Health Articles

Acute Therapy
Acute therapy for bradyarrhythmias is required if the patient has hypotension, cerebral or cardiac ischemia, heart failure, and in Che case of acute myocardial infarction, frequent ventricular ectopic beats. Placing (he patient in the supine position with Ihc legs elevated often ameliorates hypotensive sequelae acutely. Atropine given rapidly IV in a 0.5-mg bolus may be repeated at 3- to 5-min intervals until a total dose of 0.04 mg/kg has been given. If atropine is ineffective or causes intolerable side effects, an isoproterenol drip con be started at I to 4 μ^min and then titrated to produce a ventricular rale of 60 beats/min. When neither drug is successful, or if isoproterenol is coittriiiiuliciited because of ischemia or infarction, temporary Iransvenous pacing should be used.
Cardiac Pacemakers
In one series. lh of pacemakers were implanted in patients > 70 yr old; about half of ihese were implanted for high-degree atrioventricular block and the other half for sick sinus syndrome. Recent studies show that sick sinus syndrome now accounts for 48% of all pacemaker implants. Permanent ventricular pacing has eliminaled (he accelerated mortality rate formerly associated with complete heart block. However. Ihe long-term prognosis for patients with sick sinus syndrome is determined primarily by the presence and severity of underlying hear! disease. Permanent pacing for sick sinus syndrome should therefore be based on ECG documentation of symptomatic bradyarrhythmia. Pacemakers are not warranted in asymptomatic elderly patients with chronic bifascicular block, with or without a prolonged PR interval, because complete hearl block rarely occurs.
Newer types of pacemakers, such as dual-chamber atrioventricular synchronous pacemakers, improve maximal exercise cardiac oulpul and work capacity compared with traditional fixed-rale ventricular pacemakers. Therefore, such pacing modes may be extremely beneficial to active elderly patients. Although not conclusively documented, the greater dependence on the atrial contribution to ventricular filling with age means thai atrioventricular synchronous pacing should have an enhanced benefit in the elderly.
In addition, a higher incidence of atrial fibrillation and a higher mortality rate have been demonstrated in patients treated with ventricular pacemakers compared with atrial or dual-chamber atrioventricular synchronous pacemakers. In a study involving 950 patients, the benefits ol’ dual-chamber pacing were particularly prominent in patients > 70 yr old wilh sick sinus syndrome. At 7 yr postimplantation, atrial fibrillation developed in 47% of patients with ventricular pacemakers compared with only 9% of those with dual-chamber units; corresponding mortality rates were 72% vs. 51%. Thus, otherwise healthy elderly patients in sinus rhythm who require pacing for sick sinus syndrome should probably be given units that preserve atrioventricular synchrony.
A permanent pacemaker has a low but significant rate of complications. Abrupt loss of pacing—due to battery failure, fibrosis around the catheter site, myocardial perforation, lead fracture, or electrode dis-lodgment—may result in marked bradycardia or asystole. Catheter perforation of the right ventricle may cause a pericardial friction rub or, rarely, tamponade. In patients with little overlying subcutaneous tissue, the pulse generator may extrude or the pacing wire may erode through the skin. Occasionally, a patient has difficulty adjusting psychologically to pacemaker implantation. All pacemaker patients should have regular follow-up physical and ECG examinations.

Specific bradyarrhythmias include sinus bradycardia, sinoatrial block, atrioventricular block, sick sinus syndrome, and left and right bundle branch block. The prevalence and effect on mortality for some of these bradyarrhythmias are shown in TABLE 40-2.
Sinus bradycardia, ti sinus rate of< 60 bcatsimin, may indicate excellent physical conditioning; however, in the elderly it often indicates intrinsic sinus node disease. Inferior myocardial infarction, hypothermia, myxedema, or increased intracranial pressure may cause this arrhythmia. A longitudinal study of apparently healthy persons between 40 and 80 yr of age wiih sinus rales < 50 beats/min found no increase in cardiovascular morbidity or mortality over a 5-yr mean follow-up period.
Sinoatrial block occurs when sinus node impulses fail to depolarize the atria. Such block is often 2:1. resulting in a venlricular rate that is exactly one half the sinus rale. Common causes in the elderly are intrinsic conduction syslem disease, ischemia, and digitalis loxicily.
First-degree atrioventricular block, prolongation of the PR interval > 0.22 see, may be seen in heallhy persons with high vagal tone. It also may be caused by intrinsic conduction syslem disease or by various medications (eg. digoxin. β-blockers. calcium antagonisls, and class IA antiarrhythmic drugs). No therapy is required.
Second-degree atrioventricular block has three different patterns. Mobitz type I (Wenckebach) block is recognized by prolongation of the PR interval that progresses until a ventricular complex is dropped. Because this type of block is usually proximal to the His-Purkinje system, the QRS complex (ypically appears normal. Digitalis toxicity and acute inferior myocardial infarction are common precipitating factors. This conduction disturbance is usually transient and rarely requires specific therapy. In Mobitz type II block, the PR interval is fixed but QRS complexes are dropped. Because the site of block is at or below the His bundle, the QRS complex is often wide. Mobitz lypc II block is most often associated with acute anterior myocardial infarction, myocarditis, or advanced sclerodegenerative conduction system disease. Patients with this arrhythmia are usually symptomatic and often present with syncope due to inadequate cerebral perfusion (Stokes-Adams attack). Because of its symptomatic presentation and frequent progression to complete heart block, Mobitz type II block is usually treated with a permanent pacemaker. Similarly, high-grade block is often symptomatic, may progress to complete heart block, and is usually treated with permanent pacing.
Third-degree (complete) atrioventricular block is characterized by the inability of any atrial depolarizations to activate the ventricle. Block wilhin the atrioventricular node is usually associated with normal QRS complexes and an escape rale close to 60 beats/tnin. Common causes are acule inferior myocardial infarction and digitalis toxicily. In most instances, block within the atrioventricular node is transient, However, block within the ventricles is accompanied by wide QRS complexes and a slow escape rate, often < 40 beats/tnin. Such block may occur in patients with severe sclerodcgcnerative conduction system disease or extensive acute anterior myocardial infarclion. Because these patients usually respond poorly to atropine and isoproterenol, pacemaker insertion is necessary.
Sick sinus syndrome encompasses a variety of rhythm disturbances that reflecl sinoatrial node dysfunction and are often associated with dysfunction elsewhere in the conduction syslem. Although sick sinus syndrome is associaled with many different cardiac diseases, coronary artery disease or a primary sclcrodegenerative process is most often responsible. Patients may present with bradyarrhylhmias (sinus bradycardia, sinus pauses or arrest, sinoatrial exit block, or atrial fibrillation with a slow ventricular response) or with the so-called bradycardia-tachycardia syndrome, in which a supraventricular tachycardia terminates in a long period of asystole. Therefore, symptoms may consist of palpitations or chest pain during tachycardia, and dizziness or syncope during bradycardia. The tachycardia—paroxysmal supraventricular tachycardia, atrial flutter, or atrial fibrillation—is treated with digoxin, other antiarrhythmic agents, or cardioversion (as outlined above); bradycardia associated with syncope should be treated by permanent pacing.
The prevalence of bundle branch block increases with age. Although left bundle branch block is usually associaled with ischemic or hypertensive cardiac disease, complete right bundle branch block is often seen in apparently healthy older men, who appear to have a satisfactory prognosis. An analysis of the predominantly male, multicenter Coronary Artery Surgery Study population confirmed an independent adverse effect of left, but not right, bundle branch block on mortality over the subsequent 5 yr. In women, however, right and left bundle branch block are highly—ami equally—indicative of underlying cardiac disease.

Some age-related histologic changes in the conduction system are apparent on the standard 12-!ead HCG. Although resting heart rate does not change with age, the respiratory variation in resting sinus rate (known as sinus arrhythmia) decreases. In addition, measurements of heart rate variability by lime or frequency domain analyses demonstrate reduced heart rale variability in (he elderly. The PR and QT intervals are somewhal prolonged with age. but QRS duration is unchanged. High-resolulion surface electrocardiography in healthy volunteers has localized the increase in PR inlerval to a delay that is proximal lo Ihe His bundle; conduction time from the His bundle to the ventricle appears to be unrelated lo age.
The QRS frontal plane axis shifts leftward over time, probably reflecting the combined effects of fibrosis in the anterior fascicle of the left bundle branch and mild age-related left venlricular hypertrophy. In a review of BCGs from elderly persons, such left axis deviation was the most common abnormality, occurring in 51%. In patients with no organic heart disease, neither first-degree atrioventricular block nor axis deviation leftward of - 30″ is associated with increased cardiac morbidity or mortality.

Widespread histologic changes lhat occur in the conduclion system with age may help account for the striking age-related increase in the incidence of bradyarrhythmias and conduction dislurbances. The number of pacemaker cells in the sinoatrial node progressively declines beginning by age 60 yr: only about 10% of the tells are still present at age 75 yr. The sinoatrial node becomes enveloped by fat, which may partially or completely separate the node from the atrial musculature.
Age-associaled changes in the His bundle include loss of cells, more fibrous and adipose tissue, and amyloid infiltration. The lefl side of the cardiac skeleton, which includes the central fibrous body, the mitral and aortic annuli. and the proximal interventricular seplum. undergoes some degree of fibrosis. The atrioventricular node. His bundle, and proximal left and right bundle branches may be involved because of their proximity to these structures. In extreme cases, the resultant “idiopathic” fibrosis may cause atrioventricular block; it is the most common cause of chronic alrioventricular block in the elderly.

Because intrinsic conduction system disease and acute processes such as myocardial infarction and digilalis toxicity are more prevalent, bradyarrhythmias are more common in the elderly. However, sinus bradycardia < 40 bcats/min. sinus pauses > 1.6 sec, and high-degree atrioventricular block arc rare in healthy persons > 60 yr old. These conduction disturbances arc often associated with ischemic, hypertensive, or amyloid hear! disease.

The half-life of digoxin is prolonged because elderly persons have a reduced glomerular filtration rate; this reduction and a generally smaller body size result in a higher serum digoxin level in older persons. Despite the widespread availability of serum drug-level testing, digitalis toxicity continues lo be relatively common in the elderly, primarily because digoxin is oflen used to treat heart failure and atrial arrhythmias. (For a more detailed discussion of digoxin and digitalis toxieity, see Antiarrhythmics inCh. 21.) Quinidine clearance is reduced by 34% and elimination half-life is prolonged from 7.3 h to 9.7 h in persons 60 to 69 yr of age compared with those 23 to 29 yr of age. Evidence thai quinidine therapy increases serum digoxin levels by about 100% may be particularly significant in the elderly, in whom these two drugs are often co-prescribed.
Because hepatic flow decreases with age, (he infusion rate of lido-caine should be reduced to avoid CNS toxicity, which is common in the elderly. Similar dosage adjustments are necessary with propranolol and other β-blockers (hat undergo first-pass hepatic metabolism. The clinical significance of age-related decreases in the binding of propranolol to β-udrenergic receptors is unknown.

Many new antiarrhythmic drugs and several pacemaker innovations have expanded the therapeutic options for arrhythmias. Although the roles of these newer agenls and devices for the older cardiac palienl have not been completely defined, their benefits and limitations have begun lo be determined. Cardiac pacemakers are discussed under BRADYAKKHYTHMIAS, below.

Venlricular tachycardia is usually a regular tachycardia with broad QRS complexes and a rate of 100 to 200 bcats/min. Although a distinction from paroxysmal supraventricular tachycardia is often difficult when the QRS complex is widened, a diagnosis of ventricular tachycardia is strongly suggested by atrioventricular dissocialion, fusion beats, and ORS duration > 0.14 sec or a QRS axis between 90° and - 180°. Severe myocardial ischemia, acute myocardial infarction, digitalis toxicity, or heart failure commonly precipitates ventricular tachycardia in the elderly.
Sustained ventricular tachycardia requires immediate attention. If ventricular tachycardia is well tolerated hemodynamically, a rapid IV infusion (bolus) of lidocaine 50 to 75 mg, followed by anolher 50 mg 2 min later, may be given initially. Recurrent ventricular tachycardia or lidocaine-resislant ventricular tachycardia may be treated with IV procainamide or β-blocking drugs. Current data, derived largely from studies of younger patients, suggest that hrctyliurn is the most effective drug for ventricular tachycardia lhat is refractory to lidocaine. In the elderly, as in younger palienls. venlricular tachycardia associated with hypotension or syncope requires immediate electrical cardioversion.
Ventricular tachycardia precipilated by an acute event, such as myocardial infarction or digitalis toxicity, has a low recurrence and does no! require chronic prophylaxis. However, venlricular tachycardia without an obvious precipilanl is known as primary ventricular tachycardia; il has a l-yr recurrence of about 35% and requires aggressive prophylaxis. In one study, the mean age of patients who had an out-of-hospital cardiac arrest caused by a primary arrhythmia was dS.5 yr, and these patients had a l-yr mortality rate of 29%.
The most promising approach to patients wilh primary recurrent symptomatic ventricular tachycardia appears to be intracardiac programmed electrophysiologic stimulation, a technique in which the malignant arrhythmia is induced and the efficacy of various antiarrhythmic agents in preventing it is assessed in a special catheterization laboratory. In a randomized trial of 57 patients (86% men. mean age 59 yr). antiarrhythmic Iherapy determined by this method resulted in a lower rate of symptomatic ventricular tachyarrhythmia than did an empiric approach. Olhcr studies show a marked reduction in the I- to 2-yr mortalily rale when drug therapy tor recurrent ventricular tachycardia is determined by this technique. A less-invasive but similarly labor-intensive approach using ambulatory KCG monitoring with or without exercise testing has also been successful, ;is demonstrated by the preliminary results of the multicenler ESVCM (Hlectrophysiology Study Versus Electrocardiographic Monitoring) trial.
The availability of amiodarone and several other new antiarrhythmic drugs increases the likelihood that a successful medical regimen car be found. Patients in whom neither of the above approaches is successful are possible candidates for an automatic implantable cardioverter-defibrillator or endocardial resection guided by intraoperative mapping. In a large series of patients with recurrent venlricular tachycardia or venlricular fibrillation, about lh were treated wilh these invasive approaches. Long-term survival was similar in elderly and younger patients, although surgical mortalily was higher in the elderly.

Although ventricular ectopic beats, whether isolaled or frequent and complex, do noi appear Co adversely affect the long-term risk of cardiovascular mortality in clinically healthy elderly persons, even simple ventricular ectopic beals increase the risk in patients wilh documented coronary artery disease. Nevertheless, it has yet to be shown that treating isolaled ventricular eclopic beats in these patients reduces the long-term risk of death. Furthermore, the Cardiac Arrhythmia Suppression Trial (CAST) recently demonstrated that the powerful class 1C antiarrhythmic drugs f lecainide and eneainide actually increased the mortality rale in patients wilh asymptomatic or mildly symptomatic frequenl ventricular ectopic beats after acute myocardial infarction. This finding challenges the belief that suppression of ventricular eclopic beats in such patients necessarily translates into improved survival. These drugs had a similar adverse effect on survival in patients younger than <>Oyr.
Hie generally higher risk of reactions to antiarrhythmic drugs in the elderly dictates a conservative approach, starting with low doses and titrating cautiously until density of ventricular ectopic beats is reduced by 75% and ventricular tachycardia is eliminated. The combination of low-dose quinidine and tocainide was generally effective and well tolerated in a pilot study of elderly patients with coronary artery disease and frequent ventricular eclopic beats. Low-dose combination therapy with various agents probably warrants investigation to minimize the risks of adverse effects from any single drug. As wilh supraventricular ectopic beats, trealmenl should be directed at resolving underlying or exacerbating factors, such as electrolyte disturbances, hypoxia, or hearl failure.

Paroxysmal supraventricular tachycardia is characterized by a regular narrow QRS complex at 150 to 200 beats/min. Usually due to a reentrant mechanism, it can often be terminated by vagal maneuvers (eg. Valsalva’s maneuver, gagging, or carotid sinus massage). NOTE: Carotid sinus massage should not he performed on elderly patients until significant carotid stenosis has been excluded by physical examination. It should also not be performed on any patient with a bruit. If vagal rqaneuvers are unsuccessful and hypotension is absent, verapamil 5 to 10 mg IV should be given over 2.5 to 5 min. With its rapid onset of action and low risk of hypotension. IV adenosine is an alternative to verapamil. If the arrhythmia precipitates hypotension, cerebral ischemic symptoms, angina pectoris, or heart failure, immediate cardioversion is indicated, starting at 25 to 50 joules. Digoxin is the preferred prophylaxis for paroxysmal supraventricular tachycardia because of its documented efficacy and once-daily dosing. ^-Adrenergic blockers or calcium antagonists are alternalives.
Atrial tachycardia with block is usually caused by digitalis toxicity. Treatment consists of withholding digitalis and correcting hypokalemia.
Multifocal atrial tachycardia is common in elderly patients with chronic obstructive pulmonary disease. Here, the P-wave morphology. PR interval, and cycle length vary from beat to beat. Although treatment is directed at correcting Ihc underlying condition, verapamil is usually effective as short-term therapy.
Although nol usually a cause of hemodynamic impairment, accelerated junctional rhythm may be a sign of a serious underlying disorder. It is characterized by a heart rate of 70 to 130 beats/min; the P wave is usually inverted and may precede, follow, or fall wilhin the QRS complex. In the elderly, digitalis toxicity and acute inferior myocardial in-I’iirclion are the most common causes. Sudden regularization of the ventricular rate in an elderly patient receiving digoxin for chronic atrial fibrillation suggests (his diagnosis. Treatment is directed at the underlying disorder, such as digilalis toxicity, myocardial infarction, or heart failure.
Atrial flutter should be suspected if a patient has a regular tachycardia at a ventricular rate close to l50bcals/min. Carotid massage (see warning, above) should cause an abrupt slowing of the ventricular response and the emergence of “sawlooth” flutter waves at about 300/min, which confirms the diagnosis. Coronary artery disease and chronic obstructive pulmonary disease are common causes of atrial flutter in the elderly. Digoxin is (he drug of choice if the palient is hemodynamically stable. Otherwise, low-level DC cardioversion (25 to 50 joules) almost always converts flutter to sinus rhythm.
Atrial fibrillation is recognized by a lack of organized atrial activity and the totally irregular timing of (he QRS complexes. In contrast lo the other atrial tachyarrhythmias, atrial fibrillation is much more likely lo be chronic than acute. Hypertension, coronary arlcry disease, and mitral valve disease are the most common predisposing conditions in elderly and middle-aged palienls. Additional considerations include amyloidosis, sick sinus syndrome, and thyrotoxicosis.
In contrast to isolated supraventricular or venlricular ectopic beals, atrial flutter or fibrillation usually signifies organic heart disease. Hs-(ablished atrial fibrillation in otherwise healthy persons (lone atrial fibrillation) appears (o substantially increase the risk of cardiovascular morbidity and mortality. In studies, such mortality was increased two-to thirteenfold and stroke more than fivefold in men aged 40 to 65 yr. Thus, even if no organic heart disease is apparent, atrial fibrillation should never be considered benign.
As in younger patients, initial treatment of atrial fibrillation is directed toward slowing the ventricular response to 60 to 100 beats/min with digoxin. verapamil, or propranolol given IV. Long-term control of ventricular rale is also achieved with these agents, which are sometimes given in combination. Digoxin and verapamil are conlraindicated in the Wolff-Parkinson-White syndrome, which is rare in the elderly. Because of the associated atrioventricular nodal disease, about lh of older patients with atrial fibrillation have a controlled ventricular response and require no specific therapy. Before electrical cardioversion is attempted for chronic atrial fibrillation, the cause and duration of atrial fibrillation, atrial size, and the risks of alternative therapy with anticoagulants should be considered. Because chronic (and even lone) atrial fibrillation has a substantially increased risk of cerebral embolism, anticoagulation should be strongly considered in any elderly patient with this arrhythmia (see also MITRAL STENOSIS in Ch. 38). However, given the increased risk of thromboembolic events in patients with chronic atrial fibrillation, an early attempt at cardioversion (generally within a few weeks of diagnosis) is probably warranted in most elderly patients. Chemical cardioversion with quinidine or other class ! drugs may be considered in older patients with atrial fibrillation, although a recent meta-analysis suggests that patients receiving long-term quinidine therapy have an increased mortality rate. The mul-ticenler AFASAK (Atrial Fibrillation. Aspirin, and Anticoagulation [Kopenhcigen]) and SPAF (Stroke Prevention in Atrial Fibrillation) studies showed that warfarin reduced the incidence of thromboembolic events in elderly patients with nonrheumatic atrial fibrillation. In the SPAF study, low-dose aspirin also reduced such events, though only in patients ^ 75 yrofd.