Bench-to-bedside review: Vasopressin in the management of septic shock

James A Russell, James A Russell

Abstract

This review of vasopressin in septic shock differs from previous reviews by providing more information on the physiology and pathophysiology of vasopressin and vasopressin receptors, particularly because of recent interest in more specific AVPR1a agonists and new information from the Vasopressin and Septic Shock Trial (VASST), a randomized trial of vasopressin versus norepinephrine in septic shock. Relevant literature regarding vasopressin and other AVPR1a agonists was reviewed and synthesized. Vasopressin, a key stress hormone in response to hypotension, stimulates a family of receptors: AVPR1a, AVPR1b, AVPR2, oxytocin receptors and purinergic receptors. Rationales for use of vasopressin in septic shock are as follows: first, a deficiency of vasopressin in septic shock; second, low-dose vasopressin infusion improves blood pressure, decreases requirements for norepinephrine and improves renal function; and third, a recent randomized, controlled, concealed trial of vasopressin versus norepinephrine (VASST) suggests low-dose vasopressin may decrease mortality of less severe septic shock. Previous clinical studies of vasopressin in septic shock were small or not controlled. There was no difference in 28-day mortality between vasopressin-treated versus norepinephrine-treated patients (35% versus 39%, respectively) in VASST. There was potential benefit in the prospectively defined stratum of patients with less severe septic shock (5 to 14 μg/minute norepinephrine at randomization): vasopressin may have lowered mortality compared with norepinephrine (26% versus 36%, respectively, P = 0.04 within stratum). The result was robust: vasopressin also decreased mortality (compared with norepinephrine) if less severe septic shock was defined by the lowest quartile of arterial lactate or by use of one (versus more than one) vasopressor at baseline. Other investigators found greater hemodynamic effects of higher dose of vasopressin (0.06 units/minute) but also unique adverse effects (elevated liver enzymes and serum bilirubin). Use of higher dose vasopressin requires further evaluation of efficacy and safety. There are very few studies of interactions of therapies in critical care--or septic shock--and effects on mortality. Therefore, the interaction of vasopressin infusion, corticosteroid treatment and mortality of septic shock was evaluated in VASST. Low-dose vasopressin infusion plus corticosteroids significantly decreased 28-day mortality compared with corticosteroids plus norepinephrine (44% versus 35%, respectively, P = 0.03; P = 0.008 interaction statistic). Prospective randomized controlled trials would be necessary to confirm this interesting interaction. In conclusion, low-dose vasopressin may be effective in patients who have less severe septic shock already receiving norepinephrine (such as patients with modest norepinephrine infusion (5 to 15 μg/minute) or low serum lactate levels). The interaction of vasopressin infusion and corticosteroid treatment in septic shock requires further study.

Figures

Figure 1
Figure 1
Vasopressin occupies the AVPR1a receptor. Vasopressin (line and beads) occupies the AVPR1a receptor.
Figure 2
Figure 2
The hypothalamic pituitary axis and vasopressin. Provasopressin is synthesized in neurohypophyseal neurons of the paraventricular nuclei (PVN) and supraoptic nuclei (SON) of the hypothalamus. Provasopressin is transported along the supraoptic neurohypophyseal tract in neurosecretory granules to the posterior pituitary gland. Provasopressin is cleaved by enzymes to vasopressin during transport to the posterior pituitary gland. Hypotension and hyperosmolality stimulate release of stored vasopressin (immediate) and synthesis (delayed) of vasopressin. In response to hypotension, vasopressin is released into the systemic circulation and also into the pituitary portal capillaries, flows to the anterior pituitary, binds to the AVPR1b receptor of corticotrophs, and stimulates release of adrenocorticotropic hormone. MNPO, median pre-optic nucleus.
Figure 3
Figure 3
Plasma vasopressin levels in the Vasopressin and Septic Shock Trial. Plasma vasopressin levels in patients in the Vasopressin and Septic Shock Trial who were infused with vasopressin compared with norepinephrine. Plasma vasopressin levels over time in patients receiving a vasopressin infusion (n = 54, black squares), patients in the vasopressin group once vasopressin infusions had stopped (open squares), and patients in the norepinephrine group (n = 53, grey circles). Values are median and interquartile range (IQR).
Figure 4
Figure 4
Mean arterial pressure and heart rate in the Vasopressin and Septic Shock Trial. Comparison of (a) mean arterial pressure (MAP) and (b) heart rate in the norepinephrine group (grey circles) and in the vasopressin group (black squares) of the Vasopressin and Septic Shock Trial. Values are mean ± standard deviation (SD). Heart rate was significantly lower in the vasopressin group than in the norepinephrine group over the first 4 days (P < 0.001). There were no statistically significant differences between the norepinephrine and vasopressin groups in MAP.
Figure 5
Figure 5
Doses of norepinephrine infusions in the Vasopressin and Septic Shock Trial. Rates of total norepinephrine infusion (open-label and study drug) in the Vasopressin and Septic Shock Trial for the vasopressin-treated group (black squares) and for the norepinephrine-treated group (grey circles) amongst all patients who were treated with open-label norepinephrine at baseline. The rates of norepinephrine infusion were significantly lower in the vasopressin group than in the norepinephrine group over the first 4 days (P < 0.001). Values are median and interquartile range (IQR).
Figure 6
Figure 6
Survival curve for Vasopressin and Septic Shock Trial vasopressin-infused patients compared with norepinephrine-infused patients. Ninety-day Kaplan-Meier survival curves for all randomized and infused patients (P = 0.27 at day 28; P = 0.10 at day 90). Solid line, vasopressin-infused group; dotted line, norepinephrine-infused group. P values were calculated using the log-rank statistic.
Figure 7
Figure 7
Survival curve for patients with more severe and less severe septic shock. Ninety-day Kaplan-Meier survival curves for patients with more severe and less severe septic shock in the Vasopressin and Septic Shock Trial comparing vasopressin-infused patients with norepinephrine-infused patients within each stratum. (a) Patients in the more severe stratum (P = 0.77 at day 28 and P = 0.92 at day 90). (b) Patients in the less severe stratum (P = 0.05 at day 28 and P = 0.03 at day 90). Solid black line, vasopressin-treated group; dotted line, norepinephrine-treated group; vertical line, day 28. P values were calculated using the log-rank statistic.

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