Oxygen consumption during septic shock. Effects of inotropic drugs.

Abstract

Septic shock may be defined as a clinical entity wherein a patient has an inadequate peripheral metabolism in the presence of circulating bacteria. The demands for metabolic requirements of the tissues and hence for oxygen transport to these tissues are then markedly high. The average response to increased metabolism in such patients is a percentage increase in cardiac output that is comparable to the percentage increase in oxygen consumption while oxygen extraction rate does not change or even decreases in severe or/and advanced septic shock. This emphasizes the high priority placed by the body on the ability to increase blood flow from the heart in the presence of increased metabolic demands due to sepsis. Concerning the myocardium, oxygen consumption is low in hyper- and hypodynamic states of septic shock, probably and partially due to marked arterial vasodilatation. However, in hypodynamic states, the lower value of perfusion pressure may account for a decrease in myocardial oxygen supply, especially in subendocardial areas and may be responsible for myocardial ischaemia, more especially as myocardial oxygen extraction as well as systemic oxygen extraction is impaired. The goal of therapeutics is to improve oxygen availability through: (1) maintenance of haemoglobin levels and (2) increases in stroke volume using inotropic drugs since these drugs may produce a rise in myocardial oxygen supply higher than their drug-induced increase in oxygen requirements in hypodynamic states of septic shock.