Myocardial depression during acute pancreatitis: fact or fiction?

Clinical and experimental evidence suggests that myocardial depression occurs during severe pancreatitis, but this evidence is derived from techniques that are not optimal for assessing myocardial contractility (e.g., rate of rise in ventricular pressure [dP/dt]). The slope of the left ventricular (LV) and systolic pressure dimension relationship (Ees), a better indicator of myocardial function, has not been measured in pancreatitis. Ten mongrel dogs underwent surgical instrumentation to monitor systemic arterial and LV pressure, cardiac output, LV dP/dt, and anterior LV wall thickness. End of systole was defined by the peak negative dP/dt. The end-systolic points used to calculate Ees were obtained by aortic and vena caval occlusion. After surgical recovery, pancreatitis was induced via cannulation of the pancreatic duct and injection of autologous bile (1 ml/kg) at 200 mm Hg perfusion pressure. All measurements were taken during a control period and daily after pancreatitis was induced. Pancreatitis was confirmed by a significant increase in serum amylase throughout the study and by autopsy finding of hemorrhagic necrosis. Ees was increased throughout the experimental protocol (1 to 7 days) (p less than 0.05). Myocardial performance as assessed by Ees was significantly increased and myocardial depression did not occur in untreated, conscious dogs with severe pancreatitis. Peak positive LV dP/dt was a poor index of contractility during pancreatitis since it decreased while myocardial contractility was increased. Cardiac depression in pancreatitis noted in other reports was likely due to decreased preload and not to intrinsic cardiac dysfunction.