Vasopressin is a naturally occurring hormone produced in the brain, also known as antidiuretic hormone (ADH). This hormone plays a role in regulating the body’s water balance and blood pressure through its effects on blood vessels and kidneys. Advanced Cardiovascular Life Support (ACLS) provides standardized, evidence-based protocols for healthcare professionals to manage cardiac arrest and other cardiovascular emergencies, aiming to improve patient outcomes. Vasopressin was once a component of these protocols, specifically for certain cardiac arrest scenarios.
Vasopressin’s Removal from ACLS Guidelines
Vasopressin was removed from the adult cardiac arrest algorithm in the 2015 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC). The decision to remove vasopressin stemmed from a thorough review of clinical evidence, including systematic reviews and randomized controlled trials. These studies consistently indicated that vasopressin, whether used alone or in combination with epinephrine, did not offer a significant advantage over epinephrine alone in improving patient outcomes. Specifically, there was no demonstrated improvement in survival to hospital discharge or neurological outcomes for patients receiving vasopressin during cardiac arrest. The absence of clear benefit, coupled with the desire to simplify the ACLS algorithm, led to its discontinuation as a recommended drug for adult cardiac arrest.
Current Vasopressor Recommendations in ACLS
In the current ACLS adult cardiac arrest algorithm, epinephrine is the sole recommended vasopressor. It is used for both non-shockable rhythms, such as asystole and pulseless electrical activity, and for shockable rhythms like ventricular fibrillation and pulseless ventricular tachycardia if initial defibrillation attempts are unsuccessful. Epinephrine works by stimulating alpha-adrenergic receptors, which causes vasoconstriction and increases systemic vascular resistance. This action helps to improve perfusion pressure to the heart and brain during resuscitation efforts. Epinephrine also has beta-adrenergic effects, increasing heart rate and contractility, which can enhance cardiac output.
The standard dose for epinephrine in adult cardiac arrest is 1 milligram administered intravenously (IV) or intraosseously (IO) every 3 to 5 minutes. Each dose should be followed by a 20 milliliter normal saline flush and elevation of the extremity where the medication was administered for 10 to 20 seconds. If IV or IO access is not available, epinephrine may be given via an endotracheal tube at a dose of 2 to 2.5 milligrams diluted in 10 milliliters of normal saline.