Cerebrovascular reactivity to carbon dioxide is not influenced by variability in the ventilatory sensitivity to carbon dioxide

• Published in: Experimental physiology Vol. 105; no. 5; pp. 904 - 915
• Main Authors: Howe, Connor A., Caldwell, Hannah G., Carr, Jay, Nowak‐Flück, Daniela, Ainslie, Philip N., Hoiland, Ryan L.
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01-05-2020
• Subjects: Blood flow; Blood pressure; Carbon dioxide; Carotid artery; Cerebral blood flow; CO2 reactivity; Conductance; Hypercapnia; Hyperventilation; Hypoventilation; Mechanical ventilation; Skull; Ultrasound; Ventilation; Vertebrae; cerebral blood flow; hypercapnia; ventilation; CO2 reactivity
• ISSN: 0958-0670; 1469-445X
• DOI: 10.1113/EP088192

New Findings
What is the central question of this study?
Do differing magnitudes of ventilation influence cerebrovascular CO2 reactivity and the cerebral blood flow response to increases in arterial carbon dioxide?
What is the main finding and its importance?
While a greater ventilation, through voluntary hyperventilation, is associated with a higher anterior cerebral blood flow during carbon dioxide breathing, this elevated cerebral blood flow is due to a higher blood pressure and not ventilation per se. A greater ventilation, through voluntary hyperventilation, does not influence global or posterior cerebral blood flow during carbon dioxide breathing. Cerebrovascular reactivity to carbon dioxide is not influenced by an individual's ventilatory sensitivity to carbon dioxide.
Recent work demonstrated an influence of ventilation on cerebrovascular reactivity to CO2; however, the concomitant influence of changes in mean arterial blood pressure (MAP) on ventilation‐induced differences in cerebral blood flow (CBF) has yet to be examined in this context. Healthy participants (n = 15; 25 ± 3 years of age; 179 ± 6 cm height; 74 ± 10 kg weight; 3 female) underwent end‐tidal forcing to increase their partial pressure of end‐tidal CO2 by +3, +6 and +9 mmHg above baseline in 5‐min sequential steps while maintaining iso‐oxia. This protocol was then repeated twice, with participants hyperventilating and hypoventilating by ∼30% compared to the first trial. Intra‐cranial and extra‐cranial CBF were measured using ultrasound. The MAP (finger photo‐plethysmography) was higher during the hyperventilation and hypoventilation trials compared to normal ventilation (main effects, P < 0.05 for both). While internal carotid artery blood flow was higher during the hyperventilation trial compared to normal ventilation (P = 0.01), this was due to a higher MAP, as indicated by analysis of conductance values (P = 0.68) or inclusion of MAP in covariate analysis (P = 0.11). Global CBF (P = 0.11) and vertebral artery blood flow (P = 0.93) were unaffected by the magnitude of ventilation. Further, CO2 reactivity was not affected by the different breathing trials (P > 0.05 for all). Retrospective analysis of a larger data set (n = 53) confirmed these observations and demonstrated no relationships between the ventilatory and global CBF response to hypercapnia (r2 = 0.04; P = 0.14). Therefore, when differences in MAP are accounted for, cerebrovascular CO2 reactivity (assessed via end‐tidal forcing) is independent of the magnitude of ventilation.