Sinus node arrest

Encainide has been reported to cause sinus node arrest in association with prolonged sinus node recovery time (19). It also raises the pacing threshold in patients with chronic implanted pacemakers (20), although this has not been reported to increase the failure rate of pacemakers. 

III. Clinical presentation. Mild to moderate intoxication results in lethargy, muscular weakness, slurred speech, ataxia, tremor, and myoclonic jerks. Rigidity and ex-trapyramidal effects may be seen. Severe intoxication may result in agitated delirium, coma, convulsions, and hyperthermia. Recovery is often very slow, and patients may remain confused or obtunded for several days to weeks. Rarely, cerebellar and cognitive dysfunction are persistent. Cases of rapidly progressive dementia, similar to Jacob-Creutzfeldt disease, have occurred and are usually reversible. The ECG commonly shows T-wave inversions less commonly, bradycardia and sinus node arrest may occur. The white cell count is often elevated (15-20,000/mm ). 

A. Cardiotoxic effects of the type la agents include sinus bradycardia sinus node arrest or asystole PR, QRS, or QT interval prolongation sinus tachycardia (caused by anticholinergic effects) polymorphous ventricular tachycardia (torsade de pointes) and depressed myocardial contractility, which, along with alpha-adrenergic or ganglionic blockade, may result in hypotension and occasionally pulmonary edema. 

Fig. 9.1 After a premature atrial contraction (PAC), there is sinus node arrest for at least 5 s. After a long asystoUe period, the first escape heat is a junetional beat with retrograde atrial activation.

Verapamil s cardiotoxic effects are dose-related and usually avoidable. A common error has been to administer intravenous verapamil to a patient with ventricular tachycardia misdiagnosed as supraventricular tachycardia. In this setting, hypotension and ventricular fibrillation can occur. Verapamil s negative inotropic effects may limit its clinical usefulness in diseased hearts (see Chapter 12 Vasodilators the Treatment of Angina Pectoris). Verapamil can lead to atrioventricular block when used in large doses or in patients with atrio-ventricular nodal disease. This block can be treated with atropine and -receptor stimulants. In patients with sinus node disease, verapamil can precipitate sinus arrest. 

A very uncommon adverse effect involves sinus node dysfunction (extreme bradycardia, sinus arrest, sinoatrial block), which can be associated with syncopal episodes, perhaps due to hypothyroidism (119,120). In such cases, lithium must either be withdrawn or continued in the presence of a pacemaker. At therapeutic concentrations, other cardiac conduction disturbances have been reported, sometimes in conjunction with hypercalcemia (121), but are uncommon. 

Two reviews of the cardiac effects of psychotropic drugs briefly mentioned lithium and dysrhythmias, with a focus on sinus node dysfunction (122,123), reports of which, as manifested by bradycardia, sinoatrial block, and sinus arrest, continue to accumulate in association with both toxic (124) and therapeutic (125,126) serum lithium concentrations. The rhythm disturbance normalized in some cases when lithium was stopped (124,126), persisted despite discontinuation... 

Patients with impaired function of the sinus node or impaired atrioventricular conduction can develop sinus bradycardia, sinus arrest, heart block, hypotension and shock, and even asystole, with verapamil (139) or diltiazem. These drugs should not be given to patients with aberrant conduction pathways associated with broad-complex tachydysrhythmias, and they can cause severe conduction disturbances in hypertrophic cardiomyopathy. 

Four additional cases of carbamazepine-induced sinus node dysfunction (n = 3) and atrioventricular block (n = 1) were described in elderly Japanese women taking 200-600 mg/day. In two of the three patients rechallenged, sinus arrest recurred within 48 hours (8). 

The safety of oral propafenone in the treatment of dysrhythmias has been studied retrospectively in infants and children (40). There were significant electrophysiolo-gical adverse effects and prodysrhythmia in 15 of 772 patients (1.9%). These included sinus node dysfunction in four, complete atrioventricular block in two, aggravation of supraventricular tachycardia in two, acceleration of ventricular rate during atrial flutter in one, ventricular prodysrhythmia in five, and unexplained sjmcope in one. Cardiac arrest or sudden death occurred in five patients (0.6%) two had a supraventricular tachycardia due to Wolff-Parkinson-White syndrome the other three had structural heart disease. Adverse cardiac events were more common in the presence of structural heart disease and there was no difference between patients with supraventricular and ventricular dysrhythmias. 

The progressive depression of sinus node automatism and the occurrence of a progressively slower escape rhythm that leads to cardiac arrest (Figure 8.34) are usually detected in patients with... 

Another reason for paroxysmal bradycardia and sinus arrest that is not due directly to sinus node dysfunction is carotid sinus hypersen-... 

The authors of the report describing the sinoatrial arrest suggest a synergistic depression by both drugs of the sinus node. 

The sick sinus syndrome is a term that is cormnonly used to describe a wide variety of disturbances of sinus node function (28,29). More recently, the term sick sinus syndrome has been replaced by the phrase sinus node dysfunction, which will be used in this chapter. The spectrum of sinus node dysfunction includes sinus bradycardia, sinus pauses or sinus arrest, and sinoatrial exit block, which are frequently associated with atrial disease and disturbances... 

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