The "jaundiced heart": a possible explanation for postoperative shock in obstructive jaundice

Abstract

Patients with obstructive jaundice are susceptible to postoperative shock and kidney failure. The cause of these potentially fatal complications has not been fully clarified. The present study was designed to assess the role of myocardial dysfunction in the hemodynamic disturbance of obstructive jaundice. We studied the effect of isolated cholemia on left ventricular performance in five conscious dogs before and 2 weeks after choledochocaval anastomosis by using measurements of systolic time intervals (STIs) and maximal dp/dt. Mean left ventricular ejection tiem (LVET) decreased after cholemia from 159 +/- 2.8 msec to 139 +/- 2.6 msec (p less than 0.005), while mean preejection period (PEP) and mean PEP/LVET were increased from 41 +/- 8.5 msec to 87 +/- 14 msec (p less than 0.05) and from 0.39 +/- 0.06 to 0.62 +/- 0.1 (p less than 0.01), respectively. During cholemia, STIs were unchanged after intravenous administration of ouabain, whereas in the control period, there was shortening of mean PEP from 71 +/- 8.8 msec to 58 +/- 7.6 msec (p less than 0.05) and of Q-S2 from 257 +/- 12 msec to 235 +/- 14 msec (p less than 0.005) in response to ouabain. Maximal dp/dt decreased after choledochocaval anastomosis from 4543 +/- 593 mm Hg/sec to 3666 +/- 648 mm Hg/sec (p less than 0.025). We conclude that cholemia in the dog is clearly associated with impaired left ventricular performance. The present data also support a previously published in vitro study from our laboratory showing that cholemia blunts the myocardial contractile response to sympathomimetic agents. The cardiodepressor effect of cholemia may explain the increased tendency of patients with obstructive jaundice to postoperative shock and renal failure.