IAH and pulmonary mechanics:
The early effects of IAH on pulmonary function are largely mechanical. As intra-abdominal pressure increases, it pushes the diaphragms cephlad. This results in reduced intra-thoracic volume (reduced functional residual capacity, total lung capacity and residual volume), reduced chest wall compliance and increased intra-pleural pressure. Simultaneously there is alveolar collapse due to the smaller intra-thoracic space and the higher intra-thoracic pressure.[1] This leads to ventilation-perfusion mismatching, hypoxia, hypercarbia and respiratory acidosis. To maintain ventilation, airway pressures must be increased and high peak airway and plateau pressures are often generated. The combination of elevated intrathoracic pressure and hypoxic pulmonary vasoconstriction can lead to pulmonary hypertension.[2]

ACS and ARDS:
Elevated intra-abdominal pressure initially causes direct mechanical pulmonary problems as described above. However, as the pressure remains elevated and ischemic injury progresses, inflammatory mediators are released from the gut. These inflammatory mediators cause pulmonary capillary damage leading to interstitial edema and an ARDS like syndrome.[1]

The ARDS that evolves as the result of ACS is a combination of alveolar collapse, high intra-thoracic pressure and interstitial edema. Ventilatory strategies such as PEEP, inspiratory recruitment and prone positioning more effectively improve respiratory mechanics, alveolar recruitment and gas exchange in these patients than in those with direct pulmonary injury.[1]

Summary:
In summary, elevated intra-abdominal pressure causes direct mechanical effects on the lung, which result in reduced intra-thoracic volume and elevated intra-thoracic pressure. This results in reduced blood return to the heart and decreased cardiac output due to the pressure effect on preload. It also may result in hypoxia, hypercarbia, elevated peak inspiratory pressures and pulmonary barotrauma. Eventually, the ischemia that develops due to hypoxia and reduced cardiac output may cause inflammatory mediator release, which can cause an ARDS syndrome to occur.

1. Pelosi, P., et al., Pulmonary and extrapulmonary acute respiratory distress syndrome are different. Eur Respir J Suppl, 2003. 42: p. 48s-56s.
2. Hunter, J.D. and Z. Damani, Intra-abdominal hypertension and the abdominal compartment syndrome. Anaesthesia, 2004. 59(9): p. 899-907.