Peripheral Oxyhemoglobin Saturation Research Articles

Acute Hyperoxia Improves Spinal Cord Oxygenation and Circulatory Function Following Cervical Spinal Cord Injury in Rats

Spinal cord injury is associated with spinal vascular disruptions that result in spinal ischemia and tissue hypoxia. This study evaluated the therapeutic efficacy of normobaric hyperoxia on spinal cord oxygenation and circulatory function at the acute stage of cervical spinal cord injury. Adult male Sprague Dawley rats underwent dorsal cervical laminectomy or cervical spinal cord contusion. At 1–2 days after spinal surgery, spinal cord oxygenation was monitored in anesthetized and spontaneously breathing rats through optical recording of oxygen sensor foils placed on the cervical spinal cord and pulse oximetry. The arterial blood pressure, heart rate, blood gases, and peripheral oxyhemoglobin saturation were also measured under hyperoxic (50% O2) and normoxic (21% O2) conditions. The results showed that contused animals had significantly lower spinal cord oxygenation levels than uninjured animals during normoxia. Peripheral oxyhemoglobin saturation, arterial oxygen partial pressure, and mean arterial blood pressure are significantly reduced following cervical spinal cord contusion. Notably, spinal oxygenation of contused rats could be improved to a level comparable to uninjured animals under hyperoxia. Furthermore, acute hyperoxia elevated blood pressure, arterial oxygen partial pressure, and peripheral oxyhemoglobin saturation. These results suggest that normobaric hyperoxia can significantly improve spinal cord oxygenation and circulatory function in the acute phase after cervical spinal cord injury. We propose that adjuvant normobaric hyperoxia combined with other hemodynamic optimization strategies may prevent secondary damage after spinal cord injury and improve functional recovery.

The role of upper airway and facial skeleton anatomy in the evolution of obstructive sleep apnea: an 8-year follow-up.

To evaluate the role of anatomic alterations of the upper airway and facial skeleton in the evolution of obstructive sleep apnea (OSA) in a prospective population-based study with an 8-year follow-up. This was a population-based, longitudinal, prospective study, which took place from 2007 to 2015 at the Instituto do Sono, Sao Paulo, Brazil. In 2007, type I polysomnography (PSG), otorhinolaryngological examination, and collection of anthropometric measurements of all volunteers were performed. Volunteers were classified according to their anatomical features of the upper airway and facial skeleton. After 8 years, volunteers were invited for reevaluation. The relationship between anatomical characteristics and polysomnographic evolution was evaluated. The study included 554patients. After 8 years of follow-up, there was an increase in neck circumference and body mass index of the participants. There was a worsening in all polysomnographic parameters analyzed, with an increase in the apnea-hypopnea index, a decrease in minimum saturation values, and an increase in the percentage of sleep time with peripheral oxyhemoglobin saturation <90%. There was no statistical relationship between the anatomical findings considered unfavorable and the worsening of polysomnographic parameters. In a sample of the general population, after 8 years, we did not find any relationship between upper airway and facial skeleton characteristics and the progression of OSA.

Sleep and cardiometabolic comorbidities in the obstructive sleep apnoea-COPD overlap syndrome: data from the European Sleep Apnoea Database.

The impact of obstructive sleep apnoea (OSA)-COPD overlap syndrome (OVS) on sleep quality and cardiovascular outcomes has not been fully explored. We aimed to compare clinical and polysomnographic characteristics of patients with OVS versus patients with OSA, and to explore pathophysiological links between OVS and comorbidities. This cross-sectional analysis initially included data from 5600 patients with OSA and lung function in the European Sleep Apnoea Database. Two subgroups of patients with OSA (n=1018) or OVS (n=509) were matched (2:1) based on sex, age, body mass index and apnoea-hypopnea index at baseline. After matching, patients with OVS had more severe hypoxia, lower sleep efficiency and presented with higher prevalences of arterial hypertension, ischaemic heart disease and heart failure compared with patients with OSA. OVS was associated with a significant decrease in sleep efficiency (mean difference (β) -3.0%, 95% CI -4.7 to -1.3) and in nocturnal mean peripheral oxyhaemoglobin saturation (SpO2) (β -1.1%, 95% CI -1.5 to -0.7). Further analysis revealed that a decrease in forced expiratory volume in 1 s and arterial oxygen tension was related to a decrease in sleep efficiency and in mean nocturnal SpO2. A COPD diagnosis increased the odds of having heart failure by 1.75 (95% CI 1.15-2.67) and systemic hypertension by 1.36 (95% CI 1.07-1.73). Nocturnal hypoxia was strongly associated with comorbidities; the mean nocturnal SpO2 and T90 (increase in time below SpO2 of 90%) were associated with increased odds of systemic hypertension, diabetes and heart failure but the oxygen desaturation index was only related to hypertension and diabetes. Patients with OVS presented with more sleep-related hypoxia, a reduced sleep quality and a higher risk for heart failure and hypertension.

Immediate and Medium-Term Follow-Up of Patients with Obstructive Sleep Apnea Undergoing Pharyngeal and Nasal Surgery: A Pilot Study.

Objectives  To evaluate the evolution of obstructive sleep apnea (OSA), comparing data from preoperative, immediate postoperative and late postoperative, in patients undergoing pharyngeal surgery associated with nasal surgery, and to compare the findings of arterial tonometry and type 1 polysomnography in the late postoperative period. Methods  Seventeen adults with moderate or severe OSA were included in the study. They underwent clinical evaluation, surgical intervention, and sleep study preoperatively, on the 1 st night after surgery, and after a minimum period of 3 months. The data for the three moments were compared. Results  The mean age was 38.1 ± 12.5 years old (22 to 59 years old), and 82.3% were male. Body mass index (BMI) ranged from 25.6 to 45.1 kg/m2 (mean = 33.1 ± 5.8 kg/m 2 ). Fifteen patients (88.2%) were diagnosed with severe OSA. There was a progressive improvement, with a decrease in the indexes (AHI and RDI) and in the percentage of time with peripheral oxyhemoglobin saturation below 90% (tSpO < 90%), and an increase in nadir of SpO2. In the comparison between the 2 methods used in the late postoperative period - arterial tonometry and polysomnography - there was no difference in the indexes and in the tSpO < 90%. Discussion  There was a progressive and favorable impact of pharyngeal surgery on the improvement of polysomnographic and clinical respiratory parameters; however, many patients maintained residual OSA, suggesting the need for a new sleep study in the postoperative period. The arterial tonometry showed similar findings to polysomnography, which can be considered as an option in postoperative follow-up of patients.

Unstable SpO2 in preterm infants: The key role of reduced ventilation to perfusion ratio.

Introduction: Instability of peripheral oxyhemoglobin saturation (SpO2) in preterm infants is correlated with late disability and is poorly understood. We hypothesised that a reduced ventilation to perfusion ratio (VA/Q) is the key predisposing factor for SpO2 instability. Methods: We first used a mathematical model to compare the effects of reduced VA/Q or shunt on SaO2 stability (SaO2 and SpO2 are used for model and clinical studies respectively). Stability was inferred from the slope of the SaO2 vs. inspired oxygen pressure (P IO2) curve as it intersects the 21kPa P IO2 line (breathing air). Then, in a tertiary neonatal intensive care unit, paired hourly readings of SpO2 and P IO2 were recorded over a 24h period in week old extremely preterm infants. We noted SpO2 variability and used an algorithm to derive VA/Q and shunt from the paired SpO2 and P IO2 measurements. Results: Our model predicted that when VA/Q < 0.4, a 1% change in P IO2 results in >8% fluctuation in SaO2 at 21kPa P IO2. In contrast, when a 20% intrapulmonary shunt was included in the model, a 1% change in P IO2 results in <1% fluctuation in the SaO2. Moreover, further reducing the VA/Q from 0.4 to 0.3at 21kPa P IO2 resulted in a 24% fall in SaO2. All 31 preterm infants [mean gestation (±standard deviation) 26.2 (±1)week] had VA/Q < 0.74 (normal >0.85) but only two infants had increased shunt at 1.1 (±0.5)weeks' postnatal age. Median (IQR) SpO2 fluctuation was 8 (7)%. The greatest SpO2 fluctuations were seen in infants with VA/Q < 0.52 (n = 10): SpO2 fluctuations ranged from 11%-17% at a constant P IO2 when VA/Q < 0.52. Two infants had reduced VA/Q and increased shunt (21% and 27%) which resolved into low VA/Q after 3-6h. Discussion: Routine monitoring of P IO2 and SpO2 can be used to derive a hitherto elusive measure of VA/Q. Predisposition to SpO2 instability results from reduced VA/Q rather than increased intrapulmonary shunt in preterm infants with cardiorespiratory disease. SpO2 instability can be prevented by a small increase in P IO2.

Obstructive sleep apnea and pulmonary hypertension: the pendulum swings again.

Free AccessCommentaryObstructive sleep apnea and pulmonary hypertension: the pendulum swings again Jenny Z. Yang, MD, Babak Mokhlesi, MD, Omar A. Mesarwi, MD Jenny Z. Yang, MD Address correspondence to: Jenny Z. Yang, MD, 9300 Campus Point Dr., MC 7381, La Jolla, CA 92037; Email: E-mail Address: [email protected] Division of Pulmonary, Critical Care, and Sleep Medicine and Physiology, University of California, San Diego, La Jolla, California; Search for more papers by this author , Babak Mokhlesi, MD Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Rush University Medical Center, Chicago, Illinois Search for more papers by this author , Omar A. Mesarwi, MD Division of Pulmonary, Critical Care, and Sleep Medicine and Physiology, University of California, San Diego, La Jolla, California; Search for more papers by this author Published Online:February 1, 2023https://doi.org/10.5664/jcsm.10454SectionsPDF ShareShare onFacebookTwitterLinkedInRedditEmail ToolsAdd to favoritesDownload CitationsTrack Citations AboutINTRODUCTIONObstructive sleep apnea (OSA) is highly prevalent1 and has been shown to be an independent risk factor for multiple adverse cardiovascular outcomes, including hypertension, heart failure, coronary heart disease, and arrhythmias.2 However, a clear link demonstrating causality between OSA and pulmonary hypertension (PH) is less well entrenched in the literature. Over 25 years ago, a major study in which 220 patients with OSA were evaluated for PH using right heart catheterization (RHC) concluded that OSA plays only a very minor role in the development of PH.3 The authors suggested that concurrent obstructive lung disease and daytime hypoxemia were more critical for the development of PH than OSA severity. A few years later though, Sajkov et al4 carefully demonstrated that after excluding individuals with lung disease or hypoventilation, there was a persistent and perhaps clinically important association between PH and OSA, though in general OSA was only associated with mild to moderate PH, and elevations in pulmonary arterial pressures improve with the initiation of continuous positive airway pressure therapy.5 Consequently, in 1998 at the Second World Symposium of PH6, sleep-disordered breathing was classified as an associated condition of group 3 (hypoxemia-related) PH. At our institutions and many others worldwide, practice shifted toward diagnosis and treatment of sleep-disordered breathing in those with PH.Since then, multiple studies have re-evaluated the association between OSA and PH, but there remains equipoise on mechanism and controversy on causality. Samhouri et al7 attempted to address some of these issues by performing a retrospective review of PH patients who had both polysomnogram and RHC data. Sleep time spent with peripheral oxyhemoglobin saturation (SpO2) less than 90% (T90) was found to be higher among patients with all subtypes of PH and was associated with higher mean pulmonary artery pressure (mPAP), pulmonary vascular resistance (PVR), and right atrial pressure as well. However, this study was limited by a lack of comprehensive sleep data, and it remained unclear whether a higher T90 in this population was simply a marker of PH severity, instead of—or in addition to—a manifestation of OSA severity.In this issue of the Journal of Clinical Sleep Medicine, Huang et al8 provide some data in order to clarify a few of these points. In this study, patients who were suspected of having PH based on echocardiographic findings were hospitalized and then underwent both an RHC and polysomnogram. Patients were stratified by presence of OSA and PH, which was defined as mPAP ≥ 25 mm Hg. PH was further categorized as pre- or postcapillary, based on a pulmonary artery wedge pressure threshold of 15 mm Hg. Those with predominantly central sleep apnea were excluded, as were those with pulmonary disease requiring supplemental oxygen. Of the 563 patients remaining, 358 did not have OSA and 205 did have OSA. Although the authors primarily focused their attention toward those with OSA, they report data about those without OSA as well. In the OSA cohort, prevalence of PH was 65% (85% of those having precapillary PH), whereas prevalence of PH in the non-OSA cohort was somewhat surprisingly higher (84%). Similar to the study by Samhouri et al,7 T90 was closely correlated with pulmonary hemodynamics. mPAP, PVR, and right ventricular stroke work indices were all worse as a function of increasingly higher tertile of T90, and this relationship held after adjustment for common covariates (age, sex, body mass index, presence of left heart disease, etc). Correspondingly, patients with PH also had more severe hypoxemia on their sleep studies, whether quantified by mean SpO2, T90, nadir SpO2, or apnea time, although respiratory event index, a more traditional measure of OSA severity, was not worse among those with PH.One major strength of this study, compared to previous examinations of the OSA-PH relationship, is that we have some basic information about those patients without OSA too. Having these data is important, as we finally can get some insight about the “chicken or the egg” nature of the interaction between hypoxemia in OSA and PH. Is the hypoxemia in OSA, previously noted to be correlated with PH severity, occurring due to the presence of OSA pushing PA pressures higher, or is this an epiphenomenon of more severe PH? In patients without OSA from this study, there was a statistical but somewhat trivial difference in T90 among those with or without PH (0.35% vs 0%, respectively). By contrast, among those with PH, T90 was markedly higher in those with OSA (9.4%) than in those without OSA (0.3%). This finding seemingly implies that nocturnal hypoxemia resulting from PH alone is minimal, and that OSA is linked perhaps not just by association with worsened pulmonary hemodynamics. But we also note an important caveat: Looking at hypoxemia metrics other than T90 among non-OSA patients with and without PH, there is a significant difference in mean saturation (94% vs 97%, respectively). Though this outcome does not fully explain T90 findings, we believe it adds somewhat to uncertainty about the cause-effect relationship between hypoxemia in OSA and PH; PH itself may be causing mild hypoxemia, contributing somewhat to a false association between hypoxemia in OSA and PH severity, and somewhat clouding the interactions seen in this study.There are a few other limitations worth mentioning. First, all patients enrolled had a suspicion of PH based on echocardiography and were subsequently screened for OSA. Therefore, the findings are likely not generalizable to a standard OSA population, and PH prevalence data were likely higher than one would expect among a general OSA cohort. Indeed, among those even without OSA, the prevalence of PH was very high, suggesting a selection bias. Second, polysomnograms were performed as inpatient studies, which is unusual in many institutions, so this may affect the quality of sleep and recorded data. Third, while 85% of the patients with OSA and PH were deemed to have precapillary PH, when these patients were grouped by tertile, the most severely hypoxemic (tertile 3, T90 ≥ 12.25%) had a mean pulmonary arterial wedge pressure of 20.1 mm Hg, which is more consistent with postcapillary PH. Fourth, and relatedly, the subtypes of precapillary PH are unclear. Precapillary PH encompasses groups 1, 3, 4, and 5 PH, and these conditions have very different underlying pathophysiology. Finally, the 2022 European Society of Cardiology (ESC)/European Respiratory Society (ERS) guidelines on PH were released in September 2022 with some significant changes.9 The mPAP threshold was lowered to > 20 mm Hg, consistent with the Second World Symposium of PH guidelines, but the PVR threshold was also lowered from 3 Wood units to 2. In addition to changes in the hemodynamic definition of PH, there were also changes in the classification of PH; most notably, “sleep disordered breathing” was removed as a potential etiology of group 3 PH and was replaced with “hypoventilation syndromes,” with the note that “[s]ole nocturnal obstructive sleep apnoea is generally not a cause of PH.” This assertion may become more controversial in time with data such as presented by Huang et al. However, we note that this study does not report data on hypercapnia or the possibility of concurrent obesity hypoventilation syndrome.The concept of hypoxemia severity being causally related to PH has merit based on preclinical studies. Chronic hypoxia exposure has been used for decades to produce pulmonary hypertension in rodent models and is particularly successful with a “second hit” of monocrotaline or a vascular endothelial growth factor inhibitor. This exposure faithfully recapitulates hemodynamic and histologic findings of human PH.10 While some studies have demonstrated that severe intermittent hypoxia modeling OSA increases Fulton index (RV mass divided by LV plus septal mass) or right ventricular systolic pressure (RVSP), the severity of PH induced by this model is generally less than that induced by chronic sustained hypoxia.11,12 Indeed, in 1 clinical study of 43 patients with pulmonary arterial hypertension, most patients (70%) had nocturnal hypoxemia (T90 > 10%), but only 2 patients had an apnea index > 5.13 At our institutions (The University of California San Diego and Rush University Medical Center), our practice is to screen for symptoms of sleep-disordered breathing in most PH patients, and to refer symptomatic patients for sleep studies or, at a minimum, nocturnal oximetry. For new PH referrals with mildly elevated RVSP on echocardiography and high risk for OSA (eg, older males with obesity and/or cardiovascular comorbidities), we often pursue diagnostic testing for OSA, though RHC is usually not needed. And in our experience, when OSA is treated, the RVSP is typically reduced to normal on repeat echocardiography if there are no other contributing conditions. From the sleep medicine side, in the absence of clinical signs of right heart failure, or obesity hypoventilation syndrome, we do not routinely screen for PH in all OSA patients.Huang et al’s work is commendable and adds significantly to our understanding of the relationship between PH and OSA, though there is more to be said about this complex interaction. Future studies could re-evaluate T90 and invasive pulmonary hemodynamics after continuous positive airway pressure therapy specifically in OSA patients with more severe PH. Understanding the contribution of intermittent and/or sustained hypercapnia (in rodents and in humans) would also help us understand biological mechanisms in a more robust manner. We also need clinical guidelines about who specifically to refer for PH assessment in those with OSA, and who to refer for OSA assessment in those with PH. On both sides, it is becoming clear that referral of all patients is probably unnecessary. The new ESC/ERS PH guidelines will likely lead to more PH diagnoses but the ramifications of changes to the PH definition and classification, specifically in relation to those with OSA, remain to be seen. The pendulum has swung more than once on this topic, and we will likely see it happen again.DISCLOSURE STATEMENTAll authors have seen and approved this manuscript. The authors have no financial support to declare, nor any conflict of interest which could impact the manuscript as submitted.REFERENCES1. Benjafield AV, Ayas NT, Eastwood PR, et al.. Estimation of the global prevalence and burden of obstructive sleep apnoea: a literature-based analysis. Lancet Respir Med. 2019;7(8):687–698 . CrossrefGoogle Scholar2. Bradley TD, Floras JS. Obstructive sleep apnoea and its cardiovascular consequences. Lancet. 2009;373(9657):82–93 . CrossrefGoogle Scholar3. Chaouat A, Weitzenblum E, Krieger J, Oswald M, Kessler R. Pulmonary hemodynamics in the obstructive sleep apnea syndrome. Results in 220 consecutive patients. Chest. 1996;109(2):380–386 . CrossrefGoogle Scholar4. Sajkov D, Wang T, Saunders NA, Bune AJ, Neill AM, McEvoy RD. Daytime pulmonary hemodynamics in patients with obstructive sleep apnea without lung disease. Am J Respir Crit Care Med. 1999;159(5):1518–1526 . CrossrefGoogle Scholar5. Sajkov D, Wang T, Saunders NA, Bune AJ, McEvoy RD. Continuous positive airway pressure treatment improves pulmonary hemodynamics in patients with obstructive sleep apnea. Am J Respir Crit Care Med. 2002;165(2):152–158 . CrossrefGoogle Scholar6. Rich S, ed. Primary pulmonary hypertension: executive summary from the World Symposium - Primary Pulmonary Hypertension 1998. http://www.wsphassociation.org/wp-content/uploads/2019/04/Primary-Pulmonary-Hypertension-Evian-1998.pdf. Accessed January 13, 2023. Google Scholar7. Samhouri B, Venkatasaburamini M, Paz Y Mar H, Li M, Mehra R, Chaisson NF. Pulmonary artery hemodynamics are associated with duration of nocturnal desaturation but not apnea-hypopnea index. J Clin Sleep Med. 2020;16(8):1231–1239 . LinkGoogle Scholar8. Huang Z, Duan A, Hu M, et al.. Implication of prolonged nocturnal hypoxemia and obstructive sleep apnea for pulmonary hemodynamics in patients being evaluated for pulmonary hypertension: a retrospective study. J Clin Sleep Med. 2023;19(2):213–223 . LinkGoogle Scholar9. Humbert M, Kovacs G, Hoeper MM, et al. ESC/ERS Scientific Document Group. 2022 ESC/ERS guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Respir J. 2022:2200879 . Google Scholar10. Maarman G, Lecour S, Butrous G, Thienemann F, Sliwa K. A comprehensive review: the evolution of animal models in pulmonary hypertension research; are we there yet? Pulm Circ. 2013;3(4):739–756 . CrossrefGoogle Scholar11. Fagan KA. Selected contribution: pulmonary hypertension in mice following intermittent hypoxia. J Appl Physiol. 2001;90(6):2502–2507 . CrossrefGoogle Scholar12. Zhen X, Moya EA, Gautane M, et al.. Combined intermittent and sustained hypoxia is a novel and deleterious cardio-metabolic phenotype. Sleep. 2022;45:zsab290 . CrossrefGoogle Scholar13. Minai OA, Pandya CM, Golish JA, et al.. Predictors of nocturnal oxygen desaturation in pulmonary arterial hypertension. Chest. 2007;131(1):109–117 . CrossrefGoogle Scholar Next article FiguresReferencesRelatedDetails Volume 19 • Issue 2 • February 1, 2023ISSN (print): 1550-9389ISSN (online): 1550-9397Frequency: Monthly Metrics History Submitted for publicationDecember 15, 2022Accepted for publicationDecember 15, 2022Published onlineFebruary 1, 2023 Information© 2023 American Academy of Sleep MedicinePDF download

Effectiveness, implementation, and monitoring variables of intermittent hypoxic bicycle training in patients recovered from COVID-19: The AEROBICOVID study.

Hypoxic exposure is safely associated with exercise for many pathological conditions, providing additional effects on health outcomes. COVID-19 is a new disease, so the physiological repercussions caused by exercise in affected patients and the safety of exposure to hypoxia in these conditions are still unknown. Due to the effects of the disease on the respiratory system and following the sequence of AEROBICOVID research work, this study aimed to evaluate the effectiveness, tolerance and acute safety of 24 bicycle training sessions performed under intermittent hypoxic conditions through analysis of peripheral oxyhemoglobin saturation (SpO2), heart rate (HR), rate of perceived exertion (RPE), blood lactate concentration ([La-]) and symptoms of acute mountain sickness in patients recovered from COVID-19. Participants were allocated to three training groups: the normoxia group (GN) remained in normoxia (inspired fraction of O2 (FiO2) of ∼20.9%, a city with 526m altitude) for the entire session; the recovery hypoxia group (GHR) was exposed to hypoxia (FiO2 ∼13.5%, corresponding to 3,000m altitude) all the time except during the effort; the hypoxia group (GH) trained in hypoxia (FiO2 ∼13.5%) throughout the session. The altitude simulation effectively reduced SpO2 mean with significant differences between groups GN, GHR, and GH, being 96.9(1.6), 95.1(3.1), and 87.7(6.5), respectively. Additionally, the proposed exercise and hypoxic stimulus was well-tolerated, since 93% of participants showed no or moderate acute mountain sickness symptoms; maintained nearly 80% of sets at target heart rate; and most frequently reporting session intensity as an RPE of "3" (moderate). The internal load calculation, analyzed through training impulse (TRIMP), calculated using HR [TRIMPHR = HR * training volume (min)] and RPE [TRIMPRPE = RPE * training volume (min)], showed no significant difference between groups. The current strategy effectively promoted the altitude simulation and monitoring variables, being well-tolerated and safely acute exposure, as the low Lake Louise scores and the stable HR, SpO2, and RPE values showed during the sessions.

Analgesic efficacy of ultrasound-guided transversus abdominis plane block in dogs undergoing ovariectomy.

In medicine, the transversus abdominis plane (TAP) block has been shown as an effective method of analgesia in several surgical procedures. In this context, this prospective, randomized, blinded study aimed to evaluate the analgesic efficacy of TAP block, guided by ultrasound in female dogs submitted to ovariectomy. Therefore, 32 animals randomly assigned in two groups (n = 16) were used. Groups consisted of TAP block control (TBC) which received water injection (0.2 ml kg-1 point), and TAP block bupivacaine (TBB) which received bupivacaine (0.2 ml kg-1 point at 0.25%); both groups were submitted to four-point approach. Animals were pre-medicated with acepromazine (0.03 mg kg-1) and meperidine (2 mg kg-1) IM, propofol was used as anesthetic induction (3-5 mg kg-1) IV, and isoflurane was used to maintain. To standardize groups, the animals received a continuous infusion of remifentanil (0.2μg kg-1 min) and rocuronium (0.6 mg kg-1) IV in the intraoperative period. Variables measured were the heart and respiratory rates, blood pressure, temperature, peripheral oxyhemoglobin saturation, exhaled carbon dioxide concentration, exhaled isoflurane concentration, serum cortisol, analgesia, and sedation. Before the pre-anesthetic medication (Baseline) and 1, 2, 4, 6, and 8 h after extubation, pain and sedation were assessed using a numeric rating scale (NRS), Glasgow composite measure pain scale (GCMPS-SF), and sedation scale. Moreover, serum cortisol was measured at different moments. The results show that in the intraoperative period, there was no significant difference between groups. After surgery, in TBC, 13 out of 16 animals required analgesic rescue, whereas, in TBB, this occurred only in one animal. Regarding the measurement of serum cortisol, the TBC group showed a significant difference when compared to the baseline time in the traction of the first ovary (p < 0.0001), 2 h (p = 0.0441), and 8 h (p = 0.0384) after extubation. In TBB, cortisol showed a significant increase only in the traction of the first ovary and 2 h after extubation (p < 0.0001). The technique using ultrasound-guided TAP block in two points approach by hemiabdomen with 0.2 ml kg-1 bupivacaine 0.25% was effective in providing post-operative analgesia in dogs undergoing ovariectomy.

The effect of dietary intake on apneic performance, cardiovascular and splenic responses during repeated breath holds.

Static apneas performed after an overnight fast as opposed to postprandially have been evinced to improve apneic performance. However, no study has explored the effect of dietary intake on apneic performance, cardiovascular or splenic responses over a series of repeated apneas. Ten healthy adults attended the laboratory on three separate occasions (≥48-h apart): after a 14-h fast (F14), 1 h postconsumption of a high-calorie, high-carbohydrate (HCHC) meal, or 1 h postconsumption of a low-calorie, low-carbohydrate (LCLC)-based meal. During each visit, the subjects performed a hyperoxic rebreathing trial and a series of three repeated maximal static apneas. Heart rate, peripheral oxyhemoglobin saturation ([Formula: see text]), and gas exchange were monitored continuously, whereas splenic volume (SV) and hematology were assessed after the rebreathing and apneas. At rest, after HCHC, the respiratory exchange ratio (0.87 ± 0.17, P ≤ 0.043), expired minute volume of carbon dioxide (CO2; HCHC, 0.35 ± 0.09 L/min, P ≤ 0.014), and SV (227 ± 45 mL, P ≤ 0.031) were higher compared with F14 (0.71 ± 0.08; 0.23 ± 0.04 L/min; 204 ± 49 mL) and LCLC (0.72 ± 0.07; 0.25 ± 0.03 L/min; 199 ± 49 mL). A faster CO2 accumulation was recorded during the HCHC (96 ± 35 s) rebreathing trial (F14, 162 ± 42 s, P = 0.001; LCLC, 151 ± 23 s, P = 0.002). Longer apneas were reported in F14 compared with HCHC (apneas 1-3, P ≤ 0.046) and LCLC (apneas 2-3, P ≤ 0.006). After the first apnea, SV was lower in F14 (141 ± 43 mL, P = 0.015) compared with HCHC (180 ± 34 mL). Moreover, after the third apnea, end-tidal partial pressure of oxygen and nadir [Formula: see text] were lower in F14 (8.6 ± 2.2 kPa, P = 0.028; 77 ± 13%, P = 0.009) compared with HCHC (10.1 ± 1.7 kPa; 84 ± 9%). No differences were measured in end-apneic end-tidal partial pressure of CO2, heart rate nor hematology across diets. Fasting improved apneic performance with apneas being terminated at lower oxygen levels through altering the rate of CO2 accumulation but without affecting the cardiovascular responses.

Cardiopulmonary Parameters and Arterial Blood Gases During Etorphine-Medetomidine-Midazolam Immobilization in Free-Ranging Black Rhinoceroses (Diceros bicornis) Undergoing Electro-Ejaculation-A Preliminary Study.

Conservation management interventions for the critically endangered black rhinoceros (Diceros bicornis) require immobilization, which offer opportunities for semen collection and cryopreservation to establish genetic reservoirs. In free-ranging rhinoceroses, a combination of the potent opioid etorphine and the tranquilizer azaperone is routinely used for chemical immobilization but is associated with muscle rigidity and severe cardiopulmonary changes. Additionally, azaperone inhibits semen emission. Seven free-ranging, male, sexually mature black rhinoceroses were immobilized with an alternative protocol consisting of 4.5 mg etorphine, 5 mg medetomidine, 50 mg midazolam and 2,500 IU hyaluronidase delivered remotely by darting from a helicopter. During the immobilization, electro-ejaculation was performed with a portable electro-ejaculator, and a species-specific rectal probe. Animals were observed for muscle tremors. Longitudinal changes in respiratory rate, heart rate and peripheral oxyhemoglobin saturation, measured at 5 min intervals, were assessed using a general mixed model. Non-invasive oscillometric blood pressure and arterial blood gas variables were measured at first handling and before reversal and compared using the Wilcoxon rank sum test. All animals were successfully immobilized, showed no muscle tremors, presented with normal heart rates and lactate concentration (<5 mmol/L), recovered uneventfully, but experienced acidemia, hypoxemia and hypercapnia. Induction time and total time in recumbency were 4.2 ± 0.41 and 38.4 ± 6.9 min, respectively. Electro-stimulation commenced after 11.7 ± 3.98 min and completed after 24.3 ± 6.65 min. Semen-rich fractions were successfully collected from six animals. Our observations indicate that etorphine-medetomidine-midazolam provides a promising immobilization protocol for free-ranging black rhinoceroses, that allows for successful electro-ejaculation.

Pulmonary Gas Exchange Improves over the First Year in Preterm Infants with and without Bronchopulmonary Dysplasia

Background: Right shift of the peripheral oxyhaemoglobin saturation (SpO₂) versus inspired oxygen pressure (P_IO₂) curve is a sensitive marker of pulmonary gas exchange. Objectives: The aim of this study was to assess the impact of prematurity and bronchopulmonary dysplasia (BPD) on gas exchange and right-to-left shunt in the neonatal period, and its evolution over the first year of life. Method: We assessed shift and shunt in extremely preterm (EP) and very preterm (VP) infants at 36 and 44 weeks’ postmenstrual age (PMA), and at 1-year corrected postnatal age (cPNA). P_IO₂ was decreased stepwise to achieve SpO₂ between 85 and 98%. Shift and shunt were calculated from paired SpO₂/P_IO₂ measurements using customized software. Results were examined cross-sectionally at each time point, and longitudinally using generalized linear regression. Term infants were assessed at 44 wk PMA as a comparative reference. Results: Longitudinal modelling showed continuous decline in shift in EP and VP infants during the first year of life. There was no difference in shift compared to term infants at 44 wk PMA (p = 0.094). EP infants with BPD had higher shift than infants without BPD at 36 wk PMA (p < 0.001) and 44 wk PMA (p = 0.005) but not at 1-year cPNA. Conclusions: In the absence of lung disease, prematurity per se did not result in reduced gas exchange at 1-year cPNA. We report ongoing, significant improvements in pulmonary gas exchange in all preterm infants during the first year of life, despite evidence of early deficits in gas exchange in EP infants with BPD.

Digital Health and Possible Solutions to Improve the Care in the Field of Nephrology.

Digital health is an area that emerges from the association between health needs and technological solutions. With the growing access of people to the internet and the ease of acquiring equipment that allows internet connection, we are observing an exponential increase in the strategies that use technology to connect patients and healthcare providers. Telenephrology is a channel of communication that facilitates the access to the nephrologist for both primary care physicians and patients and has been implemented in several countries. Applications for smartphones are frequently used by both patients and healthcare providers, and these tools are changing the way we practice nephrology and medicine in general. Social networks emerge as an important way of communicating between healthcare professionals and patients and a source of connection for people with the same interests. Artificial intelligence, big data, and other technological solutions, including wearable devices that measure and monitor different health parameters, are revolutionizing healthcare and the field of nephrology. Implantable devices are in development, including devices to monitor electrolytes in dialysis patients, systems to track medication intake, wearables to monitor exercises, monitoring of blood pressure, heart rate, arrhythmia, and peripheral oxy-hemoglobin saturation, among others. The wearable artificial kidney, a device which would perform renal function during ambulation and social activities outside of the hospital, has been under investigation for many years. In this chapter, we highlight the most recent advances in digital health applied to nephrology.

Awake prone positioning does not reduce the risk of intubation in COVID-19 treated with high-flow nasal oxygen therapy: a multicenter, adjusted cohort study

BackgroundAwake prone positioning (awake-PP) in non-intubated coronavirus disease 2019 (COVID-19) patients could avoid endotracheal intubation, reduce the use of critical care resources, and improve survival. We aimed to examine whether the combination of high-flow nasal oxygen therapy (HFNO) with awake-PP prevents the need for intubation when compared to HFNO alone.MethodsProspective, multicenter, adjusted observational cohort study in consecutive COVID-19 patients with acute respiratory failure (ARF) receiving respiratory support with HFNO from 12 March to 9 June 2020. Patients were classified as HFNO with or without awake-PP. Logistic models were fitted to predict treatment at baseline using the following variables: age, sex, obesity, non-respiratory Sequential Organ Failure Assessment score, APACHE-II, C-reactive protein, days from symptoms onset to HFNO initiation, respiratory rate, and peripheral oxyhemoglobin saturation. We compared data on demographics, vital signs, laboratory markers, need for invasive mechanical ventilation, days to intubation, ICU length of stay, and ICU mortality between HFNO patients with and without awake-PP.ResultsA total of 1076 patients with COVID-19 ARF were admitted, of which 199 patients received HFNO and were analyzed. Fifty-five (27.6%) were pronated during HFNO; 60 (41%) and 22 (40%) patients from the HFNO and HFNO + awake-PP groups were intubated. The use of awake-PP as an adjunctive therapy to HFNO did not reduce the risk of intubation [RR 0.87 (95% CI 0.53–1.43), p = 0.60]. Patients treated with HFNO + awake-PP showed a trend for delay in intubation compared to HFNO alone [median 1 (interquartile range, IQR 1.0–2.5) vs 2 IQR 1.0–3.0] days (p = 0.055), but awake-PP did not affect 28-day mortality [RR 1.04 (95% CI 0.40–2.72), p = 0.92].ConclusionIn patients with COVID-19 ARF treated with HFNO, the use of awake-PP did not reduce the need for intubation or affect mortality.

Changes in prefrontal cerebral oxygenation and microvascular blood volume in hypoxia and possible association with acute mountain sickness.

What is the central question of this study? The role of the cerebral haemodynamic response to either normobaric or hypobaric hypoxia in people susceptible to acute mountain sickness (AMS) is still under debate. Prefrontal cortex near-infrared spectroscopy-derived parameters were monitored in normobaric hypoxia at rest and during moderate-intensity exercise in AMS-prone and non-AMS individuals. What is the main finding and its importance? The AMS-prone individuals did not increase microvascular blood volume and showed lower prefrontal cerebral oxygenation in normobaric hypoxia both at rest and during exercise compared with non-AMS subjects, suggesting that these changes might underpin later development of AMS at altitude. The aim of this study was to evaluate changes in prefrontal cerebral oxygenation and microvascular blood volume during exercise in normobaric hypoxia and to investigate possible associations with the occurrence of acute mountain sickness (AMS) at altitude. Twenty-two healthy individuals (age, 26±4years; peak oxygen uptake, 42±4mlkg-1 min-1 ) were tested in two different conditions: normoxia (NORM) and normobaric hypoxia (fraction of inspired O2 =0.13; HYPO). Data were collected at rest and during submaximal constant-speed exercise. The peripheral oxyhaemoglobin saturation was measured by finger pulse oximeter. Changes in prefrontal cerebral oxygenation (ΔHbO2 ), deoxygenation (ΔHHb) and microvascular blood volume (ΔHbtot ) were obtained by near-infrared spectroscopy. Within 2weeks after laboratory testing, subjects rapidly ascended to 3647m a.s.l., and AMS was evaluated using the Lake Louise scale. Eight subjects were AMS+ , whereas 14 were AMS- . During NORM, near-infrared spectroscopy variables did not change from baseline values both at rest and during exercise, with similar results in AMS+ and AMS- subjects. During HYPO, ΔHHb increased to a similar extent in both groups, both at rest and during exercise. The ΔHbO2 was significantly less in AMS+ compared with AMS- subjects, both at rest [-3.23±5.90 versus 1.44±2.14μm, P=0.04, effect size (ES)=1.1, respectively] and during exercise (-6.56±5.51versus 0.37±4.36μm,P<0.01,ES=1.2, respectively). Total haemoglobin did not change from baseline, both at rest (-1.67±9.53μm) and during exercise (-0.96±9.12μm) in AMS+ subjects, which was significantly different from the AMS- group (5.49±3.99μm, P=0.03, ES=1.0 and 8.17±7.34μm, P=0.02, ES=1.0, respectively). Individuals prone to AMS seem to be unable to increase microvascular blood volume and to maintain oxygenation at the cerebral level during exercise in acute normobaric hypoxia, suggesting that these changes might underpin later development of AMS.

Sleep disorders are distinctively associated with exercise intolerance and sedentary behavior in children with cystic fibrosis

ObjectiveTo evaluate the presence of sleep disorders and its associations with exercise capacity and daily physical activity levels among children and adolescents with CF. MethodsChildren age 6–18 years with a diagnosis of CF were recruited. Information regarding sociodemographic profile, pulmonary function and nutritional status were collected. Sleep disorders (polysomnography), exercise capacity (modified shuttle test - MST) and daily physical activity levels (questionnaire and five days accelerometer use) were evaluated. ResultsThirty-one patients, median age of 9.6 years and forced expiratory volume in 1 s (FEV1) of 68.1 ± 24.4%, were included. Obstructive sleep apnea syndrome (OSAS) was present in 32.3% and nocturnal hypoxemia in 29%. The MST distance correlated with the mean peripheral oxyhemoglobin saturation (SpO2) during sleep (r = 0.40) and the percent of total sleep time with SpO2<90% (r = −0.49). The final MST SpO2 correlated with the occurrence of OSAS (r = −0.48) and mean nocturnal SpO2 (r = 0.45). Sedentary activities, as measured by accelerometry, correlated with sleep architecture, including the percent of stage II (r = 0.60) and rapid eye movement (REM) stage sleep (r = −0.37). Patients with OSAS and nocturnal hypoxemia presented lower values (p < 0.05) of distance and final SpO2 in the MST. Nocturnal hypoxemia was the main variable to influence exercise capacity (r2 = 0.521). ConclusionSleep disorders are distinctively related with exercise capacity and daily physical activity levels, as nocturnal hypoxemia is associated with exercise intolerance and sleep architecture disorders are associated with sedentary physical activity levels.

Sleep-disordered breathing and markers of morbidity in children and adolescents with cystic fibrosis.

Studies have shown that sleep disorders occur in cystic fibrosis (CF) patients and may be present before daytime clinical manifestations. To evaluate the presence of sleep disorders among children and adolescents with CF, attempting to identify associations with pulmonary function, nutritional status, days in hospital, and days taking antibiotics. Individuals with a diagnosis of CF aged between 6 and 18 years were included. Information on sociodemographic, clinical profile, history of hospitalizations, and use of antibiotics in the last year were collected. Spirometry, bioimpedance, and polysomnography were performed. The presence of nocturnal hypoxemia and obstructive sleep apnea syndrome (OSAS) were evaluated and participants divided according to their presence. Thirty-one patients were included. The prevalence of OSAS was 32.3% and nocturnal hypoxemia was 29.0%. Average nocturnal peripheral oxyhemoglobin saturation (SpO2 ) correlated (P < .001) with forced vital capacity (r = .55) and forced expiratory volume in the first second (r = .62). The higher the percentage of total sleep time (TST) with SpO2 less than 90%, the lower the pulmonary function. Individuals with OSAS and nocturnal hypoxemia had lower spirometric values compared to patients without these disorders, but the nocturnal hypoxemia group also had lower Shwachman-Kulczycki score, longer hospitalization time and antibiotic use. TST with SpO2 less than 90% was associated with length of hospitalization (r2  = .53). Children and adolescents with CF have sleep disorders, including OSAS (32.3%) and nocturnal hypoxemia (29%). Individuals with nocturnal hypoxemia presented lower lung function, worse clinical score, and higher morbidity. TST with SpO2 less than 90% was associated with length of hospitalization.

A noninvasive postoperative clinical score to identify patients at risk for postoperative pulmonary complications: the Air-Test Score.

Postoperative pulmonary complications (PPCs) negatively affect morbidity, healthcare costs and postsurgical survival. Preoperative and intraoperative peripheral oxyhemoglobin saturation (SpO2) levels are independent risk factors for postoperative pulmonary complications (PPCs). The air-test assesses the value of SpO2 while breathing room-air. We aimed at building a clinical score that includes the air-test for predicting the risk for PPCs. This is a development and validation study in patients -randomly divided into two cohorts- from a large randomized clinical trial (iPROVE) that enrolled 964 intermediate-to-high risk patients scheduled for abdominal surgery. Arterial oxygenation was assessed on room-air in the preoperative period (preoperative air-test) and 3h after admission to the postoperative care unit (postoperative air-test). The air-test was defined as positive or negative if SpO2 was ≤96% or >96%, respectively. Positive air-tests were stratified into weak (93-96%) or strong (<93%). The primary outcome was a composite of moderate-to-severe PPCs during the first seven postoperative days. A total of 902 patients were included in the final analysis (542 in the development cohort and 360 in the validation cohort). Regression analysis identified five independent risk factors for PPC: age, type of surgery, pre- and postoperative air-test, and atelectasis. The area under the receiver operating characteristic curve (AUC) was 0.79 (95% CI: 0.75-0.82) when including these five independent predictors. We built a simplified score termed "air-test score" by using only the pre- and postoperative SpO2, resulting in an AUC of 0.72 (95% CI: 0.67-0.76) for the derivation and 0.72 (95% CI: 0.66-0.78) for the validation cohort, respectively. The air-test score stratified patients into four levels of risk, with PPCs ranging from <15% to >75%. The simple, non-invasive and inexpensive bedside air-test score, evaluating pre- and postoperatively SpO2 measured on room-air, helps to predict the risk for PPCs.

Effects of oxygen on post-surgical infections during an individualised perioperative open-lung ventilatory strategy: a randomised controlled trial

BackgroundWe aimed to examine whether using a high fraction of inspired oxygen (FIO2) in the context of an individualised intra- and postoperative open-lung ventilation approach could decrease surgical site infection (SSI) in patients scheduled for abdominal surgery. MethodsWe performed a multicentre, randomised controlled clinical trial in a network of 21 university hospitals from June 6, 2017 to July 19, 2018. Patients undergoing abdominal surgery were randomly assigned to receive a high (0.80) or conventional (0.3) FIO2 during the intraoperative period and during the first 3 postoperative hours. All patients were mechanically ventilated with an open-lung strategy, which included recruitment manoeuvres and individualised positive end-expiratory pressure for the best respiratory-system compliance, and individualised continuous postoperative airway pressure for adequate peripheral oxyhaemoglobin saturation. The primary outcome was the prevalence of SSI within the first 7 postoperative days. The secondary outcomes were composites of systemic complications, length of intensive care and hospital stay, and 6-month mortality. ResultsWe enrolled 740 subjects: 371 in the high FIO2 group and 369 in the low FIO2 group. Data from 717 subjects were available for final analysis. The rate of SSI during the first postoperative week did not differ between high (8.9%) and low (9.4%) FIO2 groups (relative risk [RR]: 0.94; 95% confidence interval [CI]: 0.59–1.50; P=0.90]). Secondary outcomes, such as atelectasis (7.7% vs 9.8%; RR: 0.77; 95% CI: 0.48–1.25; P=0.38) and myocardial ischaemia (0.6% [n=2] vs 0% [n=0]; P=0.47) did not differ between groups. ConclusionsAn oxygenation strategy using high FIO2 compared with conventional FIO2 did not reduce postoperative SSIs in abdominal surgery. No differences in secondary outcomes or adverse events were found. Clinical trial registrationNCT02776046.

Oxygen therapy improves cerebral oxygen delivery and neurovascular function in hypoxaemic chronic obstructive pulmonary disease patients.

What is the central question of this study? How does oxygen therapy influence cerebral blood flow, cerebral oxygen delivery and neurovascular function in chronic obstructive pulmonary disease patients? What is the main finding and its importance? Oxygen therapy improves cerebral oxygen delivery and neurovascular function in chronic obstructive pulmonary disease patients. This improvement in cerebral oxygen delivery and neurovascular function might provide a physiological link between oxygen therapy and a reduced risk of cerebrovascular disease (e.g. stroke, mild cognitive impairment and dementia) in chronic obstructive pulmonary disease. We investigated the role of hypoxaemia in cerebral blood flow (CBF), oxygen delivery (CDO2 ) and neurovascular coupling (coupling of CBF to neural activity; NVC) in hypoxaemic chronic obstructive pulmonary disease (COPD) patients (n=14). Resting CBF (duplex ultrasound), peripheral oxyhaemoglobin saturation (SpO2; pulse-oximetry) and NVC (transcranial Doppler) were assessed before and after a 20min wash-in of supplemental oxygen (∼3lmin-1 ). The peripheral oxyhaemoglobin saturation increased from 91.0±3.3 to 97.4±3.0% (P<0.01), whereas CBF was unaltered (593.0±162.8 versus 590.1±138.5mlmin-1 ; P=0.91) with supplemental O2 . In contrast, both CDO2 (98.1±25.7versus 108.7±28.4mldl-1 ; P=0.02) and NVC were improved. Specifically, the posterior cerebral artery cerebrovascular conductance was increased to a greater extent after O2 normalization (+40%, from 20.4±9.9 to 28.0±10.4% increase in conductance; P=0.04), whereas the posterior cerebral artery cerebrovascular resistance decreased to a greater extent during O2 normalization (+22%, from -16.7±7.3 to -21.4±6.6% decrease in resistance; P=0.04). The cerebral vasculature of COPD patients appears insensitive to oxygen, because CBF was unaltered in response to O2 supplementation leading to improved CDO2 . In patients, the improvements in CDO2 and neurovascular function with supplemental O2 may underlie the cognitive benefits associated with O2 therapy.

Chronic obstructive pulmonary disease-induced autonomic dysfunction may be associated with cerebral blood flow regulation and brain function.

Chronic obstructive pulmonary disease (COPD) increases the risk of cerebrovascular disease and brain dysfunction, such as ischaemic stroke and dementia, in proportion to its severity. Cerebral blood flow (CBF) regulation may be a key factor for this phenomenon, but the physiological mechanisms of COPD pathogenesis regarding cerebrovascular disease are yet to be established. Physiologically, COPD is a chronic hypoxic condition, and long-term oxygen therapy improves survival in patients with COPD and severe resting hypoxaemia. Given this background, Hoiland et al. (2018) have reported, in this issue of Experimental Physiology, the effects of oxygen therapy on cerebral oxygen delivery and neurovascular function in patients with COPD. The authors demonstrated that oxygen therapy improved cerebral oxygen delivery by increasing peripheral oxyhaemoglobin saturation () and enhanced neurovascular function in patients with COPD. These findings suggested that such oxygen delivery and functional neurovascular improvements may provide a physiological link between oxygen therapy and the reduced risk of cerebrovascular disease in patients with COPD. Thus, oxygen therapy appears beneficial for patients with COPD. On the contrary, oxygen therapy did not alter volumetric global CBF (Hoiland et al., 2018), suggesting that the cerebral vasculature has a low sensitivity to the acute normalization of . From these results, it can be suspected that the contribution of CBF regulation to COPD-induced cerebrovascular disease or brain dysfunction is likely to be minimal. In patients with COPD receiving oxygen therapy, we should consider cerebral oxygen delivery and cerebral haemodynamics and other physiological mechanisms potentially induced by hypoxaemia to understand the physiological mechanisms of this positive phenomenon. One example includes autonomic dysfunction, which is commonly observed in patients with COPD. Indeed, a previous study (van Gestel, Kohler, & Clarenbach, 2012) has demonstrated that autonomic dysfunction through sympathetic nervous system overactivity might contribute to the initiation and progression of cardiovascular disease in the examined population. However, the contributions of autonomic dysfunction to COPD-induced cerebrovascular disease and brain dysfunction may not be simple, because autonomic dysfunction modifies cerebral vasculature regulation (cerebral autoregulation and cerebral CO2 reactivity), the arterial baroreflex and the respiratory system (Ogoh & Ainslie, 2009). Indeed, baroreflex function is attenuated in patients with COPD. Importantly, the baroreflex simultaneously influences the respiratory system (ventilation and tidal volume) and the control of arterial pressure (Brunner, Sussman, Greene, Kallman, & Shoukas, 1982). Moreover, there is an interaction between cerebral vasculature regulation and the arterial baroreflex or respiratory system (Ogoh & Ainslie, 2009). Taken together, we cannot rule out the possibility that autonomic dysfunction might affect cerebral vasculature and function in the examined population both directly and indirectly. Indeed, another study (Bartels, Gonzalez, Kim, & De Meersman, 2000) demonstrated that oxygen therapy increased baroreflex sensitivity in patients with COPD, indicating that oxygen supplementation in this population significantly and favourably altered autonomic activity. Thus, oxygen therapy-modified autonomic function may be associated with improved survival in patients with COPD. Regarding this concept, the duration or severity of COPD may cause different functional autonomic adaptations and may result in different effects of oxygen therapy on the cerebral vasculature. The work of Hoiland et al. (2018) has clearly described the mechanisms through which oxygen therapy improved survival in patients with COPD. However, in order to identify the mechanisms underlying these effects, we should conduct additional, detailed investigations of the physiological regulatory mechanisms associated with various autonomic functions.