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

Abstract

Objective: 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.

Design: Prospective, observational cohort study.

Setting: Emergency Department and general Intensive Care Unit in a city hospital.

Interventions: Basic and advanced life support.

Patients and participants: 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).

Measurements and results: 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.

Conclusions: 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.