Chapter 021. Syncope (Part 7) potx

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 years of age but
decreased the incidence of syncope 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