The mechanism of sinoatrial block.

S ~NOATRIAL BLOCK is diagnosed when pauses appearing during regular heart action are approximately double the length, or a multiple, of the normal period and there is no evidence of ventricular and atria1 activity. If the pause is an exact multiple of the normal period, the disturbance is comparable to a type II atrioventricular (A-V) block; if less than double the normal period with certain irregularities, it is said to be an analog of a type I A-V block. Although sinoatrial block doubtless exists, its mechanism is difficult to explain, partly because it cannot be reproduced easily in experiments.1 This paper will consider four possible explanations, as well as a fifth modus operandi bearing on its genesis. The first possibility is that sinoatrial block results from a disturbance of impulse formation. The structure of the sinus node consists of thousands of specialized fibers possessing automaticity. Temporary failure of all these fibers to form impulses is improbable. When certain fibers cease to lead the heart, others take over. Evidence indicates that impulses may even arise in different areas of the sinus node without altering the electrocardiogram. Since it is difficult to conclude that all of the specialized fibers cease simultaneously to form an impulse for one beat, this explanation for sinoatrial block can be discarded. A second possibility, that sinoatrial block results from abnormal conduction between the sinus node and atria, is equally difficult to accept. Of the many connections between the sinus node and atria, numerous junctional fibers supplement the special preferential pathways. It is inconceivable that the impulse would be blocked in all these pathways simultaneously for one beat only. If different pathways are blocked temporarily, a continuous variation of the P waves would be expected, but in many instances of sinoatrial block the form of the P waves does not change. Anyone who has attempted to eliminate sinus node activity by clamping off the sinus node or by isolating it with ligatures knows how difficult it is to obtain a pertianent A-V junctional rhythm. Of course, a conduction disturbance must be postulated to account for beats periodically dropped between the sinus node and atria (Wenckebach periods). However, it is difficult to accept the existence of such periods as proved, for several reasons: (1) sinus node activity in our patients cannot be registered; (2) similar pauses may appear in simple respiratory arrhythmias; (3) the frequent diagnosis of periodically dropped beats between sinus node and atria in clinical tracings rests only on conjectures inferred from the duration of the atria1 periods; and (4) diagrams to indicate periodically dropped beats just because they are easily drawn do not demonstrate the presence of this conduction disturbance. The third possibility, advanced by Lewis,” is that sinoatrial block results from an increased uagal tone. He held that the long refractory period of the sinus node allowed a higher vagal tone to block the sinus node as it does the A-V node. Opposed to this explanation is the observation that the rate of the sinus beats is frequently regular in clinical instances of sino-