Cardiopulmonary Response to Shock
Abstract
A major hypothesis that clinical events such as endotoxemia and ischemia which could lead to shock stimulate platelet and white blood cell (WBC) secretions which modify cardiopulmonary function has undergone further scrutiny. Particular attention has been paid to the role of arachidonic acid derivatives. Several common events have been found which simulate the production of Tx such as exposure of blood to foreign surfaces, positive end-expiratory pressure ventilation and pulmonary embolism. The release of TxA sub 2 is associated with the formation of a circulating substance which causes a decrease in contractility and abnormalities in myocardial ATPase. Prostacyclin (PGI sub 2) has been found to be produced in large quantity following surgical trauma. Under these circumstances, endogenous PGI sub 2 which is formed, increases cardiac output and dilates the systemic vasculate. An infusion of PGI sub 2 in an experimental setting of severe cardiac depression induced by endotoxemia leads to rapid improvement of cardiac function. PGI sub 2 also has adverse effects and may paradoxically stimulate the production of TxA sub 2 in settings where blood is exposed to an artificial surface. The problem of permeability in shock states is documented and has been studied in several experimental preparations. It has been found that TxA sub 2 is centrally involved in the edema of acid aspiration, complement activation and burns. Leukotrienes are also of importance in the biochemical sequence which leads to capillary damage. The vasoactive agent serotonin (5HT) has been evaluated as a potential culprit in the induction of respiratory failure without pulmonary edema.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 30, 1982
- Accession Number
- ADA176625
Entities
People
- Herbert B. Hechtman
Organizations
- Harvard University