Hemodynamic function in acute pancreatitis

Abstract

Acute pancreatitis is often associated with impaired cardiovascular function. This study examined the systemic cardiovascular effect of acute pancreatitis induced by injection of autologous bile (0.5 ml/kg) into the canine pancreatic duct. After acute pancreatitis was induced, eight dogs were given no resuscitation (group 1, untreated pancreatitis), and lactated Ringer's solution was infused in 11 dogs (group II, treated pancreatitis) to maintain mean arterial pressure and pulmonary wedge pressure at control values. In the untreated pancreatitis group, mean arterial pressure, cardiac output, stroke volume, and stroke work values decreased (mean arterial pressure from 101 +/- 4 to 74 +/- 12 mm Hg, cardiac output from 118 +/- 7 to 56.2 +/- 1.1 ml/min/kg; stroke volume from 0.93 +/- 0.08 to 0.22 +/- 0.07 ml/beat/kg; p less than 0.05), whereas heart rate and peripheral resistance increased (heart rate from 125 +/- 7 to 185 +/- 10 beats/min, peripheral vascular resistance from 3130 +/- 410 to 4436 +/- 610 dynes/sec/cm5; p less than 0.05). Although coronary blood flow, endocardial-epicardial flow ratio, and myocardial oxygen delivery values decreased progressively in group I after induction of pancreatitis, these changes did not achieve statistical significance. All indices of cardiovascular function and coronary blood flow remained unchanged in group II. Neither dP/dt max, the maximal rate of left ventricular pressure increase, nor dP/dt at a developed pressure of 40 mm Hg (an index of myocardial contractility minimally affected by changes in preload and afterload) were depressed by bile-induced acute canine pancreatitis in either group. Our data indicate that the detrimental effects of acute pancreatitis on cardiovascular function are related solely to hypovolemia and reduced cardiac filling and not to humoral or reflex effects induced by the disease.