# Negative end-expiratory versus zero end-expiratory pressure flow-controlled ventilation in a porcine hemorrhagic shock model

## TL;DR

Using negative end-expiratory pressure in ventilation during pig hemorrhagic shock improves blood pressure but not heart function, with no impact on gas exchange.

## Contribution

Shows that negative end-expiratory pressure improves mean arterial pressure during hemorrhagic shock compared to zero end-expiratory pressure.

## Key findings

- Negative end-expiratory pressure improved mean arterial pressure in the first 15 minutes of fluid resuscitation.
- Gas exchange performance was similar between negative and zero end-expiratory pressure groups.
- Lung compliance decreased with negative end-expiratory pressure but without differences in gas exchange.

## Abstract

•Hemodynamics during hemorrhagic shock are impaired by positive pressure ventilation.•Negative compared to zero end-expiratory pressure improves mean arterial pressure.•This only applies to the hypovolemic state and diminishes during fluid resuscitation.•Gas exchange is thereby not significantly impaired.

Hemodynamics during hemorrhagic shock are impaired by positive pressure ventilation.

Negative compared to zero end-expiratory pressure improves mean arterial pressure.

This only applies to the hypovolemic state and diminishes during fluid resuscitation.

Gas exchange is thereby not significantly impaired.

Hemorrhagic shock is a life-threatening event whereby low flow may lead to end-organ dysfunction. This is aggravated by mechanical ventilation, where a positive intrathoracic pressure further deteriorates venous filling of the heart. The aim of this study was to evaluate the effects of a mild negative end-expiratory pressure (NEEP) on mean arterial pressure compared to zero end-expiratory pressure (ZEEP) in a porcine hemorrhagic shock model.

In anesthetized pigs, hemorrhagic shock was induced by a standardized lesion in the common femoral artery. After achieving half of baseline arterial pressure, hemorrhage was stopped. Ventilation was then switched to either flow-controlled ventilation with ZEEP (0 cmH2O, n = 6) or NEEP (−5 cmH2O, n = 6). After 5 min, fluid resuscitation was initiated (30 ml/kg) over 60 min and the observation period ended after 120 min.

The primary outcome parameter mean arterial pressure was significantly improved within the first 15 min with NEEP compared to ZEEP (49 vs 40 mmHg, MD 9 (95% CI 2 to 15); p = 0.031), but this effect diminished throughout fluid resuscitation. The cardiac index was similar in both groups. Evaluation of lung mechanics revealed a decrease in dynamic compliance (29 vs 44 ml/cmH2O, MD −14 (95% CI −20 to −9); p < 0.001) in the NEEP group without differences in gas exchange.

Application of −5 cmH2O NEEP improved mean arterial pressure but not cardiac index during hemorrhagic shock and the first 15 min of fluid resuscitation compared to ZEEP. Thereby gas exchange performance was similar.