The effect of Ventricular Assist Devices on cerebral autoregulation: A preliminary study
1 Department of Intensive Care, Royal Brisbane and Women's Hospital. Butterfield Street, Herston (4029), QLD, Australia
2 Critical Care Research Group and Department of Intensive Care Medicine, The Prince Charles Hospital and University of Queensland, Rode road, Brisbane, (4032), QLD, Australia
3 Biomedical Systems Laboratory, School of Electrical Engineering and Telecommunications, University of New South Wales, Sydney, NSW, 2052, Australia
4 Cardiovascular Systems Laboratory, Department of Surgery and Anesthesia, University of Otago, 23 A Mein Street, Newtown, PO Box 7343, Wellington, New Zealand
5 Department of Human Kinetics, Faculty of Health and Social Development, University of British Columbia Okanagan, Kelowna, Canada
6 Institute of Health and Biomedical Innovation & School of Public Health, Queensland University of Technology, 60 Musk Avenue, Brisbane, (4059), Australia
7 Critical Care Research Group, The Prince Charles Hospital. Medical Engineering Research Facility, Queensland University of Technology, Australia
BMC Anesthesiology 2011, 11:4 doi:10.1186/1471-2253-11-4Published: 22 February 2011
The insertion of Ventricular Assist Devices is a common strategy for cardiovascular support in patients with refractory cardiogenic shock. This study sought to determine the impact of ventricular assist devices on the dynamic relationship between arterial blood pressure and cerebral blood flow velocity.
A sample of 5 patients supported with a pulsatile ventricular assist device was compared with 5 control patients. Controls were matched for age, co-morbidities, current diagnosis and cardiac output state, to cases. Beat-to-beat recordings of mean arterial pressure and cerebral blood flow velocity, using transcranial Doppler were obtained. Transfer function analysis was performed on the lowpass filtered pressure and flow signals, to assess gain, phase and coherence of the relationship between mean arterial blood pressure and cerebral blood flow velocity. These parameters were derived from the very low frequency (0.02-0.07 Hz), low frequency (0.07-0.2 Hz) and high frequency (0.2-0.35 Hz).
No significant difference was found in gain and phase values between the two groups, but the low frequency coherence was significantly higher in cases compared with controls (mean ± SD: 0.65 ± 0.16 vs 0.38 ± 0.19, P = 0.04). The two cases with highest coherence (~0.8) also had much higher spectral power in mean arterial blood pressure.
Pulsatile ventricular assist devices affect the coherence but not the gain or phase of the cerebral pressure-flow relationship in the low frequency range; thus whether there was any significant disruption of cerebral autoregulation mechanism was not exactly clear. The augmentation of input pressure fluctuations might contribute in part to the higher coherence observed.