Chapter 021. Syncope (Part 7)

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Syncope: Treatment The treatment of syncope is directed at the underlying cause. This discussion will focus on disorders of autonomic control. Arrhythmias are discussed in Chaps. 225 and 226, valvular heart diseases in Chap. 230, and cerebrovascular disorders in Chap. 364.Certain precautions should be taken regardless of the cause of syncope. At the first sign of symptoms, patients should make every effort to avoid injury should they lose consciousness. Patients with frequent episodes, or those who have experienced syncope without warning symptoms, should avoid situations in which sudden loss of consciousness might result in injury (e.g., climbing ladders, swimming alone,...

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Chapter 021. Syncope (Part 7) Syncope: Treatment The treatment of syncope is directed at the underlying cause. This discussion will focus on disorders of autonomic control. Arrhythmias are discussed in Chaps. 225 and 226, valvular heart diseases in Chap. 230, and cerebrovascular disorders in Chap. 364.Certain precautions should be taken regardless of the cause of syncope. At the first sign of symptoms, patients should make every effort to avoid injury should they lose consciousness. Patients with frequent episodes, or those who have experienced syncope without warning symptoms, should avoid situations in which sudden loss of consciousness might result in injury (e.g., climbing ladders, swimming alone, operating heavy machinery, driving). Patients should lower their head to the extent possible and preferably should lie down. Lowering the head by bending at the waist should be
avoided because it may further compromise venous return to the heart. When appropriate, family members or other close contacts should be educated as to the problem. This will ensure appropriate therapy and may prevent delivery of inappropriate therapy (chest compressions associated with cardiopulmonary resuscitation) that may inflict trauma.Patients who have lost consciousness should be placed in a position that maximizes cerebral blood flow, offers protection from trauma, and secures the airway. Whenever possible, the patient should be placed supine with the head turned to the side to prevent aspiration and the tongue from blocking the airway. Assessment of the pulse and direct cardiac auscultation may assist in determining if the episode is associated with a bradyarrhythmia or a tachyarrhythmia. Clothing that fits tightly around the neck or waist should be loosened. Peripheral stimulation, such as sprinkling cold water on the face, may be helpful. Patients should not be given anything by mouth or be permitted to rise until the sense of physical weakness has passed.Patients with vasovagal syncope should be instructed to avoid situations or stimuli that have caused them to lose consciousness and to assume a recumbent position when premonitory symptoms occur. These behavioral modifications alone may be sufficient for patients with infrequent and relatively benign episodes of vasovagal syncope, particularly when loss of consciousness occurs in response to a specific stimulus. Tilt training (standing and leaning against a wall for progressively longer periods each day) has been used with limited success, particularly for patients with orthostatic intolerance. Episodes associated with intravascular volume depletion may be
prevented by salt and fluid loading prior to provocative events.Drug therapy may be necessary when vasovagal syncope is resistant to the above measures, when episodes occur frequently, or when syncope is associated with a significant risk for injury. β-Adrenergic receptor antagonists (metoprolol, 25–50 mg bid; atenolol, 25–50 mg qd; or nadolol, 10–20 mg bid; all starting doses), the most widely used agents, mitigate the increase in myocardial contractility that stimulates left ventricular mechanoreceptors and also block central serotonin receptors. Serotonin reuptake inhibitors (paroxetine, 20–40 mg qd; or sertraline, 25–50 mg qd), appear to be effective for some patients. Bupropion SR (150 mg qd), another antidepressant, has also been used with success. β-Adrenergic receptor antagonists and serotonin reuptake inhibitors are well tolerated and are often used as first-line agents for younger patients. Hydrofludrocortisone (0.1–0.2 mg qd), a mineralocorticoid, promotes sodium retention, volume expansion, and peripheral vasoconstriction by increasing β-receptor sensitivity to endogenous catecholamines. Hydrofludrocortisone is useful for patients with intravascular volume depletion and for those who also have postural hypotension. Proamatine (2.5–10 mg bid or tid), an α-agonist, has been used as a first-line agent for some patients. In a randomized controlled trial, proamatine was more effective than placebo in preventing syncope during an upright tilt-test. However, in some patients, proamatine and hydrofludrocortisone may increase resting supine systemic blood pressure, which may be problematic for those with hypertension.Disopyramide (150 mg bid), a vagolytic antiarrhythmic drug with
negative inotropic properties, and transdermal scopolamine, another vagolytic, have been used to treat vasovagal syncope, as have theophylline and ephedrine. Side effects associated with these drugs have limited their use for this indication. Disopyramide is a type 1A antiarrhythmic drug and should be used with great caution, if at all, in patients who are at risk for ventricular arrhythmias. Although several clinical trials have suggested that pharmacologic therapy for neurocardiogenic syncope is effective, the few long-term prospective randomized controlled trials have yielded mixed results. In the Prevention of Syncope Trial (POST), metoprolol was ineffective in patients 42, raising the possibility that there may be significant age-related differences in response to pharmacologic therapy.Studies of permanent pacing for neurocardiogenic syncope have also yielded mixed results. Dual-chamber cardiac pacing may be effective for patients with frequent episodes of vasovagal syncope, particularly for those with prolonged asystole associated with vasovagal episodes. Pacemakers that can be programmed to transiently pace at a high rate (90–100 beats/min) after a profound drop in the patient's intrinsic heart rate are most effective.Patients with orthostatic hypotension should be instructed to rise slowly and systematically (supine to seated, seated to standing) from the bed or a chair. Movement of the legs prior to rising facilitates venous return from the lower extremities. Whenever possible, medications that aggravate the problem (vasodilators, diuretics, etc.) should be
discontinued. Elevation of the head of the bed [20–30 cm (8–12 in.)] and use of compression stockings may help.Additional therapeutic modalities include salt loading and a variety of pharmacologic agents including sympathomimetic amines, monamine oxidase inhibitors, beta blockers, and levodopa. The treatment of orthostatic hypotension secondary to central or peripheral disorders of the autonomic nervous system is discussed in Chap. 370.Glossopharyngeal neuralgia is treated with carbamazepine, which is effective for syncope as well as for pain. Patients with carotid sinus hypersensitivity should be instructed to avoid clothing and situations that stimulate carotid sinus baroreceptors. They should turn their entire body, rather than just their head, when looking to the side. Those with intractable syncope due to the cardioinhibitory response to carotid sinus stimulation should undergo permanent pacemaker implantation.Patients with syncope should be hospitalized when there is a possibility that the episode may have resulted from a life-threatening abnormality or if recurrence with significant injury seems likely. These individuals should be admitted to a bed with continuous electrocardiographic monitoring. Patients who are known to have a normal heart and for whom the history strongly suggests vasovagal or situational syncope may be treated as outpatients if the episodes are neither frequent nor severe. FURTHER READINGS Grubb BP:
Neurocardiogenic syncope and related disorders of orthostatic intolerance. Circulation 111:2997, 2005 [PMID: 15939833] ———, Olshansky B (eds): Syncope: Mechanisms and Management, 2d ed. Malden, Mass., Blackwell Futura, 2005 Kapoor WN: Current evaluation in management of syncope. Circulation 106:1606, 2002 [PMID: 12270849] Kaufman H et al: Midodrine in neurally mediated syncope: A double-blind, randomized, crossover study. Ann Neurol 52:342, 2002
Kaufmann H, Bhattacharya K: Diagnosis and treatment of neurally mediated syncope. Neurologist 8:175, 2002 [PMID: 12803689] Kerr SRJ et al: Carotid sinus hypersensitivity in asymptomatic older persons: Implications for diagnosis of syncope and falls. Arch Intern Med 166:515, 2006 [PMID: 16534037] Maisel W, Stebenson W: Syncope—getting to the heart of the matter. N Engl J Med 347:931, 2002 [PMID: 12239264] Soteriades E et al: Incidence and prognosis of
syncope. N Engl J Med 347:878, 2002 [PMID: 12239256] Strickberger SA et al: AHA/ACCF scientific statement on the evaluation of syncope: From the American Heart Association Councils on Clinical Cardiology, Cardiovascular Nursing, Cardiovascular Disease in the Young, and Stroke, and the Quality of Care and Outcomes Research Interdisciplinary Working Group; and the American College of Cardiology Foundation: In collaboration with the Heart Rhythm Society: Endorsed by the American Autonomic Society. Circulation 113(2):316, 2006
Van Dijk N et al: Quality of life within one year following presentation after transient loss of consciousness. Am J Cardio 100:672, 2007