Intra-abdominal hypertension is common in critically ill patients and is associated with increased morbidity and mortality. In a previous experimental study, positive end-expiratory pressures of up to 15 cm H2O did not prevent end-expiratory lung volume decline caused by intra-abdominal hypertension. Therefore, we examined the effect of matching positive end-expiratory pressure to the intra-abdominal pressure on cardio-respiratory parameters.
Experimental pig model of intra-abdominal hypertension.
Large animal facility, University of Western Australia.
Nine anesthetized, nonparalyzed, and ventilated pigs (48 ± 7 kg).
Four levels of intra-abdominal pressure (baseline, 12, 18, and 22 mm Hg) were generated in a randomized order by inflating an intra-abdominal balloon. At each level of intra-abdominal pressure, three levels of positive end-expiratory pressure were randomly applied with varying degrees of matching the corresponding intra-abdominal pressure: baseline positive end-expiratory pressure (= 5 cm H2O), moderate positive end-expiratory pressure (= half intra-abdominal pressure in cm H2O + 5 cm H2O), and high positive end-expiratory pressure (= intra-abdominal pressure in cm H2O).
We measured end-expiratory lung volume, arterial oxygen levels, respiratory mechanics, and cardiac output 5 mins after each new intra-abdominal pressure and positive end-expiratory pressure setting.
Intra-abdominal hypertension decreased end-expiratory lung volume and PaO2 (−49% [p < .001] and −8% [p < .05], respectively, at 22 mm Hg intra-abdominal pressure compared with baseline intra-abdominal pressure) but did not change cardiac output (p = .5). At each level of intra-abdominal pressure, moderate positive end-expiratory pressure increased end-expiratory lung volume (+119% [p < .001] at 22 mm Hg intra-abdominal pressure compared with 5 cm H2O positive end-expiratory pressure) while minimally decreasing cardiac output (−8%, p < .05). High positive end-expiratory pressure further increased end-expiratory lung volume (+233% [p < .001] at 22 mm Hg intra-abdominal pressure compared with 5 cm H2O positive end-expiratory pressure) but led to a greater decrease in cardiac output (−26%, p < .05). Neither moderate nor high positive end-expiratory pressure improved PaO2 (p = .7).
Intra-abdominal hypertension decreased end-expiratory transpulmonary pressure but did not alter end-inspiratory transpulmonary pressure. Intra-abdominal hypertension decreased total respiratory compliance through a decrease in chest wall compliance. Positive end-expiratory pressure decreased the respiratory compliance by reducing lung compliance.
In a pig model of intra-abdominal hypertension, positive end-expiratory pressure matched to intra-abdominal pressure led to a preservation of end-expiratory lung volume, but did not improve arterial oxygen tension and caused a reduction in cardiac output. Therefore, we do not recommend routine application of positive end-expiratory pressure matched to intra-abdominal pressure to prevent intra-abdominal pressure–induced end-expiratory lung volume decline in healthy lungs.
From the Intensive Care Unit (AR, JC, BR, PVvH), Sir Charles Gairdner Hospital, Perth, Western Australia, Australia; Intensive Care Unit (AR, BLDK), Fremantle Hospital, Fremantle, Western Australia, Australia; Medical School (AR), The University of Notre Dame Australia, Fremantle, Western Australia, Australia; Department of Pulmonary Physiology and Sleep Medicine (BN, BS), Sir Charles Gairdner Hospital, Perth, Western Australia, Australia; and School of Medicine and Pharmacology (PVvH), The University of Western Australia, Perth, Western Australia, Australia.
*See also p. 1988.
Drs. Regli, Chakera, Singh, and van Heerden participated in the design of the study. Dr. Regli, Dr. Chakera, Mrs. Roberts, and Mr. Noffsinger contributed to data collection. Dr. Regli performed the statistical analyses. Dr. Regli drafted the manuscript. Dr. Chakera, Mrs. Roberts, Dr. Singh, Dr. Keulenaer, and Dr. van Heerden revised the manuscript. All authors read and approved the final manuscript.
Bench work trials were performed at the Sir Charles Gairdner Hospital, Perth, Australia. The animal experimental work was performed at the Large Animal Facility of The University of Western Australia, Australia.
Data analysis was performed at Fremantle Hospital, Perth, Australia.
This study was entirely financed by Sir Charles Gairdner Hospital Intensive Care Research Funds. No public funding was used.
The authors have not disclosed any potential conflicts of interest.
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