Alcohol and Syncopal Events: A Complex Connection

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.

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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. However, a recent study showed that subjects exhibited unusual alcohol-induced sinus bradycardia and hypotension, suggesting a paradoxical increase in parasympathetic activity and/or decreases in sympathetic activity.

6 This will give rise to carotid sinus hypersensitivity, which is an exaggerated response to carotid sinus baroreceptor stimulation. It results in dizziness or syncope from transient diminished cerebral perfusion. Case Report A 27-year-old, well-appearing African American female was brought to the Emergency Department by Emergency Medical Services after a witnessed syncopal episode. The only medical history is a previous alcohol-induced syncope 2 years ago. The patient does not have any past surgical history. The patient only drinks socially. She does not smoke, and she denied any drug use.

The patient lives with mother, and works as a nursing assistant in a nursing home. The patient admitted to drinking “a shot of vodka” approximately 10 minutes prior to syncopal episode. The patient fell upon standing and hit the back of her head on the floor. Patient’s significant other who witnessed the syncopal event reported that loss of consciousness (LOC) lasted about 2 minutes. EMS was consequently called. According to EMS, the patient was still on the floor, alert and oriented only to self upon their arrival. She was lethargic. The patient did not remember passing out.

She was subsequently transported to the Emergency department. Patient did improve remarkably on the way to the hospital. Upon arrival to the Emergency Department, patient was alert and oriented to person, place, and time. She answered questions appropriately. She was slightly lethargic. Her pupils were equal bilaterally, and equally responsive to light and accommodation. The patient denied any visual changes and headache. There was no facial droop, and her smile was even. Tongue was midline. There was no weakness in all extremities. Patient moved all extremities purposefully with equal grip strength in bilateral upper extremities.

There was no nausea or vomiting. Respiration was even and unlabored with respiratory rate of 20/min. Bilateral lungs were clear to auscultation. The patient denied any shortness of breath or chest pain. A 12 lead EKG showed normal sinus rhythm with heart rate of 90 beats/min. Her skin was warm and dry with axillary temperature of 98. 70 F. Small bruises were noted on the back of her head. An orthostatic blood pressure and pulse were checked with the following results; supine 132/78 mm Hg, 85 beats/min; sitting 135/80 mm Hg, 86 beats/min; standing 130/78 mm Hg, 90 beats/min.

Urine toxicity screen was negative for any drug. Blood alcohol level was not significant. Cardiac enzyme markers were negative. A basic metabolic panel study and complete blood count were done with the following results; hemoglobin 13. 9 gm/dL, hematocrit 41 percent, Potassium 3. 7 mEq/L, Sodium 140 mEq/L, Chloride 106 mEq/L, BUN 12 mg/dL, glucose 101 mg/dL and Creatinine 1. 0mg/dL. There was no electrolyte abnormality. Chest x-ray was unremarkable. Head CT was unimpressive. The patient was given 1 liter of normal saline intravenously at the rate of 250 ml/hour.

The patient did not have any other episode of syncope while in the Emergency Department. The patient reported feeling “a lot better”. The patient was admitted to the telemetry unit for overnight monitoring. The following day, the medical admitting team ran more blood tests on the patient. There was however no abnormal results. Magnetic Resonance Imaging was also done. The result was also unimpressive. Patient was subsequently discharged home with discharge teachings and instructions. Most importantly, the patient was told to remain seated for at least 30 minutes and then rise slowly after future alcohol consumption.

She was also advised to stop drinking alcohol. She was further instructed to follow up with a neurologist for possible tilt table test. Discussion This case compares well with current literature on the topic of alcohol-induced syncope. There is currently no definitive treatment for this underreported medical problem. The mainstay of treatment at this point is patient education and public health awareness. Emphasis is placed on reducing orthostatic stress after alcohol consumption in patients with this disorder. The patient is advised to avoid sudden change in position 1-2 hours after alcohol ingestion.

In addition, there seems to be a consensus among scholars that avoiding alcohol represents the best practices in avoiding this problem. Alcohol consumption is widespread among young healthy adults. This is particularly disturbing since alcohol-induced syncope is responsible for approximately 10 percent of syncope in this age group. In a double-blind study design conducted by Cooley et al. , their data demonstrated that in young subjects, short-term alcohol consumption elicits hypotension during orthostatic stress because of impairment of vasodilation. 3 The implication is that this may cause sudden death in a young healthy adult.

My patient fits the profile of this study. She is healthy and young with no significant medical problem. All the imaging and laboratory tests that were done during her hospital stay did not reveal any underlining pathology. Recent evidence shows that alcohol-induced syncope occurs in light drinkers and shows a pattern of repeated episodes of syncope after alcohol ingestion. In a landmark study done on this subject in Japan, researchers observed 2 cases of repeated syncopal episodes after alcohol ingestion. 5,6 In both cases, alcohol loading tests repeatedly induced sinus bradycardia and hypotension 1.

0-1. 5 hours after drinking alcohol. The two patients in this study were both light drinkers. This was the case with the patient that presented to us in the Emergency Department. She is not a heavy drinker. In fact, she only drinks socially. Furthermore, she had a similar syncopal event following alcohol ingestion approximately two years ago. However, it seems that her syncopal events tend to occur quicker (approximately 10-20 minutes) following alcohol ingestion, compared to the subjects of the aforementioned study. Conclusion The exact mechanism of alcohol-induced syncope is not known.

However, an impressive body of scientific and medical evidence suggests that short-term alcohol consumption elicits hypotension during orthostatic stress even in healthy young subjects. Unexplained syncope in healthy young adults after drinking alcohol in most of the studies reviewed,suggests that alcohol may play a crucial role in eliciting syncope. Alcoholism is a public health problem in the United States, especially among young adults. Alcohol-induced syncope is a direct consequence of alcohol intake. In summary, understanding the pathophysiology of alcohol-induced syncope would be a necessary first step in the fight against this problem.

References 1. Carratta R, Fabris B, Bardelli M, Muiesan S, Fischetti F, Casanelli R, Pizzolitto A, Campanacci L. Acute effects of intravenous infusions of alcohol on baroreceptor sensitivity in essential hypertension. Cardiovasc Res. 1988; 22:226-230. 2. Johnson R, Eisenhofer G, Lambra D. The effects of acute and chronic ingestion of ethanol on autonomic nervous system. Drug Alcohol Depend. 1986; 18:319-328. 3. Narkiewicz K, Cooley R, Somers V. Alcohol potentiates orthostatic hypotension: implications for alcohol-related syncope. Circulation Journal. 2000; 101:398-402. 4.

Narkiewicz K, Cooley R, Somers V, Wolk R. Alcohol and syncope.Journal of Cardiac Electrophysiology Review. 2004; 5:430-434. 5. Takahashi N, Imai S, Saitr F, Suzuki K, Tanaka H, Kushiro T, Yagi H, Hirbyama A. Alcohol produces imbalance of adrenal and neuronal sympathetic activity in patients with alcohol-induced neurocardiogenic syncope. Circulation Journal. 2008; 72:979-85.

6. Tsutsui M, Matsuguchi T, Tsutsui H, Yoshida T, Yoshihara S, Yamamoto K, Hisanou R, Shimokawa H, Okamatsu S. Alcohol-induced sinus bradycardia and hypotension in patients with syncope. Japan Heart Journal. 1992; 33:875-9. Alcohol-induced syncope: a case report Chijindu Nworgu Howard University College of medicine.