TREATMENT Sinoatrial Node Dysfunction
Since SA node dysfunction is not associated with increased mortality rates, the aim of therapy is alleviation of symptoms. Exclusion of extrinsic causes of SA node dysfunction and correlation of the cardiac rhythm with symptoms is an essential part of patient management. Pacemaker implantation is the primary therapeutic intervention in patients with symptomatic SA node dysfunction. Pharmacologic considerations are important in the evaluation and management of patients with SA nodal disease. A number of drugs modulate SA node function and are extrinsic causes of dysfunction (Table 274-1). Beta blockers and calcium channel blockers increase SNRT in patients with SA node dysfunction, and antiarrhythmic drugs with class I and III action may promote SA node exit block. In general, such agents should be discontinued before decisions regarding the need for permanent pacing in patients with SA node disease are made. Chronic pharmacologic therapy for sinus bradyarrhythmias is limited. Some pharmacologic agents may improve SA node function; digitalis, for example, has been shown to shorten SNRT in patients with SA node dysfunction. Isoproterenol or atropine administered IV may increase the sinus rate acutely. Theophylline has been used both acutely and chronically to increase heart rate but has liabilities when used in patients with tachycardia-bradycardia syndrome, increasing the frequency of supraventricular tachyarrhythmias, and in patients with structural heart disease, increasing the risk of potentially serious ventricular arrhythmias. Currently, there is only a single randomized study of therapy for SA node dysfunction. In patients with resting heart rates <50 and >30 beats/min on a Holter monitor, patients who received dual-chamber pacemakers experienced significantly fewer syncopal episodes and had symptomatic improvement compared with patients randomized to theophylline or no treatment.
In certain circumstances, sinus bradycardia requires no specific treatment or only temporary rate support. Sinus bradycardia is common in patients with acute inferior or posterior MI and can be exacerbated by vagal activation induced by pain or the use of drugs such as morphine. Ischemia of the SA nodal artery probably occurs in acute coronary syndromes more typically with involvement with the right coronary artery, and even with infarction, the effect on SA node function most often is transient.
Sinus bradycardia is a prominent feature of carotid sinus hypersensitivity and neurally mediated hypotension associated with vasovagal syncope that responds to pacemaker therapy. Carotid hypersensitivity with recurrent syncope or presyncope associated with a predominant cardioinhibitory component responds to pacemaker implantation. Several randomized trials have investigated the efficacy of permanent pacing in patients with drug-refractory vasovagal syncope, with mixed results. Although initial trials suggested that patients undergoing pacemaker implantation have fewer recurrences and a longer time to recurrence of symptoms, at least one follow-up study did not confirm these results. PERMANENT PACEMAKERS Nomenclature and Complications
The main therapeutic intervention in SA node dysfunction is permanent pacing. Since the first implementation of permanent pacing in the 1950s, many advances in technology have resulted in miniaturization, increased longevity of pulse generators, improvement in leads, and increased functionality. To better understand pacemaker therapy for bradycardias, it is important to be familiar with the fundamentals of pacemaking. Pacemaker modes and function are named using a five-letter code. The first letter indicates the chamber(s) that is paced (O, none; A, atrium; V, ventricle; D, dual; S, single), the second is the chamber(s) in which sensing occurs (O, none; A, atrium; V, ventricle; D, dual; S, single), the third is the response to a sensed event (O, none; I, inhibition; T, triggered; D, inhibition + triggered), the fourth refers to the programmability or rate response (R, rate responsive), and the fifth refers to the existence of antitachycardia functions if present (O, none; P, antitachycardia pacing; S, shock; D, pace + shock). Almost all modern pacemakers are multiprogrammable and have the capability for rate responsiveness using one of several rate sensors: activity or motion, minute ventilation, or QT interval. The most commonly programmed modes of implanted single- and dual-chamber pacemakers are VVIR and DDDR, respectively, although multiple modes can be programmed in modern pacemakers.
Although pacemakers are highly reliable, they are subject to a number of complications related to implantation and electronic function. In adults, permanent pacemakers are most commonly implanted with access to the heart by way of the subclavian–superior vena cava venous system. Rare, but possible, acute complications of transvenous pacemaker implantation include infection, hematoma, pneumothorax, cardiac perforation, diaphragmatic/phrenic nerve stimulation, and lead dislodgment. Limitations of chronic pacemaker therapy include infection, erosion, lead failure, and abnormalities resulting from inappropriate programming or interaction with the patient’s native electrical cardiac function. Rotation of the pacemaker pulse generator in its subcutaneous pocket, either intentionally or inadvertently, often referred to as “twiddler’s syndrome,” can wrap the leads around the generator and produce dislodgment with failure to sense or pace the heart. The small size and light weight of contemporary pacemakers make this a rare complication.
Complications stemming from chronic cardiac pacing also result from disturbances in atrioventricular synchrony and/or left ventricular mechanical synchrony. Pacing modes that interrupt or fail to restore atrioventricular synchrony may lead to a constellation of signs and symptoms, collectively referred to as pacemaker syndrome, that include neck pulsation, fatigue, palpitations, cough, confusion, exertional dyspnea, dizziness, syncope, elevation in jugular venous pressure, canon A waves, and stigmata of congestive heart failure, including edema, rales, and a third heart sound. Right ventricular apical pacing can induce dyssynchronous activation of the left ventricle, leading to compromised left ventricular systolic function, mitral valve regurgitation, and the previously mentioned stigmata of congestive heart failure. Maintenance of AV synchrony can minimize the sequelae of pacemaker syndrome. Selection of pacing modes that minimize unnecessary ventricular pacing or implantation of a device capable of right and left ventricular pacing (biventricular pacing) can help minimize the deleterious consequences of pacing-induced mechanical dyssynchrony at the ventricular level. Pacemaker Therapy in SA Node Dysfunction
Pacing in SA nodal disease is indicated to alleviate symptoms of bradycardia. Consensus guidelines published by the American Heart Association (AHA)/American College of Cardiology/Heart Rhythm Society (ACC/HRS) outline the indications for the use of pacemakers and categorize them by class based on levels of evidence. Class I conditions are those for which there is evidence or consensus of opinion that therapy is useful and effective. In class II conditions, there is conflicting evidence or a divergence of opinion about the efficacy of a procedure or treatment; in class IIa conditions, the weight of evidence or opinion favors treatment; and in class IIb conditions, efficacy is less well established by the evidence or opinion of experts. In class III conditions, the evidence or weight of opinion indicates that the therapy is not efficacious or useful and may be harmful.
Class I indications for pacing in SA node dysfunction include documented symptomatic bradycardia, sinus node dysfunction–associated long-term drug therapy for which there is no alternative, and symptomatic chronotropic incompetence. Class IIa indications include those outlined previously in which sinus node dysfunction is suspected but not documented and for syncope of unexplained origin in the presence of major abnormalities of SA node dysfunction. Mildly symptomatic individuals with heart rates consistently <40 beats/min constitute a class IIb indication for pacing. Pacing is not indicated in patients with SA node dysfunction who do not have symptoms and in those in whom bradycardia is associated with the use of nonessential drugs (Table 274-2).
There is some controversy about the mode of pacing that should be employed in SA node disease. A number of randomized, single-blind trials of pacing mode have been performed. There are no trials that demonstrate an improvement in mortality rate with AV synchronous pacing compared with single-chamber pacing in SA node disease. In some of these studies, the incidence of atrial fibrillation and thromboembolic events was reduced with AV synchronous pacing. In trials of patients with dual-chamber pacemakers designed to compare single-chamber with dual-chamber pacing by crossover design, the need for AV synchronous pacing due to pacemaker syndrome was common. Pacing modes that preserve AV synchrony appear to be associated with a reduction in the incidence of atrial fibrillation and improved quality of life. Because of the low but finite incidence of AV conduction disease, patients with SA node dysfunction usually undergo dual-chamber pacemaker implantation. Pacemaker Therapy in Carotid Sinus Hypersensitivity and Vasovagal Syncope
Carotid sinus hypersensitivity, if accompanied by a significant cardioinhibitory component, responds well to pacing. In this circumstance, pacing is required only intermittently and single-chamber ventricular pacing is often sufficient. The mechanism of vasovagal syncope is incompletely understood but appears to involve activation of cardiac mechanoreceptors with consequent activation of neural centers that mediate vagal activation and withdrawal of sympathetic nervous system tone. Several randomized clinical trials have been performed in patients with drug-refractory vasovagal syncope, with some studies suggesting reduction in the frequency and the time to recurrent syncope in patients who were paced compared with those who were not. A recent follow-up study to one of those initial trials, however, found less convincing results, casting some doubt on the utility of pacing for vagally mediated syncope.