Citation

Kelbaek H, Fløistrup S, Gjørup T, Christensen NJ, Hartling OJ, Godtfredsen J. Alcohol Alcohol. 1988; 23(3): 211-216.

Affiliation

Department of Clinical Physiology and Nuclear Medicine, Herlev Hospital, University of Copenhagen, Denmark.

Copyright

(Copyright © 1988, Oxford University Press)

DOI

unavailable

PMID

3202925

Abstract

Central and peripheral haemodynamic changes 1 and 8 hours after alcohol ingestion were studied in seven healthy men, aged 21-30 years, by radionuclide cardiography and strain gauge plethysmography. Heart rate (HR) increased by 12% and cardiac output (CO) by 24% 1 hour after alcohol ingestion (mean serum ethanol 35 mmol/l). Left ventricular (LV) ejection fraction (EF) decreased by 5% because of endsystolic dilation and the forearm blood flow increased by 140%. Eight hours after alcohol ingestion (serum ethanol 21 mmol/l.) hangover symptoms were present in all subjects. HR and CO remained increased by 19% and 23%, respectively. A 4% increase was recorded in LVEF. The total peripheral resistance was reduced by 25%, while the forearm blood flow had returned to baseline values. No significant changes in plasma catecholamines were recorded. Apart from a slight increase in CO at 1 hour no haemodynamic changes were recorded after ingestion of an isovolumic, isocaloric drink. The present findings suggest that acute alcohol intoxication causes impairment of LV contractility, but that tachycardia results in an increase in cardiac output accompanied by an increased blood flow in the forearm. In the early hangover phase, when the serum ethanol is still elevated, cardiac output remains enhanced because of tachycardia, although the sympathetic nervous activity as measured by the plasma norepinephrine level is not influenced. A reduced total peripheral resistance may contribute to the increase in LV contractility in spite of sustained alcohol intoxication.

Language: en