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Updated: Aug 10, 2026
Standardized Hemorrhagic Shock Induction Guided by Cerebral Oximetry and Extended Hemodynamic Monitoring in Pigs
Published on: May 21, 2019
Cardiac contractile effects of ethanolism and hemorrhagic shock
1Department of Surgery, University of Texas Southwestern Medical Center, Dallas 75235-9031.
Insights
Moderate alcohol consumption exacerbates cardiac dysfunction during hemorrhagic shock. This study found that intoxicated subjects experienced significantly worse heart problems after blood loss compared to non-intoxicated subjects.
Area of Science:
- Cardiovascular Physiology
- Toxicology
Background:
- Moderate ethanol consumption is common in trauma patients and linked to cardiac depression.
- Hemorrhagic shock, a frequent trauma complication, impairs heart function intrinsically.
Purpose of the Study:
- To investigate if acute ethanol intoxication heightens cardiovascular risks during hemorrhagic shock.
- To compare cardiac dysfunction in ethanol-intoxicated versus non-intoxicated subjects experiencing hemorrhagic shock.
Main Methods:
- An isolated guinea pig heart model was used with 116 animals divided into four groups: control, ethanol alone, hemorrhagic shock alone, and combined ethanol and hemorrhagic shock.
- Hearts underwent isolated heart studies and myocardial cell membrane integrity assessments.
- Hemorrhagic shock was induced by maintaining a mean arterial blood pressure of 30 mmHg for 2 hours.
Main Results:
- Ethanol alone reduced peak isovolumic pressure, maximal rate of left ventricular pressure (LVP) rise, and fall by 27-36%.
- Contractile depression was significantly greater in the combined ethanol and hemorrhagic shock group compared to the hemorrhagic shock alone group (P < 0.05).
- Both ethanol and hemorrhage affected myocardial cell volume regulation, but hemorrhage-induced changes were similar in both intoxicated and non-intoxicated groups.
Conclusions:
- Hemorrhagic shock leads to significantly greater cardiac contractile dysfunction in intoxicated individuals.
- Acute ethanolism increases the cardiovascular risk associated with hemorrhagic shock.
Abstract:
Moderate ethanol consumption, associated with cardiac depression, occurs in greater than 50% of trauma. Hemorrhagic shock, a significant component of trauma in the clinical setting, causes intrinsic cardiac contractile dysfunction. In this study, we used an isolated heart model to determine whether acute ethanolism increases the cardiovascular risk associated with hemorrhagic shock. We hypothesized that hemorrhagic shock in the acutely intoxicated subject would cause significantly greater cardiac dysfunction compared with that observed in a nonintoxicated subject. A total of 116 guinea pigs was divided into four groups: control (no ethanol, no shock), ethanol intoxication alone (1 mg/kg iv), hemorrhagic shock alone (mean arterial blood pressure, 30 mmHg for 2 h), and a combination of hemorrhagic shock plus ethanol. Half of the hearts in each group were used for isolated heart studies, and half were used to assess myocardial cell membrane integrity. Ethanol alone reduced peak isovolumic pressure by 36%, maximal rate of left ventricular pressure (LVP) rise by 27%, and maximal rate of LVP fall by 35%; however, contractile depression was significantly greater in the intoxicated, hemorrhaged, group compared with the nonintoxicated, hemorrhaged, group (P less than 0.05). Both ethanol and hemorrhage independently altered myocardial cell volume regulation; however, abnormalities in myocardial cell volume regulation induced by hemorrhage were similar in the intoxicated and nonintoxicated groups. Our data show that hemorrhagic shock causes significantly greater cardiac contractile dysfunction in the intoxicated subject.
