scholarly journals The Clamping of End-Tidal Carbon Dioxide Does Not Influence Cognitive Function Performance During Moderate Hyperthermia With or Without Skin Temperature Manipulation

2021 ◽  
Vol 12 ◽  
Author(s):  
Ricardo Schultz Martins ◽  
Phillip J. Wallace ◽  
Scott W. Steele ◽  
Jake S. Scott ◽  
Michael J. Taber ◽  
...  

Increases in body temperature from heat stress (i.e., hyperthermia) generally impairs cognitive function across a range of domains and complexities, but the relative contribution from skin versus core temperature changes remains unclear. Hyperthermia also elicits a hyperventilatory response that decreases the partial pressure of end-tidal carbon dioxide (PetCO2) and subsequently cerebral blood flow that may influence cognitive function. We studied the role of skin and core temperature along with PetCO2 on cognitive function across a range of domains. Eleven males completed a randomized, single-blinded protocol consisting of poikilocapnia (POIKI, no PetCO2 control) or isocapnia (ISO, PetCO2 maintained at baseline levels) during passive heating using a water-perfused suit (water temperature ~ 49°C) while middle cerebral artery velocity (MCAv) was measured continuously as an index of cerebral blood flow. Cognitive testing was completed at baseline, neutral core-hot skin (37.0 ± 0.2°C-37.4 ± 0.3°C), hot core-hot skin (38.6 ± 0.3°C-38.7 ± 0.2°C), and hot core-cooled skin (38.5 ± 0.3°C-34.7 ± 0.6°C). The cognitive test battery consisted of a detection task (psychomotor processing), 2-back task (working memory), set-shifting and Groton Maze Learning Task (executive function). At hot core-hot skin, poikilocapnia led to significant (both p < 0.05) decreases in PetCO2 (∆−21%) and MCAv (∆−26%) from baseline, while isocapnia clamped PetCO2 (∆ + 4% from baseline) leading to a significantly (p = 0.023) higher MCAv (∆−18% from baseline) compared to poikilocapnia. There were no significant differences in errors made on any task (all p > 0.05) irrespective of skin temperature or PetCO2 manipulation. We conclude that neither skin temperature nor PetCO2 maintenance significantly alter cognitive function during passive hyperthermia.

1983 ◽  
Vol 143 (6) ◽  
pp. 604-608 ◽  
Author(s):  
Roy J. Mathew ◽  
Deborah L. Barr ◽  
Maxine L. Weinman

SummaryTwo groups of normal volunteers had regional cerebral blood flow (rCBF) measured, by the 133Xenon inhalation technique, before and 30 minutes after 250 mg or 500 mg caffeine given orally. rCBF was measured in a third group of subjects, twice, at a similar interval under identical laboratory conditions. Subjects who received caffeine showed significant decreases in rCBF while the others showed no rCBF change from the first to the second measurement. However, the two caffeine groups did not differ in degrees of rCBF reduction. There were no regional variations in the post-caffeine decrease in cerebral blood flow. The three groups did not show significant changes in end-tidal carbon dioxide, pulse rate, blood pressure, forehead skin temperature and respiratory rate.


2009 ◽  
Vol 587 (15) ◽  
pp. 3921-3927 ◽  
Author(s):  
R. Matthew Brothers ◽  
Jonathan E. Wingo ◽  
Kimberly A. Hubing ◽  
Craig G. Crandall

2020 ◽  
Vol 9 (12) ◽  
pp. 4088
Author(s):  
Shyan-Lung Lin ◽  
Shoou-Jeng Yeh ◽  
Ching-Kun Chen ◽  
Yu-Liang Hsu ◽  
Chih-En Kuo ◽  
...  

Postural orthostatic tachycardia syndrome (POTS) typically occurs in youths, and early accurate POTS diagnosis is challenging. A recent hypothesis suggests that upright cognitive impairment in POTS occurs because reduced cerebral blood flow velocity (CBFV) and cerebrovascular response to carbon dioxide (CO2) are nonlinear during transient changes in end-tidal CO2 (PETCO2). This novel study aimed to reveal the interaction between cerebral autoregulation and ventilatory control in POTS patients by using tilt table and hyperventilation to alter the CO2 tension between 10 and 30 mmHg. The cerebral blood flow velocity (CBFV), partial pressure of end-tidal carbon dioxide (PETCO2), and other cardiopulmonary signals were recorded for POTS patients and two healthy groups including those aged >45 years (Healthy-Elder) and aged <45 years (Healthy-Youth) throughout the experiment. Two nonlinear regression functions, Models I and II, were applied to evaluate their CBFV-PETCO2 relationship and cerebral vasomotor reactivity (CVMR). Among the estimated parameters, the curve-fitting Model I for CBFV and CVMR responses to CO2 for POTS patients demonstrated an observable dissimilarity in CBFVmax (p = 0.011), mid-PETCO2 (p = 0.013), and PETCO2 range (p = 0.023) compared with those of Healthy-Youth and in CBFVmax (p = 0.015) and CVMRmax compared with those of Healthy-Elder. With curve-fitting Model II for POTS patients, the fit parameters of curvilinear (p = 0.036) and PETCO2 level (p = 0.033) displayed significant difference in comparison with Healthy-Youth parameters; range of change (p = 0.042), PETCO2 level, and CBFVmax also displayed a significant difference in comparison with Healthy-Elder parameters. The results of this study contribute toward developing an early accurate diagnosis of impaired CBFV responses to CO2 for POTS patients.


1996 ◽  
Vol 85 (6) ◽  
pp. 1395-1402. ◽  
Author(s):  
Antonio M. Cruz ◽  
Lucy C. Southerland ◽  
Tanya Duke ◽  
Hugh G. G. Townsend ◽  
James G. Ferguson ◽  
...  

Background Laparoscopic surgical procedures are being performed in pregnant women with increasing frequency. Maternal-fetal physiologic changes occurring during intraabdominal carbon dioxide insufflation are poorly understood, and maternal-fetal safety is of concern during carbon dioxide pneumoperitoneum. A previous pilot study using end-tidal carbon dioxide-guided ventilation resulted in maternal and fetal acidosis and tachycardia during carbon dioxide pneumoperitoneum. Using serial arterial PCO2 to guide ventilation, this study was designed to evaluate maternal-fetal cardiopulmonary status, uterine blood flow, and the intraamniotic pressure effects of intraabdominal carbon dioxide insufflation in singleton pregnant ewes between 120 and 135 days of gestation. Methods In a prospective randomized cross-over study, nine ewes were to receive either abdominal insufflation with carbon dioxide to an intraabdominal pressure of 15 mmHg (n = 9; insufflation group) or receive no insufflation (n = 9; control group). Anesthesia was induced with thiopental and maintained with end-tidal halothane (1 to 1.5 minimum alveolar concentration/100% oxygen). Mechanical ventilation was guided by serial maternal arterial blood gas analysis to maintain PaCO2 between 35 and 40 mmHg. Data from insufflated animals were collected during insufflation (60 min) and after desufflation (30 min). Control group data were collected and matched to similar time intervals for 90 min. Ewes were allowed to recover, and after a rest period (48 h) they were entered in the cross-over study. Results During insufflation there was a significant increase (P &lt; 0.05) in maternal PaCO2 to end-tidal carbon dioxide gradient and minute ventilation, with concomitant decreases in maternal end-tidal carbon dioxide and PaO2. Intraamniotic pressure increased significantly during insufflation. No significant changes were observed in maternal hemodynamic variables, fetal variables, or in uterine blood flow during the study. There were no fetal deaths or preterm labor in any of the animals during the experiment. Conclusions During the 1-h insufflation, a marked increase in PaCO2-to-end-tidal carbon dioxide gradient was observed, suggesting that capnography may be an inadequate guide to ventilation during carbon dioxide pneumoperitoneum in the pregnant patient. No other significant circulatory changes were observed.


2018 ◽  
Vol 124 (1) ◽  
pp. 225-233 ◽  
Author(s):  
Bun Tsuji ◽  
Davide Filingeri ◽  
Yasushi Honda ◽  
Tsubasa Eguchi ◽  
Naoto Fujii ◽  
...  

Elevating core temperature at rest causes increases in minute ventilation (V̇e), which lead to reductions in both arterial CO2 partial pressure (hypocapnia) and cerebral blood flow. We tested the hypothesis that in resting heated humans this hypocapnia diminishes the ventilatory sensitivity to rising core temperature but does not explain a large portion of the decrease in cerebral blood flow. Fourteen healthy men were passively heated using hot-water immersion (41°C) combined with a water-perfused suit, which caused esophageal temperature (Tes) to reach 39°C. During heating in two separate trials, end-tidal CO2 partial pressure decreased from the level before heating (39.4 ± 2.0 mmHg) to the end of heating (30.5 ± 6.3 mmHg) ( P = 0.005) in the Control trial. This decrease was prevented by breathing CO2-enriched air throughout the heating such that end-tidal CO2 partial pressure did not differ between the beginning (39.8 ± 1.5 mmHg) and end (40.9 ± 2.7 mmHg) of heating ( P = 1.00). The sensitivity to rising Tes (i.e., slope of the Tes − V̇E relation) did not differ between the Control and CO2-breathing trials (37.1 ± 43.1 vs. 16.5 ± 11.1 l·min−1·°C−1, P = 0.31). In both trials, middle cerebral artery blood velocity (MCAV) decreased early during heating (all P < 0.01), despite the absence of hyperventilation-induced hypocapnia. CO2 breathing increased MCAV relative to Control at the end of heating ( P = 0.005) and explained 36.6% of the heat-induced reduction in MCAV. These results indicate that during passive heating at rest ventilatory sensitivity to rising core temperature is not suppressed by hypocapnia and that most of the decrease in cerebral blood flow occurs independently of hypocapnia. NEW & NOTEWORTHY Hyperthermia causes hyperventilation and concomitant hypocapnia and cerebral hypoperfusion. The last may underlie central fatigue. We are the first to demonstrate that hyperthermia-induced hyperventilation is not suppressed by the resultant hypocapnia and that hypocapnia explains only 36% of cerebral hypoperfusion elicited by hyperthermia. These new findings advance our understanding of the mechanisms controlling ventilation and cerebral blood flow during heat stress, which may be useful for developing interventions aimed at preventing central fatigue during hyperthermia.


2020 ◽  
Vol 9 (24) ◽  
Author(s):  
Rachel Wells ◽  
Varun Malik ◽  
Anthony G. Brooks ◽  
Dominik Linz ◽  
Adrian D. Elliott ◽  
...  

Background The physiology underlying "brain fog" in the absence of orthostatic stress in postural tachycardia syndrome (POTS) remains poorly understood. Methods and Results We evaluated cognitive and hemodynamic responses (cardiovascular and cerebral: heart rate, blood pressure, end‐tidal carbon dioxide, and cerebral blood flow velocity (CBFv) in the middle cerebral artery at baseline, after initial cognitive testing, and after (30‐minutes duration) prolonged cognitive stress test (PCST) whilst seated; as well as after 5‐minute standing in consecutively enrolled participants with POTS (n=22) and healthy controls (n=18). Symptom severity was quantified with orthostatic hypotensive questionnaire at baseline and end of study. Subjects in POTS and control groups were frequency age‐ and sex‐matched (29±11 versus 28±13 years; 86 versus 72% women, respectively; both P ≥0.4). The CBFv decreased in both groups (condition, P =0.04) following PCST, but a greater reduction in CBFv was observed in the POTS versus control group (−7.8% versus −1.8%; interaction, P =0.038). Notably, the reduced CBFv following PCST in the POTS group was similar to that seen during orthostatic stress (60.0±14.9 versus 60.4±14.8 cm/s). Further, PCST resulted in greater slowing in psychomotor speed (6.1% versus 1.4%, interaction, P =0.027) and a greater increase in symptom scores at study completion (interaction, P <0.001) in the patients with POTS, including increased difficulty with concentration. All other physiologic responses (blood pressure and end‐tidal carbon dioxide) did not differ between groups after PCST (all P >0.05). Conclusions Reduced CBFv and cognitive dysfunction were evident in patients with POTS following prolonged cognitive stress even in the absence of orthostatic stress.


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