Hemodynamic and respiratory alterations in an experimental abdominal compartment syndrome model
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Keywords

Abdominal Compartment Syndrome
Intra-Abdominal Pressure
Abdominal Perfusion Pressure
Hemodynamics
Lung Function
Critical Care
Research
Animal Experimentation

How to Cite

1.
Díaz R. F, Donoso F. A, Carvajal B. C, Salomón S. T, Torres G. MF, Erranz M. B, Cruces R. P. Hemodynamic and respiratory alterations in an experimental abdominal compartment syndrome model. Andes pediatr [Internet]. 2012 Oct. 9 [cited 2026 May 30];83(5):454-61. Available from: https://andespediatrica.cl/index.php/rchped/article/view/2890

Abstract

Introduction: Abdominal compartment syndrome (ACS) is a severe and under-reported condition among the pediatric population due to inadequate warning and recognition. It can be caused by medical and surgical reasons, resulting in a high mortality rate. 

Objective: To determine the magnitude of the initial hemodynamic and respiratory consequences triggered by the induction of ACS in an experimental model. 

Methods: The model consisted of twelve anesthetized pigs (4.8 ± 0.1 kg). The ACS was induced by instillation of colloid solution in the peritoneal cavity to obtain an intra-abdominal pressure (IAP) of 24.9 ± 0.6 mmHg. In basal conditions and after the ACS induction, a conventional hemodynamic monitoring and transpulmonary thermodilution were performed. At the same time, arterial blood gases and lung mechanics analysis were measured. 

Results: There was a reduction of cardiac output by 16% (5.19 ± 0.33 to 4.34 ± 0.28 l/min/m2, p = 0.01) and abdominal perfusion pressure by 20% (72.3 ± 3.2 to 57.3 ± 4.0 mmHg, p <0.001) without changes in heart rate, arterial or central venous pressure. In addition there was an approximately 50% worsening of respiratory system compliance (1.28 ± 0.09 to 0.62 ± 0.04 ml/cmH2O/kg, p = 0.002) associated with a significant increase in intrathoracic pressure and slight decrease in oxygenation. 

Discussion: In this experimental model, the early development of hemodynamic and pulmonary dysfunction could be observed. A reduction of cardiac output that was not detected by conventional monitoring and a substantial deterioration of lung mechanics, characteristic of restrictive disease, associated with mild alterations in gas exchange were reported. It is essential then to monitor the IAP in patients predisposed to develop ACS, especially in the case of organ dysfunction deterioration, as severe hypotension and hypoxemia are late signs of this complication.

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