Authors

  1. Cutugno, Christine PhD, RN

Abstract

Two studies examine drug and fluid interventions by emergency personnel.

 

Article Content

Vasopressin and Epinephrine vs. Epinephrine Alone

This randomized and double-blind multicenter study, conducted in cooperation with the French Emergency Medical System, evaluated the effectiveness of vasopressin and epinephrine versus epinephrine alone in the resuscitation of patients experiencing out-of-hospital cardiac arrest.

 

Ambulance emergency medical technicians administered either vasopressin and epinephrine (n = 1,442) or epinephrine and saline (n = 1,452) to patients who suffered a cardiac arrest between May 1, 2004, and April 30, 2006. Patients were then evaluated for outcomes such as survival to hospital admission (primary) and return of spontaneous circulation, survival to hospital discharge, good neurologic recovery, and survival to one year (secondary). Neurologic recovery was evaluated on a scale of 1 (conscious and normal to near normal activity) to 5 (coma or brain death).

 

Researchers didn't find any statistically significant differences between the two groups, but noted that the incidence of ventricular fibrillation in this study population was much lower than that in previous studies. Since ventricular fibrillation is an indication for the use of vasopressin, its low incidence may have affected the study outcome.

 

The rate of survival to hospital admission in this study was similar to that in previous studies, and long-term survival without neurologic impairment was statistically better in the 17.3% of admitted patients treated immediately with hypothermia.

 

The 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care recommend that vasopressin be used instead of either the first or second dose of epinephrine for the resuscitation of cardiac arrest resulting from pulseless ventricular tachycardia and ventricular fibrillation.

 

Gueugniaud PY, et al. N Engl J Med 2008;359(1):21-30.

 

Hypertonic Resuscitation of Hypovolemic Shock

A significant number of patients who initially survive catastrophic trauma later succumb to nosocomial infections and progressive multiple organ failure, including acute respiratory distress syndrome (ARDS). Acute immune suppression often follows traumatic injury; this is thought to occur when hypovolemic shock causes "extensive activation" of the victim's inflammatory response. In a recent study, Bulger and colleagues attempted to mitigate the later effects of blunt trauma (and decrease the rate of ARDS) by administering a hypertonic saline-dextran solution to patients who suffered severe blunt trauma, in the hope that the increase in osmotic pressure would quickly restore intravascular volume and mitigate the severe immune response. Hypertonic fluids have the known benefit of decreasing the intracranial pressure resulting from concomitant head trauma.

 

The ideal fluid to resuscitate traumatic hypovolemic shock has been the subject of research for decades. In this study, a total of 209 victims of blunt trauma admitted to a level I trauma center between 2003 and 2005 were randomly assigned to receive either a 250-mL bolus of 7.5% hypertonic saline and 6% dextran 70 (HSD) or 250 mL of lactated Ringer's solution. Criteria for study admission included blunt trauma and a prehospital systolic blood pressure of less than 90 mmHg.

 

The study was stopped early when it became apparent that the HSD yielded no improvement over lactated Ringer's solution in the rate of ARDS. Although the results did not prove the efficacy of the HSD solution, they did suggest to the authors a need for further refinement of the inclusion criteria. A predetermined subset of patients receiving 10 units or more of blood (who are by definition at greater risk for ARDS) appeared to receive some benefit from HSD. A future multicenter study will examine the effects of HSD on patients with lower systolic blood pressures and those requiring surgery and multiple blood transfusions for their injuries.

 

Bulger EM, et al. Arch Surg 2008;143(2):139-48.