Hypersensitivity to carotid sinus stimulation has been shown in recent studies to be more common than previously thought. Carotid sinus stimulation may either cause a vasodepressor reaction or a predominant vasovagal reaction, or both. Drugs known to aggravate carotid sinus syncope are digitalis, beta blockers, and calcium channel blockers. The hypersensitivity may be secondary to an abnormality of the carotid sinus mechanism or to underlying conduction system disease. Diagnosis can be made with carotid massage in a head-up tilt position with blood pressure and ECG monitoring, with hypotension being a positive result.
Therapy includes patient education and evaluation of their medications, with possible carotid sinus denervation and pacemaker implantation if symptoms are refractory or associated with significant bradycardias. Dual-chamber pacing is required since single-chamber pacing commonly produces pacemaker syndrome. Pacer therapy reduces the incidence of syncope even without a direct affect on vasodepressor response.
1When should arrhythmic syncope be suspected?
Arrhythmia is more likely if the patient has underlying heart disease, symptoms of palpitations, abrupt syncope with injury, and syncope not associated with posture changes. Arrhythmic syncope is usually the result of a heart rate either too fast or slow occurring in a patient with limited cardiac reserve (secondary to valvular or myocardial disease). These patients are also more likely to have conduction abnormalities, predisposing them to low cardiac output with an arrhythmia.
What is the best approach for work-up of a suspected arrhythmic syncope?
The work-up of syncope can be costly and timely. Therefore, it should usually start with the less expensive and least invasive studies, unless special circumstances dictate otherwise.
The accompanying table shows the usual tests and how they fit into the evaluation of syncope. Obviously, if a specific exertional etiology is suspected from the history and physical examination, this should help dictate the work-up strategy. Because of the importance of left ventricular function in the prognosis of patients, we do echo-Doppler as part of the evaluation of almost all syncope patients referred to the cardiology service.
Defines conduction system disease, Wolff-Parkinson-White syndrome, myocardial infarction, left ventricular hypertrophy, atrial and ventricular ectopy, and occasionally arrhythmia.
Screens for ventricular tachycardia after myocardial infarction. Documents arrhythmia and relates to symptoms; aids in defining therapeutic response.
Evaluates for valve disease, myocardial disease, left ventricular function.
Documents paroxysmal arrhythmias in low-risk subsets. Reproduces external arrhythmia; evaluates role of ischemia. Defines conduction system disease, elicits supraventricular and ventricular tachycardia, and measures hemodynamic effect of arrhythmias and response to pharmacologic and pacing interventions.
Elicits vasodepressor or hemodynamic response to arrhythmia.
Modified from Weissler AM, Boudoulas HB, Lewis RP, et al: Syncope: Pathophysiology, recognition, and treatment. In Hurst JW (ed): The Heart, 7th ed. New York, McGraw-Hill, 1990, p 581.