Sinoatrial SA Block

The sinus node discharge must be conducted into the atria to pace the heart during sinus rhythm. If sinus node discharges are delayed or blocked in their outward propagation (exit block), then sinoatrial block is present. Sinoatrial block is divided into first-, second-, and third-degree varieties.

First-degree SA block means that the impulse is delayed in its conduction out of the sinus node into the atria—a condition that cannot be recognized on the clinical ECG.

Second-degree SA block means that some impulses get through and some are blocked. Second-degree SA block can be suspected whenever an expected P wave and the corresponding QRS complex are absent. In the variable (Wenckebach) type of second-degree SA block, the missing P wave would come after a period of progressive prolongation of the conduction time from the sinus node to the atrium, something undetectable on the clinical ECG. However, another ECG finding common to the Wenckebach phenomenon can be seen—progressive shortening of the P-P intervals prior to the missing P wave ( Fig..24:22). In the constant type of second-degree SA block, the sinoatrial conduction time remains constant before and after the blocked impulses. In this situation, the interval encompassing the missing beat is an exact or near-exact multiple of the cycle length (Fig.,.24-23).

Wenckebach

FIG. 24-22. Second-degree SA block type I (Wenckebach). (From Braunwald E: Heart Disease. A Textbook of Cardiovascular Medicine. Philadelphia, Saunders, 1980. Used by permission.)

Wenckebach Phenomenon
FIG. 24-23. Second-degree constant SA block type II (lead V4).

Third-degree SA block occurs when the sinus node discharge is completely blocked and no P wave originating from the sinus seen. There are three other causes of absent sinus P waves in addition to third-degree SA block: (1) sinus node failure, (2) a sinus node stimulus inadequate to activate the atria, and (3) atrial unresponsiveness.

CLINICAL SIGNIFICANCE Sinoatrial block usually arises from myocardial disease (acute rheumatic fever, acute inferior MI, other causes of myocarditis) or drug toxicity (digoxin, quinidine, salicylates, b-adrenergic blockers, or calcium channel blockers). In rare individuals, vagal stimulation can produce SA block.

TREATMENT

1. Treatment depends on the underlying cause, associated dysrhythmias, and whether symptoms of hypoperfusion are present.

2. Sinus node discharge rate and sinoatrial conduction can be facilitated by atropine or isoproterenol when clinically required; however, ischemia may result from a rhythm that is accelerated.

3. Cardiac pacing is indicated for recurrent or persistent symptomatic bradycardia.

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