Cardiac Defibrillation

Today, sudden cardiac arrest (death) is one of the most common causes of mortality in developed countries; 3 million people experience sudden cardiac arrest worldwide, and the annual incidence in the United States is 300,000. Sudden cardiac arrest claims more lives in the United States each year than the combination of deaths from acquired immunodeficiency syndrome (AIDS), breast cancer, lung cancer, and stroke (31).

Several studies have identified the primary risk factors for sudden cardiac arrest, including: (1) coronary artery disease;

(2) heart failure or decreased left ventricular ejection fraction;

(3) previous sudden cardiac arrest events; (4) prior episodes of ventricular tachycardia; (5) hypertrophic cardiomyopathies; and (6) long QT syndrome (32). The combination of any three of these factors increases the risk for sudden cardiac arrest significantly. Of sudden deaths, 90% occur in patients with two or more occlusions in their major coronary arteries (33).

5.1. History

The first documentation of ventricular fibrillation was noted in 1850 (34). A little over a century later, in 1962, the first direct current defibrillator was developed. Ventricular fibrillation began to be recognized as a possible cause of sudden death in the 1970s, and the first transvenous ICD was implanted in the 1990s. Since then, the medical device industry has provided dramatic reductions in ICD size and simultaneously increased safety, efficacy, battery longevity, diagnostics, and memory capabilities. Figure 18 shows the evolution in size of one manufacturer's ICD models.

5.2. Tachyarrhythmias

The commonly recognized mechanisms that lead to tachy-arrhythmias (tachycardias and fibrillation) include reentry circuits, triggered activity, and automaticity. Reentry is considered as the most common tachyarrhythmia mechanism. It can be described as an electrical loop within the myocardium that has a circular, continuous series of depolarizations and repolarizations (Fig. 19).

In general, there are three requirements for reentry to occur: (1) the presence of a substrate, for example, an area of scar tissue; (2) two parallel pathways that encircle the substrate; and (3) one pathway that conducts slowly and one that exhibits unidirectional block. An impulse reaching the substrate is slowed by the unidirectional block and is allowed to conduct slowly down the slow pathway. As the impulse continues to move around the substrate, it conducts in a retrograde manner up the fast pathway, and the impulse continues to conduct in a circular fashion.

Inappropriate atrial tachycardias and ventricular tachycardias can be either hemodynamically stable or unstable. The level of hemodynamic compromise that occurs is typically considered to depend on both the rate and the pathway of the arrhythmia. In general, atrial tachycardias usually result in fast irregular ventricular rates caused by conduction through the atrioventricular node. As atrial rates increase, the rate conducted to the ventricles may or may not be 1:1 because the atrioventricular node has inherent limitations in its ability to conduct depolarizations. If, however, an abnormal pathway exists from the atria to the ventricles, then 1:1 conduction may be possible. Nevertheless, a patient's clinical risks are related to the level of hemodynamic compromise, with the most extreme case being

Implantable Cardioverter Defibrillator
Fig. 18. The evolution of the implantable cardioverter-defibrillator (ICD). Dramatic reductions in size have occurred, with simultaneous improvements in longevity, diagnostics, functionality, and memory.
Unidirectional Block
Fig. 19. Reentrant circuits. (A) Unidirectional block; (B) slow conduction; (C) reentry circuit.

ventricular fibrillation, which if not immediately reversed, most often results in death.

Triggered activity, or hyperautomaticity, is typically not consistently spontaneous and is a less-common mechanism. Early and delayed afterdepolarizations seen in phases 3 and 4 of the action potential are associated with triggered activity. Automaticity is defined as the ability of the cell to depolarize spontaneously at regular intervals. In a diseased heart, cells exhibit abnormal automaticity that causes them to depolarize at a rate faster than the intrinsic rate (i.e., phase 4 of the action potential is accelerated).

Common symptoms seen in patients with tachyarrhythmias may include syncopal episodes, palpitations, fatigue, or dyspnea. Both invasive and noninvasive diagnostic tools are available for diagnosing tachyarrhythmias. The common noninvasive procedures include: (1) a thorough patient interview; (2) blood work; (3) a 12-lead electrocardiogram (ECG); (4) tilt table testing; (5) Holter monitoring; (6) exercise stress test; (7) echocardiography; (8) signal average ECG; and/or (9) single-photon emission computed tomography/multiple gated acquisition (SPECT/MuGA). An electrophysiological study using cardiac catheterization and insertable loop recorders is the most commonly used invasive diagnostic procedure.

Therapeutic interventions to manage tachyarrhythmias are aimed at altering the behavior of myocardial cells or the conduction of the electrical impulse in the diseased tissue. They

Table 7

Indications for Implantable Cardioverter-Defibrillator (ICD) Therapy

Class I

Class IIa

Cardiac arrest caused by ventricular fibrillation or ventricular tachycardia not because of a transient or reversible cause. Spontaneous sustained ventricular tachycardia in association with structural heart disease.

syncope of undetermined origin with clinically relevant, hemodynamically significant sustained ventricular tachycardia or ventricular fibrillation induced at electrophysiological study when drug therapy is ineffective, not tolerated, or not preferred. Nonsustained ventricular tachycardia in patients with coronary disease, prior myocardial infarction, left ventricular dysfunction, and inducible ventricular fibrillation or sustained ventricular tachycardia at electrophysiological study that is not suppressible by a class i antiarrhythmic drug.

spontaneous sustained ventricular tachycardia in patients without structural heart disease not amenable to other treatments. Patients with left ventricular ejection fraction of less than or equal to 30% at least 1 month postmyocardial infarction and 3 months postcoronary artery revascularization surgery. class iib 1. cardiac arrest presumed to be caused by ventricular fibrillation when electrophysiological testing is precluded by other medical conditions.

severe symptoms (e.g., syncope) attributable to sustained ventricular tachyarrhythmias while awaiting cardiac transplantation. Familial or inherited conditions with a high risk for life-threatening ventricular tachyarrhythmias, such as long QT syndrome or hypertrophic cardiomyopathy.

Nonsustained ventricular tachycardia with coronary artery disease, prior myocardial infarction, left ventricular dysfunction, and inducible sustained ventricular tachycardia or ventricular fibrillation at electrophysiological study. Recurrent syncope of undetermined etiology in the presence of ventricular tachyarrhythmias at electrophysiological study when other causes of syncope have been excluded.

Syncope of unexplained origin or family history of unexplained sudden cardiac arrest in association with typical or atypical right bundle branch block and sT segment elevation (Brugada syndrome).

syncope in patients with advanced structural heart disease in whom thorough invasive and noninvasive investigations have failed to define a cause.

class iii 1. syncope of undetermined cause in a patient without inducible ventricular tachyarrhythmias and without structural heart disease.

incessant ventricular tachycardia or ventricular fibrillation.

Ventricular fibrillation or ventricular tachycardia resulting from arrhythmias amenable to surgical or catheter ablation; for example, atrial arrhythmias associated with Wolfe-Parkinson-White syndrome, right ventricular outflow tract ventricular tachycardia, idiopathic left ventricular tachycardia, or fascicular ventricular tachycardia.

Ventricular tachyarrhythmias caused by a transient or reversible disorder (e.g., acute myocardial infarction, electrolyte imbalance, drugs, or trauma) when correction of the disorder is considered feasible and likely to reduce the risk or recurrent arrhythmia substantially.

significant psychiatric illnesses that may be aggravated by device implantation or may preclude systematic follow-up. Terminal illnesses with projected life expectancy of less than 6 months.

Patients with coronary artery disease with left ventricular dysfunction and prolonged QRS duration in the absence of spontaneous or inducible sustained or nonsustained ventricular tachycardia who are undergoing coronary bypass surgery. New York Heart Association class iV drug-refractory congestive heart failure in patients who are not candidates for cardiac transplantation.

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