Platelet activation with massive formation of thromboxane A2 during and after cardiopulmonary resuscitation.

Abstract

Hypoxia and ischemia cause endothelial cell damage with consequent platelet activation. The hypothesis that human cardiac arrest accelerates platelet activation and the formation of prostanoids was tested. Prospective, observational cohort study. Emergency Department and general Intensive Care Unit in a city hospital. Basic and advanced life support. Forty-seven out-of-hospital cardiac arrest patients. The patients were classified into two groups, those who were resuscitated (n = 18) and those who died (n = 29). Serial levels of platelet aggregation, thromboxane B2 (TXB2), 11-dehydro-TXB2 and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured. The results of measurements and demographic data were compared between the groups. Platelet counts decreased at the end of cardiopulmonary resuscitation (CPR), the decrease of the platelet counts showed statistical significance especially in the patients who died (p < 0.001). Platelet aggregation induced by adenosine diphosphate, epinephrine and collagen decreased to the lower limits of normal during and after CPR. Although high values of TXB2 and 11-dehydro-TXB2 continued throughout the study period in the resuscitated patients, 6-keto-PGF1 alpha decreased to the normal range (22.7 +/- 3.6 pg.ml-1. p < 0.05 at -24 h after arrival at the Emergency Department. Platelet activation with the massive formation of thromboxane A2 (TXA2) occurs in patients with out-of-hospital cardiac arrest. Successful resuscitation is not associated with the balanced production of PGI2 against the TXA2 formation.