Cerebral perfusion, cardiac output, and arterial pressure in patients with fulminant hepatic failure.
OBJECTIVE
To evaluate whether changes in cardiac output influence cerebral perfusion directly. In fulminant hepatic failure, the circulation is characterized by wide variations in cardiac output and cerebral blood flow (CBF).


METHODS
A retrospective, interindividual analysis of CBF and cardiac output (part 1) and a prospective evaluation of cerebral perfusion, cardiac output, and arterial pressure during norepinephrine infusion (part 2).


METHODS
A four-bed specialist liver failure unit.


METHODS
Twenty patients with fulminant hepatic failure (median age, 43 yrs; range, 17-54; 13 women) maintained on mechanical ventilation (Paco2, 33 torr [4.40 kPa]; range, 26-36 torr [3.47-4.80 kPa) after development of hepatic encephalopathy, stages 3 to 4, had mean arterial pressure (MAP) and cardiac output determined by radial and pulmonary artery catheters. Cerebral perfusion was measured by the 133Xenon clearance technique (n = 8) and by transcranial Doppler sonography, which was used to measure mean flow velocity (Vmean). CBF and Vmean in patients with high cardiac output (>9 L/min) were compared with those with normal or low cardiac output. In the second part of the study, cerebral autoregulation was evaluated by concomitant measurement of Vmean, cardiac output, and MAP during norepinephrine infusion in nine patients.


RESULTS
Median cardiac output was 8.5 L/min (range, 3.2-17.3), CBF was 33 mL/100 g/min (12-77 g/min), and Vmean was 45 cm/sec (22-65 cm/sec). In patients with elevated cardiac output, MAP, Vmean, and CBF were similar compared with patients with normal cardiac output. Neither CBF nor Vmean correlated to cardiac output. During norepinephrine infusion, Vmean increased from 49 cm/sec (34-69 cm/sec) to 63 cm/sec (58-90 cm/sec; p < .05), as MAP increased from 75 mm Hg (54-105 mm Hg) to 97 mm Hg (90-128 mm Hg). On average, cardiac output remained unchanged at 5.7 L/min (range, 3.2-17.3), as it increased in five patients and decreased in four patients. The change in Vmean was related to MAP (r2 = .76; p < .01) but not to cardiac output (r2 = .01).


CONCLUSIONS
This study shows that CBF correlates to arterial pressure rather than to cardiac output in patients with fulminant hepatic failure. The presence of pressure-passive cerebral circulation stresses the importance of strict cardiovascular control in securing continuous and sufficient cerebral oxygenation and in avoiding the development of cerebral hyperemia and cerebral edema.
Larsen
F S
FS
Department of Hepatology, Rigshospitalet, University of Copenhagen, Denmark. stolze@post3.tele.de
Strauss
G
G
Knudsen
G M
GM
Herzog
T M
TM
Hansen
B A
BA
Secher
N H
NH
D000293:Adolescent; D000328:Adult; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006801:Humans; D017093:Liver Failure / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000008:administration & dosage; D011446:Prospective Studies; D011877:Radionuclide Imaging; D012189:Retrospective Studies; D013997:Time Factors; D017585:Ultrasonography, Doppler, Transcranial; D014662:Vasoconstrictor Agents / Q000008:administration & dosage; D014980:Xenon Radioisotopes
D014662:Vasoconstrictor Agents; D014980:Xenon Radioisotopes; D009638:Norepinephrine