Respiratory consequences of intra-abdominal hypertension

Intra-abdominal hypertension (IAH) is a common complication in critically ill patients that may lead to multiorgan failure and is associated to worse outcome. Respiratory failure is among the most important consequences of IAH and it is originated by different mechanisms, such as chest wall elastance increase, functional residual capacity reduction, compression atelectasis and lung edema formation through reduction in lymphatic drainage. Many experimental studies showed that total lung capacity and functional residual capacity can be decreased by 40% during abdominal hypertension, while respiratory system and chest wall pressure-volume curves can be significantly shifted downward and to the right. Moreover, the relationship between intra-abdominal volume and airway pressure has been found to be exponential, meaning that small increases in volume can translate in dramatic increases in pressure. Clinical studies confirmed relevant atelectasis in dependent lung regions during IAH, with significant reductions in functional residual capacity and compromised oxygenation. Moreover, sepsis-related capillary leak and fluid overload may aggravate IAH and respiratory failure, thus establishing a dangerous vicious circle. Respiratory management of patients with IAH is challenging and there is no univocal answer. The measurement of intra-abdominal pressure and esophageal pressure (as a surrogate of pleural pressure) may be useful in assessing the condition and guiding mechanical ventilation. Positive end-expiratory pressure (PEEP) must be carefully selected to counteract IAH-related diaphragm displacement, but too high PEEP levels are associated with hemodynamic failure. Continuous negative extra-abdominal pressure is a promising approach, but its clinical application needs more investigation.