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 flaw (CBF). Design: 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). Setting: A four-bed specialist liver failure unit. Patients and Interventions: Twenty patients with fulminant hepatic failure (median age, 43 yrs; range, 17-54; 13 women) maintained on mechanical Ventilation (Paco(2) 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 (133)Xenon clearance technique (n = 8) and by transcranial Doppler sonography, which was used to measure mean flow velocity (V-mean). CBF and V-mean 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 V-mean, cardiac output, and MBP during norepinephrine infusion in nine patients. Measurements and Main 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 V-mean was 45 cm/sec (22-65 cm/sec). In patients with elevated cardiac output, MAP, V-mean, and CBF were similar compared with patients with normal cardiac output. Neither CBF nor V-mean correlated to cardiac output. During norepinephrine infusion, V-mean increased from 49 cm/sec (34-69 cm/sec) to 63 cm/sec (58-90 cm/sec; p <.05), as MBP 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 V-mean was related to MAP (r(2) =.76; p <.01) but not to cardiac output (r(2) = .01). Conclusion: 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.