Cerebrovascular and cardiovascular responses to the Valsalva manoeuvre during hyperthermia.

During hyperthermia the perturbations in mean arterial blood pressure (MAP) produced by the Valsalva manoeuvre (VM) are more severe. However, whether these more severe VM induced changes in MAP are translated to the cerebral circulation during hyperthermia is unclear. Healthy participants (n=12, 1 female, mean±SD: age 24±3 years) completed a 30 mm Hg (mouth pressure) VM for 15 s whilst supine during normothermia and mild hyperthermia. Hyperthermia was induced passively using a liquid conditioning garment with core temperature measured via ingested temperature sensor. Middle cerebral artery blood velocity (MCAv) and MAP were recorded continuously during and post VM. Tieck's autoregulatory index was calculated from the VM responses, with pulsatility index, an index of pulse velocity (pulse time) and mean MCAv (MCAvmean ) also calculated. Passive heating significantly raised core temperature from baseline (37.9±0.2 vs. 37.1±0.1°C at rest, P<0.01). MAP during phase I through III of the VM was lower during hyperthermia (interaction effect P<0.01). Although an interaction effect was observed for MCAvmean (P=0.02), post-hoc differences indicated only phase IIa was lower during hyperthermia (55±12 vs. 49.3±8 cm.s-1 for normothermia and hyperthermia respectively, P=0.03). Pulsatility index was increased 1-minute post-VM in both conditions (0.71±0.11 vs. 0.76±0.11 for pre- and post-VM during normothermia respectively P=0.02, and 0.86±0.11 vs. 0.99±0.09 for hyperthermia P<0.01), although for pulse time only main effects of time (P<0.01), and condition (P<0.01) were apparent. These data indicate that the cerebrovascular response to the VM is largely unchanged by mild hyperthermia. This article is protected by copyright. All rights reserved.