CO2 Tension Research Articles

Ventilation/carbon dioxide output relationships during exercise in health.

"Ventilatory efficiency" is widely used in cardiopulmonary exercise testing to make inferences regarding the normality (or otherwise) of the arterial CO2 tension (P aCO2 ) and physiological dead-space fraction of the breath (V D/V T) responses to rapid-incremental (or ramp) exercise. It is quantified as: 1) the slope of the linear region of the relationship between ventilation (V'E) and pulmonary CO2 output (V'CO2 ); and/or 2) the ventilatory equivalent for CO2 at the lactate threshold (V'E/V'CO2 [Formula: see text]) or its minimum value (V'E/V'CO2 min), which occurs soon after [Formula: see text] but before respiratory compensation. Although these indices are normally numerically similar, they are not equally robust. That is, high values for V'E/V'CO2 [Formula: see text] and V'E/V'CO2 min provide a rigorous index of an elevated V D/V T when P aCO2 is known (or can be assumed) to be regulated. In contrast, a high V'E-V'CO2 slope on its own does not, as account has also to be taken of the associated normally positive and small V'E intercept. Interpretation is complicated by factors such as: the extent to which P aCO2 is actually regulated during rapid-incremental exercise (as is the case for steady-state moderate exercise); and whether V'E/V'CO2 [Formula: see text] or V'E/V'CO2 min provide accurate reflections of the true asymptotic value of V'E/V'CO2 , to which the V'E-V'CO2 slope approximates at very high work rates.

Closed-Loop Dynamic Modeling of the Heart-Rate Reflex to Concurrent Spontaneous Changes of Arterial Blood Pressure and CO2 Tension: Quantification of the Effects of Mild Cognitive Impairment.

To extend closed-loop modeling of the heart-rate reflex (HRR) by including the dynamic effects of concurrent changes in blood CO2 tension. This extended dynamic model can be used to generate physio-markers of "baroreflex gain" (BRG) and "chemoreflex gain" (CRG) that allow quantitative assessment of the possible impact of pathologies upon HRR. Mild Cognitive Impairment (MCI) is used as an example. The proposed data-based closed-loop modeling methodology estimates the forward and reverse dynamic components of the model via Laguerre kernel expansions of two open-loop models using spontaneous time-series data collected in 45 MCI patients and 15 controls. The BRG and CRG physio-markers are subsequently computed for each subject via simulation of the obtained closed-loop model for unit-step change of arterial pressure or blood CO2 tension, respectively. Both open-loop and closed-loop HRR modeling revealed that MCI patients exhibit significantly smaller CRG relative to controls (p<0.001), but not significantly different BRG. Furthermore, the closed-loop model captured the dynamic effect of sympathetic activity as resonant peak around 0.1 Hz (Mayer wave) in the chemoreflex and baroreflex transfer functions (not captured via open-loop modeling). This may prove valuable in advancing our understanding of how sympathetic activity impacts HRR in various pathologies. The extended HRR model, incorporating the dynamic effects of concurrent changes of blood CO2 tension, revealed significantly reduced chemoreflex gain (but not baroreflex gain) in MCI patients. Furthermore, the closed-loop model captured the sympathetic influence around 0.1 Hz. Multivariate closed-loop dynamic modeling is valuable for understanding physiological autoregulation.

Impact of Arterial Carbon Dioxide and Oxygen Content on Cerebral Autoregulation Monitoring Among Children Supported by ECMO.

Cerebral autoregulation (CA) impairment is associated with neurological complications among children supported by extracorporeal membrane oxygenation (ECMO). Severe variations of arterial CO2 (PaCO2) and O2 (PaO2) tension after ECMO onset are common and associate with mortality and poor neurological outcome. The impact of gas exchange on CA among critically ill patients is poorly studied. Retrospective analysis of data collected prospectively from 30 children treated with veno-arterial or veno-venous ECMO in the PICU of Nantes University Hospital, France. A correlation coefficient between the variations of regional cerebral oxygen saturation (rSO2) and the variations of mean arterial blood pressure (MAP) was calculated as an index of CA (cerebral oxygenation reactivity index, COx). Cox-MAP plots were investigated allowing determining lower limit of autoregulation (LLA) and upper limit of autoregulation (ULA) limits of autoregulation. Age-based normal blood pressure was used to adjust the MAP, LLA, and ULA data from each patient and then reported as percentage (nMAP, nLLA, and nULA, respectively). RSO2, COx, nMAP, nLLA, and nULA values were averaged over one hour before each arterial blood gas (ABG) sample during ECMO run. Thirty children (median age 4.8months [Interquartile range (IQR) 0.7-39.1], median weight 5kg [IQR 4-15]) experiencing 31 ECMO runs were included in the study. Three hundred and ninety ABGs were analyzed. The highest values of COx were observed on day 1 (D1) of ECMO. The relationship between COx and PaCO2 was nonlinear, but COx values tended to be lower in case of hypercapnia compared to normocapnia. During the whole ECMO run, a weak but significant correlation between PaCO2 and nULA was observed (R = 0.432, p = 0.02). On D1 of ECMO, this correlation was stronger (R = 0.85, p = 0.03) and a positive correlation between nLLA and PaCO2 was also found (R = 0.726, p < 0.001). A very weak negative correlation between PaO2 and nULA was observed within the whole ECMO run and on D1 of ECMO (R = -0.07 p = 0.04 and R = -0.135 p = <0.001, respectively). The difference between nULA and nLLA representing the span of the autoregulation plateau was positively correlated with PaCO2 and negatively correlated with PaO2 (R = 0.224, p = 0.01 and R = -0.051, p = 0.004, respectively). We observed a complex relationship between PaCO2 and CA, influenced by the level of blood pressure. Hypercapnia seems to be globally protective in normotensive or hypertensive condition, while, in case of very low MAP, hypercapnia may disturb CA as it increases LLA. These data add additional arguments for very cautiously lower PaCO2, especially after ECMO start.

Comparison of pulmonary function in isoflurane anaesthetized ventilated sheep (Ovis aries) following administration of intravenous xylazine versus medetomidine.

Alpha2 receptor agonists (alpha2-agonists) are useful sedative and analgesic agents in sheep, but have adverse pulmonary effects, which are reportedly similar between different alpha2-agonists. This randomized crossover study compared pulmonary function after intravenous administration of an alpha2-agonist, either xylazine or an equipotent dose of medetomidine in 34 female sheep anaesthetized twice. Pulmonary function was assessed using spirometry, volumetric capnography, arterial blood gas analysis 1 min prior to, and 5 and 10 min after administration of the allocated alpha 2 agonist drug. Pulmonary structural changes were subsequently assessed using computed tomography (CT). Tachypnoea or hypoxaemia prompted reversal with atipamezole and exclusion of data. Data were analysed for a fixed effect of drug using a mixed effect linear model with significance set at p < 0.05. Ten sheep administered xylazine required atipamezole while none of sheep receiving medetomidine did. Xylazine produced significantly higher respiratory frequency, airway pressures, airway resistance and arterial carbon dioxide (CO2), and lower dynamic compliance, tidal volume, CO2 elimination and end tidal CO2 tension and arterial oxygen tension than medetomidine. This was associated with a significantly lower % of aerated tissue and higher % poorly and non-aerated tissue in CT images of sheep receiving xylazine versus medetomidine. In conclusion, xylazine administration produced marked decreases in pulmonary function, in ventilated isoflurane anaesthetized sheep, when compared to an equipotent dose of medetomidine when administered as an intravenous bolus supporting the use of medetomidine when alpha2-agonists are required.

The effects of wearing facemasks on oxygenation and ventilation at rest and during physical activity.

BackgroundFacemasks are recommended to reduce the spread of SARS-CoV-2, but concern about inadequate gas exchange is an often cited reason for non-compliance.Research questionAmong adult volunteers, do either cloth masks or surgical masks impair oxygenation or ventilation either at rest or during physical activity?Study design and methodsWith IRB approval and informed consent, we measured heart rate (HR), transcutaneous carbon dioxide (CO2) tension and oxygen levels (SpO2) at the conclusion of six 10-minute phases: sitting quietly and walking briskly without a mask, sitting quietly and walking briskly while wearing a cloth mask, and sitting quietly and walking briskly while wearing a surgical mask. Brisk walking required at least a 10bpm increase in heart rate. Occurrences of hypoxemia (decrease in SpO2 of ≥3% from baseline to a value of ≤94%) and hypercarbia (increase in CO2 tension of ≥5 mmHg from baseline to a value of ≥46 mmHg) in individual subjects were collected. Wilcoxon signed-rank was used for pairwise comparisons among values for the whole cohort (e.g. walking without a mask versus walking with a cloth mask).ResultsAmong 50 adult volunteers (median age 33 years; 32% with a co-morbidity), there were no episodes of hypoxemia or hypercarbia (0%; 95% confidence interval 0–1.9%). In paired comparisons, there were no statistically significant differences in either CO2 or SpO2 between baseline measurements without a mask and those while wearing either kind of mask mask, both at rest and after walking briskly for ten minutes.InterpretationThe risk of pathologic gas exchange impairment with cloth masks and surgical masks is near-zero in the general adult population.

Comparative Analysis of Acid-base Status Parameters in Newborn with Congenital Surgical Malformations During Perioperative Care Based on Types of Anesthesia

Introduction: Congenital malformations (CM) are most common in newborns and infants in the first year of life and require surgical correction in the first hours, days, months of life. Surgical interventions in severely ill babies with malformations can lead to catabolic stress, circulatory and respiratory disorders, metabolism shifts, water-electrolyte, protein, and acid-base status disorders.&#x0D; This study aimed to compare acid-base status in newborns and infants with congenital surgical pathology under different types of combined anesthesia. &#x0D; Materials and methods: This retrospective study included 150 newborns and infants with CM who required surgery. The patients were divided into three groups based on types of provided anesthesia: inhalation by Sevoran (sevoflurane) and regional anesthesia (group I); inhalation of Sevoran and intravenous anesthesia by Fentanyl (group II); and intravenous combination of Fentanyl and 20% Sodium Oxybutyrate (group III). The analysis included: acid-base status, peripheral oximetry, and the need for an oxygen mixture inhaled by the patient.&#x0D; Results In group I, there was a significant reduction in partial tension of CO2 and increased pH from the pre-surgical status, at the time of induction of anesthesia, during the most painful, traumatic stage, and after surgery compared to group II and III. Peripheral O2 saturation was not critically reduced at all stages of observation except in babies of group I compared to group III at the stage of induction of anesthesia (97.79 ± 2.45 vs. 98.79 ± 1.63, p = 0.0194) and at the most painful period of surgery (96.29 ± 3.47 vs. 98.10 ± 2.47, p = 0.0368). In group I, newborns and infants required higher oxygen concentrations in the inhalation mixture. There was a significant difference in FiO2 between groups I and III during the most painful stage of surgery (0.47 ± 0.29 and 0.33 ± 0.2, p = 0.0071), and immediately after surgery (0.34 ± 0, 19 and 0.26 ± 0.13, p = 0.0246).&#x0D; Conclusion: Among the newborns and infants with CM requiring surgical intervention and combined anesthesia, the most substantial acid-base status changes were observed in the group where anesthesia was provided by Sevoran (sevoflurane) and regional anesthesia (Group I).

Respiratory Acid-Base Disorders: Respiratory Acidosis and Respiratory Alkalosis

Respiratory acid-base disorders are divided into respiratory acidosis (which can be acute or chronic), and respiratory alkalosis (which also can be acute or chronic). The diagnosis is made after obtaining arterial blood gases (ABGs). Respiratory acidosis is also known as primary hypercapnia and is due to an increase in carbon dioxide (CO2) tension in bodily fluids. The metabolic compensation is an increase in serum bicarbonate (HCO3−), the increase is more pronounced in chronic respiratory acidosis. Oxygen administration (O2) is critical in the management of respiratory acidosis. Respiratory alkalosis or primary hypocapnia is due to a decrease in CO2 tension in bodily fluids. The metabolic compensation is a decrease in HCO3−, the decrease is more pronounced in chronic respiratory alkalosis. Rapid correction of respiratory alkalosis should be avoided, and the underlying etiology should be addressed.

Comparisons of the Nonlinear Relationship of Cerebral Blood Flow Response and Cerebral Vasomotor Reactivity to Carbon Dioxide under Hyperventilation between Postural Orthostatic Tachycardia Syndrome Patients and Healthy Subjects.

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.

Increased ratio of P[v-a]CO2 to C[a-v]O2 without global hypoxia: the case of metformin-induced lactic acidosis

The ratio of venoarterial CO2 tension to arteriovenous O2 content difference (P[v-a]CO2/C[a-v]O2) increases when lactic acidosis is due to inadequate oxygen supply (hypoxia); we aimed to verify whether it also increases when lactic acidosis develops because of mitochondrial dysfunction (dysoxia) with constant oxygen delivery. Twelve anaesthetised, mechanically ventilated pigs were intoxicated with IV metformin (4.0 to 6.4 g over 2.5 to 4.0 h). Saline and norepinephrine were used to preserve oxygen delivery. Lactate and P[v-a]CO2/C[a-v]O2 were measured every one or two hours (arterial and mixed venous blood). During metformin intoxication, lactate increased from 0.8 (0.6−0.9) to 8.5 (5.0−10.9) mmol/l (p < 0.001), even if oxygen delivery remained constant (from 352 ± 78 to 343 ± 97 ml/min, p = 0.098). P[v-a]CO2/C[a-v]O2 increased from 1.6 (1.2–1.8) to 2.3 (1.9−3.2) mmHg/ml/dl (p = 0.004). The intraclass correlation coefficient between lactate and P[v-a]CO2/C[a-v]O2 was 0.72 (p < 0.001). We conclude that P[v-a]CO2/C[a-v]O2 increases when lactic acidosis is due to dysoxia. Therefore, a high P[v-a]CO2/C[a-v]O2 may not discriminate hypoxia from dysoxia as the cause of lactic acidosis.

PNIPAAM/SA pH-responsive microcapsules based on chemical and non-covalent crosslinking

Abstract A triple interpenetrating polymer network (IPN) with dual responses to temperature and pH was constructed based on chemical crosslinking and electrostatic interaction. In this IPN, CaCO3 microspheres were used as the kernel and PNIPAAM/sodium alginate microcapsules were prepared by the inverse emulsion polymerization method. Research results demonstrated that CaCO3 kernels were decomposed into Ca2+ and CO2 at pH 1.2. Such decomposition facilitated the formation of triple IPN of Ca2+ crosslinking. Moreover, microcapsules were expanded by tension of CO2 and the volume increased to 3.55 × 105 times that of the original microcapsules, with capsules remaining an intact morphology. These microcapsules loading doxorubicin hydrochloride (DOX) stability and responses to environment were investigated. No drug overflow was observed at pH 7.4, indicating the high stability of microcapsules. However, DOX was released gradually in the simulated human stomach acid with a weak solution of hydrochloric acid (pH 1.2, 37 °C). This showed that the prepared microcapsules were feasible for drug-loaded capsules and the controlled drug release behavior could relieve side effects of drugs to human body. Moreover, it will help to increase the drug utilization and realize accurate treatment.

The impact of damage-associated molecular patterns on the neurotransmitter release and gene expression in the ex vivo rat carotid body.

What is the central question of this study? Are carotid bodies (CBs) modulated by the damage-associated molecular patterns (DAMPs) and humoral factors of aseptic tissue injury? What are the main findings and their importance? DAMPs (HMGB1, S100 A8/A9) and blood plasma from rats subjected to tibia surgery, a model of aseptic injury, stimulate the release of neurotransmitters (ATP, dopamine) and TNF-α from ex vivo rat CBs. All-thiol HMGB1 mediates upregulation of immune-related biological pathways. These data suggest regulation of CB function by endogenous mediators of innate immunity. The glomus cells of carotid bodies (CBs) are the primary sensors of arterial partial O2 and CO2 tensions and moreover serve as multimodal receptors responding also to other stimuli, such as pathogen-associated molecular patterns (PAMPs) produced by acute infection. Modulation of CB function by excessive amounts of these immunomodulators is suggested to be associated with a detrimental hyperinflammatory state. We have hypothesized that yet another class of immunomodulators, endogenous danger-associated molecular patterns (DAMPs), released upon aseptic tissue injury and recognized by the same pathogen recognition receptors as PAMPs, might modulate the CB activity in a fashion similar to PAMPs. We have tested this hypothesis by exposing rat CBs to various DAMPs, such as HMGB1 (all-thiol and disulfide forms) and S100 A8/A9 in a series of ex vivo experiments that demonstrated the release of dopamine and ATP, neurotransmitters known to mediate CB homeostatic responses. We observed a similar response after incubating CBs with conditioned blood plasma obtained from the rats subjected to tibia surgery, a model of aseptic injury. In addition, we have investigated global gene expression in the rat CB using an RNA sequencing approach. Differential gene expression analysis showed all-thiol HMGB1-driven upregulation of a number of prominent pro-inflammatory markers including Il1α and Il1β. Interestingly, conditioned plasma had a more profound effect on the CB transcriptome resulting in inhibition rather than activation of the immune-related pathways. These data are the first to suggest potential modulation of CB function by endogenous mediators of innate immunity.

Biofilm Production by Enterotoxigenic Strains of Bacillus cereus in Different Materials and under Different Environmental Conditions.

Foodborne illnesses, such as infections or food poisoning, can be caused by bacterial biofilms present in food matrices or machinery. The production of biofilms by several strains of Bacillus cereus on different materials under different culture conditions was determined, as well as the relationship of biofilms with motility, in addition to the enterotoxigenic profile and candidate genes that participate in the production of biofilms. Biofilm production of B. cereus strains was determined on five materials: glass, polystyrene, polyethylene, polyvinylchloride (PVC), PVC/glass; in three culture media: Phenol red broth, tryptic soy broth, and brain heart infusion broth; in two different temperatures (37 °C and 25 °C), and in two different oxygen conditions (oxygen and CO2 tension). Furthermore, the strains were molecularly characterized by end-point polymerase chain reaction. Motility was determined on semi-solid agar. The B. cereus strains in this study were mainly characterized as enterotoxigenic strains; statistically significant differences were found in the PVC material and biofilm production. Motility was positively associated with the production of biofilm in glass/PVC. The sipW and tasA genes were found in two strains. The results of this study are important in the food industry because the strains carry at least one enterotoxin gene and produce biofilms on different materials

Cerebral Autoregulation Is Not Different Between Hot And Thermoneutral Head-Out Water Immersion In Healthy Participants

Recurring hot head-out water immersion (HOWI) enhances peripheral vascular function and cerebral blood velocity during non-immersion conditions (i.e., rest, aerobic exercise, and heat stress). However, it is not known if an acute bout of hot HOWI alters cerebrovascular function (i.e., cerebral autoregulation). PURPOSE: We tested the hypothesis that dynamic cerebral autoregulation is improved during and following an acute bout of hot (HOT) vs. thermoneutral (TN) HOWI. METHODS: Seventeen healthy participants (age: 23±2 y, 5 females) completed two randomized trials which consisted of 30 min of HOT (39°C) or TN (35°C) HOWI. Beat-to-beat blood pressure (MAP), middle cerebral artery blood velocity (MCAv), and end-tidal CO2 tension (PETCO2) were recorded continuously. After 5 min of seated rest, participants breathed through a respiratory impedance device for 5 min while maintaining PETCO2 values to assess cerebral autoregulation using Fourier transformation (n = 11). Cerebral autoregulation testing was completed pre, 30 min into HOWI (during), and immediately post HOWI. Values are reported as a change from baseline (α: mean ± SD). RESULTS: MAP, MCAv, PETCO2, gain, and phase were not different between HOT and TN at pre (P > 0.23 for all). αMAP was lower in HOT vs. TN during (-3±6 vs. 9±5 mmHg; P<0.01) and post (0±5 vs. 10±7 mmHg; P<0.01). αMCAv was lower in HOT vs. TN during (-3±5 vs. 4±4 cm/s; P<0.01) and post (-5±7 vs. 0±5 cm/s; P<0.01). αPETCO2 was lower in HOT vs. TN during (1±2 vs. 2±2 mmHg; P<0.01) and post (-3±2 vs. -1±2 mmHg; P<0.01). αGain was not different between HOT and TN during (HOT: -0.03±0.15 vs. TN: -0.08±0.05 cm/s/mmHg; P=0.18) or post (HOT: 0.04±0.12 vs. TN: -0.03±0.07 cm/s/mmHg; P=0.18). αPhase was not different between HOT and TN during (HOT: 2.9±9.0 vs. TN: 1.0±8.8°; P=0.74) or post (HOT: -1.2±12.8 vs. TN: -2.0±9.7°; P=0.74) CONCLUSION: These data indicate that an acute bout of hot water immersion attenuates cerebral blood velocity vs. thermoneutral water immersion. This response is likely due to the differences in arterial blood pressure and/or arterial carbon dioxide between conditions. However, cerebral autoregulation during and following hot water immersion is not different compared to thermoneutral water immersion in healthy participants. Supported by Office of Naval Research Award N00014-17-1-2665

Patterns and Impact of Arterial CO2 Management in Patients With Acute Respiratory Distress Syndrome: Insights From the LUNG SAFE Study

Considerable variability exists regarding CO2 management in early ARDS, with the impact of arterial CO2 tension on management and outcomes poorly understood. To determine the prevalence and impact of hypocapnia and hypercapnia on the management and outcomes of patients with early ARDS enrolled in the Large Observational Study to Understand the Global Impact of Severe Acute Respiratory Failure (LUNG SAFE) study, an international multicenter observational study. Our primary objective was to examine the prevalence of day 1 and sustained (day 1 and 2) hypocapnia (Paco2< 35mmHg), normocapnia (Paco2 35-45mmHg), and hypercapnia (Paco2 > 45mmHg) in patients with ARDS. Secondary objectives included elucidating the effect of CO2 tension on ventilatory management and examining the relationship with ARDS outcome. Of 2,813 patients analyzed, 551 (19.6%; 95%CI, 18.1-21.1) were hypocapnic, 1,018 (36.2%; 95%CI, 34.4-38.0) were normocapnic, and 1,214 (43.2%; 95%CI, 41.3-45.0) were hypercapnic, on day 1. Sustained hypocapnia was seen in 252 (9.3%; 95%CI, 8.2-10.4), sustained normocapnia in 544 (19.3%; 95%CI, 17.9-20.8), and sustained hypercapnia in 654 (24.1%; 95%CI, 22.5-25.7) patients. Hypocapnia was more frequent and severe in patients receiving noninvasive ventilation but also was observed in patients on controlled mechanical ventilation. Sustained hypocapnia was more frequent in middle-income countries, whereas sustained hypercapnia was more frequent in Europe. ARDS severity profile was highest in sustained hypercapnia, and these patients received more protective ventilation. No independent association was seen between arterial CO2 and outcome. In propensity-matched analyses, the hospital mortality rate was 36%in both sustained normocapnic and hypercapnic patients (P= 1.0). ICU mortality was higher in patients with mild to moderate ARDS receiving sustained hypocapnia (38.1%) compared with normocapnia (27.1%). No evidence was found for benefit or harm with hypercapnia. Of concern, ICU mortality was higher with sustained hypocapnia in mild to moderate ARDS.

Optimal ventilator settings after return of spontaneous circulation.

To describe current practice, recent advances in knowledge and future directions for research related to the post return of spontaneous circulation (ROSC) ventilatory management of cardiac arrest patients. Out-of-hospital cardiac arrest (OHCA) is a major public health problem with an estimated incidence of approximately one per 1000 persons per year. A priority of intensive care management of resuscitated OHCA patients is to reduce secondary reperfusion injury. Most OHCA patients are mechanically ventilated. Most of these require mechanical ventilation as they are unconscious and for oxygen (O2) management and carbon dioxide (CO2) control. Low levels of O2 and CO2 following OHCA is associated with poor outcome. Recently, very high fraction of inspired oxygen has been associated with poor outcomes and elevated CO2 levels have been associated with improved neurological outcomes. Moreover, it is increasingly being appreciated that the ventilator may be a tool to adjust physiological parameters to enhance the chances of favourable outcomes. Finally, ventilator settings themselves and the adoption of protective ventilation strategies may affect lung-brain interactions and are being explored as other avenues for therapeutic benefit. Current evidence supports the targeting of normal arterial O2 and CO2 tensions during mechanical ventilation following ROSC after cardiac arrest. Use of protective lung strategies during mechanical ventilation in resuscitated cardiac arrest patients is advocated. The potential therapeutic benefits of conservative O2 therapy, mild hypercapnia and the optimal ventilator settings to use post-ROSC period will be confirmed or refuted in clinical trials.

Fluid administration for acute circulatory dysfunction using basic monitoring.

This review aims at evaluating the role and the effectiveness of basic hemodynamic monitoring to guide and to titrate fluid administration during acute circulatory dysfunction. Fluid infusion is a cornerstone of the management of acute circulatory dysfunction. This is a time-related situation, which should be promptly faced to avoid multi organ dysfunction. For this purpose, the recognition of clinical signs of acute circulatory dysfunction is of pivotal importance. A prompt fluid resuscitation in the early phase of acute circulatory failure is a key and recommended intervention, on the other hand the hemodynamic targets and the safety limits indicating whether or not stopping this treatment in already resuscitated patients are still undefined. Bedside clinical examination has been demonstrated to be a reliable instrument to recognize the mismatch between cardiac function and peripheral oxygen demand. Mottling skin and capillary refill time have been recently proposed using a semi-quantitative approach as reliable tool to guide shock therapy; lactate level, central venous oxygen saturation and venous-to-arterial CO2 tension difference are also useful to track the effect of the therapies overtime. Finally, the availability of echocardiography miniaturization of the machines has boosted this technique as part of the daily clinical assessment of patient, inside and outside the intensive care units (ICUs).

Extracorporeal membrane oxygenation and V/Q ratios: an ex vivo analysis of CO2 clearance within the Maquet Quadrox-iD oxygenator.

While hypercapnia is typically well treated with modern membrane oxygenators, there are cases where respiratory acidosis persists despite maximal extracorporeal membrane oxygenation support. To better understand the physiology of gas exchange within the membrane oxygenator, CO2 clearance within an adult Maquet Quadrox-iD oxygenator was evaluated at varying blood CO2 tensions and V/Q ratios in an ex vivo extracorporeal membrane oxygenation circuit. A closed blood-primed circuit incorporating two Maquet Quadrox-iD oxygenators in series was attached to a Maquet PLS Rotaflow pump. A varying blend of CO2 and air was connected to the first oxygenator to provide different levels of pre-oxygenator blood CO2 levels (PvCO2) to the second oxygenator. Varying sweep gas flows of 100% O2 were connected to the second oxygenator to provide different V/Q ratios. Exhaust CO2 was directly measured, and then VCO2 and oxygenator dead space fraction (VD/VT) were calculated. VCO2 increased with increasing gas flow rates with plateauing at V/Q ratios greater than 4.0. Exhaust CO2 increased with PvCO2 in a linear fashion with the slope of the line decreasing at high V/Q ratios. Oxygenator dead space fraction varied with V/Q ratio-at lower ratios, dead space fraction was 0.3-0.4 and rose to 0.8-0.9 at ratios greater than 4.0. Within the Maquet Quadrox-iD oxygenator, CO2 clearance is limited at high V/Q ratios and correlated with elevated oxygenator dead space fraction. These findings have important implications for patients requiring high levels of extracorporeal membrane oxygenation support.

Cardiac Baroreflex Sensitivity during Mild Hypercapnia Following Acute Beetroot Juice Consumption

IntroductionPatients with obstructive sleep apnea often exhibit augmented arterial carbon dioxide tension (CO2) and autonomic dysfunction, which result in increased sympathetic activity and reduced baroreflex sensitivity. Beetroot juice (BRJ) is a popular nutraceutical that decreases resting sympathetic nerve activity and improves vascular function. However, the effects of acute BRJ consumption on cardiac baroreflex sensitivity (cBRS) in healthy individuals with elevated arterial CO2 is unknown.PurposeWe tested the hypothesis that acute BRJ consumption will decrease cBRS during mild hypercapnia.MethodsThirteen healthy adults (age: 26±4 years; 5 females) participated in two oscillatory lower body negative pressure (OLBNP) protocols while breathing a mild hypercapnic gas (3% CO2; 21% O2; 76% N2) during one study visit. OLBNP protocols were completed before (PRE) and 3 hours after consuming 500 mL of beetroot juice (BRJ). After a 5 min resting baseline (BL), the OLBNP protocols consisted of alternating 30 s intervals between −70 mmHg and 0 mmHg for a total of 5 min. Blood pressure (finger photoplethysmography), heart rate (HR; ECG), and end‐tidal CO2 tension (PETCO2; capnography) were continuously recorded and mean values across the −70 mmHg and 0 mmHg intervals during OLBNP were calculated. The sequence method (WinCPRS) was used to calculate cBRS from the obtained beat‐to‐beat blood pressure and R‐R interval data at PRE and BRJ throughout the 5 min BL and 5 min of OLBNP. cBRS was represented by Up‐cBRS and Down‐cBRS sequences and overall cBRS gain.ResultsAt BL, there were no differences in HR (PRE: 65±9 vs BRJ: 66±9 bpm; P=0.69), systolic blood pressure (SBP; PRE: 132±10 vs BRJ: 130±10 mmHg; P=0.17), diastolic blood pressure (DBP; PRE: 74±8 vs BRJ: 72±5 mmHg; P=0.14) and PETCO2 (PRE: 49±4 vs BRJ: 49±4 mmHg; P=0.45). At BL, mean arterial pressure (MAP) was lower with BRJ (96±8 vs 93±7 mmHg; P=0.01). At BL, there were no differences in Up‐BRS (PRE: 27±16 vs BRJ: 26±14 ms/mmHg; P=0.93), Down‐BRS (PRE: 22±11 vs BRJ: 20±9 ms/mmHg; P=0.65), or cBRS Gain (PRE: 17±8 vs BRJ: 19±8 ms/mmHg; P=0.18). During 0 mmHg of OLBNP, there were no differences in HR (PRE: 62±8 vs BRJ: 63±9 bpm; P=0.38), MAP (PRE: 98±7 vs BRJ: 97±6 mmHg; P=0.73), SBP (PRE: 133±7 vs BRJ: 133±10 mmHg; P=0.79), DBP (PRE 73±9 vs BRJ 74±5 mmHg; P=0.48), and PETCO2 (PRE 48±3 vs BRJ 48±4 mmHg; P=0.86). During −70 mmHg of OLBNP, there were no differences in DBP (PRE: 71±12 vs BRJ: 72±9 mmHg; P=0.48) or PETCO2 (PRE: 46±3 vs BRJ: 46±4 mmHg; P=0.86). During −70 mmHg of OLBNP with BRJ, HR was higher (77±10 vs 81±13 bpm; P&lt;0.01), MAP was lower (90±10 vs 88±10 mmHg; P=0.01), and SBP was lower (123±13 vs 120±16 mmHg; P=0.01). During OLBNP, there were no differences in Up‐BRS (PRE: 15±8 vs BRJ: 16±8 ms/mmHg; P=0.94), Down‐BRS (PRE: 14±7 ms/mmHg vs BRJ: 13±5 ms/mmHg; P=0.65), or cBRS Gain (PRE 13±6 vs BRJ 11±6 ms/mmHg P=0.18).ConclusionsDespite slight reductions in MAP following a single bolus of BRJ, there was no difference in cBRS in healthy participants while breathing a hypercapnic gas during an orthostatic challenge. Further research is warranted to determine the effects of chronic BRJ consumption on cBRS.

Glycophorin B‐A‐B Variant GP.Mur, a Chaperone for Erythroid SLC4A Transporter, Supports Gas Exchange during Exhaustive Exercise

The main function of glycophorin A is to stabilize protein complex expression of SLC4A (band 3) and to facilitate its Cl−/HCO3− antiporter activity across human red blood cell (RBC) membrane. Anion exchange through SLC4A on the RBC surface is physiologically critical for blood CO2 transport. We previously found that glycophorin B‐A‐B hybrid protein GP.Mur, a special blood type unique to people of Southeast Asian origins, further promotes erythroid expression of SLC4A. People with GP.Mur phenotype not only express more band 3 on their RBCs but also exhibit more efficient blood CO2 expiration when challenged with a mild stepping exercise test. We have noticed a disproportional number of elite athletes in Taiwan bearing the GP.Mur phenotype. The goal of this study was thus to verify whether GP.Mur expression could indeed support the respiratory function of elite athletes during exhaustive exercise. Here we recruited GP.Mur+ and GP.Mur‐young elite/professional athletes in Taiwan and challenged them with a graded, exhaustive protocol of cardiopulmonary exercise testing (CPET). As revealed by CPET, compared to the athletes lacking the special blood type, GP.Mur+ athletes showed smaller respiratory quotient (RQ) and lower arterial CO2 tension throughout the graded test before exhaustion. This suggests relative easiness on the respiratory function for athletes with GP.Mur phenotype during exhaustive exercise. We are currently exploring the possibility of utilizing one’s GP.Mur/band 3 expression levels in personalized athletic training.Support or Funding InformationTaiwan Ministry of Science &amp; Technology (MOST 108‐2628‐B‐195‐001)

Effect of dexmedetomidine on dynamic cerebral autoregulation and carbon dioxide reactivity during sevoflurane anesthesia in healthy patients.

BackgroundThere are conflicting opinions on the effect of dexmedetomidine on cerebral autoregulation. This study assessed its effect on dynamic cerebral autoregulation (dCA) using a transcranial Doppler (TCD).MethodsThirty American Society of Anesthesiologists physical status I and II patients between 18 and 60 years, who underwent lumbar spine surgery, received infusions of dexmedetomidine (Group D) or normal saline (Group C), followed by anesthesia with propofol and fentanyl, and maintenance with oxygen, nitrous oxide and sevoflurane. After five minutes of normocapnic ventilation and stable bispectral index value (BIS) of 40–50, the right middle cerebral artery flow velocity (MCAFV) was recorded with TCD. The transient hyperemic response (THR) test was performed by compressing the right common carotid artery for 5–7 seconds. The lungs were hyperventilated to test carbon dioxide (CO2) reactivity. Hemodynamic parameters, arterial CO2 tension, pulse oximetry (SpO2), MCAFV and BIS were measured before and after hyperventilation. Dexmedetomidine infusion was discontinued ten minutes before skin-closure. Time to recovery and extubation, modified Aldrete score, and emergence agitation were recorded.ResultsDemographic parameters, durations of surgery and anesthesia, THR ratio (Group D: 1.26 ± 0.11 vs. Group C: 1.23 ± 0.04; P = 0.357), relative CO2 reactivity (Group D: 1.19 ± 0.34 %/mmHg vs. Group C: 1.23 ± 0.25 %/mmHg; P = 0.547), blood pressure, SpO2, BIS, MCAFV, time to recovery, time to extubation and modified Aldrete scores were comparable.ConclusionsDexmedetomidine administration does not impair dCA and CO2 reactivity in patients undergoing spine surgery under sevoflurane anesthesia.