Groth, CG

Halgrimson, CG

Martineau, GL

Palmer, WM

Pappas, G

Penn, I

Starzl, TE

English

PubMed

D-Scholarship@Pitt

HEMODYNAMIC CHANGES IN CLINICAL ORTHOTOPIC LIVER TRANSPLANTATION GEORGE PAPPAS, M.D., \VILLIAM M. PALMER, M.D., GERARD L. MARTINEAU, M.D., CHARLES G. HALGRIMSON, M.D., ISRAEL PENN, M.D., F.A.C.S., CARL G. GROTH, M.D., AND THOMAS E. STARZL, M.D., F.A.C.S. SERIAL CHANGES were measured in the cardiohemodynamics of 7 pa-tients undergoing orthotopic liver transplantation, with the specific objective of determining the effects of simultaneously cross-clamping the portal vein and inferior vena cava before, during, and after the anhepatic phase. METHODS Cardiac output (with cardiogreen dye dilution), heart rate, stroke volume, mean arterial pressure, and central venous pressure (SVC) were measured': I) following induction of anesthesia while the ab-domen was being opened, 2) during mobilization of the recipient'S liver, 3) shortly following cross-clamping the inferior vena cava and portal vein (early anhepatic phase), 4) just prior to revascularization of the donor liver (late anhepatic phase), 5) one hr later, and, 6) sev-eral hours following transplantation with the recipient awake. Each patient suffered from cirrhosis, portal hypertension, and extensive venous collaterals. There were two children (ages 3Y2 and 3Y2 years) with biliary atresia; 3 adolescents (ages II, lSY2 and 16 years) with chronic aggressive hepatitis, \Vilson's disease and chronic aggressive hepatitis, respectively; and 2 adults (ages 47 and 47 years) with Laennec's cirrhosis. RESULTS Intermittent decreases in cardiac index, stroke volume, and ar-terial blood pressure were observed before the anhepatic phase apparently because of displac'ement of the native liver and partial From the Department of Surgery, University of Colorado School of !lJedicine, and the Denver Veterans Administration Hospital, Denver, Colorado. Supported by research grants from the Veterans Administration, grants RR-0005J and RR-00069 from the general clinical research centers program of the Division of Research Resources, National Institutes of Health, and grants £11-10176-01, AI· AM-08898, £1M-07772, GM-01686, HE-09110 of the U.S. Public Health Service. Reprint from Surgical Forum Vofume XXII, 1971 interruption of the venous return. These changes became pro-nounced during the ensuing 52 to 116 min of the anhepatic phase (average 71 min) with the cross-damping of the portal vein and in-ferior vena cava. The average maximum decrements wer.e 47'70 ± 15 (SD)'70 of cardiac index 4R~~ ± 26 (SD)'70 of stroke volume, and 19'70 ± 13 (SD)% of mean arterial blood pressure. The peripheral vascular resistance index increased by 95% ± 78 (SD)% whereas the heart rate increased by only 7% ± II (SD)'70. During the late anhepatic phase, the alterations in hemodynamics were less noticeable than at the beginning, probably due to an intentional overtrans-fusion of blood in anticipation of blood loss incurred during re-vascularization of the new organ. The central venous pressure (SVC) did not change significantly during the operation. The transfusion of blood was insufficient in one severely ill child (3 V2 years). The control cardiac index was only 1.3 LjminjM2 which fell to 0.7 Ljminj.wp during the anhepatic phase. After revascularization of the new liver in this patient, cardiac arrest occurred which was im-mediately reversed by external cardiac massage, adequate blood replacement, and administration of inotropic drugs. The alterations of hemodynamics noted during mobilization of the recipient's liver and during the anhepatic phase reverted to control levels shortly after revascularization of the new organ in this patient as well as in the other 6. SUMMARY In spite of pre-existing hepatic disease, portal hypertension, and extensive venous collaterals, significant cardiohemodynamic depres-sion occurred during the anhepatic phase of liver replacement. With simultaneous cross-clamping of the portal vein and inferior vena cava, there was a moderate reduction in arterial blood pressure and a minimal increase in the pulse rate, but the cardiac index and stroke index fell sharply along with a substantial increase in peripheral vascular resistance. These changes were promptly reversed with re-vascularization of the homograft. A highly significant pooling with consequent reduction of venous return during cross-damping of the great veins is offered as an explanation. The acute insult appeared to be well tolerated as previously reported (1), but the anhepatic period is potentially dangerous unless appropriate monitoring and therapy are provided at this critical intra-operative time. REFERENCE 1. Starzl TE (with assistance of Putnam CW): Experience in Hepatic Trans-plantation. Philadelphia, W.B. Saunders Company, 1969 

Hemodynamic changes in clinical orthotopic liver transplantation

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Hemodynamic changes in clinical orthotopic liver transplantation

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