In the previous issue of Critical Care, Krebs and colleagues systematically studied the effects of intra-abdominal hypertension (IAH) inhibitor Ponatinib on cardiopulmonary function [1]. Such studies are very much needed for a number of reasons. Traditionally, trauma surgeons witnessed improvements in urinary output following laparatomy; but medical intensivists were slower to appreciate the importance of intra-abdominal pressure (IAP). IAH is highly prevalent, however, in both surgical and medical intensive care units [2], although the causes may differ. IAH may become an even greater issue in the medical intensive care unit with the obesity pandemic, since body mass index is the best independent predictor of IAP [2].Furthermore, several studies have shown that IAH has prognostic importance through effects on both intra-abdominal and intrathoracic organ function [3].

That is, increased IAP causes pleural pressure elevations that affect cardiopulmonary function [4]. Hepatic and renal compromise has been reported, presumably through compression of venules. We have previously observed patients with presumed hepatorenal syndrome (a diagnosis with ostensibly up to 100% mortality) who were markedly improved by lowering IAP via paracentesis, suggesting IAH as a cause for their renal failure [5]. In addition, marked elevations in intracranial pressure have been observed with increasing IAP, presumably through reductions in venous return from the head [6]. Beyond these end organ effects, elevations in IAP can also impact measurement of respiratory and hemodynamic parameters [7].

For example, the central venous pressure – typically measured with reference to atmosphere – can be elevated in patients with IAH. These elevated values of central venous pressure do not reflect excess preload, however, but instead reflect external compression of the right atrium (by elevated pleural pressure in the setting of IAH) that raises central venous pressure even with very little volume within the atrium. Based on the appreciation of the importance of IAP, there is now renewed interest in the measurement of intrathoracic pressure.How to incorporate these pressure measurements into clinical practice raises several issues. First, the use of esophageal pressure to estimate pleural pressure has been questioned [8], since elevated values were presumed to be an artifact of cardiac weight.

Sustained elevations in pleural Carfilzomib pressure would imply negative transpulmonary pressure (classically defined as airway opening pressure minus pleural pressure [9]), which some individuals have argued cannot occur. These negative values (pleural pressure in excess of the airway opening pressure) are routinely seen during forced exhalation, however, and are commonly observed with the development of atelectasis, airway closure, alveolar flooding and/or expiratory flow limitation [10].