Efficacy of vasopressin on systemic hemodynamics in catecholamine-resistant septic and postcardiotomy shock have been studied and published first in 2001[8] Later, the group concluded the ischemic skin lesions (ISL) developed in patients with catecholamine-resistant vasodilatory shock have multi-factorial cause and shall not necessarily been seen a side effect of AVP solely.

The presence of septic shock and a history of peripheral arterial occlusive disease are independent risk factors for the development of ISL.

[9] In the last decade, in early hyperdynamic septic shock, the administration of high-dose AVP as a single agent proved to fail to increase mean arterial pressure in the first hour but maintains it above 70mmHg in two-thirds of patients at 48h.

AVP decreases NE exposure, has no effect on the PrCO(2) - PaCO(2 )difference, and improves renal function and SOFA score.

[13] Modern interest in vasopressors as a treatment for cardiac arrest stem mostly from canine studies performed in the 1960s by anesthesiologists Dr. John W. Pearson and Dr. Joseph Stafford Redding in which they demonstrated improved outcomes with the use of adjunct intracardiac epinephrine injection during resuscitation attempts after induced cardiac arrest.

[18] This idea has led to the advent of several studies searching for the presence of a clinical difference in benefit of these two treatment choices.

Several randomized controlled trials have been unable to reproduce positive results with vasopressin treatment in both return of spontaneous circulation (ROSC) and survival to hospital discharge,[19][20][21][22] including a systematic review and meta-analysis completed in 2005 that found no evidence of a significant difference with vasopressin in five studied outcomes.

[17] There is no current evidence of significant survival benefit with improved neurological outcomes in patients given combinations of both epinephrine and vasopressin during cardiac arrest.

[22][24] A more recently published clinical trial out of Singapore has shown similar results, finding combination treatment to only improve the rate of survival to hospital admission, especially in the subgroup analysis of patients with longer "collapse to emergency department" arrival times of 15 to 45 minutes.

Copeptin, a more stable and easily measured product of pro-AVP processing, may be a means of identifying patients with low endogenous vasopressin concentrations.