TY - JOUR
T1 - Alcohol potentiates orthostatic hypotension
T2 - Implications for alcohol- related syncope
AU - Narkiewicz, Krzysztof
AU - Cooley, Ryan L.
AU - Somers, Virend K.
PY - 2000/2/1
Y1 - 2000/2/1
N2 - Background - Alcohol consumption may be linked to syncopal events. The mechanisms by which alcohol may induce syncope are unknown. Impairment of the response to orthostatic stress may be involved. Using a double-blind, randomized, placebo-controlled study, we tested the hypothesis that short- term alcohol intake causes orthostatic hypotension because of an impairment in the vasoconstrictor response to orthostatic stress. Methods and Results - We examined the effects of alcohol on blood pressure, heart rate, and forearm vascular resistance (FVR) during orthostatic stress achieved by stepwise increases in lower-body negative pressure (LBNP) in 14 healthy young volunteers. During the placebo session, blood pressure did not change significantly during LBNP at -5, -10, and -20 mm Hg. A significant decrease in blood pressure was evident only at -40 mm Hg. In contrast, blood pressure fell significantly at all levels of LBNP during the alcohol session. Compared with placebo, alcohol potentiated the hypotensive responses to LBNP, particularly at -40 mm Hg, when the decrease in systolic blood pressure after alcohol intake (-14 mm Hg) was double that after placebo intake (-7 mm Hg). FVR increased with LBNP after placebo. However, after alcohol intake, FVR did not increase during LBNP despite the potentiated decrease in blood pressure. FVR responses during LBNP were reduced during alcohol compared with placebo consumption (P=0.04). Conclusions - Short-term alcohol consumption elicits hypotension during orthostatic stress because of impairment of vasoconstriction. These findings have implications for the understanding of the hemodynamic effects of alcohol and, in particular, for understanding syncopal events that occur in association with alcohol intake.
AB - Background - Alcohol consumption may be linked to syncopal events. The mechanisms by which alcohol may induce syncope are unknown. Impairment of the response to orthostatic stress may be involved. Using a double-blind, randomized, placebo-controlled study, we tested the hypothesis that short- term alcohol intake causes orthostatic hypotension because of an impairment in the vasoconstrictor response to orthostatic stress. Methods and Results - We examined the effects of alcohol on blood pressure, heart rate, and forearm vascular resistance (FVR) during orthostatic stress achieved by stepwise increases in lower-body negative pressure (LBNP) in 14 healthy young volunteers. During the placebo session, blood pressure did not change significantly during LBNP at -5, -10, and -20 mm Hg. A significant decrease in blood pressure was evident only at -40 mm Hg. In contrast, blood pressure fell significantly at all levels of LBNP during the alcohol session. Compared with placebo, alcohol potentiated the hypotensive responses to LBNP, particularly at -40 mm Hg, when the decrease in systolic blood pressure after alcohol intake (-14 mm Hg) was double that after placebo intake (-7 mm Hg). FVR increased with LBNP after placebo. However, after alcohol intake, FVR did not increase during LBNP despite the potentiated decrease in blood pressure. FVR responses during LBNP were reduced during alcohol compared with placebo consumption (P=0.04). Conclusions - Short-term alcohol consumption elicits hypotension during orthostatic stress because of impairment of vasoconstriction. These findings have implications for the understanding of the hemodynamic effects of alcohol and, in particular, for understanding syncopal events that occur in association with alcohol intake.
KW - Alcohol
KW - Blood pressure
KW - Hypotension
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U2 - 10.1161/01.CIR.101.4.398
DO - 10.1161/01.CIR.101.4.398
M3 - Article
C2 - 10653831
AN - SCOPUS:0034141731
SN - 0009-7322
VL - 101
SP - 398
EP - 402
JO - Circulation
JF - Circulation
IS - 4
ER -