Hyperventilation-induced intracranial pressure reduction might be impaired in cerebral venous thrombosis (CVT) patients. Using transcranial Doppler, we assessed carbon dioxide-vasomotor reactivity (CO2-VMR) within 24 hours of admission in CVT patients and studied its correlation with patient outcomes. Adult moderate-severe CVT patients (participants of another large observational study) were included. CO2-VMR was calculated as the percentage change in peak flow velocities during maximal hypercapnia and hypocapnia. Outcome was assessed with the modified Rankin scale (mRS) at one - month post-discharge, dichotomized into favourable (mRS≤2) and unfavourable (mRS>2). Twenty patients\' data was analysed. Impaired CO2-VMR (<70 %) was observed in 13 patients in the affected hemisphere; among them, 10 had impairments in both hemispheres. CO2-VMR correlated negatively with mRS (Rho = -0.688, p = 0.001). Odds for unfavourable outcomes were reduced by 92 % in patients with intact VMR on the ipsilateral hemisphere (Odds ratio (OR) 0.08, Confidence interval (CI) 0.006---0.636, p = 0.027) and by 94 % with VMR intact on the contralateral hemisphere (OR 0.063, CI 0.003---0.569, p = 0.03). Thus, impaired CO2-VMR in moderate to severe CVT patients is associated with unfavourable outcomes, and has the potential to prognosticate CVT patients objectively.

Prior studies have identified variable effects of aging on neurovascular coupling (NVC). Carbon dioxide (CO2) affects both cerebral blood velocity (CBv) and NVC, but the effects of age on NVC under different CO2 conditions are unknown. Therefore, we investigated the effects of aging on NVC in different CO2 states during cognitive paradigms. Seventy-eight participants (18-78 yr), with well-controlled comorbidities, underwent continuous recordings of CBv by bilateral insonation of middle (MCA) and posterior (PCA) cerebral arteries (transcranial Doppler), blood pressure, end-tidal CO2, and heart rate during poikilocapnia, hypercapnia (5% CO2 inhalation), and hypocapnia (paced hyperventilation). Neuroactivation via visuospatial (VS) and attention tasks (AT) was used to stimulate NVC. Peak percentage and absolute change in MCAv/PCAv, were compared between CO2 conditions and age groups (≤30, 31-60, and >60 yr). For the VS task, in poikilocapnia, younger adults had a lower NVC response compared with older adults [mean difference (MD): -7.92% (standard deviation (SD): 2.37), P = 0.004], but comparable between younger and middle-aged groups. In hypercapnia, both younger [MD: -4.75% (SD: 1.56), P = 0.009] and middle [MD: -4.58% (SD: 1.69), P = 0.023] age groups had lower NVC responses compared with older adults. Finally, in hypocapnia, both older [MD: 5.92% (SD: 2.21), P = 0.025] and middle [MD: 5.44% (SD: 2.27), P = 0.049] age groups had greater NVC responses, compared with younger adults. In conclusion, the magnitude of NVC response suppression from baseline during hyper- and hypocapnia, did not differ significantly between age groups. However, the middle age group demonstrated a different NVC response while under hypercapnic conditions, compared with hypocapnia.NEW & NOTEWORTHY This study describes the effects of age on neurovascular coupling under altered CO2 conditions. We demonstrated that both hypercapnia and hypocapnia suppress neurovascular coupling (NVC) responses. Furthermore, that middle age exhibits an NVC response comparable with younger adults under hypercapnia, and older adults under hypocapnia.

OBJECTIVE: The purpose of this study was to investigate whether people with fibromyalgia (FM) have dysfunctional breathing by examining acid-base balance and comparing it with healthy controls.
METHODS: Thirty-six women diagnosed with FM and 36 healthy controls matched for age and gender participated in this cross-sectional study. To evaluate acid-base balance, arterial blood was sampled from the radial artery. Carbon dioxide, oxygen, bicarbonate, base excess, pH and lactate were analysed for between-group differences. Blood gas analyses were performed stepwise on each individual to detect acid-base disturbance, which was categorized as primary respiratory and possible compensation indicating chronicity. A three-step approach was employed to evaluate pH, carbon dioxide and bicarbonate in this order.
RESULTS: Women with FM had significantly lower carbon dioxide pressure (p = 0.013) and higher lactate (p = 0.038) compared to healthy controls at the group level. There were no significant differences in oxygen pressure, bicarbonate, pH and base excess. Employing a three-step acid-base analysis, 11 individuals in the FM group had a possible renally compensated mild chronic hyperventilation, compared to only 4 among the healthy controls (p = 0.042).
CONCLUSIONS: In this study, we could identify a subgroup of individuals with FM who may be characterized as mild chronic hyperventilators. The results might point to a plausible dysfunctional breathing in some women with FM.

Background: This study aimed to investigate the associations between dyscapnia, ventilatory variables, and mortality. We hypothesized that the association between mechanical power or ventilatory ratio and survival is mediated by dyscapnia. Methods: Patients with moderate or severe acute respiratory distress syndrome (ARDS), who received mechanical ventilation within the first 48 h after admission to the intensive care unit for at least 48 h, were included in this retrospective single-center study. Values of arterial carbon dioxide (PaCO2) were categorized into \"hypercapnia\" (PaCO2 ≥ 50 mm Hg), \"normocapnia\" (PaCO2 36-49 mmHg), and \"hypocapnia\" (PaCO2 ≤ 35 mm Hg). We used path analyses to assess the associations between ventilatory variables (mechanical power and ventilatory ratio) and mortality, where hypocapnia or hypercapnia were included as mediating variables. Results: Between December 2017 and April 2021, 435 patients were included. While there was a significant association between mechanical power and hypercapnia (BEM = 0.24 [95% CI: 0.15; 0.34], P < .01), there was no significant association between mechanical power or hypercapnia and ICU mortality. The association between mechanical power and intensive care unit (ICU) mortality was fully mediated by hypocapnia (BEM = -0.10 [95% CI: -0.19; 0.00], P = .05; BMO = 0.38 [95% CI: 0.13; 0.63], P < .01). Ventilatory ratio was significantly associated with hypercapnia (B = 0.23 [95% CI: 0.14; 0.32], P < .01). There was no significant association between ventilatory ratio, hypercapnia, and mortality. There was a significant effect of ventilatory ratio on mortality, which was fully mediated by hypocapnia (BEM = -0.14 [95% CI: -0.24; -0.05], P < .01; BMO = 0.37 [95% CI: 0.12; 0.62], P < .01). Conclusion: In mechanically ventilated patients with moderate or severe ARDS, the association between mechanical power and mortality was fully mediated by hypocapnia. Likewise, there was a mediating effect of hypocapnia on the association between ventilatory ratio and ICU mortality. Our results indicate that the debate on dyscapnia and outcome after ARDS should consider the impact of ventilatory variables.

Orthostatic hypotension (OH) is a form of orthostatic intolerance (OI) and a key physiological indicator of autonomic dysfunction that is associated with an increased risk of major cerebrocardiovascular events. Symptoms of cerebral hypoperfusion have been reported in patients with OH, which worsens symptoms and increases the risk of syncope. Since pharmacological interventions increase blood pressure (BP) independent of posture and do not restore normal baroreflex control, nonpharmacological treatments are considered the foundation of OH management. While reductions in cerebral blood flow velocity (CBFv) during orthostatic stress are associated with a decrease in end-tidal CO2 (EtCO2) and hypocapnia in patients with OI, their contribution to the severity of OH is not well understood. These measures have been physiological targets in a wide variety of biofeedback interventions. This study explored the relationship between cardiovascular autonomic control, EtCO2 and cerebral hypoperfusion in patients (N = 72) referred for OI. Patients with systolic OH were more likely to be male, older, demonstrate reduced adrenal and vagal baroreflex sensitivity, and reduced cardiovagal control during head-up tilt (HUT) than patients without systolic OH. Greater reduction in CBFv during HUT was associated with a larger reduction in ETCO2 and systolic BP during HUT. While deficits in cardiovascular autonomic control played a more important role in systolic OH, reduced EtCO2 was a major contributor to orthostatic cerebral hypoperfusion. These findings suggest that biofeedback treatments targeting both the autonomic nervous system and EtCO2 should be part of nonpharmacological interventions complementing the standard of care in OH patients with symptoms of cerebral hypoperfusion.

暂无摘要。

OBJECTIVE: Both hypercapnia and hypocapnia are common in patients with acute heart failure (AHF), but the association between partial pressure of arterial carbon dioxide (PaCO2) and AHF prognosis remains unclear. The objective of this study was to investigate the connection between PaCO2 within 24 h after admission to the intensive care unit (ICU) and mortality during hospitalization and at 1 year in AHF patients.
RESULTS: AHF patients were enrolled from the Medical Information Mart for Intensive Care IV database. The patients were divided into three groups by PaCO2 values of <35, 35-45, and >45 mmHg. The primary outcome was to investigate the connection between PaCO2 and in-hospital mortality and 1 year mortality in AHF patients. The secondary outcome was to assess the prediction value of PaCO2 in predicting in-hospital mortality and 1 year mortality in AHF patients. A total of 2374 patients were included in this study, including 457 patients in the PaCO2 < 35 mmHg group, 1072 patients in the PaCO2 = 35-45 mmHg group, and 845 patients in the PaCO2 > 45 mmHg group. The in-hospital mortality was 19.5%, and the 1 year mortality was 23.9% in the PaCO2 < 35 mmHg group. Multivariate logistic regression analysis showed that the PaCO2 < 35 mmHg group was associated with an increased risk of in-hospital mortality [hazard ratio (HR) 1.398, 95% confidence interval (CI) 1.039-1.882, P = 0.027] and 1 year mortality (HR 1.327, 95% CI 1.020-1.728, P = 0.035) than the PaCO2 = 35-45 mmHg group. The PaCO2 > 45 mmHg group was associated with an increased risk of in-hospital mortality (HR 1.387, 95% CI 1.050-1.832, P = 0.021); the 1 year mortality showed no significant difference (HR 1.286, 95% CI 0.995-1.662, P = 0.055) compared with the PaCO2 = 35-45 mmHg group. The Kaplan-Meier survival curves showed that the PaCO2 < 35 mmHg group had a significantly lower 1 year survival rate. The area under the receiver operating characteristic curve for predicting in-hospital mortality was 0.591 (95% CI 0.526-0.656), and the 1 year mortality was 0.566 (95% CI 0.505-0.627) in the PaCO2 < 35 mmHg group.
CONCLUSIONS: In AHF patients, hypocapnia within 24 h after admission to the ICU was associated with increased in-hospital mortality and 1 year mortality. However, the increase in 1 year mortality may be influenced by hospitalization mortality. Hypercapnia was associated with increased in-hospital mortality.

Rationale: Adult and pediatric studies provide conflicting data regarding whether post-cardiac arrest hypoxemia, hyperoxemia, hypercapnia, and/or hypocapnia are associated with worse outcomes. Objectives: We sought to determine whether postarrest hypoxemia or postarrest hyperoxemia is associated with lower rates of survival to hospital discharge, compared with postarrest normoxemia, and whether postarrest hypocapnia or hypercapnia is associated with lower rates of survival, compared with postarrest normocapnia. Methods: An embedded prospective observational study during a multicenter interventional cardiopulmonary resuscitation trial was conducted from 2016 to 2021. Patients ⩽18 years old and with a corrected gestational age of ≥37 weeks who received chest compressions for cardiac arrest in one of the 18 intensive care units were included. Exposures during the first 24 hours postarrest were hypoxemia, hyperoxemia, or normoxemia-defined as lowest arterial oxygen tension/pressure (PaO2) <60 mm Hg, highest PaO2 ⩾200 mm Hg, or every PaO2 60-199 mm Hg, respectively-and hypocapnia, hypercapnia, or normocapnia, defined as lowest arterial carbon dioxide tension/pressure (PaCO2) <30 mm Hg, highest PaCO2 ⩾50 mm Hg, or every PaCO2 30-49 mm Hg, respectively. Associations of oxygenation and carbon dioxide group with survival to hospital discharge were assessed using Poisson regression with robust error estimates. Results: The hypoxemia group was less likely to survive to hospital discharge, compared with the normoxemia group (adjusted relative risk [aRR] = 0.71; 95% confidence interval [CI] =  0.58-0.87), whereas survival in the hyperoxemia group did not differ from that in the normoxemia group (aRR = 1.0; 95% CI = 0.87-1.15). The hypercapnia group was less likely to survive to hospital discharge, compared with the normocapnia group (aRR = 0.74; 95% CI = 0.64-0.84), whereas survival in the hypocapnia group did not differ from that in the normocapnia group (aRR = 0.91; 95% CI = 0.74-1.12). Conclusions: Postarrest hypoxemia and hypercapnia were each associated with lower rates of survival to hospital discharge.

A given dose of hypoxia causes a greater increase in pulmonary ventilation during physical exercise than during rest, representing an exercise-induced potentiation of the acute hypoxic ventilatory response (HVR). This phenomenon occurs independently from hypoxic blood entering the contracting skeletal muscle circulation or metabolic byproducts leaving skeletal muscles, supporting the contention that neural mechanisms per se can mediate the HVR when humoral mechanisms are not at play. However, multiple neural mechanisms might be interacting intricately. First, we discuss the neural mechanisms involved in the ventilatory response to hypoxic exercise and their potential interactions. Current evidence does not support an interaction between the carotid chemoreflex and central command. In contrast, findings from some studies support synergistic interactions between the carotid chemoreflex and the muscle mechano- and metaboreflexes. Second, we propose hypotheses about potential mechanisms underlying neural interactions, including spatial and temporal summation of afferent signals into the medulla, short-term potentiation and sympathetically induced activation of the carotid chemoreceptors. Lastly, we ponder how exercise-induced potentiation of the HVR results in hyperventilation-induced hypocapnia, which influences cerebral blood flow regulation, with multifaceted potential consequences, including deleterious (increased central fatigue and impaired cognitive performance), inert (unchanged exercise) and beneficial effects (protection against excessive cerebral perfusion).

BACKGROUND: In-hospital cardiac arrest (IHCA) continues to be associated with high morbidity and mortality. The objective of this study was to study the association of arterial carbon dioxide tension (PaCO2) on survival to discharge and favorable neurologic outcomes in adults with IHCA.
METHODS: The study population included 353 adults who underwent resuscitation from 2011 to 2019 for IHCA at an academic tertiary care medical center with arterial blood gas testing done within 24 hours of arrest. Outcomes of interest included survival to discharge and favorable neurologic outcome, defined as Glasgow outcome score of 4-5.
RESULTS: Of the 353 patients studied, PaCO2 classification included: hypocapnia (PaCO2 <35 mm Hg, n = 89), normocapnia (PaCO2 35-45 mm Hg, n = 151), and hypercapnia (PaCO2 >45 mm Hg, n = 113). Hypercapnic patients were further divided into mild (45 mm Hg < PaCO2 ≤55 mm Hg, n = 62) and moderate/severe hypercapnia (PaCO2 > 55 mm Hg, n = 51). Patients with normocapnia had the highest rates of survival to hospital discharge (52.3% vs. 32.6% vs. 30.1%, P < 0.001) and favorable neurologic outcome (35.8% vs. 25.8% vs. 17.9%, P = 0.005) compared those with hypocapnia and hypercapnia respectively. In multivariable analysis, compared to normocapnia, hypocapnia [odds ratio (OR), 2.06; 95% confidence interval (CI), 1.15-3.70] and hypercapnia (OR, 2.67; 95% CI, 1.53-4.66) were both found to be independently associated with higher rates of in-hospital mortality. Compared to normocapnia, while mild hypercapnia (OR, 2.53; 95% CI, 1.29-4.97) and moderate/severe hypercapnia (OR, 2.86; 95% CI, 1.35-6.06) were both independently associated with higher in-hospital mortality compared to normocapnia, moderate/severe hypercapnia was also independently associated with lower rates of favorable neurologic outcome (OR, 0.28; 95% CI, 0.11-0.73), while mild hypercapnia was not.
CONCLUSIONS: In this prospective registry of adults with IHCA, hypercapnia noted within 24 hours after arrest was independently associated with lower rates of survival to discharge and favorable neurologic outcome.