ARRHYTHMIAS in ACUTE MYOCARDIAL MFARCTION



Arrhythmias occurring in patients with acute myocardial infarction should be treated if they cause hemodynamic compromise, augment my­ocardial oxygen requirements, or predispose to more malignant arrhythmias such as sustained ventricular tachycardia or fibrillation. Some rhythms not ordinarily deleterious may decrease cardiac output in patients who have stiff, non-compliant ventricles by the loss of atrioventric­ular synchrony. Reversible causes of ventricular ectopy, for example, digitalis excess or metabolic abnormalities, should be considered.

Ventricular premature complexes (PVC’s) are very common following acute myocardial infarc­tion. Unless very frequent, they usually cause no problem in themselves but may be forerunners of more serious sustained ventricular tachyarrhyth­mias. The danger of “R on T” PVC’s (a ventricular premature complex occurring during the T wave of a previous complex) has probably been over­estimated in the past and probably does not carry any worse prognosis than any other PVC. Even though PVC’s are sometimes considered a warn­ing arrhythmia for the subsequent development of ventricular tachycardia or fibrillation, many episodes of ventricular fibrillation occur without any warning arrhythmia. Approximately half of those patients who develop ventricular fibrilla­tion have no warning PVC’s, while half of those with warning PVC’s do not develop a sustained ventricular tachyarrhythmia. If ventricular tachy­cardia is not suppressed by lidocaine, intrave­nous procainamide can be substituted or added to lidocaine. Intravenous bretylium may also be useful to prevent recurrence of sustained or symp­tomatic ventricular tachyarrhythmias. High-dose or multiple antiarrhythmic drug therapy in pa­tients with simple ventricular ectopy is not war­ranted. If sustained ventricular tachycardia oc­curs, it should be cardioverted immediately if hemodynamic compromise occurs. If it is well-tolerated for a short period of time, a limited trial of lidocaine for termination may be tried. The pa­tient with acute infarction should not be allowed to continue having sustained ventricular tachy­cardia for a prolonged period of time. Ventricular fibrillation occurs in 2 to 3 per cent of hospital­ized patients with acute myocardial infarction and should be promptly defibrillated with 200 to 400 joules.

Ventricular tachycardia and fibrillation during the first 36 to 48 hours of acute myocardial in­farction do not carry the same prognosis as when they occur later in the recovery period. These early ventricular arrhythmias appear to be due to acute ischemia and do not necessitate long-term, chronic antiarrhythmic therapy. On the other hand, ventricular tachycardia or fibrillation oc­curring more than 48 hours after infarction are probably due to different electrophysiological mechanisms and may be forerunners of severe, chronic arrhythmias.

Accelerated idioventricular rhythm with rates of 60 to 100 beats/minute occurs commonly dur­ing the acute infarction period. This arrhythmia probably does not increase the incidence of more rapid ventricular tachyarrhythmias. It usually does not cause hemodynamic deterioration unless cardiovascular compensation is tenuous and de­pendent upon normal atrioventricular synchrony. If the rhythm appears to be affecting hemodynam­ics adversely or increasing the incidence of ven­tricular ectopy, it can be treated by lidocaine or in some instances by accelerating the sinus rate slightly with atropine or atrial pacing.

Sinus tachycardia that persists in a patient with acute infarction after relief of pain and anxiety is often due to inability of the ventricle to maintain an adequate stroke volume. Not only is it a sign of hemodynamic impairment in some patients but also is detrimental by increasing oxygen demand. Pericarditis, pulmonary embolus, and fever com­monly cause sinus tachycardia. The treatment of sinus tachycardia is directed at the underlying cause.

Sinus bradycardia often occurs early after acute inferior myocardial infarction and may be related to ischemia of the sinus node or abnormally ele­vated vagal tone. If asymptomatic and hemody-namically tolerated, it should not be treated. If it creates symptoms, atropine or temporary pacing may be required.

A rapid ventricular response caused by atrial flutter or fibrillation should be treated vigorously because of the increase in myocardial oxygen con­sumption. If the ventricular rate cannot be slowed pharmacologically, early electrical cardioversion should be considered. The treatment of atrial tachyarrhythmias is discussed in Chapter 8. Atrial tachyarrhythmias also may be features of pericar­ditis or pulmonary embolus.

First-degree AV block requires no therapy; if digitalis is thought to be the etiology, it should be discontinued. Second-degree AV block of the Mobitz type I (Wenckebach) type (see Chapter 8) is common in patients with inferior myocardial infarction due to increased vagal tone and/or is­chemic involvement of the AV node. It is usually temporary and, if asymptomatic, requires no ther­apy. If hemodynamic compromise occurs, atro­pine is effective; if sustained improvement does not occur, temporary pacing may be needed. Type I AV block usually does not lead to high-degree AV block; if it does, the ventricular escape is junc­tional and usually reliable at reasonable rates (40 to 60/minute). Mobitz type II second-degree AV block is an indication for prophylactic pacing. Type I second-degree AV block is more common with inferior and type II more common with an­terior myocardial infarctions. - A prophylactic temporary pacemaker is usually recommended for any patient who has developed complete heart block with an acute myocardial infarction, especially if the infarction is anterior and the site of the heart block likely to be in the His-Purkinje system. Complete AV block should be differentiated from AV dissociation, common in inferior myocardial infarction due to sinus bra­dycardia with junctional escape or accelerated junctional rhythms.

The occurrence of new intraventricular con­duction defects (left or right bundle branch block, or right bundle branch block with left anterior or posterior fascicular block) are associated with an­terior more often than inferior infarction. The prognosis of these patients, as in those with Mob-itz II second degree heart block, is poor, reflecting the extensive infarction rather than the conduc­tion disturbance itself. Even though temporary pacing in these patients has not been shown def­initely to increase survival, it is still reasonable to insert a temporary pacemaker if heart block is deemed likely. Therefore, temporary prophylactic pacing is indicated in patients who develop new trifascicular block. Temporary prophylactic pac­ing in patients who have a new right bundle branch block and a normal axis or a new left bun­dle branch block with a normal PR interval is more controversial. Patients who have pre-exist­ing left or right bundle branch block with or with­out axis deviation probably do not require pro­phylactic pacing with acute infarction.