The effect of vasopressin on gastric perfusion in catecholamine-dependent septic shock patients

Introduction

Vasopressin increases blood pressure and decreases catecholamine requirements in septic shock patients [1–3]. Few clinically relevant data are available on the effect of vasopressin on the splanchnic circulation.

Objective

To study the effect of continuous infusion of vasopressin on the splanchnic circulation in septic shock patients.

Design

Prospective clinical study.

Setting

Intensive care unit in a teaching hospital.

Patients

Eleven consecutive patients with documented septic shock who remained hypotensive despite norepinephrine infusion at a rate of ≥ 0.2 μg/kg per min.

Interventions

Insertion of a gastric tonometry catheter; continuous infusion of vasopressin 0.04 U/min during 4 hours.

Measurements and main results

P(g–a)CO₂ gap, blood pressure and cardiac index were recorded at baseline and after 15, 30, 60, 120 and 240 min.

The median P(g–a)CO₂ gap increased from 5 mmHg at baseline to 19 mmHg after 4 hours (P = 0.022; Fig. 1). Blood pressure (mean ± SD) increased from 61 ± 13 mmHg at baseline to 68 ± 9 mmHg after 4 hours (P = 0.055). No significant changes in cardiac index were noted (P = 0.978). There was a strong correlation between median plasma levels of vasopressin and the median P(g–a)CO₂ gap (r² = 0.98) as is shown in Fig. 2.

Figure 1

Median P(g–a)CO₂ gap (mmHg) with 25th and 75th percentiles.

Figure 2

Relationship between median plasma levels of vasopressin and median P(g–a)CO₂ gap.

Conclusions

In norepinephrine-dependent septic shock patients, continuous infusion of low-dose vasopressin results in a significant and dose-dependent increase of the P(g–a)CO₂ gap compatible with gastrointestinal hypoperfusion.