Anesthesia for Correction of Cardiac Arrhythmias

Historical Perspectives

The treatment of cardiac arrhythmias with device-based therapy may have begun in 1899, when Prevost and Batteli noted almost as an afterthought that direct electric shock could terminate ventricular fibrillation in dogs. Hooker and colleagues showed three decades later that the passage of electric current across the heart can initiate and terminate ventricular fibrillation. In 1947, Beck saved the first human life by the successful use of cardiac defibrillation in a 14-year-old boy who developed ventricular fibrillation during a thoracic procedure and went on to achieve full recovery. These early achievements provided the foundation for the landmark work of Mirowski and Mower which ultimately led to the development of ICDs in humans in 1980. During the past three decades, an increase has occurred in the numbers of patients with pacemakers and ICDs for the correction of cardiac arrhythmias.

Scope of Cardiac Arrhythmias

Cardiac arrhythmias are common. Some cardiac arrhythmias are life-threatening, and others are merely a nuisance. Cardiac arrhythmias are caused by abnormalities in impulse formation or conduction that lead to slow or fast, regular or irregular heart rhythms. At the present time, it is not difficult to treat slow rhythms because available pacemakers are able to adapt slow function to the needs of the body. The situation is different, however, for patients with rapid rhythms. Rapid rhythms may originate anywhere in the heart and result from various mechanisms. These mechanisms may be focal, meaning that the abnormal impulse formation is confined to a small area, or they may be the result of an impulse running in a circuit composed of several interconnected cardiac cells. Such a circuit may be small or large, as in atrial flutter and in arrhythmias in which the normal atrioventricular conduction system and an extra connection between the atrium and the ventricle are incorporated into the circuit of the arrhythmia.

Pharmacologic interventions originally were used to terminate and prevent rapid rhythms. However, antiarrhythmic drugs may have serious side effects and sometimes may even be responsible for the occurrence of life-threatening arrhythmias and sudden death. As a result of these effects, techniques were developed for localizing the site of origin or pathway of an arrhythmia and then isolating or destroying the tissue that is responsible. By employing an intracardiac catheter, the site of origin or pathway of an arrhythmia can be identified and the rhythm disturbance corrected by applying radiofrequency, laser, ultrasound, microwave energy, or freezing temperatures to the tissue causing the arrhythmia.

Heart failure is a major problem in older patients. Although pharmacologic treatment of heart failure has improved, outcome generally remains poor. New pacing technologies may be used to treat selected patients with heart failure. For many years, permanent pacing has been used to treat symptomatic bradycardia, and pacing may alleviate heart failure when associated with heart block. Several studies have examined the use of conventional dual-chamber atrioventricular–right ventricular pacing for treatment of heart failure in the absence of symptomatic bradycardia or heart block. Biventricular pacing aims to restore synchronous cardiac contraction. When ventricular dyssynchrony is reduced, the heart is able to contract more efficiently and increase left ventricular ejection fraction and cardiac output, while working less and consuming less oxygen. In addition, reestablishment of left ventricular synchrony can increase left ventricular filling times, decrease pulmonary capillary wedge pressure, and reduce mitral regurgitation.

Normal Cardiac Rhythm

In the normal heart, the dominant impulse arises in the sinus node with a rate of 60 to 100 beats/min ( Fig. 55.1 ). During sleep, the rate may decrease to 30 to 50 beats/min. Episodes of sinus pauses up to 3 seconds, sinoatrial block, junctional rhythms, and first-degree and second-degree atrioventricular nodal block that occur quite often (especially in trained athletes) are considered to be normal variants.

The impulses generated from the sinoatrial node propagate along three intraatrial conduction pathways: the anterior, middle, and posterior internodal tracts. These tracts are not discrete pathways, but groups of cells that conduct slightly faster than the atrial myocardium. The internodal tracts give rise to interatrial fibers. The electric impulse, whether propagated in the atrial myocardium or along the internodal tracts, converges on the atrioventricular junction. The atrioventricular node located in the atrioventricular junction ultimately receives the impulses generated from the sinoatrial node. The impulses are delayed in the atrioventricular node before they are finally distributed to the ventricular myocardium via the His-Purkinje system.

Normally, the heart rate increases with exercise to at least 85% of the age-predicted maximum of 220 minus age in years; failure to do so is termed chronotropic incompetence. Sinus arrhythmia is defined as sinus rhythm with P-to-P variations of more than 10% ( Fig. 55.2 ). Sinus arrhythmia is due to cyclic variations in vagal tone commonly related to respiration (the rate is faster with inspiration and slower with expiration). Sinus arrhythmia disappears with exercise, breath-holding, and atropine, and is more likely to be seen in individuals who do not have heart disease.

Cardiac Arrhythmias

Cardiac arrhythmia is caused by a disorder of impulse generation, impulse conduction, or a combination of both. Cardiac arrhythmia may be life-threatening because of a reduction in cardiac output, reduction in myocardial blood flow, or precipitation of a more serious arrhythmia. Arrhythmias may be described based on (1) rate (bradycardia or tachycardia), (2) rhythm (regular or irregular), (3) origin of impulse (supraventricular, ventricular, or artificial pacemaker), (4) impulse conduction (atrioventricular, ventriculoatrial, or block), (5) ventricular rate, or (6) special phenomena (e.g., preexcitation).

Reentry is a common electrophysiologic mechanism that predisposes to most ventricular arrhythmias and to most supraventricular tachyarrhythmias. The most common mechanism of reentry is based on the model originally proposed by Erlanger and Schmitt and later modified by Wit. This model postulates the presence of a ring or loop of cardiac tissue that is functionally separate from neighboring tissue and the presence of transient or permanent unidirectional block in a portion of the loop. Unidirectional block may be anatomic in origin (e.g., bundle branches, fibrosis, dual pathways, atrioventricular node plus accessory pathway) or functional (e.g., ischemia, drug effect).

Atrial flutter is a macro-reentrant arrhythmia identified by flutter waves, often best seen in the inferior leads at 250 to 350 beats/min ( Fig. 55.3 ). Patients often present with a 2:1 atrioventricular conduction with a ventricular rate of 150 beats/min, although the atrioventricular conduction ratio can change abruptly. Atrial fibrillation is a narrow-complex tachyarrhythmia and is the most common in the general population ( Fig. 55.4 ). It is associated with significant morbidity. The prevalence of atrial fibrillation in the general population increases exponentially with age, from 0.9% in individuals 40 years of age to 5.9% in individuals older than age 65 years. The most important risk factors for development of atrial fibrillation in the general population are structural heart disease, valvular heart disease, and left ventricular hypertrophy. Atrial fibrillation is a significant contributor to the development of angina and stroke, with an estimated stroke risk in untreated individuals of 3% to 5%.

Ventricular tachyarrhythmia is defined as three or more consecutive ectopic beats at a rate more rapid than 100 beats/min ( Fig. 55.5 ). Ventricular tachyarrhythmia is traditionally classified as nonsustained or sustained. Sustained ventricular tachyarrhythmia is defined as ventricular tachyarrhythmia lasting more than 30 seconds. Nonsustained ventricular tachyarrhythmia is defined as ventricular tachyarrhythmia that terminates spontaneously within 30 seconds. Sustained ventricular tachyarrhythmia also is traditionally classified as monomorphic (one site of origin) or polymorphic (two or more sites of origin). Monomorphic ventricular tachyarrhythmia usually results from reentry, and the site of reentry depends in part on the type of heart disease. In patients with coronary artery disease, the reentry circuit is usually located in ventricular myocardium, whereas in dilated cardiomyopathy with left bundle branch block, bundle branch reentry is common. Monomorphic ventricular tachyarrhythmia may occur in individuals with an otherwise normal heart, whereas polymorphic ventricular tachyarrhythmia may occur in acquired states that produce a marked prolongation of the Q-T interval. Nonsustained ventricular tachyarrhythmia is frequently asymptomatic, but may produce palpitations, weakness, and presyncope.

Torsade de pointes is a French term translated as “twisting of the points.” It is a syndrome composed of polymorphic ventricular tachyarrhythmia ( Fig. 55.6 ). It may be due to various medications or electrolyte imbalances. Torsade de pointes is usually paroxysmal, but is frequently symptomatic and often produces loss of consciousness. It occasionally degenerates to ventricular fibrillation. Ventricular fibrillation accounts for 80% to 85% of sudden cardiac deaths.

Ventricular fibrillation is usually preceded by ventricular tachyarrhythmia, but also may occur as a primary arrhythmia ( Fig. 55.7 ). More recent studies suggest that ventricular fibrillation results from multiple wavelengths that disperse randomly, using the leading circle form of reentry. The most common cause of ventricular fibrillation is acute myocardial infarction. It also is observed in patients with chronic ischemic heart disease, hypoxia resulting from any cause, acidosis, hypokalemia, and massive hemorrhage.

Permanent Pacing

Indications for pacemaker therapy have increased in recent years and now include the treatment of bradyarrhythmias and heart failure according to the American College of Cardiology and American Heart Association guidelines. These guidelines discuss indications for pacing in patients with sinus node dysfunction, acquired atrioventricular block, chronic bifascicular and trifascicular block, hypersensitive carotid sinus, and neurally mediated syndromes. The guidelines direct the treating physician in selecting patients who would benefit from device therapy.

A Swedish team led by Sennings and Elmqvist implanted the first pacemaker in 1958. A thoracotomy was required, and pacing was done through electrodes sutured to the epicardium. In these early systems, significant problems with changes in pacing threshold, lead infection, and lead breakage were common. Transvenous lead implantation subsequently developed by Furman and colleagues would resolve many of these issues. In 1958, Furman successfully paced an elderly patient with a catheter electrode inserted transvenously. Other investigators took on the challenge of solving various technical problems, such as device miniaturization; longer-life batteries; and stable, reliable lead material. As the indication for implantation expanded from atrioventricular conduction disturbances to management of sinus node dysfunction, the need for implantable pacemakers grew in proportion. Technology evolved rapidly with the development of lithium-iodide batteries that had greater longevity. Electronic advances then led to major miniaturization using integrated circuits as opposed to discrete components. Lead materials used in today’s pacemaker rely on silicone and polyurethane, which are more biocompatible and reliable than earlier materials. With these technical refinements, present-day pacemakers are small and can pace reliably for 8 to 10 years before generator replacement is needed. The primary functional challenge for contemporary pacemakers is to maintain the heart rate based on circulatory needs, pacing in a manner that mimics the natural physiology of excitation and conduction. In a healthy heart, the sinus node is modulated by the autonomic nervous system, and its rate is determined by a multiplicity of factors, such as physical activity, emotion, and blood pressure. Not only the rate, but also the activation sequence and atrioventricular conduction time vary with demand; these requirements also must be considered. Rate is controlled by pacemaker discharge, and the excitation and conduction sequence depends on the placement of pacing electrodes. Approximately 120,000 pacemakers are implanted each year in the United States. Indication for implantation for most of these cases is sick sinus syndrome. Other indications include atrioventricular block, carotid sinus hypersensitivity, malignant vasodepressor syndrome, and hypertrophic cardiomyopathy. The primary purpose of implantable pacemakers is to treat symptomatic bradycardia. With the extraordinary developments that have occurred in pacemaker therapy for the traditional indication—bradycardia—new uses are now beginning to be explored. Pacemakers have progressed from large, fixed-rate, single-chamber devices to multiprogrammable, multichamber devices with the ability to respond to changing hemodynamic demands. As technology advances, other possible uses are likely to be conceived.