Abstract
ObjectiveTo investigate spontaneous variability in the time and frequency domain in mean flow velocity (MFV) and mean arterial pressure (MAP) in comatose patients after cardiac arrest, and determine possible differences between survivors and non-survivors. MethodsA prospective observational study was performed at the ICU of a tertiary care university hospital in the Netherlands. We studied 11 comatose patients and 10 controls. MFV in the middle cerebral artery was measured with simultaneously recording of MAP. Coefficient of variation (CV) was used as a standardized measure of dispersion in the time domain. In the frequency domain, the average spectral power of MAP and MFV were calculated in the very low, low and high frequency bands. ResultsIn survivors CV of MFV increased from 4.66 [3.92–6.28] to 7.52 [5.52–15.23] % at T=72h. In non-survivors CV of MFV decreased from 9.02 [1.70–9.36] to 1.97 [1.97–1.97] %. CV of MAP was low immediately after admission (1.46 [1.09–2.25] %) and remained low at 72h (3.05 [1.87–3.63] %) (p=0.13). There were no differences in CV of MAP between survivors and non-survivors (p=0.30). We noticed significant differences between survivors and non-survivors in the VLF band for average spectral power of MAP (p=0.03) and MFV (p=0.003), whereby the power of both MAP and MFV increased in survivors during admission, while remaining low in non-survivors. ConclusionsCerebral blood flow is altered after cardiac arrest, with decreased spontaneous fluctuations in non-survivors. Most likely, these changes are the consequence of impaired intrinsic myogenic vascular function and autonomic dysregulation.
Highlights
The incidence of post-anoxic encephalopathy after cardiac arrest is high, resulting in high mortality and morbidity.[1]
The spontaneous variability of MFVMCA was low after cardiac arrest
The average power in the VLF spectrum of the MFVMCA was low after cardiac arrest and restored towards normal values in survivors
Summary
The incidence of post-anoxic encephalopathy after cardiac arrest is high, resulting in high mortality and morbidity.[1] Crucial in the ICU treatment after cardiac arrest is to create an optimal environment, for cerebral recovery including adequate cerebral blood flow (CBF). CBF exhibits rapid spontaneous fluctuations, in order to maintain cerebrovascular homeostasis. The adaptation of CBF to perturbations in cerebral perfusion pressure is regulated by central control mechanisms[2,3] and by an intrinsic variation via myogenic vasoconstriction.[4,5]. J.M.D. van den Brule et al / Resuscitation 111 (2017) 110–115 dependent on pressure variability is a matter of debate in healthy subjects and yet unknown in patients after cardiac arrest.[10]
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