Intraabdominal Pressure

The IAP is the pressure generated inside the abdomen and depends on the status of diaphragm, the abdominal wall, and the viscera [17]. The abdomen and its contents should be considered as non-compressive and primarily fluid, that follow Pascal's law. The normal pressure in humans is between 5-15 cmH2O. The two most common methods to measure the IAP are direct measurement of the gastric pressure and the measurement of bladder pressure [18]. The bladder pressure is usually measured by inflating the bladder through a bladder catheter with 50-200 ml of saline [17]. However, in the presence of bladder trauma, pelvic hematoma or in cases of low bladder compliance, the bladder pressure is not a reliable indicator ofthe IAP and the gastric pressure is better [19].

An increase in IAP can occur in the presence of hemorrhage, ascites, bowel edema, orexternal compression [17]. The incidence of an increase in the IAP (above 15 cmH2O) varies according to the underlying diseases but seems to be around 30 % in the surgical intensive care population [20].

The most important side effects of an elevated IAP are on: 1) respiratory mechanics and gas exchange; 2) hemodynamics and; 3) edema formation

Respiratory Mechanics and Gas Exchange

The increase in IAP increases the gravitational gradient of pleural pressure especially in the dependent lung regions, inducing an increase in the volume of airway closure, and a decrease in the FRC, with possible risk of compressive atelectasis due to the upward push of the diaphragm to the lung. Mutho et al. evaluated the effect of abdominal distension on the lung and chest wall mechanics in anesthetized pigs [21]. The abdominal distension caused a rightward and downward shift of the pressure volume curve (PV curve) of the respiratory system and the chest wall by a stiffening of the diaphragm/abdomen and by a reduction in lung expansion. Similarly Ranieri et al. found that surgical ARDS patients presented a rightward shift of the thoracic and abdominal PV curves compared to medical ARDS patients, related to abdominal distension [22]. When these patients underwent abdominal decompression, the PV curve of the thorax and abdomen moved upward and leftward.

Our group showed that ARDSexp, due to intraabdominal pathologic conditions, presented a higher IAP compared to ARDSp [14]. We found a direct correlation between the IAP and the chest wall elastance, i.e., patients with a higher IAP have a higher chest wall elastance which reflected the increase stiffness of the thoracic rib cage.

We analyzedthe sonographic findings ofthe abdomen in normal spontaneously breathing subjects, in patients with ARDSexp due to abdominal sepsis, and in patients with ARDSp due to community acquired pneumonia [23]. In the normal subjects it was difficult to recognize the abdominal wall and the gut anatomical structure. In the patients with ARDSexp and with related abdominal problems, the increased dimension and thickness of the gut due to intraluminal debris and fluid and also with reduced peristaltic movements were visible. In the patients with ARDSp, the dimensions of the gut were slightly increased while the gut wall thickness was not increased, without any consistent debris or fluid.

These findings, thus, suggest that in ARDS the increase in respiratory system elastance may be produced by two different mechanisms: in ARDSp a high lung elastance is the major component, whereas in ARDSexp the lung and the chest wall elastance equally contribute to the increase in the respiratory system elastance.

Abdominal distension can also impair gas exchange. Mure et al., evaluating the effects of abdominal distension in anesthetized pigs, found that animals with abdominal distension presented a lower arterial oxygenation, higher ventilation/perfusion (V/Q) heterogeneity and dead space compared to normal animals [24].

We performed a prospective observational multicenter Italian study on IAP in critically ill patients [17]. The IAP was significantly increased in intubated compared to non-intubated patients (14.6±6 vs 12.3±7 cmH2O). Considering three ranges of IAP: patients with IAP < 10 cmH2O, patients with IAP between 10 and 20 cmH2O and patients > 20 cmH2O, the PaO2/FiO2 significantly decreased from 322±138 to 286±126 to 235±136 mm Hg while the PaCO2 did not change.


An elevated IAP may cause hypoperfusion, because the diaphragm is pushed upward transmitting the abdominal pressure to the heart and big vessels causing a decrease in cardiac output [17, 20, 24, 25]. Further, several studies have shown a reduction in renal blood flow with consequent increase in serum creatinine due to a direct compression of renal parenchyma or to a compression of renal veins when the IAP was increased [17, 20, 26, 27].

The intracardiac pressures (central venous or wedge pressure) used as an estimation of the preload, could be falsely elevated in the presence of an elevated IAP [17,20]. Consequently, for a correct evaluation ofthe preload, the intracardiac pressures should be measured against the intrathoracic pressure and not, as is usually done, against the atmospheric pressure [17, 20]. In such situations the estimation of the preload by the volume indexes should be more accurate.

Edema Formation

Recently we investigated the impact of changes in IAP due to pneumoperitoneum, in healthy animals and in an oleic acid animal model by CT scan analysis (Luecke T, et al, unpublished data). In the healthy group, an IAP of 20 cmH2O significantly decreased the gas volume compared to IAP of 0 cmH2O. In the oleic acid group at IAP of 0 cmH2O the gas volume was lower and despite the edema formation the total lung volume decreased compared to the healthy lung group. This may suggest that the edema increase did not fully compensate for the reduction in gas volume. On raising the IAP to 20 cmH2O, the tissue increased by almost threefold. The edema formation at the highest IAP was due to concomitant effects: 1) an increase in the central venous pressure, 2) a blood shift from the abdomen to the thorax, and 3) a reduction of edema clearance due to the increase in the pleural pressure.

These data clearly stress the importance of measuring IAP at the bedside in critically ill patients as an invaluable tool to optimize the clinical management.

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  • Selassie
    What are signs of increased intraabdominal pressure patient on ventilator?
    1 month ago

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