Search

Key points Arterial CO2 serves as a mediator of cerebral blood flow, and its relative influence on the regulation of cerebral blood flow is defined as cerebral CO2 reactivity., Because of methodological limitations, almost all previous studies have evaluated the response of blood flow velocity in the middle cerebral artery to changes in CO2 as a measure of CO2 reactivity across the whole brain., We found that the vertebral artery has lower CO2 reactivity than the internal carotid artery. Moreover, CO2 reactivity in the external carotid artery was markedly lower than in the cerebral circulation., These results demonstrate regional differences in CO2 regulation of blood flow between the internal carotid, external carotid, and vertebro-basilar circulation., Abstract Arterial CO2 serves as a mediator of cerebral blood flow (CBF), and its relative influence on the regulation of CBF is defined as cerebral CO2 reactivity. Our previous studies have demonstrated that there are differences in CBF responses to physiological stimuli (i.e. dynamic exercise and orthostatic stress) between arteries in humans. These findings suggest that dynamic CBF regulation and cerebral CO2 reactivity may be different in the anterior and posterior cerebral circulation. The aim of this study was to identify cerebral CO2 reactivity by measuring blood flow and examine potential differences in CO2 reactivity between the internal carotid artery (ICA), external carotid artery (ECA) and vertebral artery (VA). In 10 healthy young subjects, we evaluated the ICA, ECA, and VA blood flow responses by duplex ultrasonography (Vivid-e, GE Healthcare), and mean blood flow velocity in middle cerebral artery (MCA) and basilar artery (BA) by transcranial Doppler (Vivid-7, GE healthcare) during two levels of hypercapnia (3% and 6% CO2), normocapnia and hypocapnia to estimate CO2 reactivity. To characterize cerebrovascular reactivity to CO2, we used both exponential and linear regression analysis between CBF and estimated partial pressure of arterial CO2, calculated by end-tidal partial pressure of CO2. CO2 reactivity in VA was significantly lower than in ICA (coefficient of exponential regression 0.021 ± 0.008 vs. 0.030 ± 0.008; slope of linear regression 2.11 ± 0.84 vs. 3.18 ± 1.09% mmHg−1: VA vs. ICA, P < 0.01). Lower CO2 reactivity in the posterior cerebral circulation was persistent in distal intracranial arteries (exponent 0.023 ± 0.006 vs. 0.037 ± 0.009; linear 2.29 ± 0.56 vs. 3.31 ± 0.87% mmHg−1: BA vs. MCA). In contrast, CO2 reactivity in ECA was markedly lower than in the intra-cerebral circulation (exponent 0.006 ± 0.007; linear 0.63 ± 0.64% mmHg−1, P < 0.01). These findings indicate that vertebro-basilar circulation has lower CO2 reactivity than internal carotid circulation, and that CO2 reactivity of the external carotid circulation is markedly diminished compared to that of the cerebral circulation, which may explain different CBF responses to physiological stress. [ABSTRACT FROM AUTHOR]

Key points Acute hypoxia increases pulmonary arterial (PA) pressures, though its effect on right ventricular (RV) function is controversial. The objective of this study was to characterize exertional RV performance during acute hypoxia. Ten healthy participants (34 ± 10 years, 7 males) completed three visits: visits 1 and 2 included non‐invasive normoxic (fraction of inspired oxygen (FiO2${F_{{\mathrm{i}}{{\mathrm{O}}_{\mathrm{2}}}}}$) = 0.21) and isobaric hypoxic (FiO2${F_{{\mathrm{i}}{{\mathrm{O}}_{\mathrm{2}}}}}$ = 0.12) cardiopulmonary exercise testing (CPET) to determine normoxic/hypoxic maximal oxygen uptake (V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$). Visit 3 involved invasive haemodynamic assessments where participants were randomized 1:1 to either Swan–Ganz or conductance catheterization to quantify RV performance via pressure–volume analysis. Arterial oxygen saturation was determined by blood gas analysis from radial arterial catheterization. During visit 3, participants completed invasive submaximal CPET testing at 50% normoxic V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$ and again at 50% hypoxic V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$ (FiO2${F_{{\mathrm{i}}{{\mathrm{O}}_{\mathrm{2}}}}}$ = 0.12). Median (interquartile range) values for non‐invasive V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$ values during normoxic and hypoxic testing were 2.98 (2.43, 3.66) l/min and 1.84 (1.62, 2.25) l/min, respectively (P < 0.0001). Mean PA pressure increased significantly when transitioning from rest to submaximal exercise during normoxic and hypoxic conditions (P = 0.0014). Metrics of RV contractility including preload recruitable stroke work, dP/dtmax, and end‐systolic pressure increased significantly during the transition from rest to exercise under normoxic and hypoxic conditions. Ventricular–arterial coupling was maintained during normoxic exercise at 50% V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$. During submaximal exercise at 50% of hypoxic V̇O2max${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{max}}}}$, ventricular–arterial coupling declined but remained within normal limits. In conclusion, resting and exertional RV functions are preserved in response to acute exposure to hypoxia at an FiO2${F_{{\mathrm{i}}{{\mathrm{O}}_{\mathrm{2}}}}}$ = 0.12 and the associated increase in PA pressures. The healthy right ventricle augments contractility, lusitropy and energetics during periods of increased metabolic demand (e.g. exercise) in acute hypoxic conditions. During submaximal exercise, ventricular–arterial coupling decreases but remains within normal limits, ensuring that cardiac output and systemic perfusion are maintained. These data describe right ventricular physiological responses during submaximal exercise under conditions of acute hypoxia, such as occurs during exposure to high altitude and/or acute hypoxic respiratory failure. [ABSTRACT FROM AUTHOR]