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DIAGNOSIS AND MANAGEMENT OF BRADYCARDIA AND ATRIOVENTRICULAR BLOCK ASSOCIATED WITH ACUTE CORONARY ISCHEMIA

2001; Elsevier BV; Volume: 19; Issue: 2 Linguagem: Inglês

10.1016/s0733-8627(05)70189-9

1558-0539

William J. Brady, Richard A. Harrigan,

Cardiac pacing and defibrillation studies

Bradyarrhythmias arising in the setting of myocardial infarction (MI) occur in 25% to 30% of patients with acute myocardial infarction (AMI) and result from abnormalities either of impulse formation (i.e., automaticity) or of impulse conduction. In most cases, these abnormalities are due to myocardial ischemia or infarction with necrosis of the cardiac pacemaker sites or conduction system. Other factors responsible for these bradyarrhythmias include altered autonomic influence, systemic hypoxia, electrolyte disturbances, acid–base disorders, and complications of various medical therapies. The incidence of the various bradyarrhythmias in the setting of AMI, including both bradycardia and conduction block, is reported to be 25% to 30%. Of the rhythm disturbances, sinus bradycardia (SB) is found in approximately 40% of patients, representing the most commonly encountered bradyarrhythmia in patients with AMI.1, 9 Junctional rhythm is noted in 20% of patients, whereas idioventricular rhythm occurs in 15% of such cases. Both junctional and idioventricular rhythms occur with failure of higher pacemaker site function or as escape rhythms in the setting of atrioventricular block (AVB). AV conduction disturbances are classified into first-degree AVB, second-degree (types I and II) AVB, and third-degree (complete) AVB— also known as complete heart block. Of the AVBs, first-degree and second-degree, type I AV blocks are found in 15% and 12% of patients with AMI, respectively. Complete heart block (third-degree AVB) complicates 8% of infarctions. Second-degree, type II AV block is rare. In the realm of unstable bradyarrhythmias complicating AMI, complete heart block is most often encountered, with an incidence of 40%. Sinus bradycardia (25%) and junctional rhythm (20%) are the next most commonly encountered hemodynamically compromising bradycardic rhythms in AMI patients.1, 9 The pathophysiologic mechanisms underlying most bradyarrhythmic episodes in AMI patients involve either reversible ischemic injury or irreversible necrosis of the conduction system, as well as altered autonomic function. Additional mechanisms include myocardial hyperkalemia, local increases in adenosine, metabolic acidosis, systemic hypoxia, and the complications of medical therapy, in particular both beta- and calcium channel–blocking agents. Perhaps the most useful method of approach to a discussion of the pathophysiology involves a categorization of the bradyarrhythmias relative to the anatomic location of the infarction. Using this perspective, the clinician can predict the likelihood in many cases of arrhythmia development, the expected time of onset, the associated risk of hemodynamic compromise, the response to acute therapy, the need for long-term treatment, and the ultimate prognosis. Inferior, inferolateral, and inferoposterior AMIs resulting from occlusion of the right coronary artery (RCA) are frequently complicated by bradyarrhythmias.3 The common association of inferior wall ischemic events and compromising bradyarrhythmias can be due to increased parasympathetic influence, especially early in the course of the infarction. Such patients tend to develop rhythm disturbances abruptly, within 6 hours of the onset of infarction, have relatively slow ventricular escape rates, and respond rapidly to atropine or isoproterenol therapy.3 Patients who develop bradyarrhythmia after 6 hours of infarction usually do so gradually, with an equally slow return to normal sinus rhythm. The escape rhythm is usually of ventricular origin, with a relatively high rate and poor response to medical therapy. These patients most likely experience the rhythm disturbance because reversible ischemia of the conduction system.3 In patients with inferior AMI, irreversible damage of the AV node (i.e., necrosis of this structure) is rare owing to the presence of both extensive collateral circulation (i.e., right coronary artery and left anterior descending artery contributions in the most patients), as well as a relatively low metabolic rate with high glycogen reserves of such myocardial conducting tissue. Third-degree AVB patients with inferior AMI are said to develop a “proximal” third-degree AVB owing to ischemic damage to the AV node or increased parasympathetic influence. In contrast, patients with anterior wall infarctions suffer “distal” third-degree AVB as a result of dysfunction of the trifascicular intraventricular conduction system. Patients with inferior AMI and its anatomic variants, who develop compromising bradyarrhythmias, have a higher in-hospital mortality rate—approaching 20%—compared with patients without arrhythmic complications. This increased mortality rate does not necessarily result from the bradyarrhythmia itself but rather from a generally larger MI. Patients with RCA-related infarctions also are at risk for developing sinus node dysfunction, manifested primarily by SB and sinus arrest. SB is a common bradyarrhythmia encountered in AMI patients, particularly in patients with inferior wall involvement. In cases of sinus arrest, the escape rhythm originates from either the AV node, producing the narrow-complex junctional rhythm with ventricular rates of 45 to 60 bpm, or from the intraventricular conduction system, resulting in the wide-QRS complex idioventricular rhythm, with rates of 30 to 45 bpm. In many cases, patients have either a prior history of sick sinus syndrome or are using cardioactive medications such as beta-blocking agents, calcium antagonists, and cardiac glycosides, which suppress SA node function. With the acute ischemic syndrome, either ischemic injury to the SA node or heightened parasympathetic tone are responsible for the clinical expression of the bradyarrhythmia. Patients with anterior and anteroseptal infarctions most often have occlusion of the left main coronary artery, the proximal LAD, and the LAD-derived branches. AVBs that develop in this setting respond poorly to therapy, and these patients have a poor prognosis. Autopsy studies show extensive septal necrosis often accompanied by irreversible malfunction of the His bundle and the bundle branches. In these cases, the AV node is often normal without evidence of necrosis, indicating the distal nature of the complete AVB in these patients. Patients with conduction disturbances occurring in the setting of anterior AMI most often do not respond to medical therapy (e.g., atropine or isoproterenol). Perfusion actually can be further impaired by the vasodilating effects of isoproterenol, without an accompanying increase in the escape rhythm rate. Ventricular pacing, either by the transcutaneous or transvenous routes, is required in compromised patients. The prophylactic presence of a ventricular pacer is encouraged in those patients who are hemodynamically stable on presentation.