Theoretical Analysis of the Relative Impact of Obesity on Hemodynamic Stability During Acute Hemorrhagic Shock

Background: Evidence suggests that morbid obesity may be an independent risk factor for adverse outcomes in patients with traumatic injuries. Objectives: In this study, a theoretic analysis using a derivation of the Guyton model of cardiovascular physiology examines the expected impact of obesity on hemodynamic changes in Mean Arterial Pressure (MAP) and Cardiac Output (CO) during Hemorrhagic Shock (HS). Patients and Methods: Computer simulation studies were used to predict the relative impact of increasing Body Mass Index (BMI) on global hemodynamic parameters during HS. The analytic procedure involved recreating physiologic conditions associated with changing BMI for a virtual subject in an In Silico environment. The model was validated for the known effect of a BMI of 30 on iliofemoral venous pressures. Then, the relative effect of changing BMI on the outcome of target cardiovascular parameters was examined during simulated acute loss of blood volume in class II hemorrhage. The percent changes in these parameters were compared between the virtual nonobese and obese subjects. Model parameter values are derived from known population distributions, producing simulation outputs that can be used in a deductive systems analysis assessment rather than traditional frequentist statistical methodologies. Results: In hemorrhage simulation, moderate increases in BMI were found to produce greater decreases in MAP and CO compared to the normal subject. During HS, the virtual obese subject had 42% and 44% greater falls in CO and MAP, respectively, compared to the nonobese subject. Systems analysis of the model revealed that an increase in resistance to venous return due to changes in intra-abdominal pressure resulting from obesity was the critical mechanism responsible for the differences. Conclusions: This study suggests that obese patients in HS may have a higher risk of hemodynamic instability compared to their nonobese counterparts primarily due to obesity-induced increases in intra-abdominal pressure resulting in reduced venous return.