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Pharmacology of Vasopressin For Cardiac Arrest

Jimmy September 4, 2021

Early Years of Vasopressin

Vasopressin is an endogenous peptide vasopressor agent which vasopressin-secreting neurons in the hypothalamus normally release into the general circulation in large amounts when blood pressure falls. Vasopressin is also called antidiuretic hormone (ADH), arginine vasopressin (AVP), or argipressin. Oliver Kamm isolated and purified vasopressin in 1928.

In 1992, Lindner et al. noticed that in patients that in cardiac arrest that arginine vasopressin levels were significantly higher in the patients that survived compared to those that didn't.

-Lindner KH et al. Stress hormone response during and after cardiopulmonary resuscitation. Anesthesiology. 1992 Oct;77(4):662-8. PMID: 1329579.
  • Lindner et al stuudied this phenomonon again in 1996 and found that in patients succesfully resusicitated compared to those who failed resusicitation had 3 times the concentration of aginen vasopressin.

Early Studies of Vasopressin in Cardiac Arrest

  • Karl Lindner published a study in 1993 looking at the use of vasopressin in cardiac arrest models in pigs, wihch reported improved outcomes compared epinpehrine.
  • Lindner et published the first case series using vasopressin in cardiac arrest in 1996
    • Study results display that in 8 patients, vasopressin administration led to return of spontaneous circulation all patients and discharge from hospital with intact neurological function in 3 patients.
  • In 1998, Wenzel et al studied vasopressin as an adjunct to epinpephrine and monotherapy as a vasopressor for cardiopulmonary resuscitation (CPR) in pigs. In the study, vasopressin monotherapy was found to be comparable in left ventricular myocardiac blood floow but significantly increase cerebral perfusion compared to epinpenhrine with vasopressin.

Vasopressin and The ACLS Guidelines

Vasopressin was added to the AHA Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care in 2000.

Vasopressin is an effective and can be used as an alternative to epinpehrine in patients with shock-resistant ventricular fibrillation

2000 AHA Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

Vasopressin Removed From the ACLS Alorighthm

Vasopressin offers no advantage as a substitute for epinephrine in cardiac arrest (Class IIb, LOE B-R). The removal of vasopressin has been noted in the Adult Cardiac Arrest Algorithm

2015 AHA Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

Rationale For Vasopressin

  • Vasopressin dilates cerebral blood vessels to a greater extent than epinephrine, it has a longer half-life, and its effect is not diminished by acidosis, common in prolonged cardiac arrest compared to epinephrine.
    • All of these pharmacologic effects makes vasopressin an ideal candidate for blood pressure augmentation in cardiac arrest

  • Vasopressin

    Vasopressin Mechanism of Action

    • Vasopressin causes vasoconstriction of skin, skeletal muscle, and splanchnic circulation, thus increasing peripheral arterial resistance via V1 receptors and increases smooth muscle responsiveness to catecholamines.
      • Vasopressin activated V2 receptors which are located within the distal convoluted tubule of the kidney and regulates water resorption.
    • Vasopressin does not impact the heart directly, therefore there’s no chronotropic nor inotropic effects on the heart and is not associated with myocardial ischemia, myocardial dysfunction, or arrhythmias.

Vasopressin Dose

  • 20-40 international units IV
    • Most studies utilized 40 units except for one conducted by Mentzelopoulos SD, et al which used 20 units in additonal to steroids and epinephrine saw a mortality and neurological benefit.


  • Onset
    • 5-15 minutes
  • Duration
    • 15-30 minutes
  • Metabolism
    • metabolized by vasopressinases which are found in the liver and kidney.
  • Excretion
    • 5% as unchanged drug
  • Half Life:
    •  10-35 minutes