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The coronary circulation in human septic shock
Insights
In human septic shock, myocardial depression is not caused by reduced coronary blood flow. Coronary flow remained adequate, suggesting other mechanisms are responsible for this cardiac dysfunction.
Area of Science:
- Cardiology
- Critical Care Medicine
- Physiology
Background:
- Reversible myocardial depression, characterized by ventricular dilatation and reduced ejection fraction, is a frequent complication of human septic shock.
- Animal studies suggest myocardial ischemia due to insufficient coronary blood flow as a potential cause, but this remains unconfirmed in humans.
Purpose of the Study:
- To investigate the relationship between myocardial depression and coronary blood flow in human septic shock.
- To determine if reduced coronary flow contributes to cardiac dysfunction during septic shock.
Main Methods:
- Seven patients with septic shock underwent measurements of coronary flow and myocardial metabolism using thermodilution coronary sinus catheters.
- Coronary flow, myocardial lactate production, and arterial-coronary sinus oxygen differences were assessed.
Main Results:
- Four of seven patients developed myocardial depression, but their coronary flow was similar to or higher than controls and patients without depression.
- No patients exhibited net myocardial lactate production, indicating no anaerobic metabolism.
- Oxygen extraction was diminished, suggesting disordered coronary autoregulation, similar to arteriovenous shunting in other septic organs.
Conclusions:
- Preserved coronary blood flow and myocardial lactate extraction in septic shock patients with myocardial depression argue against global ischemia.
- The findings suggest that mechanisms other than reduced coronary flow are responsible for myocardial depression in human septic shock.
- Disordered coronary autoregulation, rather than ischemia, may play a role in septic myocardial dysfunction.
Abstract:
Reversible myocardial depression, manifested by ventricular dilatation and decreased ejection fraction, is common in human septic shock. A proposed mechanism, based on animal studies, is myocardial ischemia resulting from inadequate coronary blood flow. Coronary flow observations have not been reported for human septic shock. To determine whether myocardial depression in human septic shock is associated with reduced coronary flow, thermodilution coronary sinus catheters were placed in seven patients with septic shock for measurements of coronary flow and myocardial metabolism. Four of the seven patients developed myocardial depression. These patients had coronary flow similar to or higher than that of control subjects and similar to that of the other three patients, who did not develop myocardial depression. None of the patients had net myocardial lactate production. In general, compared with values in control subjects, the oxygen content difference (arterial minus coronary sinus) was narrowed, and the fractional extraction of arterial oxygen was diminished. This pattern of disordered coronary autoregulation is analogous to the pattern of arteriovenous shunting in other organs in patients with septic shock. The preservation of coronary flow, the net myocardial lactate extraction, and the increased availability of oxygen to the myocardium argue against global ischemia as the cause of myocardial depression in human septic shock.