Iii this study, 39 patients with blood culture-positive septic shock and a characteristic hyperdynamic hemodynamic profile were found to have biventricular cardiac dysfunction. This was characterized by depression of both the right and left ventricular ejection fractions with simultaneous dilatation of both ventricles. In the survivors, these abnormalities were severe at shock onset, but returned toward normal (for both ventricles) as the patients recovered. The septic shock-induced serial changes for the right ventricle usually paralleled those of the left ventricle, demonstrating that the myocardial depression and ventricular dilatation seen in humans with septic shock is a biventricular phenomenon. It is not clear why a small number of patients had changes in right ventricular size or function in a direction that was opposite the changes in left ventricular size or function. All of these patients were critically ill, and it is possible that a number of different factors acted together to produce different responses of the ventricles in individual patients.
In the nonsurvivors, the initial right and left ventricular ejection fractions were minimally depressed (not statistically significantly different from the survivors); there was no significant change in ventricular function or size in the nonsurvivors during their course, in contrast to the survivors.
The fact that septic shock produces both biventricular depression of function and biventricular dilatation has several potential clinical implications. Both right and left heart filling pressures and/or end-diastolic volume may be important in determining how much volume resuscitation a patient requires to optimize cardiac function. In some patients, the biventricular depression may progress, leading ultimately to an inadequate cardiac output and a cardiogenic shocklike state. Understanding the biventricular nature of myocardial depression in septic shock may help in formulating decisions regarding the use of vasopressors and/or inotropic agents. For example, in volume unresponsive patients with a persistently low systemic vascular resistance, vasopressors with potent vaso- constricting activity may be an appropriate choice, while patients with a falling cardiac output due to persistent myocardial depression may do better with administration of inotropic agents.
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The pulmonary artery mean pressure and pulmonary vascular resistance index did not correlate with the right ventricular ejection fraction in this study. This suggests that the depression of right ventricular ejection fraction in these patients is most likely related to septic shock and not to changes in pulmonary afterload on the right ventricle. However, the pulmonary vascular resistance index did correlate negatively with the right ventricular end-diastolic volume index in the survivors, but not in the nonsurvivors. The reason for this finding is not clear. In fact, pathophy- siologically one would expect the opposite correlation (a higher resistance producing a more dilated ventricle). Pulmonary hypertension has been reported to be common in experimental endotoxemia and also in the presence of sepsis and the adult respiratory distress syndrome. In the present series of patients, pulmonary hypertension was uncommon. In fact, there was no difference in any hemodynamic parameter, right ventricular size, or right ventricular function between those patients with respiratory failure (due to pneumonia or the adult respiratory distress syndrome) and those without significant pulmonary disease. In another recent study, pulmonary hypertension was not seen in a population of normal volunteers who received small doses of intravenous endotoxin. Animal models of endotoxin-induced shock or respiratory failure have clearly demonstrated a marked species variability in sensitivity to endotoxin. In humans, pulmonary hypertension has primarily been reported in association with severe respiratory failure. Reports of septic shock in humans without severe respiratory failure do not emphasize the presence of pulmonary hypertension. Pulmonary hypertension does not seem to be an essential part of the pathophysiology of septic shock in humans. It is likely, then, that the pulmonary pressures and pulmonary vascular resistance were not the major causal determinants of right ventricular size and function in this series of patients with septic shock.