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Matching positive end-expiratory pressure to intra-abdominal pressure improves oxygenation in a porcine sick lung model of intra-abdominal hypertension

Adrian Regli123*, Rohan Mahendran1, Edward T Fysh24, Brigit Roberts4, Bill Noffsinger5, Bart L De Keulenaer1, Bhajan Singh5 and Peter V van Heerden246

Author Affiliations

1 Intensive Care Unit, Fremantle Hospital, Alma Street, Fremantle 6160, Australia

2 School of Medicine and Pharmacology, The University of Western Australia, 35 Stirling Highway, 6009 Crawley, Australia

3 Medical School, The University of Notre Dame Australia, 19 Mouat Street, 6959 Fremantle, Australia

4 Intensive Care Unit, Sir Charles Gairdner Hospital, Hospital Avenue, 6009 Nedlands, Australia

5 Department of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital, Hospital Avenue, 6009 Nedlands, Australia

6 Medical Intensive Care Unit, Hadassah University Hospital, Ein Kerem, 91120 Jerusalem, Israel

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Critical Care 2012, 16:R208  doi:10.1186/cc11840


See related commentary by Pelosi and Vargas, http://ccforum.com/content/16/6/187

Published: 26 October 2012

Abstract

Introduction

Intra-abdominal hypertension (IAH) causes atelectasis, reduces lung volumes and increases respiratory system elastance. Positive end-expiratory pressure (PEEP) in the setting of IAH and healthy lungs improves lung volumes but not oxygenation. However, critically ill patients with IAH often suffer from acute lung injury (ALI). This study, therefore, examined the respiratory and cardiac effects of positive end-expiratory pressure in an animal model of IAH, with sick lungs.

Methods

Nine pigs were anesthetized and ventilated (48 +/- 6 kg). Lung injury was induced with oleic acid. Three levels of intra-abdominal pressure (baseline, 18, and 22 mmHg) were randomly generated. At each level of intra-abdominal pressure, three levels of PEEP were randomly applied: baseline (5 cmH2O), moderate (0.5 × intra-abdominal pressure), and high (1.0 × intra-abdominal pressure). We measured end-expiratory lung volumes, arterial oxygen levels, respiratory mechanics, and cardiac output 10 minutes after each new IAP and PEEP setting.

Results

At baseline PEEP, IAH (22 mmHg) decreased oxygen levels (-55%, P <0.001) and end-expiratory lung volumes (-45%, P = 0.007). At IAP of 22 mmHg, moderate and high PEEP increased oxygen levels (+60%, P = 0.04 and +162%, P <0.001) and end-expiratory lung volume (+44%, P = 0.02 and +279%, P <0.001) and high PEEP reduced cardiac output (-30%, P = 0.04). Shunt and dead-space fraction inversely correlated with oxygen levels and end-expiratory lung volumes. In the presence of IAH, lung, chest wall and respiratory system elastance increased. Subsequently, PEEP decreased respiratory system elastance by decreasing chest wall elastance.

Conclusions

In a porcine sick lung model of IAH, PEEP matched to intra-abdominal pressure led to increased lung volumes and oxygenation and decreased chest wall elastance shunt and dead-space fraction. High PEEP decreased cardiac output. The study shows that lung injury influences the effects of IAH and PEEP on oxygenation and respiratory mechanics. Our findings support the application of PEEP in the setting of acute lung injury and IAH.