Sinus node dysfunction

Many individuals, particularly those who partake in regular vigorous exercise, have heart rates less than 60 bpm. For those individuals, sinus bradycardia is normal and healthy, and does not require evaluation or treatment. However, some individuals develop symptomatic sinus node dysfunction. In the absence of correctable underlying causes, idiopathic sinus node dysfunction is referred to as sick sinus syndrome,12 and occurs with greater frequency with advancing age. The prevalence of sick sinus syndrome is approximately 1 in 600 individuals over the age of 65 years.12... 

Sick sinus syndrome Idiopathic sinus node dysfunction leading to symptomatic sinus bradycardia. 

Asymptomatic sinus bradyarrhythmias (heart rate less than 60 beats/min) are common especially in young, athletically active individuals. However, some patients have sinus node dysfunction (sick sinus syndrome) because of underlying organic heart disease and the normal aging process, which... 

Treatment of sinus node dysfunction involves elimination of symptomatic bradycardia and possibly managing alternating tachycardias such as AF. Asymptomatic sinus bradyarrhythmias usually do not require therapeutic intervention. 

Cardiovascular effects If a ventricular pacemaker is operative, patients with seconder third-degree heart block may be treated with mexiletine if continuously monitored. Exercise caution in such patients or in patients with preexisting sinus node dysfunction or intraventricular conduction abnormalities. 

Oral Severe sinus-node dysfunction, causing marked sinus bradycardia second-and third-degree AV block when episodes of bradycardia have caused syncope (except when used in conjunction with a pacemaker). 

Chronic heart failure is associated with intrinsic sinus node dysfunction that can be demonstrated on careful electrophysiologic studies [22, 23]. Patients with chronic heart failure have longer intrinsic sinus cycle... 

Ideally, if symptomatic sinus node dysfunction occurs in the presence of drugs known to impair sinus node function, the first treatment is to discontinue the offending drug [29]. However, this is typically not feasible in patients with heart failure who are dependent on several medications to improve long-term outcomes, or may need antiarrhythmic drug therapy for symptomatic arrhythmias. Accordingly, the treatment usually becomes a question of whether to apply pacing to increase heart rate. This is further complicated by the appropriate pacemaker prescription once the decision to pace has been made. 

Benditt DG, Sakaguchi S, Goldstein MA, et al. Sinus node dysfunction, pathophysiology, clinical features, evaluation, and treatment. In Zipes DP, Jalife J, eds. Cardiac electrophysiology from cell to bedside. 2nd ed. Philadelphia WB Saunders, 1995 1215-47. 

Sinus rhythm with a rate of less than 60/min is defined as sinus bradycardia. This bradycardia is usually a physiological response. Pathological and/or symptomatic sinus bradycardia may suggest sinus node dysfunction (see sick sinus syndrome). Vagally induced sinus bradycardia may be responsive to atropine, but only needs to be treated if symptomatic. Atropine doses of less than 0.5 mg may cause a paradoxical increase in vagal bradycardia. 

Mexiletine is contraindicated in the presence of cardiogenic shock or preexisting second- or third-degree heart block in the absence of a cardiac pacemaker. Caution must be exercised in administration of the drug to patients with sinus node dysfunction or disturbances of intraventricular conduction. 

Propafenone is contraindicated in the presence of severe or uncontrolled congestive heart failure cardiogenic shock sinoatrial, A-V, and intraventricular disorders of conduction and sinus node dysfunction, such as sick sinus syndrome. Other contraindications include severe bradycardia, hypotension, obstructive pulmonary disease, and hepatic and renal failure. Because of its weak (3-blocking action, propafenone may cause possible dose-related bronchospasm. This problem is greatest in patients who are slow metaboUzers. 

Patients with underlying sinus node dysfunction tend to have signihcant worsening of nodal function, frequently requiring pacemaker implantation. Corneal microdeposits develop in most adults receiving amiodarone. As many as 10% of patients complain of halos or blurred vision. The corneal microdeposits are reversible with stoppage of the drug. 

Contraindications Bradycardia-induced syncope (except in the presence of a pacemaker), second-and third-degree AVblock, severe hepatic disease, severe sinus-node dysfunction... 

Use with caution in older patients with Hepatic impairment Patients taking diuretics, NSAIDs or with nephropathy Sinus node dysfunction or Heart block, Osteoporosis, Unsteady gait, Urinary incontinence... 

Lithium should not be administered to patients with fluctuating or unstable renal function. Because hthium may affect functioning of the cardiac sinus node, patients with sinus node dysfunction (e.g., sick sinus syndrome) should not receive hthium. Although hthium also has acute and chronic effects on the thyroid, patients with hypothyroidism may receive hthium if the thyroid disease is adequately treated and monitored. Laboratory tests that should be performed before initiation of hthium are listed in Table 5-1. 

Lithium Neurological tremor, ataxia, seizures Endocrine hypothyroidism Cardiovascular T wave changes, sinus node dysfunction Renal polyuria, nephrogenic diabetic insipidus Dermatological hair loss, acne, psoriasis, rash Gastrointestinal nausea, diarrhea Miscellaneous fluid retention, weight gain, weakness... 

Perrild H, Hegedus L, Baastrup PC, et al. Thyroid function and ultrasonically determined thyroid size in patients receiving long-term lithium treatment. Am J Psychiatry 1990 147 1518-1521. Rosenquist M, Bergfeldt H, Aili H, et al. Sinus node dysfunction during long-term lithium treatment. Br Heart J 1993 70 371-375. 

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... 

There have been several reports of bradycardia and sinus node dysfunction. 

A 52-year-old man took an overdose of lithium (serum concentration 4.58 mmol/1) and developed asymptomatic sinus bradycardia with sinus node dysfunction and multiple atrial extra beats, which resolved after hemodialysis (132). 

A 44-year-old woman developed atropine-resistant but isoprenaline-sensitive bradycardia (36 beats/minute), thought to be due to sinus node dysfunction related to lithium, fentanyl, and propofol (120). 

A 52-year-old man with a serum lithium concentration of 4.58 mmol/1 had sinus node dysfunction with multiple atrial extra beats and an intraventricular conduction delay, which normalized following hemodialysis (132). Two patients, a 58-year-old woman and a 74-year-old woman, developed sick sinus syndrome while taking lithium but were able to continue taking it after pacemaker implantation (135,136). 

The authors discussed the difficulty of the differential diagnosis between lithium intoxication and other neurological disorders, such as strokes. What they did not discuss was the possibility that the presentation was caused by sinus node dysfunction, which has been reported as a complication of lithium treatment. 

A case report suggested an association between lithium and carbamazepine in causing sinus node dysfunction (124). 

Terao T, Abe H, Abe K. Irreversible sinus node dysfunction induced by resumption of lithium therapy. Acta Psychiatr Scand 1996 93(5) 407-8. 

Lai CL, Chen WJ, Huang CH, Lin FY, Lee YT. Sinus node dysfunction in a patient with lithium intoxication. J Formos Med Assoc 2000 99(l) 66-8. 

Numata T, Abe H, Terao T, Nakashima Y. Possible involvement of hypothyroidism as a cause of lithium-induced sinus node dysfunction. Pacing Clin Electrophysiol 1999 22(6 Part l) 954-7. 

Moltedo JM, Porter GA, State MW, Snyder CS. Sinus node dysfunction associated with lithium therapy in a child. Tex Heart Inst J 2002 29(3) 200-2. 

The causes of syncope in patients with Alzheimer s disease treated with donepezil have been reported in 16 consecutive patients (12 women, 4 men) with Alzheimer s disease, mean age 80 years, who underwent staged evaluation, ranging from physical examination to electrophy-siological testing (54). The mean dose of donepezil was 7.8 mg/day and the mean duration of donepezil treatment at the time of syncope was 12 months. Among the causes of syncope, carotid sinus syndrome (n = 3), complete atrioventricular block (n = 2), sinus node dysfunction (n = 2), and paroxysmal atrial fibrillation (n = 1) were diagnosed. No cause of syncope was found in six patients. Non-invasive evaluation is recommended before withdrawing cholinesterase inhibitors in patients with Alzheimer s disease and unexplained syncope. 

Ajmaline occasionally causes cardiac dysrh5dhmias (SEDA-17, 219). Of 1995 patients who were given ajmaline 1 mg/kg intravenously during an electrophysiological study, 63 developed a supraventricular tachydysrhythmia (atrial flutter, fibrillation, or tachycardia), and seven an atrioventricular re-entrant tachycardia (2). Those most at risk were older patients, those with underlying cardiac disease, and those with a history of dysrhythmias or sinus node dysfunction. 

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). 

A 42-year-old woman developed sinus node dysfunction during lithium toxicity (serum concentration 3.4 mmol/1) (99). The authors suggested that concomitant carbamazepine therapy (serum concentration 22 pmol/l) had exacerbated the effect of lithium on the sinus node. 

Takayanagi K, Hisauchi I, Watanabe J, Maekawa Y, Fujito T, Sakai Y, Hoshi K, Kase M, Nishimura N, Inoue T, Hayashi T, Morooka S. Carbamazepine-induced sinus node dysfunction and atrioventricular block in elderly women. Jpn Heart J 1998 39(4) 469-79. 

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