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Cerebral perfusion, cardiac output, and arterial pressure in patients with fulminant hepatic failure
F S Larsen1, G Strauss, G M Knudsen
1Department of Hepatology, Rigshospitalet, University of Copenhagen, Denmark. stolze@post3.tele.de
Insights
In fulminant hepatic failure, cerebral blood flow (CBF) is linked to arterial pressure, not cardiac output. Maintaining strict cardiovascular control is vital for adequate cerebral oxygenation and preventing complications like cerebral edema.
Area of Science:
- Hepatology
- Neurology
- Critical Care Medicine
Background:
- Fulminant hepatic failure (FHF) presents circulatory instability with variable cardiac output and cerebral blood flow (CBF).
- Understanding the determinants of cerebral perfusion is crucial for managing FHF patients.
Purpose of the Study:
- To investigate the relationship between cardiac output and cerebral perfusion in patients with FHF.
- To assess the influence of arterial pressure on cerebral blood flow in this population.
Main Methods:
- A retrospective analysis of CBF and cardiac output was performed.
- A prospective study evaluated cerebral perfusion, cardiac output, and arterial pressure during norepinephrine infusion.
- Cerebral perfusion was measured using 133Xenon clearance and transcranial Doppler (TCD) for mean flow velocity (Vmean).
Main Results:
- Neither CBF nor Vmean correlated with cardiac output in FHF patients.
- Cerebral blood flow demonstrated a correlation with mean arterial pressure (MAP), not cardiac output.
- Norepinephrine infusion increased Vmean and MAP, with Vmean changes related to MAP, not cardiac output.
Conclusions:
- Cerebral blood flow in FHF is primarily pressure-dependent, not flow-dependent.
- Maintaining adequate arterial pressure is critical for ensuring sufficient cerebral oxygenation in FHF.
- Close cardiovascular management is essential to prevent cerebral hyperemia and edema in FHF.
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).
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 (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.
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 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).
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.
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