Document Detail


Matching positive end-expiratory pressure to intra-abdominal pressure prevents end-expiratory lung volume decline in a pig model of intra-abdominal hypertension.
MedLine Citation:
PMID:  22488004     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
OBJECTIVE:: 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. DESIGN:: Experimental pig model of intra-abdominal hypertension. SETTING:: Large animal facility, University of Western Australia. SUBJECTS:: Nine anesthetized, nonparalyzed, and ventilated pigs (48 ± 7 kg). INTERVENTIONS:: 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: positive end-expiratory pressure = 5 cm H2O (baseline positive end-expiratory pressure), positive end-expiratory pressure = half intra-abdominal pressure (cm H2O) + 5 cm H2O (moderate positive end-expiratory pressure), and positive end-expiratory pressure = intra-abdominal pressure (cm H2O) (high positive end-expiratory pressure). MEASUREMENTS:: 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. MAIN RESULTS:: 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. CONCLUSIONS:: 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.
Authors:
Adrian Regli; Jakob Chakera; Bart L De Keulenaer; Brigit Roberts; Bill Noffsinger; Bhajan Singh; Peter van Heerden
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-4-6
Journal Detail:
Title:  Critical care medicine     Volume:  -     ISSN:  1530-0293     ISO Abbreviation:  -     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-4-10     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0355501     Medline TA:  Crit Care Med     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
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.
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