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

Adrian Regli,Rohan Mahendran,Bart L De Keulenaer,Brigit Roberts,Bill Noffsinger,Edward T Fysh,Peter V Van Heerden,Bhajan Singh

doi:10.1186/cc11840

Abstract

IntroductionIntra-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.MethodsNine 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.ResultsAt 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.ConclusionsIn 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.

Highlights

Intra-abdominal hypertension (IAH) causes atelectasis, reduces lung volumes and increases respiratory system elastance
In a porcine sick lung model of IAH, Positive end-expiratory pressure (PEEP) matched to intra-abdominal pressure led to increased lung volumes and oxygenation and decreased chest wall elastance shunt and dead-space fraction
After the generation of acute lung injury (ALI), the measured parameters including the P/F ratio, End-expiratory lung volume (EELV), cardiac output (CO), and Mean arterial blood pressure (MAP) remained stable over four hours in the two control animals

Summary

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. Critically ill patients with IAH often suffer from acute lung injury (ALI). This study, examined the respiratory and cardiac effects of positive end-expiratory pressure in an animal model of IAH, with sick lungs. IAH is associated with atelectasis and impaired lung function, resulting from a cephalad shift of the diaphragm [7,8,9,10]. IAH has been reported to reduce lung volumes and increase trans-diaphragmatic pressures, inspiratory airway pressures and chest wall elastance [8,10,11,12,13]. In injured lungs IAH can substantially impair oxygenation [8,15] that is probably due to an increase in pulmonary edema [8]

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