Sick Sinus Syndrome

At a glance

Abnormality of sinoatrial node (SAN) function or atrial conduction and associated with clinical symptoms or prolonged period of asystole predominantly in the elderly.

Incidence

Approximately 1:1,000 in patients older than 45 years of age. Increased in Caucasian and patients with cardiovascular risk factors (hypertension, obesity, and diabetes).

Genetic inheritance

The syndrome may be acquired or congenital. Between 2 and 6% of cases are familial and inherited as an autosomal dominant trait.

Pathophysiology

Sinoatrial node depolarization is irregular or fails, resulting in bradycardia or sinus arrest. In the presence of sinus arrest or extreme sinus bradycardia, a junctional escape rhythm may develop. Irregular depolarization of the sinus node, however, causes paroxysms of tachycardia (supraventricular tachycardia/atrial fibrillation) between episodes of bradycardia. Acquired causes include surgical trauma, fibrous, inflammatory, or degenerative infiltration of the sinus node and ischemia.

Diagnosis

Clinical history, ECG with or without Holter monitoring.

Clinical aspects

May remain asymptomatic. Symptoms include dizziness, syncope, palpitations, and chest pain. A 12-lead ECG should be examined for sinus bradycardia, sinus arrest, and junctional escape rhythm; however, a single recording may appear normal. Continuous monitoring may be necessary to demonstrate alternating episodes of bradycardia and tachycardia. Episodes of tachycardia may be controlled with digoxin or beta blockade. If beta blockade is used, cardiac pacing (dual-mode, dual-pacing, dual-sensing) usually becomes necessary to prevent profound bradycardia. Acquired Sick Sinus Syndrome may be caused by lithium and carbamazepine therapy.

Precautions before anesthesia

Obtain a complete medical history of frequency of syncope/palpitations, drug history, and pacemaker details. Attempt to define etiology of the Sick Sinus Syndrome in the individual patient may be impossible. If the syndrome is newly diagnosed, consider temporary pacing. Cardiovascular assessment: review recent ECG(s). Further investigations must be carried on medical grounds. Metabolic considerations: check serum electrolytes.

Anesthetic considerations

Decreased systemic vascular resistance caused by volatile agents or major regional blockade may result in profound hypotension because a reflex tachycardia is not generated. Stroke volume is the primary determinant of cardiac output, therefore myocardial contractility and optimal filling pressures should be maintained. Complete atrioventricular block during anesthesia is also reported.

Pharmacological implications

Atropine will not treat the bradycardia. Chronotropic agents have minimal effect on heart rate.

References