Release of vasoactive hormones and circulatory changes in shock

Abstract

Circulatory shock mechanisms that may result in the acute renal failure (ARF) syndrome are summarized. Both circulatory and neurohumoral mechanisms leading to the shock state and ARF are emphasized. Release of vasoactive hormones, with a review of vasodilators and vasoconstrictors, is discussed in terms of release mechanisms, onset of release, magnitude and duration of plasma elevation, and the basal plasma level of each. Hemodynamic diagnoses in shock in both the classical low cardiac output and the early sepsis high cardiac output syndromes are commented upon with emphasis on the importance of early diagnosis and adequate measurements of the circulatory state for optimum therapy. The septic hyperdynamic syndrome is reviewed with particular regard to changes in the renal circulation and function. Mechanisms of lactic acidemia in the hyperdynamic syndrome in the presence of adequate nutrient tissue flow are discussed. Elevations of vasoactive hormones and their relationship to the early shock state are mentioned. Their elevations in late shock are reviewed with critical comments given as to the possible interactions and importance of the vasodilator and vasoconstrictor actions on organ function and survival. Blood pressure alone is not a good indicator of progress in the management of septic shock.