Spontaneous oscillations of arterial blood pressure, cerebral and peripheral blood flow in healthy and comatose subjects

Abstract

Slow and rhythmic spontaneous oscillations of cerebral and peripheral blood flow occur within frequencies of 0.5-3 min-1 (0.008-0.05 Hz, B-waves) and 3-9 min-1 (0.05-0.15 Hz, M-waves). The generators and pathways of such oscillations are not fully understood. We compared the coefficient of variance (CoV), which serves as an indicator for the amplitude of oscillations and is calculated as the percent standard deviation of oscillations within a particular frequency band from the mean, to study the impairment of generators or pathways of such oscillations in normal subjects and comatose patients in a controlled fashion. With local ethic committee approval, data were collected from 19 healthy volunteers and nine comatose patients suffering from severe traumatic brain injury (n = 3), severe subarachnoid hemorrhage (n = 3), and intracerebral hemorrhage (n = 3). Cerebral blood flow velocities were measured by transcranial Doppler ultrasound (TCD), peripheral vasomotion by finger tip laser Doppler flowmetry (LDF), and ABP by either non-invasive continuous blood pressure recordings (Finapres method) in control subjects, or by direct radial artery recordings in comatose patients. Each recording session lasted approximately 20-30 min. Data were stored in the TCD device for offline analysis of CoV. For CoV in the cerebral B-wave frequency range there was no difference between coma patients and controls, however there was a highly significant reduction in the amplitude of peripheral B-wave LDF and ABP vasomotion (3.8 +/- 2.1 vs. 28.2 +/- 16.1 for LDF, p < 0.001; and 1.2 +/- 0.7 vs. 4.6 +/- 2.8 for ABP, p < 0.001). This observation was confirmed for spontaneous cerebral and peripheral oscillations in the M-wave frequency range. The CoV reduction in peripheral LDF and ABP oscillations suggest a severe impairment of the proposed sympathetic pathway in comatose patients. The preservation of central TCD oscillations argues in favor of different pathways and/or generators of cerebral and peripheral B- and M-waves.

Effects of positive end-expiratory pressure on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation*

“…Patients suffering from severe SAH present with systemic and cardiovascular problems that might cause unforeseen hemodynamic effects like a systemic vasoregulatory disorder. This is in line with a previous publication suggesting that the sympathetic pathway is impaired in this group (18). In contrast, a deterioration of the hemodynamic variables with the application of PEEP was not detected in animals.…”

Spinal CSF absorption in healthy individuals

“…The physiological mechanisms behind B-waves are still obscure (1,15,29). Originally, Lundberg (32) proposed that B-waves persisting for a long period probably always could be regarded as a sign of cerebral dysfunction, even though some of the recorded patients had a ICP Ͻ11 mmHg.…”

Short pressure reactivity index versus long pressure reactivity index in the management of traumatic brain injury

“…6,11 They can be categorized into two groups: 1) the B waves that occur at approximately 0.5-3 cycles per minute, which corresponds to a frequency of 0.008-0.05 Hz;5,16,23 and 2) M waves, which occur at approximately 4-9 cycles per minute, which corresponds to a frequency of 0.07-0.15 Hz. 7,12,22 The 6 ventiabbreviatioNs ABP = arterial blood pressure; CPPopt = optimal cerebral perfusion pressure; GCS = Glasgow Coma Scale; GOS = Glasgow Outcome Scale; ICP = intracranial pressure; IQR = interquartile range; L-PRx = long pressure reactivity index; PVS = persistent vegetative state; TBI = traumatic brain injury.…”