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Intrinsic myocardial function in hemorrhagic shock
K H McDonough1, M Giaimo, M Quinn
1Department of Physiology, Louisiana State University Medical Center, New Orleans 70112, USA.
Insights
Hemorrhagic shock impacts cardiovascular function. Guinea pig hearts maintained normal function for up to 2 hours of shock, but function declined after 3 hours, indicating a loss of cardiac reserve.
Area of Science:
- Cardiovascular Physiology
- Hemorrhagic Shock Research
Background:
- Hemorrhage poses a significant stress to the cardiovascular system, reducing cardiac preload and blood pressure.
- The heart's response involves sympathetic activation and altered preload/afterload dynamics.
- The capacity of the heart to maintain contractile function during prolonged hemorrhagic shock remains unclear.
Purpose of the Study:
- To investigate the effects of varying durations of hemorrhagic shock on intrinsic cardiac contractile function.
- To determine the threshold at which prolonged hemorrhagic shock impairs myocardial function.
Main Methods:
- Guinea pigs underwent surgical preparation for hemodynamic monitoring (blood pressure, heart rate, cardiac output).
- Fifty percent of blood volume was removed to induce hemorrhagic shock.
- Animals were observed for 1, 2, or 3 hours post-hemorrhage.
- Cardiac function was assessed ex vivo after the shock period.
Main Results:
- Hearts from animals subjected to 1 or 2 hours of hemorrhagic shock demonstrated normal ventricular function.
- Hearts from animals exposed to 3 hours of hemorrhagic shock exhibited impaired ventricular function.
- Metabolic indices indicated cardiovascular stress during shock.
Conclusions:
- The heart can maintain normal contractile function for up to 2 hours of hemorrhagic shock.
- Prolonged shock (3 hours) leads to a disruption of the balance between myocardial oxygen demand and supply, resulting in loss of contractile reserve.
- Adequate physiological modulation of coronary blood flow likely supports cardiac function during the initial 2 hours of shock.
Abstract:
Hemorrhage is a stress on the cardiovascular system that results in decreased loading of the heart but also decreased blood pressure and thus decreased perfusion pressure for tissue blood flow. The heart's response to hemorrhage is governed by both an increase in sympathetic nervous system activation of the heart and decreased preload and afterload for the heart. Whether the heart can maintain normal contractile function and reserves under conditions of prolonged hemorrhagic shock is not clear. To assess the effects of hemorrhagic shock of different lengths on intrinsic cardiac contractile function, guinea pigs were surgically prepared for the measurement of blood pressure, heart rate, and cardiac output and blood samples were taken for the measurement of metabolic indices of cardiovascular stress. Fifty percent of the animals' blood volume was removed and then animals were followed for 1, 2, or 3 h of hemorrhagic shock. Hearts were then removed for measurement of intrinsic contractile function. Hearts from animals exposed to 1 or 2 h of shock exhibited normal ventricular function although hearts removed after 3 h exhibited changes in ventricular function. Maintenance of normal cardiac function through at least 2 h of shock must represent adequate physiologic modulation of coronary blood flow to deliver adequate oxygen to match the myocardial oxygen demands under conditions of severe blood loss. This balance may be disrupted by 3 h of shock thus resulting in loss of contractile reserve.