Is epinephrine contraindicated during cardiopulmonary resuscitation?

Area of Science:

• Cardiopulmonary Physiology
• Pharmacology
• Critical Care Medicine

Background:

• Pulmonary gas exchange impairment after epinephrine administration during cardiopulmonary resuscitation (CPR) is not well understood.
• Epinephrine's role in altering lung function during resuscitation requires further investigation.

Purpose of the Study:

• To investigate the effects of epinephrine on pulmonary gas exchange during experimental ventricular fibrillation and CPR.
• To compare the effects of epinephrine with methoxamine, a pressor agent lacking beta-adrenergic activity, on gas exchange during CPR.

Main Methods:

• Anesthetized swine underwent induced ventricular fibrillation and CPR.
• Infusion of inert gases was used to determine ventilation-perfusion (VA/Q) distributions via the multiple inert gas elimination technique.
• Measurements included cardiac output, blood pressure, pH, and arterial oxygen saturation following administration of saline, epinephrine, or methoxamine.

Main Results:

• Ventricular fibrillation and CPR significantly decreased cardiac output, blood pressure, and pH.
• Epinephrine administration led to a significant increase in intrapulmonary shunt (approximately 300% more than saline) and a marked reduction in arterial oxygen saturation (SaO2).
• Methoxamine increased diastolic blood pressure similarly to epinephrine but did not worsen intrapulmonary shunt or SaO2.

Conclusions:

• Epinephrine significantly increases intrapulmonary shunt and reduces SaO2 during CPR, likely by attenuating hypoxic pulmonary vasoconstriction due to its beta-adrenergic activity.
• Methoxamine is an effective pressor agent for CPR and does not cause the detrimental pulmonary gas exchange abnormalities seen with epinephrine.
• Consideration of methoxamine or similar agents instead of epinephrine for CPR is recommended to improve outcomes.