Physiology

The carotid sinus reflex is an integral component of the homeostatic mechanisms of blood pressure regulation.¹⁵ Increases in intrasinus pressure stimulate mechanoreceptors, which participate in an afferent arc terminating in the brainstem. The efferent arc travels to peripheral end organs through vagal efferents, which augment cardiac vagal input and slow heart rate, and through the spinal cord to inhibit peripheral sympathetic activity in skeletal vasculature, resulting in peripheral vasodilatation. This reflex maintains blood pressure within a narrow range.

An abnormal carotid sinus reflex can cause exaggerated responses of heart rate and blood pressure. Some evidence suggests that the major defect in carotid sinus hypersensitivity does not reside in the carotid sinus or in its neural efferents,^16,17 or in the brainstem. Rather, the neuromuscular structures surrounding the carotid sinus may be involved in CSS. Blanc et al.¹⁸ found similar results in 30 patients without known carotid sinus hypersensitivity or syncope. Abnormal sternocleidomastoid electromyograms were associated with abnormal responses to CSM. Because the denervated sternocleidomastoid muscle cannot provide or contribute information to the central nervous system baroreflex centers, any output from the carotid sinus is inappropriately interpreted as increased blood pressure.

Other Therapies

When CSS is the likely cause of syncopal episodes, the initial treatment recommendation should be simple elimination of any recognized maneuvers that may precipitate an event. Discontinuation of wearing tight collars and ties and shaving more carefully may help. Hypovolemia should be corrected. The addition of high salt intake, volume expanders such as fludrocortisone acetate (Florinef),¹⁹ or oral vasopressors such as midodrine (ProAmatine) may be helpful, but these interventions are frequently limited in older patients by comorbidities (e.g., hypertension, heart failure).

In the pre–pacemaker era, recalcitrant cases of carotid sinus syncope were treated with carotid sinus denervation by surgical technique.²⁰ Surgical sinus denervation currently is reserved for cases secondary to head or neck tumors or lymphadenopathy, or it is performed in conjunction with carotid endarterectomy or in patients with severe refractory carotid sinus syncope of the purely vasodepressor type.

Observational Studies

Table 15-2 summarizes studies of pacing for CSS.^13,21–25 Earlier studies tended to be retrospective reports of pacing practices for CSS and therefore were inherently biased toward patients with a clear diagnosis of CSS who would truly benefit from pacing.

TABLE 15-2 Clinical Studies of Pacing for Carotid Sinus Syncope*

Randomized Trials

More recently, prospective, randomized trials have examined outcomes on the basis of presence of pacing and mode. A prospective, randomized Italian trial reaffirmed the important role of permanent pacing; 60 patients with CSS were randomized to pacing (32) or no pacing (28) therapy.¹⁴ During a follow-up of about 3 years, syncope recurred in 16 patients of the no-pacing group (51%) and in three (9%) of the pacing group (P = .002). This finding somewhat confirms the usefulness of pacing for the prevention of carotid sinus syncope, although potent placebo effects cannot be ruled out (see later).

Physiologic Responses

Carotid sinus massage elicits both cardioinhibitory and vasodepressor responses (Fig. 15-1). A cardioinhibitory response to CSM is defined as 3 seconds or longer of ventricular standstill or asystole. Ventricular asystole usually results from a sinus pause caused by sinus node exit block,³⁵ but it can result from atrioventricular (AV) block as well. A vasodepressor response to CSM is defined as a drop in systolic blood pressure of 50 mm Hg or more during massage; this may be difficult to demonstrate in patients who have a significant cardioinhibitory component. In contrast to the induced cardioinhibitory component of carotid sinus hypersensitivity, the vasodepressor response may have a slower, more insidious onset and a more prolonged resolution.

Figure 15-1 Combined cardioinhibitory and vasodepressor response to carotid sinus massage (CSM). Note slow return of blood pressure despite resolution of asystole.

(From Almquist A, Gornick C, Benson W, et al: Carotid sinus hypersensitivity: evaluation of the vasodepressor component. Circulation 71:927, 1985. Copyright 1985 American Heart Association.)

Carotid Sinus Hypersensitivity and Carotid Sinus Syncope

Carotid sinus hypersensitivity denotes abnormal physiologic responses to CSM, either cardioinhibitory or vasodepressor (or both). The presence of asymptomatic carotid sinus hypersensitivity is quite common in older adults. For example, a positive cardioinhibitory response to CSM was noted in 32% of patients undergoing coronary angiography.³⁶ CSS is the syndrome of syncope in association with carotid sinus hypersensitivity, and in the absence of other apparent causes of syncope.

Complications

Carotid sinus massage is safe if done carefully. CSM is contraindicated in patients with a history of cerebrovascular disease or carotid bruits, because it can cause cerebrovascular accident (CVA, stroke). In a review of 3100 episodes of CSM performed on 1600 patients, the seven complications (0.14%) were neurologic and transient.³⁷ In another review of CSM on 4000 patients, complications were observed in 11 patients (0.28%);³⁸ all were neurologic. After 1 month, nine patients had made a full recovery; neurologic symptoms persisted in two patients. Rare, arrhythmic complications include asystole and ventricular fibrillation.³⁹

Epidemiology

About 40% of people faint at least once in their life, and at least 20% of adults faint more than once.^48,49 Fainters usually present first in their teenage years and 20s and may faint sporadically for decades. This long, usually benign, and sporadic history can make for difficult decisions about therapy. Syncope is responsible for 1% to 6% of emergency room visits and 1% to 3% of hospital admissions.^50–52 Tilt tests are often used as a diagnostic tool, although they are limited by difficulties with sensitivity, specificity, and reproducibility, and with little evidence-based agreement on methodologic details and outcome criteria. Positive tilt tests are characterized by presyncope, syncope, bradycardia, and hypotension, as well as a reproduction of the patient’s perisyncopal symptoms^53,54 (Fig. 15-2).

Figure 15-2 Hypotension and bradycardia induced during a positive drug-free passive tilt-table test. HR, Heart rate; MAP, mean arterial pressure.

Although many patients of all ages simply have vasovagal syncope, clinicians need to remain vigilant and look for other causes, including valvular and structural heart disease, sick sinus syndrome, CSS, and orthostatic hypotension.

Symptom Burden and Quality of Life

The vasovagal syncope syndrome has an extremely wide range of symptoms. The symptom burden varies from a single syncopal spell in a lifetime to daily faints. Some patients have very sporadic presentations, with periods of intense symptoms interspersed with long periods of quiescence. Other patients faint at more regular intervals, although they may be months or years apart. Several observational studies and randomized clinical trials reported that patients have a median of 5 to 15 syncopal spells, with fainting episodes occurring over 2 to 60 years.^55–58 Patients with recurrent syncope are impaired similar to those with severe rheumatoid arthritis or chronic low back pain and psychiatric inpatients.⁵⁵ The quality of life decreases as the frequency of syncopal spells increases.⁵⁶

After clinical assessment, many patients continue to do poorly. After 1, 2, and 3 years, 28%, 38%, and 49% of patients faint again, respectively.⁵⁹ Interestingly, several groups reported a 90% reduction in the total number of faints in this patient population after the tilt test. The reason for this apparently great reduction in syncope frequency after assessment is unknown, but it does lead to a large number of patients who request further treatment. Therefore, when assessing syncope patients, clinicians need to be alert to the surprising impairment of quality of life that many patients endure, to provide a perspective that lasts decades, and to remember that the patient’s clinical state will probably fluctuate.

Evidence for Bradycardia

Permanent pacemaker therapy could be effective if bradycardia is a common and symptomatically important feature of vasovagal syncope. The evidence for clinically important bradycardia comes from studies that have used tilt tests, pacemaker memory, and implantable loop recorders to record heart rate during syncopal spells.

Reassurance and Education

Most patients with vasovagal syncope simply require reassurance and education. Many of the patients with more frequent syncope also benefit from these conservative measures. In particular, patients should be taught to recognize their prodromal symptoms and to sit or lie down as quickly as possible to minimize injury during recurrences and lessen the severity of attacks.

Salt and Fluids

Blood volume is an important factor in the pathophysiology of vasovagal syncope. Syncope almost only occurs in the upright position, and many patients faint only from orthostatic stress in situations such as attending religious services, parades, or outdoor events and taking showers. Prolonged drug-free head-up tilt provokes syncope in a large number of syncope patients; this depends on the duration and angle of head-up tilt.⁶⁹ Finally, many patients report avoiding dietary salt and have low daily urinary sodium excretion.⁷⁰

Physical Counterpressure Maneuvers

Physical counterpressure maneuvers may be quite helpful, although no blinded, controlled studies have been reported. Patients must have a prodrome long enough that they can react by isometrically tightening muscles using maneuvers such as squatting, leg crossing, and fist clenching. Van Dijk et al.⁷¹

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