Alcohol Syncope

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Alcohol consumption may be linked to syncopal events. The mechanism by which alcohol may induce syncope is not well understood. Impairment of the response to orthostatic stress may be involved. A growing body of medical evidence suggests that short-term alcohol consumption elicits hypotension during orthostatic stress because of impairment of vasoconstriction. These findings have implications for understanding of hemodynamic effects of alcohol and, in particular, for understanding syncopal events that occur in association with alcohol intake. A 27-year-old African American female with a previous syncopal event following alcohol consumption was brought to the Emergency Department by ambulance after a witnessed syncopal episode. The patient admitted to drinking “a shot of vodka” 10 minutes prior to the syncopal event. Loss of consciousness was reported as lasting approximately 2 minutes, prompting family to call 911. Imaging studies and blood tests did not show any abnormalities. Patient was discharged home the next day after one night of observation in the medical unit. Since alcohol abuse and alcoholism are the greatest substance abuse problems in the United States today, it is of paramount importance to understand the pathophysiological basis and the implications of alcohol related syncope. Introduction

Syncope is defined as a transient loss of consciousness with an accompanying loss of postural tone.2 Although, by definition, it is followed by spontaneous recovery, in many instances it may be the only harbinger of sudden cardiac death. Syncope is a common disorder with many different etiologies, and can compromise the quality of life and lead to significant morbidity. It accounts for 1-6 percent of hospital admissions annually and the cost of diagnosis and treatment of patients with syncope reaches 800 million dollars.4 The incidence of alcohol-related syncope varies across different subpopulations studied. In young adults, it has been incriminated in approximately 10 percent of all syncopal events.3 Studies of unexplained syncope implicate alcohol dependence or alcohol ingestion shortly before syncope. Short-term alcohol administration impairs baroreflex sensitivity.2 Direct vascular effects of alcohol would elicit vasodilatation.5 The impaired peripheral vasoconstriction caused by alcohol is compounded by the direct vasodilator effects of alcohol. This may result in hypotension during orthostatic stress especially upon standing. Standing results in pooling of up to 800ml of blood to the lower extremities.1 Consequently, venous return, cardiac output and blood pressure decrease, with a potential risk of cerebral hypoperfusion. These changes induce complex autonomic responses that attempt to preserve cerebral perfusion. Specifically, the decrease in venous return and blood pressure are detected by cardiopulmonary and arterial baroreceptor, respectively. The information is then relayed to the central nervous system, which initiates a number of neurohumoral responses in order to restore arterial pressure and maintain adequate cerebral perfusion. These compensatory responses may cause an increase in heart rate and stroke volume, peripheral arterial and venous vasoconstriction, as well as water and sodium re-absorption in the kidneys. Impairment of one or more of these compensatory responses may result in hypotension and possibly syncope during standing. Short-term alcohol intake impairs this vasoconstrictive response to orthostatic stress in humans.2 This effect may be brought about by effects of alcohol on central brainstem mechanisms or sensory afferents of the baroreceptor reflex. Alcohol may also cause sinus bradycardia, with a resultant hypotension. Hypotension will consequently cause cerebral hypoperfusion, and syncope may result. Acute alcohol ingestion usually increases heart rate with variable effects on blood pressure....
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