HEART BLOCK



Heart block refers to a disturbance of impulse conduction and should be distinguished from in­terference, a normal phenomenon in which im­pulse conduction is blocked owing to physiolog­ical refractoriness in the wake of a preceding impulse. Heart block may occur anywhere in the heart but is commonly recognized electrocardi-ographically in the AV node, His bundle, or bun­dle branches. In first-degree AV heart block, AV conduction time is prolonged (PR interval so.20 sec), but all impulses are conducted.

Second-de­gree heart block occurs in two forms: type I sec­ond-degree heart block (Wenckebach) is charac­terized by a progressive lengthening of the PR interval until a P wave is not conducted. Type II second-degree AV heart block denotes occasional or repetitive sudden block of a P wave without prior measurable lengthening of the PR interval. Type II AV block often antedates the development of Stokes-Adams syncope and complete AV block, while type I AV block with a normal QRS complex is usually more benign and does not progress to advanced forms of AV conduction disturbances. In the patient with acute myocardial infarction, type I AV block usually accompanies inferior in­farction, is transient, and does not require tem­porary pacing, whereas type II AV block usually accompanies anterior myocardial infarction, may require temporary or permanent pacing, and is as­sociated with a high mortality, mostly due to pump failure. First-degree or type I second-degree AV block can occur in healthy young people, es­pecially well-trained athletes. Any medication that affects AV nodal conduction (for example, digitalis, beta blockers, or verapamil) may cause first- or second-degree AV block.

Type I AV block with a normal QRS complex is usually at the level of the AV node proximal to the His bundle. Type II AV block usually occurs in association with a bundle branch block and is localized to the His-Purkinje system. Type I AV block in a patient with a bundle branch block may represent block in either the AV node or the His-Purkinje system. Type II AV block in a patient with a normal QRS complex may be due to intra-His block but is more likely to be type I AV nodal block that exhibits small increments in AV con­duction time. Note that 2:1 AV block may rep­resent either AV nodal or His-Purkinje block.

Complete AV block occurs when no atrial ac­tivity conducts to the ventricles. The atria and ventricles are controlled by independent pace­makers, and thus complete AV block is one cause of AV dissociation. The ventricular rhythm is usu­ally regular. If the AV block is at the level of the AV node (for example, congenital AV block), the QRS complexes are normal in morphology and duration, with rates of 40 to 60 per minute, and respond to autonomic influences. If the AV block is in the His-Purkinje system [usually acquired), the escape rhythm originates within the ventricle, has a wide QRS and a slower rate, and is less re­liable and under less autonomic influence. Causes of AV block include surgery, electrolyte disturb­ances, endocarditis, tumor, Chagas’ disease, rheu­matoid nodules, calcific aortic stenosis, myx­edema, polymyositis, infiltrative processes such as amyloid, sarcoid, or scleroderma, drug toxicity, coronary disease, and degenerative processes. In children the most common cause of AV block is congenital and is usually asymptomatic; in some, however, symptoms eventually develop, requir­ing pacemaker implantation. The indications for pacemaker therapy in heart block are summarized in Table 8-5. Atropine (for AV nodal block) and isoproterenol (for heart block at any site) may be used transiently while preparations are made for ventricular pacing. Drugs cannot be relied on to increase the heart rate for more than several hours to a few days without producing significant side effects.

The term AV dissociation describes indepen­dent depolarization of the atria and ventricles. AV dissociation is not a primary disturbance of rhythm but is a “symptom” of an underlying rhythm disturbance produced by one or a com­bination of three causes that prevent the normal transmission of impulses from atrium to ventricle: (1) Slowing of the dominant pacemaker of the heart (usually the sinus node), allowing escape of a subsidiary or latent pacemaker. This is AV dis­sociation by default of the primary pacemaker and is often a normal phenomenon, e.g., sinus bra­dycardia and a junctional escape rhythm. (2) Ac­celeration of a latent pacemaker that usurps con­trol of the ventricles. This abnormally enhanced discharge rate of a usually slower subsidiary pace­maker is pathological, e.g., junctional or ventric­ular tachycardia. (3) Block at the AV junction that prevents impulses formed at a normal rate in a dominant pacemaker from reaching the ventricles so that the ventricles beat under the control of a subsidiary pacemaker, e.g., complete AV block with a ventricular escape rhythm. It is important to remember that complete AV dissociation is not synonymous with complete AV block.