Changes in human cerebral blood flow due to step changes in P_AO2 and P_ACO2

Abstract

The effect of moderate hypoxia on cerebral blood flow (CBF) in man has not been well described, and little is known about the interaction of changes in arterial PO2 and PCO2 as regards CBF. Using a non-invasive doppler ultrasound method we have measured the instantaneous mean blood velocity (which is proportional to CBF as long as the cross-section of the vessel is constant) in the carotid artery in four healthy unanaesthetized subjects. We found in all subjects that a reduction in alveolar PO2 from about 13 to about 8.7 kPa with maintained constant alveolar PCO2 (PA, CO2) caused CBF to increase gradually over 10 min (half-time about 4 min) to about 125% of control. The CBF decreased quickly (half-time about 45 s) towards control when alveolar PO2 was reset to 13 kPa. As measured 5 min after a step-change in PA, O2, the change in CBF was independent of PA, CO2 within the range 3.3-6.7 kPa. An increase in PA, O2 to about 33 kPa reduced CBF only if PA, CO2 was in the hypercapnic range. Unexpectedly we found that the CBF response showed 'adaptation' during both maintained increase and decrease in PA, CO2. The CBF started to return towards control level within 10 min after induction of hypo- or hypercapnia. We conclude that also moderate hypoxia causes increased CBF in unanaesthetized man within a wide range of PA, CO2.

Sustained moderate reductions in arterial CO2 after brain trauma Time-course of cerebral blood flow velocity and intracranial pressure

“…It could be argued that hyperventilation leads to cerebral activation that is at least partly responsible for the observed recovery of CBF. However, we used passive hyperventilation in our volunteers [19] and the rate of recovery that we saw using this method is comparable to earlier studies using active hyperventilation [1,2]. This makes it unlikely that the observed difference is due to this methodological aspect.…”

“…When healthy volunteers hyperventilate for a prolonged time-interval their cerebral blood flow (CBF) shows a relatively rapid adaptation starting almost immediately after onset of hyperventilation [1,2], with recovery of CBF to approximately 90% of baseline values within 4 h of sustained hypocapnia [3]. This recovery is thought to be due to the return of cerebral vascular calibre towards baseline, following the normalisation of intracellular, and perivascular pH [4].…”

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

“…Below a threshold of PaO 2 of 50 mmHg, CBF increases to maintain adequate cerebral oxygen delivery. Unlike CO 2 vasoreactivity, the equilibration of CBF is longer and takes approximately 6 minutes after the establishment of hypoxemia [51,52].…”

Heart rate response to therapeutic hypothermia in infants with hypoxic–ischaemic encephalopathy

“…5 There are few reports on variability in HR response to the induction of TH. Here we report variability in HR response, and that this variability represents important clinical differences due to severity of the underlying hypoxic-ischaemic insult and inotropic support.…”