Effect of Vasopressin on Kidney and Cardiac Function in Septic Shock

Septic shock is a syndrome characterized by tissue hypoperfusion and hypotension secondary to an uncontrolled infection. It is a frequent cause of admission to the intensive care unit (ICU) and has an associated mortality around 40%. Around 50 % of septic shock patients exhibit early acute kidney injury and 30 to 40% will require renal replacement therapy. After initial fluid resuscitation most of the patients with septic shock become hyperdynamic but still require norepinephrine (NE) to maintain a mean arterial pressure (MAP) above 65 mmHg. The optimal perfusion pressure may vary, specially in previously hypertensive patients as they may have a shift to the right in their kidney auto-regulatory curve. In a previous study in patients with chronic hypertension and septic shock, increasing MAP from 65 mmHg to 85 mmHg with NE was associated with improved renal function. However, the incidence of tachyarrhythmias increased, associated to the higher NE doses required, which has raised some concerns about the safety of this strategy. In this setting, the addition of vasopressin (AVP), a drug used as a vasopressor but with cathecholamine independent mechanisms, may allow to prevent this side effect by decreasing NE dose requirements. Low doses of AVP appear to be safe and when combined with NE in septic shock patients, it resulted in increased creatinine clearance and decreased use of renal replacement therapy, compared to NE alone. Theoretically, AVP can improve glomerular filtration rate. Therefore, the addition of AVP to NE in previously hypertensive septic shock patients should be a reasonable strategy to improve organ perfusion. Furthermore, AVP could be an important step towards decatecholaminization in the management of septic shock patients. However, its effect on cardiac performance and stroke volume when targeting high MAP is unclear.