VASOPRESSIN CAN INCREASE CORONARY PERFUSION-PRESSURE DURING HUMAN CARDIOPULMONARY-RESUSCITATION

Objectives: To determine the hemodynamic effect of vasopressin on coro nary perfusion pressure (CPP) in prolonged human cardiac arrest. Metho ds: A prospective, open-label clinical trial of vasopressin during car diac resuscitation was performed. Ten patients presenting in cardiac a rrest initially received resuscitative measures by emergency physician s according to Advanced Cardiac Life Support (ACLS) guidelines. A cent ral venous catheter for fluid and drug administration and a femoral ar tery catheter for measurement of CPP (aortic minus right atrial relaxa tion phase pressures) were placed. When each patient was deemed nonsal vageable, 1.0 mg epinephrine was given and CPP was measured for 5 minu tes, followed by a dose of vasopressin (1.0 U/kg). CPP measurements we re continued for another 5 minutes. Results: The mean duration of card iac arrest (out-of-hospital interval plus duration of ED ACLS) was 39. 6 +/- 16.5 min. There was no improvement in CPP after 1.0 mg of epinep hrine. Vasopressin administration resulted in a significant increase o f CPP in 4 of the 10 patients. Patients responding to vasopressin had a mean increase in CPP of 28.2 +/- 16.4 mm Hg (range: 10-51.5), with t hese peak increases occurring at 15 seconds to 4 minutes after adminis tration. The increases in the vasopressin levels after administration did not differ between the responders and nonresponders. Conclusions: In this human model of prolonged cardiac arrest, 40% of the patients r eceiving vasopressin had a significant increase in CPP. This pilot stu dy suggests that investigation of earlier use of vasopressin as a ther apeutic alternative in the treatment of cardiac arrest is warranted.