsuccessful in maintaining sinus rhythm following cardioversion.
- Originally published on 1 May 2000
1. Lown B. Electrical reversion of cardiac arrhythmias. Brit Heart J. 1967; 29: 469.
2. Lown B, Perlroth MG, Kaidbey S, et al. Cardioversion of atrial fibrillation. N Engl J Med. 1963; 269:325.
3. Klainer MJ, Altschule MD. Prolongation of the P-R interval in patients with auricular fibrillation and flutter following myocardial infarction. Am J Med Sci. 1942;203:215.
4. Altschule MD. The relation between vagal activity and auricular fibrillation in various clinical conditions. N Engl J Med. 1945;233:265.
Date Posted: 13 September 2008