Edema is a common morbidity following cardiopulmonary bypass (CPB) and can result in injury to many organs, including the heart, lungs, and brain. Generalized edema is also common and can lead to increased post-operative hospital stay and other morbidities. Pediatric patients are more susceptible to post-CPB edema and the consequences are more severe for this population. Hemodilution and systemic inflammatory responses are two suspected causes of CPB-related edema; however, the mechanisms involved are far from understood. Also, the common strategies to improve edema have not been completely successful and there is a need for new strategies at maintaining a fluid balance of patients as close to physiological as possible, especially for pediatric patients. An integrative approach to understanding edema is necessary as the forces involved in fluid homeostasis are dynamic and interdependent. Therefore, this review will focus on the physiology of fluid homeostasis and the pathologies of fluid shifts during CPB which lead to general edema as well as tissue-specific edema.

Aged individuals have impaired diastolic relaxation–lusitropic function. Dobutamine, a selective B1-adrenergic agonist, is used to augment systolic cardiac function at the termination of cardiopulmonary bypass (CPB). However, our question is whether dobutamine will also enhance the lusitropic function in the aged individual. The myocyte mechanism for the rate of ventricular relaxation is dependent on the velocity of calcium removal from the myocyte contractile elements by sarcoplasmic reticulum (SR) Ca2+–ATPase (SERCA2a), which is regulated by an inhibitory protein, phospholamban (PLB). Ventricular tissues harvested from young (4 month) and aged (20 months) mice were analyzed to compare the protein levels of SERCA2a and PLB with immunoblot and gene expression for PLB with reverse-transcriptase-polymerase chain reaction. The molecular analyses were compared with in vivo left ventricular function in the young and old mice before and during an intravenous infusion of dobutamine (5 μg/kg/min). The SERCA2a levels were not different between the groups; however, there was a 2-fold increase in PLB in the aged group compared with the young group (p < .05). The gene expression for PLB was increased by 5-fold in the aged group compared with the young group (p < .01). There were significant differences between the young and aged groups related to the lusitropic parameters, tau (τ) and dP/dtmin, and dobutamine infusion increased these parameters in the aged group to that of the young group. This report supports the concept that altered PLB levels correspond with the respective lusitropic function and that dobutamine administration in the aged group increased lusitropic function that was comparable with the young group. Because the patient population requiring CPB is aging, these data suggest that the use of dobutamine at the terminal phase of CPB is warranted to increase systolic and diastolic function.