Two Case Studies of Cardiopulmonary Effects of Intra-abdominal Hypertension
ABSTRACT Intra-abdominal hypertension falsely elevates the pulmonary artery pressure. Volumetric pulmonary artery catheter monitoring is an optionfor estimating preload in this condition. Treatment of intra-abdominal hypertension begins with medical therapy but once abdominal compartment syndrome develops it requires decompressive laparotomy for definitive management. Pulmonary hypertension reduces cardiac function which may be improved with inotropes that simultaneously reduce pulmonary artery pressure. Oxygenation may be improved with elevated PEEP and FiO(2).
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ABSTRACT: Cardiovascular dysfunction and failure are commonly encountered in patients with intra-abdominal hypertension or abdominal compartment syndrome. Accurate assessment and optimization of preload, afterload, and contractility are essential to restoring end-organ perfusion and maximizing patient survival. Application of a goal-directed resuscitation strategy, including abdominal decompression, when indicated, improves cardiac function, reverses end-organ failure, and minimizes intra-abdominal hypertension-related patient morbidity and mortality.Surgical Clinics of North America 04/2012; 92(2):207-20, vii. DOI:10.1016/j.suc.2012.01.009 · 1.88 Impact Factor
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ABSTRACT: Abdominal compartment syndrome (ACS) and intra-abdominal hypertension (IAH) are increasingly recognized as potential complications in intensive care unit (ICU) patients. ACS and IAH affect all body systems, most notably the cardiac, respiratory, renal, and neurologic systems. ACS/IAH affects blood flow to various organs and plays a significant role in the prognosis of the patients. Recognition of ACS/IAH, its risk factors and clinical signs can reduce the morbidity and mortality associated. Moreover, knowledge of the pathophysiology may help rationalize the therapeutic approach. We start this article with a brief historic review on ACS/IAH. Then, we present the definitions concerning parameters necessary in understanding ACS/IAH. Finally, pathophysiology aspects of both phenomena are presented, prior to exploring the various facets of ACS/IAH management.Journal of Emergencies Trauma and Shock 04/2011; 4(2):279-91. DOI:10.4103/0974-2700.82224
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ABSTRACT: Increased intra-abdominal pressure (IAP) compromises cardiopulmonary function and visceral perfusion. Our goal was to characterize acute changes in these subsystems associated with operative abdominal decompression. A series of 11 consecutive injured patients monitored with a pulmonary artery catheter and nasogastric tonometer in whom operative decompression was performed. Indications for decompression included oliguria or progressive acidosis despite aggressive resuscitation in the presence of elevated IAP (>25 mm Hg). Studied hemodynamic variables included pulmonary artery occlusion pressure (PAOP), right ventricular end-diastolic volume index (RVEDVI), and cardiac index (CI). Pulmonary variables included shunt fraction (Qs/Qt) and dynamic compliance (Cdyn). Visceral perfusion was assessed using hourly urine output 4 hours before and after decompression (UOP) and gastric intramucosal pH (pHi). Mean values before and after decompression were compared using the paired t test. Linear regression and Fisher's z transformation were used to evaluate the relationships between RVEDVI, PAOP, CI, and IAP. IAP was transduced via bladder pressures. Significance was defined as p < 0.05. Data are expressed as means+/-SD. IAP decreased with decompression (49+/-11 to 19+/-6.8 mm Hg; p < 0.0001). RVEDVI improved independent of CI and correlated better (p < 0.01) with CI (r =0.49, p=0.04) than PAOP did (r=-0.36, p=0.09). PAOP correlated significantly with IAP (r=0.45, p=0.04). Decompression resulted in significant improvements in Qs/Qt, Cdyn, UOP, and pHi. Abdominal decompression in patients with increased IAP improves preload, pulmonary function, and visceral perfusion. Elevated IAP has important effects on PAOP, which makes the PAOP an unreliable index of preload in these patients.The Journal of trauma 03/1998; 44(3):440-5. DOI:10.1097/00005373-199803000-00002 · 2.96 Impact Factor