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2.
Eur Heart J Acute Cardiovasc Care ; 10(5): 497-502, 2021 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-34192746

RESUMO

AIMS: Although both hypercapnia and hypocapnia are common in acute heart failure (AHF) patients, routine assessment of arterial blood gas is not recommended. Additionally, no association between hypercapnia and increased mortality has been found, and the prognostic value of hypocapnia in AHF patients remains to be elucidated. In this observational study, we aimed to investigate the relationship between partial pressure of arterial carbon dioxide (PaCO2), especially low PaCO2, and long-term mortality in AHF patients. METHODS AND RESULTS: Acute heart failure patients hospitalized in the cardiac intensive care unit of our institution between 2007 and 2011 were screened. All eligible patients were divided into two groups based on the inflection point (i.e. 31.0 mmHg) of the 3-knot cubic spline curve of the hazard ratio (HR), with a PaCO2 of 40 mmHg as a reference. The association between PaCO2 levels and all-cause mortality was assessed using Cox proportional hazards regression models. Among 435 patients with a median follow-up of 1.8 years, 115 (26.4%) died. Adjusted analysis with relevant variables as confounders indicated that PaCO2 <31 mmHg was significantly associated with increased all-cause mortality [HR 1.71, 95% confidence interval (CI) 1.05-2.79; P = 0.032]. When PaCO2 was considered as a continuous variable, the lower was the log-transformed PaCO2, the greater was the increased risk of mortality (HR 0.71, 95% CI 0.52-0.96; P = 0.024). CONCLUSIONS: In AHF patients, lower PaCO2 at admission was associated with increased long-term mortality risk.


Assuntos
Dióxido de Carbono , Insuficiência Cardíaca , Hipocapnia , Insuficiência Cardíaca/diagnóstico , Humanos , Hipocapnia/diagnóstico , Unidades de Terapia Intensiva , Prognóstico
3.
Can J Anaesth ; 68(10): 1497-1506, 2021 10.
Artigo em Inglês | MEDLINE | ID: mdl-34105067

RESUMO

PURPOSE: Anesthesia is associated with alterations in end-tidal (ET) respiratory gases from the awake state. These alterations result in marked vasoactive changes in regional cerebral blood flow (rCBF). Altered regional cerebrovascular reactivity (rCVR) is linked to neurologic dysfunction. We examined these differences in reactivity from prior work by focusing on the ratio of vasoconstriction with hyperoxia/hypocapnia (HO/hc):vasodilation with hypercapnia (HC) using magnetic resonance imaging pseudo-continuous arterial spin labelling (pCASL) to measure rCBF and compare rCVR The distribution and magnitude of these ratios could provide insights into rCBF during clinical anesthesia and inform future research into the origins of postoperative delirium (POD). METHODS: Ten healthy subjects underwent cerebral blood flow (CBF) studies using pCASL with computer-controlled delivery of ET gases to assess flow effects of hyperoxia, hypercapnia, and hyperoxia/hypocapnia as part of a larger study into cerebrovascular reactivity. The vasoconstrictor stimulus was compared with the vasodilator stimulus by the ratio HO/hc:HC. RESULTS: Hyperoxia minimally decreased whole brain CBF by - 0.6%/100 mm Hg increase in ETO2. Hypercapnia increased CBF by +4.6%/mm Hg carbon dioxide (CO2) and with HO/hc CBF decreased by - 5.1%/mm Hg CO2. The brain exhibited markedly different rCVR-regional HO/hc:HC ratios varied from 7.2:1 (greater response to vasoconstriction) to 0.49:1 (greater response to vasodilation). Many of the ratios greater than 1, where vasoconstriction predominated, were seen in regions associated with memory, cognition, and executive function, including the entorhinal cortex, hippocampus, parahippocampus, and dorsolateral prefrontal cortex. CONCLUSIONS: In awake humans, marked rCBF changes occurred with alterations in ET respiratory gases common under anesthesia. Such heterogeneous reactivity may be relevant to future studies to identify those at risk of POD.


Assuntos
Circulação Cerebrovascular , Gases , Dióxido de Carbono , Voluntários Saudáveis , Humanos , Hipercapnia , Hipocapnia
4.
J Physiol ; 599(15): 3663-3676, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-34107079

RESUMO

KEY POINTS: We investigated the influence of arterial P C O 2 ( P aC O 2 ) with and without acute experimental metabolic alkalosis on neurovascular coupling (NVC). We assessed stepwise iso-oxic alterations in P aC O 2 prior to and following intravenous NaHCO3 to acutely elevate arterial pH and [HCO3 - ]. The NVC response was not altered following NaHCO3 between stepwise P aC O 2 stages; therefore, NVC is acutely mediated by P aC O 2 rather than the prevailing arterial [H+ ]/pH. The NVC response was attenuated by 27-38% with -10 mmHg P aC O 2 and the absolute peak change was reduced by -19% with +10 mmHg P aC O 2 irrespective of acutely elevated arterial pH/[HCO3 - ]. The NVC kinetics (i.e. time to peak) were markedly slower with hypercapnia versus hypocapnia (24 ± 5 vs. 7 ± 5 s, respectively) likely indicating an influence of resting cerebrovascular tone on NVC responsiveness. ABSTRACT: Elevations in cerebral metabolism necessitate appropriate coordinated and localized increases in cerebral blood flow (i.e. neurovascular coupling; NVC). Recent pre-clinical work indicates that arterial P C O 2 ( P aC O 2 ) mediates NVC independently of arterial/extracellular pH; this has yet to be experimentally tested in humans. The goal of this study was to investigate the hypotheses that: (1) the NVC response would be unaffected by acute experimentally elevated arterial pH; rather, P aC O 2 would regulate any changes in NVC; and (2) stepwise respiratory alkalosis and acidosis would each progressively reduce the NVC response. Ten healthy males completed a standardized visual stimulus-evoked NVC test during matched stepwise iso-oxic alterations in P aC O 2 (hypocapnia: -5, -10 mmHg; hypercapnia: +5, +10 mmHg) prior to and following intravenous NaHCO3 (8.4%, 50 mEq/50 ml) that elevated arterial pH (7.406 ± 0.019 vs. 7.457 ± 0.029; P < 0.001) and [HCO3 - ] (26.2 ± 1.5 vs. 29.3 ± 0.9 mEq/l; P < 0.001). Although the NVC response was collectively attenuated by 27-38% with -10 mmHg P aC O 2 (stage post hoc: all P < 0.05), this response was unaltered following NaHCO3 (all P > 0.05) irrespective of the higher pH (P = 0.002) at each matched stage of P aC O 2 (P = 0.417). The absolute peak change was reduced by -19 ± 41% with +10 mmHg P aC O 2 irrespective of acutely elevated arterial pH/[HCO3 - ] (stage post hoc: P = 0.022). The NVC kinetics (i.e. time to peak) were markedly slower with hypercapnia versus hypocapnia (24 ± 5 vs. 7 ± 5 s, respectively; stage effect: P < 0.001). Overall, these findings indicate that temporal patterns in NVC are acutely regulated by P aC O 2 rather than arterial pH per se in the setting of acute metabolic alkalosis in humans.


Assuntos
Dióxido de Carbono , Acoplamento Neurovascular , Circulação Cerebrovascular , Humanos , Concentração de Íons de Hidrogênio , Hipocapnia , Cinética , Masculino
5.
Auton Neurosci ; 234: 102826, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34058717

RESUMO

High dietary sodium impairs cerebral blood flow regulation in rodents and is associated with increased stroke risk in humans. However, the effects of multiple days of high dietary sodium on cerebral blood flow regulation in humans is unknown. Therefore, the purpose of this study was to determine whether ten days of high dietary sodium impairs cerebral blood flow regulation. Ten participants (3F/7M; age: 30 ± 10 years; blood pressure (BP): 113 ± 8/62 ± 9 mmHg) participated in this randomized, cross-over design study. Participants were placed on 10-day diets that included either low- (1000 mg/d), medium- (2300 mg/d) or high- (7000 mg/d) sodium separated by ≥four weeks. Urinary sodium excretion, beat-to-beat BP (finger photoplethysmography), middle cerebral artery velocity (transcranial Doppler), and end-tidal carbon dioxide (capnography) was measured. Dynamic cerebral autoregulation during a ten-minute baseline was calculated and cerebrovascular reactivity assessed by determining the percent change in middle cerebral artery blood flow velocity to hypercapnia (8% CO2, 21% oxygen, balance nitrogen) and hypocapnia (via mild hyperventilation). Urinary sodium excretion increased in a stepwise manner (ANOVA P = 0.001) from the low, to medium, to high condition. There were no differences in dynamic cerebral autoregulation between conditions. While there was a trend for a difference during cerebrovascular reactivity to hypercapnia (ANOVA P = 0.06), this trend was abolished when calculating cerebrovascular conductance (ANOVA: P = 0.28). There were no differences in cerebrovascular reactivity (ANOVA P = 0.57) or conductance (ANOVA: P = 0.73) during hypocapnia. These data suggest that ten days of a high sodium diet does not impair cerebral blood flow regulation in healthy adults.


Assuntos
Sódio na Dieta , Adulto , Velocidade do Fluxo Sanguíneo , Pressão Sanguínea , Dióxido de Carbono , Circulação Cerebrovascular , Dieta , Humanos , Hipercapnia , Hipocapnia , Ultrassonografia Doppler Transcraniana
6.
J Appl Physiol (1985) ; 131(1): 119-130, 2021 07 01.
Artigo em Inglês | MEDLINE | ID: mdl-34013755

RESUMO

The purpose of this study was to test the hypothesis that changes in cerebral vasomotor reactivity (CVMR) after 1-yr aerobic exercise training (AET) are associated with cognitive performances in individuals with amnestic mild cognitive impairment (MCI). Seventy sedentary patients with amnestic MCI were randomized to 1-yr moderate-to-vigorous intensity AET or stretching and toning (SAT) interventions. Cerebral blood flow velocity (CBFV) with transcranial Doppler, mean arterial pressure (MAP) with finapres plethysmograph, and EtCO2 with capnography were measured during hyperventilation (hypocapnia) and a modified rebreathing protocol (hypercapnia) to assess CVMR. Cerebrovascular conductance index (CVCi) was calculated by CBFV/MAP, and CVMR by ΔCBFV/ΔEtCO2 and ΔCVCi/ΔEtCO2. Episodic memory and executive function were assessed using standard neuropsychological tests (CVLT-II and D-KEFS). Cardiorespiratory fitness was assessed by peak oxygen uptake (V̇o2peak). A total of 37 patients (19 in SAT and 18 in AET) completed 1-yr interventions and CVMR assessments. AET improved V̇o2peak, increased hypocapnic CVMR, but decreased hypercapnic CVMR. The effects of AET on cognitive performance were minimal when compared with SAT. Across both groups, there was a negative correlation between changes in hypocapnic and hypercapnic CVMRs in CBFV% and CVCi% (r = -0.741, r = -0.725, P < 0.001). Attenuated hypercapnic CVMR, but not increased hypocapnic CVMR, was associated with improved cognitive test scores in the AET group. In conclusion, 1-yr AET increased hypocapnic CVMR and attenuated hypercapnic CVMR which is associated cognitive performance in patients with amnestic MCI.NEW & NOTEWORTHY One-year moderate-to-vigorous intensity aerobic exercise training (AET) improved cardiorespiratory fitness (V̇o2peak), increased hypocapnic cerebral vasomotor reactivity (CVMR), whereas it decreased hypercapnic CVMR when compared with stretching and toning in patients with amnestic mild cognitive impairment (MCI). Furthermore, changes in hypercapnic CVMR with AET were correlated with improved memory and executive function. These findings indicate that AET has an impact on cerebrovascular function which may benefit cognitive performance in older adults who have high risk of Alzheimer's disease.


Assuntos
Disfunção Cognitiva , Exercício Físico , Idoso , Circulação Cerebrovascular , Humanos , Hipercapnia , Hipocapnia
7.
Physiol Meas ; 42(5)2021 06 17.
Artigo em Inglês | MEDLINE | ID: mdl-33853052

RESUMO

Objective.Cerebral autoregulation impairment in acute neurovascular disease is well described. The recent BREATHE-ICH study demonstrated improvements in dynamic cerebral autoregulation, by hypocapnia generated by hyperventilation, in the acute period following intracranial haemorrhage (ICH). This exploratory analysis of the BREATHE-ICH dataset aims to examine the differences in hypocapnic responses between healthy controls and patients with ICH, and determine whether haemodynamic indices differ between baseline and hypocapnic states.Approach.Acute ICH patients were recruited within 48 h of onset and healthy volunteers were recruited from a university setting. Transcranial Doppler measurements of the middle cerebral artery were obtained at baseline and then a hyperventilation intervention was used to induce hypocapnia. Patients with ICH were then followed up at 10-14 D post-event for repeated measurements.Main results.Data from 43 healthy controls and 12 patients with acute ICH met the criteria for statistical analysis. In both normocapnic and hypocapnic conditions, significantly higher critical closing pressure and resistance area product were observed in patients with ICH. Furthermore, critical closing pressure changes were observed to be sustained at 10-14 D follow up. During both the normocapnic and hypocapnic states, reduced autoregulation index was observed bilaterally in patients with ICH, compared to healthy controls.Significance.Whilst this exploratory analysis was limited by a small, non-age matched sample, significant differences between ICH patients and healthy controls were observed in factors associated with cerebrovascular tone and resistance. These differences suggest underlying cerebral autoregulation changes in ICH, which may play a pivotal role in the morbidity and mortality associated with ICH.


Assuntos
Circulação Cerebrovascular , Hipocapnia , Velocidade do Fluxo Sanguíneo , Hemorragia Cerebral/diagnóstico por imagem , Humanos , Artéria Cerebral Média
8.
Neuropsychopharmacol Hung ; 23(1): 215-220, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33835043

RESUMO

Here we propose that the Western world lifestyle disrupts phosphate metabolism and homeostasis due to caloric or acidic hyperphagia. Psychic factors such as social defeat due to stressed social coexistence characterized by reduced activity and chronic hypoventilation (hypercapnia) also play a role. At least two mechanisms mediate the harmful vascular effects of phosphates with intracellular acidosis being a feature in both of them. First, insufficient lifestyle and adjacent diet together with the psychosomatic mechanism of social defeat (mainly through chronic hypercapnic acidosis) lead to insulin resistance characterized by the classical Cardiometabolic Syndrome. Secondly, overload with fixed acids caused by renal insufficiency or acidic diet (due to intracellular metabolic acidosis) leads to our here proposed Exhausting Buffer Syndrome (EBS) which tends to elevate serum inorganic phosphate levels. These two mechanisms overlap and are regulated through genetically determined processes that drive the disruption of phosphate metabolism and lead to vascular calcification. To have a lower intake of calories and less acidic foods combined with low-grade hypocapnia, might be one of several solutions. (Neuropsychopharmacol Hung 2021; 23(1): 215-220)


Assuntos
Acidose , Hipocapnia , Cátions , Humanos , Hipercapnia
9.
J Appl Physiol (1985) ; 130(6): 1705-1715, 2021 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-33703943

RESUMO

Rapid ascent to high altitude imposes an acute hypoxic and acid-base challenge, with ventilatory and renal acclimatization countering these perturbations. Specifically, ventilatory acclimatization improves oxygenation, but with concomitant hypocapnia and respiratory alkalosis. A compensatory, renally mediated relative metabolic acidosis follows via bicarbonate elimination, normalizing arterial pH(a). The time course and magnitude of these integrated acclimatization processes are highly variable between individuals. Using a previously developed metric of renal reactivity (RR), indexing the change in arterial bicarbonate concentration (Δ[HCO3-]a; renal response) over the change in arterial pressure of CO2 (Δ[Formula: see text]; renal stimulus), we aimed to characterize changes in RR magnitude following rapid ascent and residence at altitude. Resident lowlanders (n = 16) were tested at 1,045 m (day [D]0) prior to ascent, on D2 within 24 h of arrival, and D9 during residence at 3,800 m. Radial artery blood draws were obtained to measure acid-base variables: [Formula: see text], [HCO3-]a, and pHa. Compared with D0, [Formula: see text] and [HCO3-]a were lower on D2 (P < 0.01) and D9 (P < 0.01), whereas significant changes in pHa (P = 0.072) and RR (P = 0.056) were not detected. As pHa appeared fully compensated on D2 and RR did not increase significantly from D2 to D9, these data demonstrate renal acid-base compensation within 24 h at moderate steady-state altitude. Moreover, RR was strongly and inversely correlated with ΔpHa on D2 and D9 (r ≤ -0.95; P < 0.0001), suggesting that a high-gain renal response better protects pHa. Our study highlights the differential time course, magnitude, and variability of integrated ventilatory and renal acid-base acclimatization following rapid ascent and residence at high altitude.NEW & NOTEWORTHY We assessed the time course, magnitude, and variability of integrated ventilatory and renal acid-base acclimatization with rapid ascent and residence at 3,800 m. Despite reductions in [Formula: see text] upon ascent, pHa was normalized within 24 h of arrival at 3,800 m through renal compensation (i.e., bicarbonate elimination). Renal reactivity (RR) was unchanged between days 2 and 9, suggesting a lack of plasticity at moderate steady-state altitude. RR was strongly correlated with ΔpHa, suggesting that a high-gain renal response better protects pHa.


Assuntos
Aclimatação , Altitude , Bicarbonatos , Humanos , Hipocapnia , Hipóxia
10.
J Appl Physiol (1985) ; 130(5): 1427-1435, 2021 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-33764171

RESUMO

A minimal model of cerebral blood flow and respiratory control was developed to describe hypocapnic and hypercapnic responses. Important nonlinear properties such as cerebral blood flow changes with arterial partial pressure of carbon dioxide ([Formula: see text]) and associated time-dependent circulatory time delays were included. It was also necessary to vary cerebral metabolic rate as a function of [Formula: see text]. The cerebral blood flow model was added to a previously developed respiratory control model to simulate central and peripheral controller dynamics for humans. Model validation was based on previously collected data. The variable time delay due to brain blood flow changes in hypercapnia was an important determinant of predicted instability due to nonlinear interaction in addition to linear loop gain considerations. Peripheral chemoreceptor gains above a critical level, but within normal limits, were necessary to produce instability. Instability was observed in recovery from hypercapnia and hypocapnia. The 20-s breath-hold test appears to be a simple test of brain blood flow-mediated instability in hypercapnia. Brain blood flow was predicted to play an important role with nonlinear properties. There is an important interaction predicted by the current model between central and peripheral control mechanisms related to instability in hypercapnia recovery. Posthyperventilation breathing pattern can also reveal instability tied to brain blood flow. Previous data collected in patients with chronic obstructive lung disease were closely fitted with the current model and instability predicted. Brain vascular volume was proposed as a potential cause of instability despite cerebral autoregulation promoting constant brain flow.NEW & NOTEWORTHY Prior models of brain blood flow and respiratory control have not focused on instability. Time varying time delay resulting from brain blood flow changes due to carbon dioxide (CO2) and peripheral chemoreceptor gain were predicted to be important determinants of instability due to nonlinear interaction in addition to linear control loop gain. Time delay was assumed to be set by the ratio of brain arterial vascular volume and blood flow. This vascular volume was predicted to also significantly change with CO2.


Assuntos
Dióxido de Carbono , Circulação Cerebrovascular , Humanos , Hipercapnia , Hipocapnia , Respiração
11.
Respir Med ; 179: 106329, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33610050

RESUMO

BACKGROUND: The hyperventilation syndrome (HVS) is characterized by somatic/ psychological symptoms due to sustained hypocapnia and respiratory alkalosis without any organic disease. OBJECTIVE: The purpose of this study was to compare ventilatory parameters and symptoms reproducibility during the hyperventilation provocation test (HVPT) and cardiopulmonary exercise test (CPET) as diagnostic tools in patients with HVS, and to identify the most frequent etiologies of the HVS by a systematic assessment. METHODS: After exclusion of organic causes, 59 patients with HVS according to Nijmegen's questionnaire (NQ) score ≥23 with associated hypocapnia (PaCO2/PETCO2<35 mm Hg) were studied. RESULTS: The most frequent comorbidities of HVS were anxiety and asthma (respectively 95% and 73% of patients). All patients described ≥3 symptoms of NQ during the HVPT vs 14% of patients during the CPET (p<0.01). For similar maximal ventilation (61 L/min during HVPT vs 60 L/min during CPET), the median level of PETCO2 decreased from 30 mmHg at baseline to 15 mmHg during hyperventilation and increased from 31 mmHg at baseline to 34 mmHg at peak exercise (all p<0.01). No significant difference for the ventilatory parameters was found between patients with HVS (n = 16) and patients with HVS + asthma (n = 43). CONCLUSIONS: In term of symptoms reproducibility, HVPT is a better diagnostic tool than CPET for HVS. An important proportion of patients with HVS has an atypical asthma previously misdiagnosed. The exercise-induced hyperventilation did not induce abnormal reduction in PETCO2, suggesting that the exercise could be a therapeutic tool in HVS.


Assuntos
Testes de Provocação Brônquica , Hiperventilação/diagnóstico , Adulto , Alcalose Respiratória/complicações , Ansiedade/epidemiologia , Asma/epidemiologia , Comorbidade , Teste de Esforço , Terapia por Exercício , Feminino , Humanos , Hiperventilação/epidemiologia , Hiperventilação/etiologia , Hiperventilação/terapia , Hipocapnia/complicações , Masculino , Pessoa de Meia-Idade , Espirometria , Inquéritos e Questionários , Síndrome
12.
J Cereb Blood Flow Metab ; 41(8): 1924-1938, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-33444092

RESUMO

Traumatic Brain Injury (TBI) is associated with both diffuse axonal injury (DAI) and diffuse vascular injury (DVI), which result from inertial shearing forces. These terms are often used interchangeably, but the spatial relationships between DAI and DVI have not been carefully studied. Multimodal magnetic resonance imaging (MRI) can help distinguish these injury mechanisms: diffusion tensor imaging (DTI) provides information about axonal integrity, while arterial spin labeling (ASL) can be used to measure cerebral blood flow (CBF), and the reactivity of the Blood Oxygen Level Dependent (BOLD) signal to a hypercapnia challenge reflects cerebrovascular reactivity (CVR). Subjects with chronic TBI (n = 27) and healthy controls (n = 14) were studied with multimodal MRI. Mean values of mean diffusivity (MD), fractional anisotropy (FA), CBF, and CVR were extracted for pre-determined regions of interest (ROIs). Normalized z-score maps were generated from the pool of healthy controls. Abnormal ROIs in one modality were not predictive of abnormalities in another. Approximately 9-10% of abnormal voxels for CVR and CBF also showed an abnormal voxel value for MD, while only 1% of abnormal CVR and CBF voxels show a concomitant abnormal FA value. These data indicate that DAI and DVI represent two distinct TBI endophenotypes that are spatially independent.


Assuntos
Axônios/patologia , Biomarcadores/metabolismo , Lesões Encefálicas Traumáticas/diagnóstico por imagem , Lesão Encefálica Crônica/diagnóstico por imagem , Circulação Cerebrovascular/fisiologia , Adulto , Anisotropia , Encéfalo/irrigação sanguínea , Encéfalo/fisiopatologia , Encéfalo/ultraestrutura , Lesões Encefálicas Traumáticas/patologia , Lesão Encefálica Crônica/patologia , Mapeamento Encefálico , Estudos de Casos e Controles , Feminino , Humanos , Hipercapnia/diagnóstico por imagem , Hipocapnia/fisiopatologia , Processamento de Imagem Assistida por Computador , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Marcadores de Spin
13.
J Crit Care ; 61: 207-215, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33186827

RESUMO

Serum levels of carbon dioxide (CO2) closely regulate cerebral blood flow (CBF) and actively participate in different aspects of brain physiology such as hemodynamics, oxygenation, and metabolism. Fluctuations in the partial pressure of arterial CO2 (PaCO2) modify the aforementioned variables, and at the same time influence physiologic parameters in organs such as the lungs, heart, kidneys, and the gastrointestinal tract. In general, during acute brain injury (ABI), maintaining normal PaCO2 is the target to be achieved. Both hypercapnia and hypocapnia may comprise secondary insults and should be avoided during ABI. The risks of hypocapnia mostly outweigh the potential benefits. Therefore, its therapeutic applicability is limited to transient and second-stage control of intracranial hypertension. On the other hand, inducing hypercapnia could be beneficial when certain specific situations require increasing CBF. The evidence supporting this claim is very weak. This review attempts providing an update on the physiology of CO2, its risks, benefits, and potential utility in the neurocritical care setting.


Assuntos
Dióxido de Carbono , Hipocapnia , Encéfalo , Circulação Cerebrovascular , Humanos , Hipercapnia
14.
J Physiol ; 599(4): 1097-1113, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33185896

RESUMO

KEY POINTS: Cognitive function depends on adequate cerebrovascular perfusion and control. However, it is unknown whether acutely-reduced cerebral blood flow (CBF) impairs cognition in healthy adults. In the present study, we used a placebo-controlled, single-blinded, randomized cross-over design to test the hypothesis that acutely-reduced CBF (using a pharmacological aid; indomethacin) would impair cognition in young and older healthy adults. At baseline, older adults had lower cognitive performance and CBF, but similar cerebrovascular reactivity to CO2 and dynamic cerebral autoregulation compared to young adults. In both young and older adults, cognitive performance on a mental switching task was slightly (7%) reduced after indomethacin, but not significantly associated with reductions in CBF (∼31%). These results indicate that cognitive performance is broadly resilient against a ∼31% reduction in CBF per se in healthy young and older adults. ABSTRACT: Cognitive function depends on adequate cerebrovascular perfusion and control. However, it is unknown whether acutely-reduced cerebral blood flow (CBF) impairs cognition in healthy adults. Using a placebo-controlled, single-blinded, randomized cross-over design, we tested the hypothesis that acutely-reduced CBF (using indomethacin [1.2 mg kg-1 oral dose]) would impair cognition in young (n = 13; 25 ± 4 years) and older (n = 12; 58 ± 6 years) healthy adults. CBF and cerebrovascular control were measured using middle cerebral artery blood velocity (MCAvmean ) and its reactivity to hypercapnia (CVRHYPER ) and hypocapnia (CVRHYPO ), respectively. Cognitive function was assessed using a computerized battery including response time tasks. Baseline comparisons revealed that older adults had 14% lower MCAvmean and 15% lower cognitive performance (all P ≤ 0.048), but not lower CVRHYPER/HYPO (P ≥ 0.26). Linear and rank-based mixed models revealed that indomethacin decreased MCAvmean by 31% (95% confidence interval = -35 to -26), CVRHYPER by 68% [interquartile range (IQR) = -94 to -44] and CVRHYPO by 50% (IQR = -83 to -33) (treatment-effect; all P < 0.01), regardless of age. Baseline CVRHYPER/HYPO values were strongly associated with their indomethacin-induced reductions (r = 0.70 to 0.89, P < 0.01). Mental switching performance was impaired 7% (IQR = 0-19) after indomethacin (P = 0.04), but not significantly associated with reductions in MCAvmean (Young: rho = -0.31, P = 0.30; Older: rho = 0.06, P = 0.86). In conclusion, indomethacin reduced MCAvmean and impaired cognition slightly; however, no clear association was evident in younger or older adults. Older adults had poorer cognition and lower MCAvmean , but similar CVRHYPER/HYPO .


Assuntos
Circulação Cerebrovascular , Indometacina , Idoso , Cognição , Humanos , Hipocapnia , Perfusão , Adulto Jovem
15.
Eur J Sport Sci ; 21(8): 1148-1155, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-32814502

RESUMO

AbstractTwenty minutes of voluntary hypocapnic hyperventilation prior to exercise reduces the aerobic metabolic rate with a compensatory increase in the anaerobic metabolic rate without affecting exercise performance during the Wingate anaerobic test (WAnT). Thus, pre-exercise hypocapnic hyperventilation may be a useful means of stressing the anaerobic energy system during training, ultimately improving anaerobic exercise performance. However, it remains unclear whether a shorter (e.g., 5 min) pre-exercise hypocapnic hyperventilation is sufficient to reduce the aerobic metabolic rate during high-intensity exercise. We therefore compared the effects of 5-min and 20-min pre-exercise hypocapnic hyperventilation on aerobic metabolism during the 30-s WAnT. Ten healthy young males and one female performed the WAnT following 20 min of spontaneous breathing (control trial) or 5 or 20 min of voluntary hypocapnic hyperventilation. Both the 5-min and 20-min hyperventilation reduced end-tidal CO2 partial pressure (an index of arterial CO2 partial pressure) to ∼23 mmHg, whereas it remained unchanged during the spontaneous breathing. The peak, mean and minimum power outputs during the WAnT did not differ among the three trials. Oxygen uptake during the WAnT was lower in both the 5-min (1493 ± 257 mL min-1) and 20-min (1397 ± 447 mL min-1) hyperventilation trials than during the control trial (1847 ± 286 mL min-1), and was similar in the two hyperventilation trials. These results suggest that 5 min of pre-exercise hypocapnic hyperventilation reduces aerobic metabolism during the 30-s WAnT to a level similar to that seen with the 20-min hyperventilation. Moreover, exercise performance was unaffected, which implies anaerobic metabolism was enhanced.


Assuntos
Desempenho Atlético/fisiologia , Metabolismo Energético , Exercício Físico/fisiologia , Hiperventilação/fisiopatologia , Hipocapnia/fisiopatologia , Anaerobiose , Exercícios Respiratórios/métodos , Teste de Esforço/métodos , Feminino , Frequência Cardíaca , Humanos , Masculino , Consumo de Oxigênio , Percepção/fisiologia , Esforço Físico/fisiologia , Adulto Jovem
17.
Physiol Rep ; 8(19): e14585, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-33038066

RESUMO

A high sodium (Na+ ) meal impairs peripheral vascular function. In rodents, chronic high dietary Na+ impairs cerebral vascular function, and in humans, habitual high dietary Na+ is associated with increased stroke risk. However, the effects of acute high dietary Na+ on the cerebral vasculature in humans are unknown. The purpose of this study was to determine if acute high dietary Na+ impairs cerebrovascular reactivity in healthy adults. Thirty-seven participants (20F/17M; 25 ± 5 years; blood pressure [BP]: 107 ± 9/61 ± 6 mm Hg) participated in this randomized, cross-over study. Participants were given a low Na+ meal (LSM; 138 mg Na+ ) and a high Na+ meal (HSM; 1,495 mg Na+ ) separated by ≥ one week. Serum Na+ , beat-to-beat BP, middle cerebral artery velocity (transcranial Doppler), and end-tidal carbon dioxide (PET CO2 ) were measured pre- (baseline) and 60 min post-prandial. Cerebrovascular reactivity was assessed by determining the percent change in middle cerebral artery velocity to hypercapnia (via 8% CO2 , 21% oxygen, balance nitrogen) and hypocapnia (via mild hyperventilation). Peripheral vascular function was measured using brachial artery flow-mediated dilation (FMD). Changes in serum Na+ were greater following the HSM (HSM: Δ1.6 ± 1.2 mmol/L vs. LSM: Δ0.7 ± 1.2 mmol/L, p < .01). Cerebrovascular reactivity to hypercapnia (meal effect: p = .41) and to hypocapnia (meal effect: p = .65) were not affected by the HSM. Contrary with previous findings, FMD was not reduced following the HSM (meal effect: p = .74). These data suggest that a single high Na+ meal does not acutely impair cerebrovascular reactivity, and suggests that despite prior findings, a single high Na+ meal does not impair peripheral vascular function in healthy adults.


Assuntos
Circulação Cerebrovascular/efeitos dos fármacos , Hipocapnia/fisiopatologia , Artéria Cerebral Média/fisiopatologia , Cloreto de Sódio na Dieta/farmacologia , Adolescente , Adulto , Velocidade do Fluxo Sanguíneo/efeitos dos fármacos , Artéria Braquial/efeitos dos fármacos , Dióxido de Carbono/sangue , Estudos Cross-Over , Feminino , Humanos , Hipercapnia/fisiopatologia , Masculino , Artéria Cerebral Média/fisiologia , Adulto Jovem
19.
Arch Argent Pediatr ; 118(5): 332-336, 2020 10.
Artigo em Inglês, Espanhol | MEDLINE | ID: mdl-32924396

RESUMO

Introduction: Cerebral edema (CE) is the most severe complication of diabetic ketoacidosis (DKA) in children. There is no accurate knowledge of CE pathogenesis and its onset has been related to intravenous rehydration therapy during the initial treatment. Objectives: To estimate the prevalence of CE among DKA patients treated at Hospital General de Niños Pedro de Elizalde with intravenous rehydration and analyze potential risk factors for the development of CE. Materials and methods: Cross-sectional prevalence study and exploratory analysis to compare clinical and laboratory characteristics between patients with and without CE. Patients aged 1-18 years hospitalized with the diagnosis of DKA between January 1st, 2005 and December 31st, 2014 were included. Results: A total of 693 DKA events from 561 medical records were analyzed. Ten patients had evidence of CE (1.44 %; 95 % confidence interval: 0.8-2.6). Patients with CE had higher serum urea levels (p < 0.001), lower carbon dioxide pressure (p < 0.001), and lower serum sodium levels (p < 0.001) than those without CE. Conclusion: The prevalence of CE among DKA patients was 1.44 %, smaller than that reported in our country (1.8 %). The risk factors at admission associated with CE development were high serum urea levels, hyponatremia, and hypocapnia.


Assuntos
Edema Encefálico/etiologia , Cetoacidose Diabética/complicações , Hidratação/efeitos adversos , Adolescente , Argentina , Edema Encefálico/epidemiologia , Criança , Pré-Escolar , Estudos Transversais , Cetoacidose Diabética/epidemiologia , Cetoacidose Diabética/terapia , Feminino , Hidratação/métodos , Humanos , Hipocapnia/epidemiologia , Hiponatremia/epidemiologia , Lactente , Masculino , Prevalência , Fatores de Risco , Ureia/sangue
20.
J Neurol Sci ; 418: 117139, 2020 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-32949919

RESUMO

BACKGROUND: An association between spontaneous hyperventilation, delayed cerebral ischemia, and poor clinical outcomes has been reported in subarachnoid hemorrhage. We evaluated the relationship between early pCO2 changes, ischemic lesions and outcomes in patients with intracerebral hemorrhage (ICH). METHODS: Consecutive patients with spontaneous ICH were enrolled in an observational cohort study conducted between 2006 and 2019. Patient characteristics and discharge outcome were prospectively recorded. Arterial blood gas (ABG) measurements and mechanical ventilation settings in the first 72 h of admission were retrospectively collected. MRI images were adjudicated for diffusion-restricted lesions consistent with ischemia and distant from the hematoma. We examined the associations between pCO2 changes, ischemic lesions, and discharge outcomes by univariate and adjusted analyses. RESULTS: ABG data were available for 220 patients. Hyperventilation occurred in 52 (28%) cases and was not associated with clinical severity. Lower initial pCO2 was associated with greater risk of in-hospital death (OR 0.94 per mmHg, 95%CI [0.89, 0.996], p = 0.042) after adjustment for ICH Score, pneumonia and mechanical ventilation requirements. MRI data were available for 33 patients. Lower pCO2 was associated with a higher risk of ischemic lesions, except in patients with low initial systolic blood pressure (p < 0.05 for main and blood pressure interaction effects), after adjustment for other predictors. CONCLUSIONS: In ICH patients with spontaneous ventilation, lower pCO2 was independently associated with greater risk of in-hospital death. In patients with elevated initial blood pressure, who undergo blood pressure reduction per guideline recommendations, lower pCO2 was associated with increased risk to develop ischemic lesions.


Assuntos
Hemorragia Cerebral , Hipocapnia , Hemorragia Cerebral/complicações , Hemorragia Cerebral/diagnóstico por imagem , Hemorragia Cerebral/epidemiologia , Mortalidade Hospitalar , Humanos , Hipocapnia/epidemiologia , Isquemia , Estudos Retrospectivos
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