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Clinical Investigations in Critical Care |

The Effect of Vasopressin on Gastric Perfusion in Catecholamine-Dependent Patients in Septic Shock*

Frank M. P. van Haren; Frans W. Rozendaal; Johannes G. van der Hoeven
Author and Funding Information

*From the Department of Intensive Care Medicine (Drs. van Haren and Rozendaal), Jeroen Bosch Hospital, ‘s-Hertogenbosch; and Department of Intensive Care Medicine (Dr. van der Hoeven), University Medical Hospital St. Radboud, the Netherlands.

Correspondence to: Frank M. P. van Haren, MD, Department of Intensive Care Medicine, Jeroen Bosch Hospital, PO Box 90153, 5200 ME ‘s-Hertogenbosch, the Netherlands; e-mail: fvharen@planet.nl



Chest. 2003;124(6):2256-2260. doi:10.1378/chest.124.6.2256
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Published online

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

Design: Prospective clinical study.

Setting: ICU in a teaching hospital.

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

Interventions: Insertion of a gastric tonometry catheter, and continuous infusion of vasopressin 0.04 U/min during 4 h.

Measurements and main results: Difference between gastric and arterial CO2 partial pressure (P[g-a]CO2 gap), mean arterial pressure, and cardiac index were recorded at baseline and after 15 min, 30 min, 60 min, 120 min, and 240 min.

Results: The median P(g-a)CO2 gap increased from 5 mm Hg at baseline to 19 mm Hg after 4 h (p = 0.022). Mean arterial pressure increased from 61 ± 13 mm Hg at baseline to 68 ± 9 mm Hg after 4 h (p = 0.055). No significant changes in cardiac index were noted.

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

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