That is, we have observed normal respiratory system compliance in obesity, despite markedly shifted curves (baseline pleural pressure elevations but a normal slope) [10,12,13]. Both the slope and the pressure intercept of the pressure-volume curve are therefore needed to define the mechanical behavior of the respiratory system.Third, the transmission of IAP to the thorax may depend on the disease STI571 state and/or chronicity. As such, it is unknown whether acute elevations in IAP (as seen in trauma or surgical intensive care unit patients) would have the same impact on intrathoracic pressures as would chronic elevations (due to obesity or cirrhosis with ascites, for example), since diaphragm remodeling may occur over time [14].

Moreover, in nonparalyzed patients, ongoing diaphragmatic activity could attenuate pressure transmission from the abdomen to the thorax. Careful attention to these physiological issues is required when examining the clinical literature.In their study, Krebs and colleagues report minimal effect of IAP on respiratory function, gas exchange, and hemodynamic function. The findings are very interesting and somewhat surprising. The lack of observed effect of IAP on pleural pressure may reflect the relatively modest elevations in IAP. In addition, given that these IAH patients were primarily surgical and were relatively lean (by US standards), the findings may have been different in more obese patients with more marked and sustained elevations in abdominal (and thus pleural) pressure.

In addition, we are unclear as to whether ongoing diaphragmatic activity was present in this study – which may have increased the tension across the diaphragm and perhaps minimized the influence of IAP on pleural pressure.These results raise some important issues. For the clinician, the take-home message from the present paper might be that the correlation between IAP and pleural pressure is poor within the range studied, necessitating direct measurement of intrathoracic pressure if this value is required. Further work will be necessary to determine the utility of these measurements in influencing patient outcome, particularly in patients with acute respiratory distress syndrome [15,16]. In the Krebs and colleagues study population, more marked IAP elevations may be required to have an important clinical impact.

For the scientist, careful studies on diaphragm remodeling in the setting of obesity and critical illness would be of interest. In addition, regional variations in pleural pressure and their influences Anacetrapib on local pulmonary mechanics should be assessed. Finally, although cardiac weight has only a minor effect on esophageal pressure measurements in normal subjects [17], further validation of these techniques in critically ill patients would be of interest.