OBJECTIVE: In patients affected by intra-abdominal hypertension, bladder or gastric pressure measurement may be usefully integrated by ultrasounds in order to detect early hemodynamic impairment. The purpose of this study was to search for changes in abdominal vein size and flow induced by intra-abdominal hypertension. DESIGN: Physiologic study. SETTING: Postoperative intensive care unit of a university hospital. SUBJECTS: Sixteen healthy volunteers. INTERVENTIONS: Four echographic assessments of vessel sizes and blood velocities were randomly performed in the following settings: 1) baseline, 2) intra-abdominal hypertension simulated by a tight pelvic stabilizer around the waist, 3) noninvasive ventilation with a facial mask, and 4) intra-abdominal hypertension plus noninvasive ventilation. MEASUREMENTS AND MAIN RESULTS: The model of intra-abdominal hypertension was validated in eight subjects by measuring gastric pressure. During intra-abdominal hypertension, 1) the inferior vena cava was compressed (significant decrease of both anteroposterior and lateral diameters) and deformed (decreased anteroposterior/lateral diameter ratio), and deformation, but not compression, was attenuated by noninvasive ventilation associated with intra-abdominal hypertension; 2) the portal vein was also compressed (decreased diameter); and 3) blood velocities did not change significantly in the inferior vena cava, portal vein, right suprahepatic vein, or right external iliac vein. In the receiver operating characteristic curve analysis, an inferior vena cava section area (normalized for body surface) of lower than 1 cm²/m² discriminated between intra-abdominal hypertension presence and absence with a sensitivity of 65.6% and a specificity of 87.5% (p = .0001). Noninvasive ventilation alone did not significantly affect vein sizes and velocities. The resistive index, calculated by pulse wave Doppler signal from segmental branches of the right renal artery, increased slightly, but significantly, during intra-abdominal hypertension alone, suggesting an increase of intrarenal pressure. CONCLUSIONS: Simulated intra-abdominal hypertension was associated with decreased inferior vena cava section area and increased resistive index in renal arteries. Further studies are now needed to investigate whether these changes may be of value to integrate bladder or gastric pressure measurement in clinical practice.
OBJECTIVE: In patients affected by intra-abdominal hypertension, bladder or gastric pressure measurement may be usefully integrated by ultrasounds in order to detect early hemodynamic impairment. The purpose of this study was to search for changes in abdominal vein size and flow induced by intra-abdominal hypertension. DESIGN: Physiologic study. SETTING: Postoperative intensive care unit of a university hospital. SUBJECTS: Sixteen healthy volunteers. INTERVENTIONS: Four echographic assessments of vessel sizes and blood velocities were randomly performed in the following settings: 1) baseline, 2) intra-abdominal hypertension simulated by a tight pelvic stabilizer around the waist, 3) noninvasive ventilation with a facial mask, and 4) intra-abdominal hypertension plus noninvasive ventilation. MEASUREMENTS AND MAIN RESULTS: The model of intra-abdominal hypertension was validated in eight subjects by measuring gastric pressure. During intra-abdominal hypertension, 1) the inferior vena cava was compressed (significant decrease of both anteroposterior and lateral diameters) and deformed (decreased anteroposterior/lateral diameter ratio), and deformation, but not compression, was attenuated by noninvasive ventilation associated with intra-abdominal hypertension; 2) the portal vein was also compressed (decreased diameter); and 3) blood velocities did not change significantly in the inferior vena cava, portal vein, right suprahepatic vein, or right external iliac vein. In the receiver operating characteristic curve analysis, an inferior vena cava section area (normalized for body surface) of lower than 1 cm²/m² discriminated between intra-abdominal hypertension presence and absence with a sensitivity of 65.6% and a specificity of 87.5% (p = .0001). Noninvasive ventilation alone did not significantly affect vein sizes and velocities. The resistive index, calculated by pulse wave Doppler signal from segmental branches of the right renal artery, increased slightly, but significantly, during intra-abdominal hypertension alone, suggesting an increase of intrarenal pressure. CONCLUSIONS: Simulated intra-abdominal hypertension was associated with decreased inferior vena cava section area and increased resistive index in renal arteries. Further studies are now needed to investigate whether these changes may be of value to integrate bladder or gastric pressure measurement in clinical practice.