Hyperventilation, cerebral perfusion, and syncope

Abstract

This review summarizes evidence in humans for an association between hyperventilation (HV)-induced hypocapnia and a reduction in cerebral perfusion leading to syncope defined as transient loss of consciousness (TLOC). The cerebral vasculature is sensitive to changes in both the arterial carbon dioxide (PaCO2) and oxygen (PaO2) partial pressures so that hypercapnia/hypoxia increases and hypocapnia/hyperoxia reduces global cerebral blood flow. Cerebral hypoperfusion and TLOC have been associated with hypocapnia related to HV. Notwithstanding pronounced cerebrovascular effects of PaCO2 the contribution of a low PaCO2 to the early postural reduction in middle cerebral artery blood velocity is transient. HV together with postural stress does not reduce cerebral perfusion to such an extent that TLOC develops. However when HV is combined with cardiovascular stressors like cold immersion or reduced cardiac output brain perfusion becomes jeopardized. Whether, in patients with cardiovascular disease and/or defect, cerebral blood flow cerebral control HV-induced hypocapnia elicits cerebral hypoperfusion, leading to TLOC, remains to be established.

Assessment of middle cerebral artery diameter during hypocapnia and hypercapnia in humans using ultra-high-field MRI

“…ments. In a fixed body position, the PET CO 2 -Pa CO 2 relation is linear (10,11,17). In the present study, the subjects remained in the supine position, and breathing rate and depth were controlled by visual and auditory stimuli.…”

Influence of intranasal and carotid cooling on cerebral temperature balance and oxygenation

“…Furthermore, the hyperventilation-induced hypocapnia was associated with increased lactate release from the brain indicating that reduced CBF and consequently lower cerebral oxygen delivery may have compromised aerobic metabolism and we observed that the mean capillary and venous oxygen tension were reduced following the period with nasal ventilation. All subjects tolerated the 5 min period with nasal ventilation without reporting signs of dizziness, but the hypocapnic level and marked reduction in MCA V mean indicate that they were close to levels that may lead to syncope (Immink et al, in press). If normal alveolar ventilation and consequently also P a CO 2 had been maintained during the nasal ventilation, it is almost certain that cerebral oxygenation had also remained stable, however, we asked the subjects to inhale forcefully through the nose to maximize the potential cooling effects this could have on the upper respiratory tract.…”

Arterial pressure variations as parameters of brain perfusion in response to central blood volume depletion and repletion

“…The mechanisms that drive breathing during postural stress are not well understood but likely find their origin in both the brain and the periphery. We earlier considered that in the upright position the larger BP variability and less stable blood flow enhance fluctuation of PaCO 2 as an input signal to the carotid body chemoreceptors (Immink et al, 2013). The interaction of enhanced baroreceptor activity and carotid body chemoreceptor stimulation may modify the respiratory drive (Biscoe and Purves, 1967a,b).…”

“…Nevertheless, postural stress elicits reductions in indices of CBF irrespective of the fact that CPP remains within the so called autoregulatory range, challenging the concept of CA as a plateau (Immink et al, 2010; Lucas et al, 2010). In fact, constant CBF would require an infinite gain which is generally not operative in humans (Van Lieshout et al, 2003; Panerai, 2004; Immink et al, 2013; Willie et al, 2014). Assessment of CA is based on introducing CCP fluctuations and quantifying their transfer to the blood velocity in a large cerebral artery in terms of phase angle and gain.…”