Background and Goal of Study  Cerebral perfusion is challenged during surgery and anaesthesia. Cardiac output (CO) influences cerebral blood flow independently of mean arterial blood pressure (MAP). A linear relationship was found between cerebral blood flow and CO1 during simulated hypovolemia induced by lower body negative pressure. We now have studied the response of internal carotid artery blood flow (ICABF) to non-pharmacological CO elevations in healthy humans.
Materials and Methods A -10° head-down tilt (HDT) alone or combined with a 3-min isometric handgrip (HDT+HG) of 30% maximal voluntary contraction were used in thirteen subjects (4 males, 9 females) after 5 minutes of rest to increase central blood volume and CO. Each subject repeated the procedure twice. ICA blood velocity (Doppler ultrasound), MAP and CO (Finometer), and end-tidal CO2 (ETCO2) were recorded. ICABF was calculated beat-by-beat. The ICABF response to CO was modelled by linear mixed-effects multiple regression (SAS JMP 12, USA) during HDT and HDT+HG. ETCO2, MAP and CO were continuous covariates. Due to the repeated-measures design of the study, each subject contributed with more than one observation. In order to account for the correlation among the within-subject repeated observations, Subject Identity was entered as random effect in the model. 
Results and Discussion During HDT and HDT+HG, none of the covariates contributed significantly to ICABF variance (p>0.2 for all covariates). Figure 1B and 1C show the absence of relationship between CO and ICABF during volume loading (B) and sympathetic activation combined with volume loading (C). MAP did not change from Rest to HDT, but increased from Rest to HDT+HG (+12%, p=0.007) due to sympathetic activation without affecting ICABF though. These findings in combination with previous work from our group (Figure 1A) imply that cerebrovasculature can buffer effectively CO elevations but not CO reductions. Cerebral vasoconstriction due to sympathetic activation might have counteracted the increase in CO during HDT+HG, while it may have contributed to ICABF decrease during LBNP. 
Conclusions Cerebral blood flow responds differently to CO changes with a linear response to CO drops and no change during mild CO elevations. Cerebrovasculature cannot fully compensate for a decrease in CO despite a preserved MAP, which should be considered in the treatment of hemodynamically compromised patients.


1. Skytioti et al. Internal carotid artery blood flow in healthy awake subjects is reduced by simulated hypovolemia and noninvasive mechanical ventilation. DOI: 10.14814/phy2.12969


02 / Differential response of internal carotid artery blood flow to cardiac output changes.