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. This led to development of a large trial to see theeffect of arginin vasopressin as add-on to norepinephrine in septic shock. It could be shown, if giving vasopressin in early stage of septic shock (norepinephrin < 15 microgramm/min and lactate < 1.4 mmol/L) there is a statistically significant interaction between vasopressin and corticosteroids. The combination of low-dose vasopressin and corticosteroids was associated with decreased 28 and 90 days mortality and organ dysfunction compared with norepinephrine and corticosteroids. 2018 Surviving Sepsis Campaign Guidelines The Surviving Sepsis Campaign guidelines recommend the very early management of the sepsis focusing on the hour-1 bundle. This includes use of Vasopressin 0.03 units/minute as add-on to norepinephrine (NE) with intent of either raising the mean arterial pressure or decreasing the norepinephrine dosage (i.e. de-catecholaminization). Cardiac arrest 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. Also contributing to the idea that vasopressors may be useful treatments in cardiac arrest are studies performed in the early to mid 1990s that found significantly higher levels of endogenous serum vasopressin in adults after successful resuscitation from out-of-hospital cardiac arrest compared to those who did not live. Results of animal models have supported the use of either vasopressin or epinephrine in cardiac arrest resuscitation attempts, showing improved coronary perfusion pressure and overall improvement in short-term survival as well as neurological outcomes. Vasopressin vs. epinephrine Although both vasopressors, vasopressin and epinephrine differ in that vasopressin does not have direct effects on cardiac contractility as epinephrine does. Thus, vasopressin is theorized to be of increased benefit over epinephrine in cardiac arrest due to its properties of not increasing myocardial and cerebral oxygen demands. 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. Initial small studies demonstrated improved outcomes with vasopressin in comparison to epinephrine. However,