Although this chapter emphasizes VT and VF, an important minority of SCD events begin with a bradyarrhythmia14 or an organized rhythm without a pulse (e.g., pulseless electrical activity, or PEA). Bradyasystole refers to a cardiac rhythm that has a ventricular rate below 60 beats per minute in adults and/or periods of absent heart rhythm (asystole). Bradyasystolic states are clinical situations during which bradyasystole is the dominant heart rhythm.
Bradyasystolic rhythms other than asystole can either be accompanied by a pulse or there can be no discernible pulse with each QRS (PEA). Bradyasystole with a pulse is often accompanied by a significant decrease in cardiac output, leading to hypotension and/or syncope. Bradycardia with or without a pulse occurs frequently during cardiac arrest, either as the initial rhythm, during the course of resuscitation, or following electrical defibrillation. Obviously, asystole occurs eventually in all dying patients.
Ewy et al.15 have shown that electrically induced coarse VF in dogs can have a direction or vector. When recordings are made using an ECG lead perpendicular to the main axis of the coarse fibrillation in experimental models, tracings show what appears to be asystole or fine VF. To ensure that VF is not masquerading as asystole, the American Heart Association recommends confirmation of asystole by switching to another lead whenever a "flat line" is recorded on the ECG during resuscitation. Although there are anecdotal case reports in the literature suggesting that this phenomenon can occur in humans, "masquerading" VF probably occurs rarely during clinical resuscitation and is not responsible for the misdiagnosis of large numbers of cases of asystole. 16
Bradyasystole can be either primary or secondary. Primary bradyasystole occurs when the heart's electrical system intrinsically fails to generate and/or propagate an adequate number of ventricular depolarizations per minute to sustain consciousness and other vital functions. Secondary bradyasystole is present when factors external to the heart's electrical system cause it to fail (e.g., hypoxia). It is unclear why conventional treatment of bradyasystolic cardiac arrest with atropine, epinephrine, or electrical pacemakers rarely results in survival to hospital discharge.
Cellular metabolic functions must be intact for normal electrical impulse generation and propagation to occur. Severe ischemia of the sinoatrial (SA) node can disable cellular metabolism, preventing pacemaker cells from actively transporting the ions necessary to control the transmembrane action potential. Proximal occlusion of the right coronary artery (RCA) can cause ischemia and/or infarction of both the SA and atrioventricular (AV) nodes, since the SA node is supplied by a branch from the proximal RCA 55 percent of the time and the AV node receives its nourishment from a branch of the distal RCA 90 percent of the time. Ischemia or infarction of the AV node can disrupt normal conduction, causing bradycardia due to AV block. Because the bundle branches receive their blood supply from multiple coronary arteries, bradyasystole caused by ischemic bilateral bundle branch block is rare and generally only occurs when there is extensive myocardial infarction due to severe, multivessel coronary artery disease.
The spectrum of disorders affecting the heart's primary pacemaker, known as the sick sinus syndrome, can cause intermittent lightheadedness, syncope, or SCD. The disorder affects both men and women. Although it is more common with advancing age, primary electrical failure of the heart can even occur in infants and children. The precise cause of sick sinus syndrome is unknown. Pathologic studies usually reveal histologic degeneration of the SA node. In addition, the disorder often involves the AV node and the conduction tissue between the SA and AV nodes. Thus, sick sinus syndrome should be thought of as a diffuse degenerative disease of the heart's electrical generation and conduction system. Idiopathic sclerodegeneration of the AV node and the bundle branches (Lenegre's disease) or invasion of the conduction system by fibrosis or calcification spreading from adjacent cardiac structures (Lev's disease) can lead to bradyasystolic heart block with or without cardiac arrest. In rare cases, a clinical presentation resembling the sick sinus syndrome can occur when the heart's electrical system is affected by systemic disease, vascular compromise, or tumor (e.g., melanoma metastatic to the AV node).
Atropine, transcutaneous pacing, dopamine, or epinephrine can be used to treat acute, symptomatic bradyasystole (including cardiac arrest) that is due to the sick sinus syndrome. Permanent ventricular or AV sequential pacing is usually necessary for patients with persistent symptomatic bradycardia. Patients who manifest the tachycardia-bradycardia variant (periods of supraventricular tachycardia followed by prolonged sinus arrest or bradycardia) may also require antiarrhythmic therapy or radiofrequency ablation.
Pacemaker cells and conducting tissue can be affected by a variety of endogenous chemical, hormonal, pharmacologic, toxicologic, and neurogenic influences. Hypoxia and hypercarbia due to respiratory arrest cause bradyasystole frequently, due to both a direct depressant effect on cardiac pacemaker cells and increased parasympathetic discharge. Common clinical conditions that often cause bradyasystole include suffocation, near drowning, stroke, and opiate overdose. Beta-adrenergic blocking agents, calcium channel blockers, digitalis glycosides, parasympathomimetic agents (e.g., edrophonium), hypoxia, hypercarbia, adenosine, and adenosine triphosphate can also cause bradyasystole.
Endogenous adenosine that is released when there is myocardial hypoxia and ischemia relaxes vascular smooth muscle, decreases atrial and ventricular contractility, depresses pacemaker automaticity, and impairs AV conduction. During normal aerobic metabolism, adenosine is formed primarily by intracellular degradation of S-adenosylhomocysteine (SAH), catalyzed by the enzyme SAH hydrolase (SAH pathway). During myocardial ischemia, adenosine is formed primarily by dephosphorylation of adenosine monophosphate (AMP), catalyzed by the enzyme 5' nucleotidase (adenosine triphosphate [ATP] pathway).
The cellular electrophysiologic effects of adenosine can be antagonized competitively by methylxanthines but not by atropine. A specific adenosine antagonist (BW-A1433U) has been shown to reverse and prevent postdefibrillation bradyasystole and hemodynamic depression in a domestic pig model. In small pilot studies, aminophylline, a competitive nonspecific adenosine antagonist, restored cardiac electrical activity within 30 s in more than half of the bradyasystolic cardiac arrest patients who were refractory to atropine and epinephrine. —I8
Myocardial ischemia excites cardiac vagal and sympathetic afferents, leading to vagally mediated depressor reflexes and/or sympathetic reflex cardioexcitation. In addition, myocardial infarction can interrupt afferent and efferent neural transmission, potentially triggering dysrhythmias. Autonomic disturbances have been documented in the majority of AMI patients, especially during the first 30 to 60 min after coronary artery occlusion. Stimulation of afferent vagal cardiac receptors, particularly those located in the posterior left ventricle, during ischemia or infarction can trigger sympathetic inhibition, vasodilation, bradycardia, and hypotension (the Bezold-Jarisch reflex). Activation of this reflex may explain the higher incidence of nausea and vomiting in patients with inferior (69 percent) compared to anterior (29 percent) infarction. Bradyasystole triggered by the Bezold-Jarisch reflex is usually short-lived and often responds to atropine.
One of the most baffling mysteries of bradyasystolic cardiac arrest relates to myocardial mechanics. Bradyasystole, unlike ventricular fibrillation, is accompanied by very little myocardial oxygen consumption in animal models. Because of this, myocardial high-energy phosphate stores should decay relatively slowly during bradyasystole. This should theoretically result in a high incidence of return of spontaneous circulation following restoration of a more normal rhythm (e.g., with the early use of electrical pacing). However, return of spontaneous circulation is infrequent, and long-term neurologically intact survival is rare in bradyasystolic cardiac arrest.
These findings strongly suggest that other factors must play a determining role in the pathophysiology and subsequent outcome of bradyasystolic cardiac arrest. Bradyasystolic arrest is not just a disorder of rhythm generation or propagation: it is a perplexing syndrome characterized by such rhythm disturbances accompanied, in many cases, by profound depression of myocardial and vascular function. The causes of the latter derangements have yet to be elucidated. Suspected causes include endogenous myocardial depressants (including downregulation of catecholamine receptors and/or toxic influences of intense sympathetic stimulation), neurogenic influences, postischemic myocardial stunning, and/or free radical injury.
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