Myocardial oxygen delivery after experimental hemorrhagic shock
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Hemorrhagic shock impairs myocardial oxygen delivery. Even after reinfusion, impaired oxygen diffusion and subendocardial ischemia contribute to cardiac dysfunction and irreversibility.
Area of Science:
- Cardiovascular Physiology
- Myocardial Metabolism
- Hemorrhagic Shock Research
Background:
- Myocardial oxygen delivery is crucial for cardiac function, involving both coronary blood flow and diffusion.
- Hemorrhagic shock significantly impacts circulatory dynamics and organ perfusion.
- Understanding the mechanisms of myocardial dysfunction during and after shock is vital for improving patient outcomes.
Purpose of the Study:
- To investigate the components of myocardial oxygen delivery during hemorrhagic shock and post-resuscitation.
- To determine the relationship between coronary blood flow, oxygen diffusion, and cardiac performance.
- To elucidate the causes of left ventricular dysfunction and irreversibility following shock.
Main Methods:
- Studied myocardial oxygen delivery in six dogs under four conditions: pre-shock, during shock (MAP 40 torr), after reinfusion, and during irreversible shock.
- Measured total and regional left ventricular coronary blood flow.
- Assessed myocardial oxygen delivery to capillaries and the diffusion area to distance ratio.
Main Results:
- Hemorrhagic shock caused maldistribution of coronary flow, leading to subendocardial ischemia.
- Cardiac performance was significantly impaired post-resuscitation, with all dogs becoming irreversible.
- Myocardial oxygen diffusion, indicated by the area to distance ratio, was reduced post-resuscitation, suggesting impaired diffusion.
Conclusions:
- Subendocardial ischemia during shock likely contributes to left ventricular dysfunction.
- Impaired myocardial oxygen diffusion post-resuscitation may play a role in cardiac dysfunction and irreversibility.
- Both impaired diffusion and cellular oxygen utilization could be etiological factors in post-shock cardiac failure.
Abstract:
The two components of myocardial oxygen delivery, coronary blood flow to capillaries and diffusion from capillaries to mitochondria, were studied in six dogs, (1) prior to shock, (2) after three hours of hemorrhage shock at a mean systemic arterial pressure of 40 torr, (3) after reinfusion of shed blood, and (4) during the irreversible late posttransfusion stage. There was a maldistribution of left ventricular coronary flow during late shock consistent with subendocardial ischemia. Cardiac performance was significantly impaired after resuscitation and all dogs became irreversible. Total and regional left ventricular coronary blood flow and myocardial oxygen delivery to capillaries were significantly greater than preshock values in (3) but not different from preshock values in (4). However, the myocardial oxygen diffusion area to distance ratio was significantly lower than preshock values in (3), and slightly lower in (4). These data suggest that myocardial oxygen diffusion may be impaired in the early post transfusion period, (3). Accordingly, the probable etiology of left ventricular dysfunction and possibly irreversibility after resuscitation from hemorrhagic shock is subendocardial ischemia during shock with either post-resuscitation impairment of myocardial oxygen diffusion, or in cellular oxygen utilization, or both.