Tidal volume, cardiac output and functional residual capacity determine end‐tidal CO<sub>2</sub> transient during standing up in humans

Gisolf, Janneke; Wilders, Ronald; Immink, Rogier V.; Lieshout, Johannes J. van; Karemaker, John M.

doi:10.1113/jphysiol.2003.056895

Cited by 73 publications

(62 citation statements)

References 30 publications

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“…Possibly, the decrease in CBFV could also be induced by reduction in arterial carbon dioxide pressure, because arterial carbon dioxide pressure is one of the strongest influences on CBF [11,12]. The present results demonstrated a stepwise decrease in ETCO 2 and an unchanged respiratory rate, especially with levels of hypergravity, probably implying increases in tidal volume [13,14]. The increased tidal volume would contribute to decreases in arterial carbon dioxide pressure, leading to decreases in CBFV.…”

Section: Discussionmentioning

confidence: 48%

The relationship between widespread changes in gravity and cerebral blood flow

Ogawa

Yanagida

Ueda

et al. 2016

Environ Health Prev Med

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Objectives We investigated the dose-effect relationship between wide changes in gravity from 0 to 2.0 Gz (D0.5 Gz) and cerebral blood flow (CBF), to test our hypothesis that CBF has a linear relationship with levels of gravity. Subjects and methods Ten healthy seated men were exposed to 0, 0.5, 1.0, 1.5, and 2.0 Gz for 21 min, by using a tilt chair and a short-arm human centrifuge. Steady-state CBF velocity (CBFV) in the middle cerebral artery by transcranial Doppler ultrasonography, mean arterial pressure (MAP) at the heart level (MAP Heart ), heart rate, stroke volume, cardiac output and respiratory conditions were obtained for the last 6 min at each gravity level. Then, MAP in the middle cerebral artery (MAP MCA ), reflecting cerebral perfusion pressure, was estimated. Results Steady-state CBFV decreased stepwise from 0.5 to 2.0 Gz. Steady-state heart rate, stroke volume, estimated MAP MCA and end-tidal carbon dioxide pressure (ETCO 2 ) also changed stepwise from hypogravity to hypergravity. On the other hand, steady-state MAP Heart and cardiac output did not change significantly. Steady-state CBFV positively and linearly correlated with estimated MAP MCA and ETCO 2 in most subjects. ConclusionThe present study demonstrated stepwise gravity-induced changes in steady-state CBFV from 0.5 to 2.0 Gz despite unchanged steady-state MAP Heart . The combined effects of reduced MAP MCA and ETCO 2 likely led to stepwise decreases in CBFV. We caution that a mild increase in gravity from 0 to 2.0 Gz reduces CBF, even if arterial blood pressure at the heart level is maintained.

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Section: Discussionmentioning

confidence: 48%

The relationship between widespread changes in gravity and cerebral blood flow

Ogawa

Yanagida

Ueda

et al. 2016

Environ Health Prev Med

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“…Also supporting the idea that changes in whole body blood flow distribution might play a role in postural hypocapnia, Anthonisen and Milic-Emili (2) found that the decrease in Pa CO 2 did not occur when the tilt was performed while subjects were submerged in water to the xiphoid process to prevent venous pooling. Similarly, Gisolf et al (12), using a theoretical model, demonstrated that decreases in cardiac output were responsible for ϳ20% of the decrease in PET CO 2 during standing.…”

Section: Discussionmentioning

confidence: 99%

Cerebral blood flow during orthostasis: role of arterial CO₂

Serrador

Hughson²,

Kowalchuk³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Reductions in end-tidal PCO2 (PETCO 2 ) during upright posture have been suggested to be the result of hyperventilation and the cause of decreases in cerebral blood flow (CBF). The goal of this study was to determine whether decreases in PETCO 2 reflected decreases in arterial PCO2 (PaCO 2 ) and their relation to increases in alveolar ventilation (V A) and decreases in CBF. Fifteen healthy subjects (10 women and 5 men) were subjected to a 10-min head-up tilt (HUT) protocol. PaCO 2 , V A, and cerebral flow velocity (CFV) in the middle and anterior cerebral arteries were examined. In 12 subjects who completed the protocol, reductions in PETCO 2 and PaCO 2 (Ϫ1.7 Ϯ 0.5 and Ϫ1.1 Ϯ 0.4 mmHg, P Ͻ 0.05) during minute 1 of HUT were associated with a significant increase in V A (ϩ0.7 Ϯ 0.3 l/min, P Ͻ 0.05). However, further decreases in Pa CO 2 (Ϫ0.5 Ϯ 0.5 mmHg, P Ͻ 0.05), from minute 1 to the last minute of HUT, occurred even though V A did not change significantly (Ϫ0.2 Ϯ 0.3 l/min, P ϭ not significant). Similarly, CFV in the middle and anterior cerebral arteries decreased (Ϫ7 Ϯ 2 and Ϫ8 Ϯ 2%, P Ͻ 0.05) from minute 1 to the last minute of HUT, despite minimal changes in PaCO 2 . These data suggest that decreases in PET CO 2 and PaCO 2 during upright posture are not solely due to increased V A but could be due to ventilation-perfusion mismatch or a redistribution of CO2 stores. Furthermore, the reduction in PaCO 2 did not fully explain the decrease in CFV throughout HUT. These data suggest that factors in addition to a reduction in PaCO 2 play a role in the CBF response to orthostatic stress. transcranial Doppler; cerebral vasoconstriction; head-up tilt IT HAS BEEN WIDELY NOTED that orthostatic stress in humans decreases end-tidal PCO 2 (PET CO 2 ) or arterial PCO 2 (Pa CO 2 ) (1,4,17,27,36,38,41). Because Pa CO 2 is known to be critical in control of cerebral blood flow (CBF) (30), decreased Pa CO 2 during tilt could play a role in orthostatic intolerance through inappropriate cerebral vasoconstriction. It has been hypothesized that hyperventilation in the upright posture reduces Pa CO 2 , compromising CBF and leading to syncope (27).One inherent problem with this previous work is the use of PET CO 2 to represent Pa CO 2 . Previous work has found that although, in the supine position, PET CO 2 is closely matched to Pa CO 2 (i.e., ϳ0.8 mmHg greater), the assumption of the upright posture resulted in the PET CO 2 being ϳ2.9 mmHg lower than Pa CO 2 (4).No studies have directly measured alveolar ventilation (V A) and CBF during head-up tilt (HUT) and characterized their association to Pa CO 2 . On the basis of our previous findings that decreases in PET CO 2 did not relate to changes in minute ventilation (V E) (36), we hypothesized that Pa CO 2 decreases would be attenuated compared with PET CO 2 and would not be the predominant factor in reduced CBF during HUT. METHODS Subjects.Fifteen subjects [10 women and 5 men, averaging 25.3 yr of age (range 21-32 yr), 64.3 Ϯ 20.5 (SD) kg body wt, 174 Ϯ 9 cm] with no history of card...

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“…These data, although limited by the small number of subjects, suggest that changes in PaCO 2 during LBNP, if any, are likely to be overestimated by changes in ETCO 2 , probably reflecting a ventilation/perfusion mismatch (eg, an increase in V A /Q) during orthostasis. 24 In a previous study, a small (1.6 mm Hg) but statistically significant reduction in PaCO 2 has been observed during Ϫ60 mm Hg LBNP. 25 We have considered that given the small number of subjects in this study, such a small reduction in PaCO 2 may not be distinguished from background noise.…”

Section: Arterial Comentioning

confidence: 99%

Autonomic Ganglionic Blockade Does Not Prevent Reduction in Cerebral Blood Flow Velocity During Orthostasis in Humans

Zhang

Levine

2007

Stroke

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Background and Purpose-The underlying mechanisms for reductions in cerebral blood flow (CBF) during orthostasis are not completely understood. This study tested the hypothesis that sympathetic activation causes cerebral vasoconstriction leading to reductions in CBF during lower body negative pressure (LBNP). Methods-CBF velocity, arterial pressure, and end-tidal CO 2 were measured during LBNP (Ϫ30 to Ϫ50 mm Hg) in 11 healthy subjects before and after autonomic ganglionic blockade with trimethaphan. Arterial partial pressure of CO 2 also was measured in a subgroup of 5 subjects. Mean arterial pressure during LBNP after blockade was maintained by infusion of phenylephrine. Results-Before blockade, mean arterial pressure did not change during LBNP. However, CBF velocity was reduced in all subjects by 14% (PϽ0.05). Systolic and pulsatile (systolic-diastolic) CBF velocity were reduced by 18% and 28%, respectively, associated with significant reductions in pulse arterial pressure and end-tidal CO 2 (all PϽ0.05). After blockade, mean arterial pressure during LBNP was well-maintained and even increased slightly with infusion of phenylephrine. However, reductions in mean, systolic, and pulsatile CBF velocity, pulse arterial pressure, and ETCO 2 were similar to those before blockade. In contrast to reductions in end-tidal CO 2 , arterial partial pressure of CO 2 did not change during LBNP. Conclusions-These data, contrary to our hypothesis, demonstrate that sympathetic vasoconstriction is not the primary mechanism underlying reductions in CBF during moderate LBNP. We speculate that diminished pulse arterial pressure or pulsatile blood flow may reduce cerebral vessel wall shear stress and contribute to reductions in CBF during orthostasis through flow mediated regulatory mechanisms.

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Tidal volume, cardiac output and functional residual capacity determine end‐tidal CO₂ transient during standing up in humans

Cited by 73 publications

References 30 publications

The relationship between widespread changes in gravity and cerebral blood flow

The relationship between widespread changes in gravity and cerebral blood flow

Cerebral blood flow during orthostasis: role of arterial CO₂

Autonomic Ganglionic Blockade Does Not Prevent Reduction in Cerebral Blood Flow Velocity During Orthostasis in Humans

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Tidal volume, cardiac output and functional residual capacity determine end‐tidal CO2 transient during standing up in humans

Cited by 73 publications

References 30 publications

The relationship between widespread changes in gravity and cerebral blood flow

The relationship between widespread changes in gravity and cerebral blood flow

Cerebral blood flow during orthostasis: role of arterial CO2

Autonomic Ganglionic Blockade Does Not Prevent Reduction in Cerebral Blood Flow Velocity During Orthostasis in Humans

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Tidal volume, cardiac output and functional residual capacity determine end‐tidal CO₂ transient during standing up in humans

Cerebral blood flow during orthostasis: role of arterial CO₂