Arterial Oxyhemoglobin Saturation Research Articles

Ventilatory Responsiveness during Exercise and Performance Impairment in Acute Hypoxia.

An adequate increase in minute ventilation to defend arterial oxyhemoglobin saturation (SpO2) during hypoxic exercise is commonly viewed as an important factor contributing to large inter-individual variations in the degree of exercise performance impairment in hypoxia. Although the hypoxic ventilatory response (HVR) could provide insight into the underpinnings of such impairments, it is typically measured at rest under isocapnic conditions. Thus, we aimed to determine whether 1) HVR at rest and during exercise are similar and 2) exercise HVR is related to the degree of impairment in cycling time trial (TT) performance from normoxia to acute hypoxia (∆TT). Sixteen endurance-trained men (V˙O2peak, 62.5 ± 5.8 mL·kg-1·min-1) performed two poikilocapnic HVR tests: one during seated rest (HVRREST) and another during submaximal cycling (HVREX). On two separate visits, subjects (n = 12) performed a 10-km cycling TT while breathing either room air (FiO2 = 0.21) or hypoxic gas mixture (FiO2 = 0.16) in a randomized order. HVREX was significantly (P < 0.001) greater than HVRREST (1.52 ± 0.47 and 0.22 ± 0.13 L·min-1·%SpO2-1, respectively), and these measures were not correlated (r = -0.16, P = 0.57). ∆TT was not correlated with HVRREST (P = 0.70) or HVREX (P = 0.54), but differences in ventilation and end-tidal CO2 between hypoxic and normoxic TT and the ventilatory equivalent for CO2 during normoxic TT explained ~85% of the variance in performance impairment in acute hypoxia (P < 0.01). We conclude that 1) HVR is not an appropriate measure to predict the exercise ventilatory response or performance impairments in acute hypoxia and 2) an adequate and metabolically matched increase in exercise ventilation, but not the gain in the ventilatory response to hypoxia, is essential for mitigating hypoxia-induced impairments in endurance cycling performance.

Inverse relationship of subjective daytime sleepiness to mortality in heart failure patients with sleep apnoea.

AimsPatients with sleep apnoea (SA) and heart failure (HF) are less sleepy than SA patients without HF. HF and SA both increase sympathetic nervous system activity (SNA). SNA can augment alertness. We previously showed that in HF patients, the degree of daytime sleepiness was not related to the severity of SA but was inversely related to SNA. Elevated SNA is associated with increased mortality in HF. Therefore, we hypothesized that in HF patients with SA, the degree of daytime sleepiness will be inversely related to mortality.Methods and resultsIn a prospective cohort study, 218 consecutive patients with systolic HF had overnight polysomnography. Among them, 80 subjects with SA (apnoea–hypopnoea index ≥15) were followed for a mean of 28 months to determine all‐cause mortality rate. Subjective daytime sleepiness was assessed by the Epworth Sleepiness Scale (ESS). During follow‐up, 20 patients died. The 5 year death rate in patients with ESS less than 6 (i.e. less sleepy) was significantly higher than in patients with an ESS at or above the median of 6 (i.e. sleepier) [21.3 deaths/100 patient‐years vs. 6.2 deaths/100 patient‐years, unadjusted hazard ratio (HR) 2.94, 95% confidence interval (CI) 1.20 to 7.20, P = 0.018]. After adjusting for confounding factors that included sex, history of hypertension, and mean arterial oxyhaemoglobin saturation, compared with the sleepier patients, less sleepy patients had greater risk of mortality (HR 2.56, 95% CI 1.01 to 6.47, P = 0.047). As a continuous variable, ESS scores were inversely related to mortality risk (HR 0.86, 95% CI 0.75 to 0.98, P = 0.022).ConclusionsIn patients with HF and SA, the degree of subjective daytime sleepiness is inversely related to the mortality risk, suggesting that among HF patients with SA, those with the least daytime sleepiness are at greater risk of death. They may therefore have greater potential for mortality benefit from therapy of SA than those with greater daytime sleepiness.

Non-optimal effectiveness of convalescent plasma transfusion and hydroxychloroquine in treating COVID-19: a case report

BackgroundConvalescent plasma (CP) transfusion was reported to be effective in treating critically ill patients with COVID-19, and hydroxychloroquine could potently inhibit SARS-CoV-2 in vitro. Herein, we reported a case receiving combination therapy with CP transfusion and hydroxychloroquine for the first time.Case presentationLaboratory findings showed high lactic acid level (2.1 mmol/L) and C-reactive protein (CRP, 48.8 mg/L), and low white blood cell count (1.96 × 109/L) in a 65-year-old Chinese man, who was diagnosed with severe COVID-19. CP was intravenously given twice, and hydroxychloroquine was orally administrated for a week (0.2 g, three times a day). The lactic acid and C-reactive protein levels remained high (2.1 mmol/L and 73.23 mg/L, respectively), while the arterial oxyhemoglobin saturation decreased to 86% with a low oxygenation index (OI, 76 mmHg) on day 4 after CP transfusion. His temperature returned to normal and the OI ascended above 300 on day 11. Moreover, the RNA test remained positive in throat swab, and computed tomography revealed severe pulmonary lesions on day 11 after admission.ConclusionThese findings suggested that the effectiveness of combination therapy with CP and hydroxychloroquine may be non-optimal, and specific therapy needs to be explored.

Alveolar Dead-Space Fraction and Arterial Saturation Predict Postoperative Course in Fontan Patients.

Fontan surgery, the final surgical stage in single ventricle palliation, redirects systemic venous blood into the pulmonary circulation for gas exchange. A decrease in pulmonary blood flow can lead to major complications and grave outcomes. Alveolar dead-space fraction represents the portion of inhaled air that does not participate in gas exchange and hence quantifies ventilation-perfusion abnormalities in the lung. Increased alveolar dead-space fraction has been associated with prolonged mechanical ventilation and worse outcome after congenital heart surgery. The association of alveolar dead-space fraction with clinical outcomes in patients undergoing Fontan operation has not been reported. None. A retrospective charts review of all pediatric patients who underwent Fontan surgery during June 2010-November 2018 in a tertiary-care pediatric hospital. Associations between alveolar dead-space fraction and arterial oxyhemoglobin saturation to a composite outcome (surgical or catheter-based intervention, extracorporeal membrane oxygenation use, prolonged ventilation, prolonged hospital length of stay, or death) were explored. Secondary endpoints were parameters of severity of illness, chest drainage duration, and length of stay. Of 128 patients undergoing Fontan operation, 34 met criteria for composite outcome. Alveolar dead-space fraction was significantly higher in the composite (0.33 ± 0.14) versus control (0.25 ± 0.26; p = 0.016) group. Alveolar dead-space fraction greater than or equal to 0.29 indicated a 37% increase in risk to meet composite criteria. Admission arterial oxygen saturation was significantly lower in composite versus control group (93.4% vs 97.1%; p = 0.005). Alveolar dead-space fraction was significantly associated with increased durations of mechanical ventilation, ICU length of stay, duration of thoracic drainage, and parameters of severity of illness. Alveolar dead-space fraction and arterial saturation may predict complicated postoperative course in patients undergoing the Fontan operation.

Impact of the superior cavopulmonary anastomosis on cerebral oxygenation.

Patients with univentricular heart disease may undergo a superior cavopulmonary anastomosis, an operative intervention that raises cerebral venous pressure and impedance to cerebral venous return. The ability of infantile cerebral autoregulation to compensate for this is not well understood. We identified all patients undergoing a superior cavopulmonary anastomosis (cases) and compared metrics of cerebral oxygenation upon admission to the ICU with patients following repair of tetralogy of Fallot or arterial switch operation (controls). The primary endpoint was cerebral venous oxyhaemoglobin saturation measured from an internal jugular venous catheter. Other predictor variables included case-control assignment, age, weight, sex, ischemic times, arterial oxyhaemoglobin saturation, mean arterial blood pressure, and superior caval pressure. A total of 151 cases and 350 controls were identified. The first post-operative cerebral venous oxyhaemoglobin saturation was significantly lower following superior cavopulmonary anastomosis than in controls (44 ± 12 versus 59 ± 15%, p < 0.001), as was arterial oxyhaemoglobin saturation (81 ± 9 versus 98 ± 5%, p < 0.001). Cerebral venous oxyhaemoglobin saturation correlated poorly with superior caval pressure in both groups. When estimated by linear mixed effects model, arterial oxyhaemoglobin saturation was the primary determinant of central venous oxyhaemoglobin saturation in both groups (β = 0.79, p = 3 × 10-14); for every 1% point increase in arterial oxyhaemoglobin saturation, there was a 0.79% point increase in venous oxyhaemoglobin saturation. In this model, no other predictors were significant, including superior caval pressure and case-control assignment. Cerebral autoregulation appears to remain intact despite acute imposition of cerebral venous hypertension following superior cavopulmonary anastomosis. Following superior cavopulmonary anastomosis, cerebral venous oxyhaemoglobin saturation is primarily determined by arterial oxyhaemoglobin saturation.

Comparing the Liquid Heparin Syringe with Dry Bound Heparin Syringe for Blood Gas Analysis

Abstract Background Blood gas (BG) analysis is routine today for patient management in intensive care units. Accurate analysis of different parameters in the BG is essential for managing critical patients. Errors in BG analysis can happen at many levels, with one of them being at sampling and heparinization. We compared self-prepared heparinized syringes rinsed with liquid heparin (LH) and the standard commercially available syringes with dry bound heparin (DBH) for arterial BG analysis of postoperative cardiac surgical patients. Methods This prospective observational study was conducted in 100 consecutive adult cardiac surgical patients in the cardiac surgical intensive care unit. Paired samples were collected, analyzed immediately, and statistically compared for pH, partial pressure of arterial oxygen (pO2), partial pressure of arterial carbon dioxide (pCO2), oxyhemoglobin saturation (SaO2), HCO, Na+, K+, Cl–, Ca2+, Mg2+, base excess (BE), hemoglobin (Hb), hematocrit, glucose, and lactate. Paired parameters were compared and agreement was evaluated using Bland–Altman difference plots. The 95% limits of absolute agreement (LOA) were compared with total allowable error (TEa). Results The BG parameters analyzed by two types of heparinized (LH and DBH) syringes were found to be comparable with a negligible mean difference and had an agreement outside the TEa of 8% for pO2, pCO2, and hematocrit, 7% for BE, 6% for Mg2+, 5% for K+, Ca2+, and lactate, 4% for HCOand Na+, 3% for pH, Cl–, Hb, and glucose, and zero for SaO2. The two types of syringes did not show clinically relevant discrepancies among many different parameters as per LOA and TEa limits. Conclusion In this study, we found that the BG parameters—respiratory, metabolic, and electrolytes—were comparable between the two types of syringes used for sampling. Unlike some previous studies, we did not find statistically significant differences among these analytes, which might have been due to appropriate self-preparation of heparin syringes.

Dissociating the effects of oxygen pressure and content on the control of breathing and acute hypoxic response.

Arterial oxygen tension and oxyhemoglobin saturation () decrease in parallel during hypoxia. Distinguishing between changes in oxygen tension and oxygen content as the relevant physiological stimulus for cardiorespiratory alterations remains challenging. To overcome this, we recruited nine individuals with hemoglobinopathy manifesting as high-affinity hemoglobin [HAH; partial pressure at 50% (P50) = 16 ± 0.4 mmHg] causing greater at a given oxygen partial pressure compared with control subjects (n = 12, P50 = 26 ± 0.4 mmHg). We assessed ventilatory and cardiovascular responses to acute isocapnic hypoxia, iso-oxic hypercapnia, and 20 min of isocapnic hypoxia (arterial Po2 = 50 mmHg). Blood gas alterations were achieved with dynamic end-tidal forcing. When expressed as a function of the logarithm of oxygen partial pressure, ventilatory sensitivity to hypoxia was not different between groups. However, there was a significant difference when expressed as a function of . Conversely, the rise in heart rate was blunted in HAH subjects when expressed as a function of partial pressure but similar when expressed as a function of . Ventilatory sensitivity to hypercapnia was not different between groups. During sustained isocapnic hypoxia, the rise in minute ventilation was similar between groups; however, heart rate was significantly greater in the controls during 3 to 9 min of exposure. Our results support the notion that oxygen tension, not content, alters cellular Po2 in the chemosensors and drives the hypoxic ventilatory response. Our study suggests that in addition to oxygen partial pressure, oxygen content may also influence the heart rate response to hypoxia.NEW & NOTEWORTHY We dissociated the effects of oxygen content and pressure of cardiorespiratory regulation studying individuals with high-affinity hemoglobin (HAH). During hypoxia, the ventilatory response, expressed as a function of oxygen tension, was similar between HAH variants and controls; however, the rise in heart rate was blunted in the variants. Our work supports the notion that the hypoxic ventilatory response is regulated by oxygen tension, whereas cardiovascular regulation may be influenced by arterial oxygen content and tension.

Sequencing Analysis at 8p23 Identifies Multiple Rare Variants in DLC1 Associated with Sleep-Related Oxyhemoglobin Saturation Level

Average arterial oxyhemoglobin saturation during sleep (AvSpO2S) is a clinically relevant measure of physiological stress associated with sleep-disordered breathing, and this measure predicts incident cardiovascular disease and mortality. Using high-depth whole-genome sequencing data from the National Heart, Lung, and Blood Institute (NHLBI) Trans-Omics for Precision Medicine (TOPMed) project and focusing on genes with linkage evidence on chromosome 8p23,1,2 we observed that six coding and 51 noncoding variants in a gene that encodes the GTPase-activating protein (DLC1) are significantly associated with AvSpO2S and replicated in independent subjects. The combined DLC1 association evidence of discovery and replication cohorts reaches genome-wide significance in European Americans (p = 7.9× 10-7). A risk score for these variants, built on an independent dataset, explains 0.97% of the AvSpO2S variation and contributes to the linkage evidence. The 51 noncoding variants are enriched in regulatory features in a human lung fibroblast cell line and contribute to DLC1 expression variation. Mendelian randomization analysis using these variants indicates a significant causal effect of DLC1 expression in fibroblasts on AvSpO2S. Multiple sources of information, including genetic variants, gene expression, and methylation, consistently suggest that DLC1 is a gene associated with AvSpO2S.

Inspiratory Muscle Training: Improvement of Exercise Performance With Acute Hypoxic Exposure.

To determine whether chronic IMT improves submaximal-exercise performance with acute hypoxic exposure. A total of 14 endurance-trained men completed a 20-km cycling time trial (TT) in normobaric hypoxia (fraction of inspired oxygen [FiO2] = 0.16) before and after either 6 wk of an IMT protocol consisting of inspiratory loads equivalent to 80% of sustained maximal inspiratory pressure (n = 9) or a SHAM protocol (30% of sustained maximal inspiratory pressure; n = 5). In the IMT group, 20-km TT performance significantly improved by 1.45 (2.0%), P = .03, after the 6-wk intervention. The significantly faster TT times were accompanied by a higher average V˙E (pre vs post: 99.3 [14.5] vs 109.9 [18.0]L·min-1, P = .01) and absolute oxygen uptake (pre vs post: 3.39 [0.52] vs 3.60 [0.58]L·min-1, P = .010), with no change in ratings of perceived exertion or dyspnea (P > .06). There were no changes in TT performance in the SHAM group (P = .45). These data suggest that performing 6 wk of IMT may benefit hypoxic endurance exercise performance lasting 30-40min.

Inspiratory muscle training effects on oxygen saturation and performance in hypoxemic rowers: Effect of sex

ABSTRACTExercise-induced arterial hypoxemia (EIAH) has been consistently reported in elite endurance athletes. This study examined the effects of an inspiratory muscle training protocol (IMT) on resting pulmonary function, end-exercise arterial oxygen saturation and performance in hypoxemic rowers. Twenty male and sixteen female well-trained hypoxemic rowers were divided into four groups: IMT-male, control-male, IMT-female and control-female. The IMT groups, additionally to the regular training, performed IMT (30 min/day, 5 times/week, 6 weeks). Before and after training, groups underwent an incremental rowing test, a 2000-m time trial and a 5-min “all-out” race. IMT increased respiratory strength in the IMT-male (135 ± 31 vs. 180 ± 22 cmH2O) and IMT-female (93 ± 19 vs. 142 ± 22 cmH2O) (P < 0.05). The IMT-female group exhibited lower EIAH and improved rowing performance in the 2000-m time trial (487 ± 32 vs. 461 ± 34 sec) and in the 5-min “all-out” test (1,285 ± 28 vs. 1,310 ± 36m) (P < 0.05). IMT protocol improved performance in IMT-male only in the 5-min test (1,651 ± 31 vs. 1,746 ± 37m) (P < 0.05). IMT may be a useful tool for increasing respiratory strength and enhancing performance in hypoxemic rowers, especially for women.Abbreviations: EIAH: Exercise-induced arterial hypoxemia; IMT: inspiratory muscle training protocol; PaO2: partial pressure of arterial oxygen; SaO2: arterial oxyhemoglobin saturation; VO2max: maximal oxygen consumption; [(A-a)DO2]: alveolar-to-arterial oxygen difference; VA/Q: ventilation-perfusion inequality/mismatching; PImax: maximal inspiratory pressure; BMI: body mass index; BSA: body surface area; FVC: vital capacity; FEV1: forced expiratory volume in 1 sec; VCin: vital capacity; MVV12: maximal voluntary ventilation in 12 sec

Benefit of Intensive Atorvastatin Therapy in Sleep Apnea Syndrome with Cardiovascular Disease

Background: In addition to its hypolipidemic effect, atorvastatin therapy has multiple beneficial effects in patients with cardiovascular disorders. We evaluated the effect of intensive atorvastatin therapy on sleep apnea syndrome (SAS). Methods: Eighteen patients with apnea-hypopnea index (AHI) ≥5, as assessed by portable monitor, received oral atorvastatin 10 mg/d in the first week and 20 mg/d in the second and third weeks as the preliminary group. Sixteen patients with AHI≥15, as assessed by laboratory polysomnography, received 20 mg/d for two months followed by 40 mg/d for the next two months as the intensive group. If AHI did not reduce by half or to < 15, patients received 60 mg/d from the 5th month onwards. Results: In the preliminary group, after short-term moderate-dose therapy, AHI was significantly decreased (21.7±13.6 vs. 13.6±12.9, P=0.015), along with a significant increase in average arterial oxyhemoglobin saturation (SaO2) (93.1±2.0 % vs. 93.8±1.2 %, P=0.039). In the intensive group, after mid-term titrated intensive therapy, there was a significantly greater reduction in AHI (36.6±19.8 vs. 11.5±11.5, P=0.0004) with increase in average SaO2 (93.6±2.1% vs. 94.0±1.2%, P=0.017) and minimum SaO2 (71.3±9.5 % vs. 84.3±7.7%, P<0.0001). During follow-up of intensive therapy group, 8 patients (50%) showed a decrease in AHI to < 5 events/h. The degree of AHI reduction and SaO2 amelioration in the intensive group was greater than that in the preliminary group (P<0.01). Conclusions: Atorvastatin therapy may help reduce AHI and ameliorate hypoxia in patients with SAS. Mid-term intensive dose atorvastatin therapy may be better than short-term moderate dose in this respect. Funding Statement: Financial support was granted by a Natural Science Fund (09ZR1427500) of the Science and Technology Commission of Shanghai Municipality and a Project for Public Technology Study and Social Development (2010C33SA390002) of Zhejiang Province. Declaration of Interests: No conflict of interest exists for any of the authors. Ethics Approval Statement: Our study was approved by Local Ethical Committee in April 1st 2010 (No 201003, Ethical Committee, Yueqing Hospital, Wenzhou Medical University).

Mechanical Unloading of the Respiratory System during 5km Cycling Time Trials in Hypoxia

In trained endurance athletes, the ability to defend arterial oxy-hemoglobin saturation (SaO2) during high intensity constant-workload exercise in moderate hypoxia depends in part on the ability to increase minute ventilation (V̇E). Previous data have shown, however, that despite the existence of a substantial amount of ventilatory reserve (V̇Eres) in some cyclists, V̇E surprisingly does not increase during 5km time trials (5kTT) in hypoxia, despite a significant decrease in both SaO2 and mean power output (PTT) from normoxia. PURPOSE: To determine the effect of reducing the work of breathing (Wb) on V̇E, breathlessness (RPB), and PTT during a 5kTT in hypoxia in highly trained cyclists. We hypothesized no change in RPB, while V̇E would increase with an attenuated decrement in SaO2 and PTT from normoxia. METHODS: Fourteen trained male cyclists (V̇O2max = 58.7 ± 4.7 ml·kg-1·min-1) performed a 5kTT under 3 conditions at sea level: ‘CON’ (FiO2 = 0.21), ‘HYP’ (FiO2 = 0.16), and ‘HYP+He’ (FiO2 = 0.16, with balance helium). Esophageal balloons were used to assess Wb in each condition. Inspiratory capacity maneuvers were performed at each km, and flow-volume loop analyses were used to assess the %EFL and V̇Eres. The modified Borg scale (0-10) was used to assess RPB at each km. RESULTS: Wb decreased from HYP to HYP+He by 30 ± 18% (p < 0.01). Despite a substantial V̇Eres throughout CON (52 ± 44 L·min-1), V̇E was not different between CON (117.4 ± 17.9 L·min-1) and HYP (124.8 ± 17.9 L·min-1) but increased during HYP+He (139.5 ± 22.0 L·min-1; p < 0.05). While SaO2 decreased from CON to HYP by 10 ± 1% (p < 0.01), SaO2 increased by 4 ± 1% from HYP to HYP+He (p < 0.01). PTT decreased from CON to HYP (-14.2%; p < 0.01) and increased from HYP to HYP+He (+5.5%; p < 0.01). When comparing HYP to HYP+He, a significant correlation was observed between ΔSaO2 and ΔPTT (r = 0.69; p < 0.05). RPB increased from CON (6.0 ± 2.0) to HYP (7.0 ± 2.0; p < 0.05) and was unchanged from HYP to HYP+He (6.6 ± 2.0). CONCLUSIONS: In moderate hypoxia, a low ventilatory reserve does not limit 5km time trial performance, where by design, individuals are free to adjust power output. The ability to utilize ventilatory reserve while remaining below a critical threshold of perceived breathlessness appears conducive to maintaining aerobic exercise performance in moderate hypoxia.

Effect of hypobaria on maximal ventilation, oxygen uptake, and exercise performance during running under hypobaric normoxic conditions.

During exposure to high altitude, hypoxia develops because of reductions in barometric pressure and partial pressure of O2. Although several studies have examined the effects of hypoxia on exercise performance and physiological responses, such as maximal minute ventilation (V· Emax) and maximal oxygen uptake (V·O2max), how barometric pressure reduction (hypobaria) modulates them remains largely unknown. In this study, 11 young men performed incremental treadmill running tests to exhaustion under three conditions chosen at random: normobaric normoxia (NN; 763 ± 5 mmHg of barometric pressure, equivalent to sea level), hypobaric hypoxia (HH; 492 ± 1 mmHg of barometric pressure, equivalent to 3500 m above sea level (m a.s.l.)), and hypobaric normoxia (HN; 492 ± 1 mmHg of barometric pressure while breathing 32.2 ± 0.1% O2 to match the inspiratory O2 content under NN). V· Emax was higher in HN than in NN (160.9 ± 10.7 vs. 150.7 ± 10.0 L min−1, P < 0.05). However, no differences in V·O2max and arterial oxyhemoglobin saturation were observed between NN and HN (all P > 0.05). Time to exhaustion was longer in HN than in NN (932 ± 83 vs. 910 ± 79 s, P < 0.05). These results suggest that reduced air density during exposure to an altitude of 3500 m a.s.l. increases maximal ventilation and extends time to exhaustion without affecting oxygen consumption or arterial oxygen saturation.

Incidence and Impact of Hypoalbuminaemia on Outcomes Following Acute Pulmonary Embolism

Clinical features and outcomes of patients with hypoalbuminaemia in acute pulmonary embolism (PE) have never been studied. The present study investigated the incidence and determined the prognostic significance of hypoalbuminaemia in patients with confirmed acute PE. From a dedicated tertiary-referral centre database involving 1,426 consecutive patients admitted with confirmed PE (2000-2012), 1,032 patients had serum albumin assessed on admission (day-1). Patients were stratified into hypoalbuminaemia (<35 g/L) or normal serum albumin (≥35 g/L). Multivariable logistic and Cox proportional-hazards regression methods were used to assess 30-day and 90-day all-cause mortality. Hypoalbuminaemia was present in 160 (15.5%) patients at day-1 and was associated with higher mean (±SD) heart rate (94.4 ± 21.8 vs 87.8 ± 21.5 bpm), lower systolic blood pressure (131.0 ± 24.7 vs 142.3 ± 24.7 mmHg), lower arterial oxyhaemoglobin saturation (93.3 ± 6.1% vs 95.6 ± 4.0%), lower day-1 serum sodium (137.0 ± 4.7 vs 138.8 ± 3.8 mmol/L) and haemoglobin levels (114.4 ± 20.7 vs 131.5 ± 18.7 g/L). Patients with hypoalbuminaemia had higher incidence of malignancy (44.4% vs 18.8%) and chronic renal disease (9.4% vs 5.2%), and at admission were less likely to be taking aspirin/clopidogrel (19.3% vs 27.7%) and more likely to be using enoxaparin (6.7% vs 3.0%). During a mean follow-up of 5.0 ± 4.0 years, patients with hypoalbuminaemia had higher 30-day (16.3% vs 3.6%) and 90-day (26.3% vs 6.2%) mortality. Multivariable analyses showed hypoalbuminaemia independently predicted both 30-day (odds ratio 2.57, 95% confidence interval [CI] 1.03-6.41) and 90-day (hazard ratio 2.42 95% CI 1.38-4.22) mortality. Hypoalbuminaemia is an independent predictor of mortality following PE and may improve risk stratification of patients in risk prediction models.

Incidence and risk factors of hypoxaemia after preoxygenation at induction of anaesthesia

The incidence of hypoxaemia related to airway management is still a matter of concern. Our aim was to determine the factors that contribute to hypoxaemia during induction of anaesthesia after a standardised preoxygenation procedure. The study was a multicentre and prospective observational trial. It evaluated the incidence of hypoxaemia at induction of anaesthesia in adult patients. The primary endpoint was the incidence of hypoxaemia defined as pulse oximetry of arterial oxyhaemoglobin saturation (SpO2) <95%. Of 2398 patients, hypoxaemia was observed in 158 (6.6%). We identified five preoperative independent risk factors: chronic obstructive pulmonary disease, hypertension, anticipated difficult mask ventilation and difficult tracheal intubation, and emergency surgery. There were also three pre-induction independent risk factors: difficult preoxygenation, difficult mask ventilation, and difficult tracheal intubation. We found a high negative predictive value of preoperative risk factors for difficult mask ventilation of 0.96 (0.95-0.96), and for difficult tracheal intubation (0.95 [0.94-0.96]). A total of 723 patients (30%) experienced difficult preoxygenation (FeO2 <90% at the end of preoxygenation). Male sex, chronic obstructive pulmonary disease, hypertension, emergency surgery, and predictable difficult mask ventilation were independent patient risk factors for difficult preoxygenation. Difficult mask ventilation and difficult tracheal intubation are risk factors for hypoxaemia at induction of general anaesthesia. Difficult preoxygenation was observed in 30% of patients and was also identified as a risk factor for hypoxaemia. This suggests that techniques improving preoxygenation should be implemented in daily practice.

Exercise-induced arterial hypoxemia; some answers, more questions.

Exercise-induced arterial hypoxemia (EIAH) is characterized by the decrease in arterial oxygen tension and oxyhemoglobin saturation during dynamic aerobic exercise. Since the time of the initial observations, our knowledge and understanding of EIAH has grown, but many unknowns remain. The purpose of this review is to provide an update on recent findings, highlight areas of disagreement, and identify where information is lacking. Specifically, this review will place emphasis on (i) the occurrence of EIAH during submaximal exercise, (ii) whether there are sex differences in the development and severity of EIAH, and (iii) unresolved questions and future directions.

Changes in tissue oxygen tension, venous saturation, and Fick-based assessments of cardiac output during hyperoxia.

Hyperoxemia (arterial oxygen tension >100mmHg) may occur in critically ill patients and have effects on mixed venous saturation (SvO2 ) and on Fick-based estimates of cardiac output (CO). We investigated the effect of hyperoxemia on SvO2 and on assessments of CO using the Fick equation. Yorkshire swine (n=14) were anesthetized, intubated, and paralyzed for instrumentation. SvO2 (co-oximetry) and tissue oxygen tension (tPO2 , implantable electrodes) in brain and myocardium were measured during systematic manipulation of arterial oxygen tension (PaO2 ) using graded hyperoxia (fraction of inspired oxygen 0.21 → 0.8). Secondarily, oxygen- and carbon dioxide-based estimates of CO (FickO2 and FickCO2 , respectively) were compared with measurements from a flow probe placed on the aortic root. Independent of changes in measured oxygen delivery, cerebral and myocardial tPO2 increased in proportion to PaO2 , as did SvO2 (P<0.001 for all). Based on mixed model analysis, each 100mmHg increase in PaO2 resulted in a 4.8±0.9% increase in SvO2 under the conditions tested. Because neither measured oxygen consumption, arterial oxyhemoglobin saturation or cardiac output varied significantly during hyperoxia, changes in SvO2 resulted in successively increasing errors in FickO2 during hyperoxia (34% during normoxia, 72% during FiO2 0.8). FickCO2 lacked the progressively worsening errors present in FickO2 , but correlated poorly with CO. SvO2 acutely changes following changes in PaO2 even absent changes in measured DO2 . This may lead to errors in FickO2 estimates of CI. Further work is necessary to understand the impact of this phenomenon in disease states.

Impaired left ventricular filling is associated with decreased pulse oximetry values

Objectives. The aim of this study was to investigate the association between echocardiographic measures of diastolic left ventricular dysfunction and decreased arterial oxyhaemoglobin saturation measured with pulse oximetry (SpO2). Design. This is a cross-sectional population-based survey of Norwegian adults. Values obtained using echocardiography, pulse oximetry, and spirometry were included. The primary outcome was abnormal mitral Doppler inflow, defined as normal: E/A ratio 0.75–1.5 and EDT ≥ 140 ms; abnormal: E/A ratio <0.75 or >1.5 or EDT <140 ms. The associations between this outcome and possible predictors, including SpO2 ≤ 95%, were analysed using univariable and multivariable logistic regression. Results. A total of 1782 participants aged 50 years or older (54% women, mean age 67.5 years) were included in the analysis. Abnormal mitral Doppler inflow was found in 595 participants. After adjusting for age, gender, previous myocardial infarction, smoking history, dyspnoea, obesity, and decreased lung function, SpO2 ≤ 95% predicted abnormal mitral Doppler flow with an odds ratio (OR) of 1.6 [95% confidence interval (CI) 1.1–2.4]. Hypertension and BMI > =30 were also significant predictors of impaired filling, with OR of 1.7 (95% CI 1.1–2.7) OR and 1.5 (95% CI 1.2–1.9), respectively. Conclusion. Decreased SpO2 was a significant predictor of abnormal mitral Doppler flow. Diastolic dysfunction should be considered when SpO2 ≤ 95% is found.

Impact of Arterial Stiffness on WatchPAT Variables in Patients With Obstructive Sleep Apnea.

The WatchPAT is a wrist-worn portable device that creates integration data regarding peripheral arterial tone (PAT), oxyhemoglobin saturation, heart rate, and actigraphy to diagnose or screen for obstructive sleep apnea (OSA). Previous studies have demonstrated the efficacy and validity of respiratory variables measured by the WatchPAT compared to those using polysomnography (PSG). However, the effects of arterial stiffness or atherosclerosis on WatchPAT parameters remain to be elucidated. Sixty-one consecutive patients with suspected OSA who underwent home-based testing with the WatchPAT 200, standard in-laboratory overnight polysomnography (PSG), and pulse wave velocity (PWV) as an index of arterial stiffness were studied. All PSG recordings were scored manually using the American Academy of Sleep Medicine criteria, whereas WatchPAT data were analyzed by an automatic algorithm. We evaluated how arterial stiffness affected respiratory event index data in WatchPAT (WP-AHI), because WP-AHI could be partly influenced by PAT, comparing WP-AHI and the apneahypopnea index measured by PSG (PSG-AHI) in consideration of PWV result. Overall, WP-AHI was moderately correlated to PSG-AHI, but WP-AHI was significantly lower than PSG-AHI (28.4 ± 19.2 versus 53.6 ± 30.2 events/h, P < .0001). For the lower PWV group, there was a significant correlation and good agreement between the WP-AHI and PSG-AHI, but as the PWV increased, there was low correlation between the WP-AHI and PSG-AHI. Arterial stiffness may affect the respiratory variables measured by WatchPAT in patients with OSA. A commentary on this article appears in this issue on page 301.

Measurement of Dead Space Fraction Upon ICU Admission Predicts Length of Stay and Clinical Outcomes Following Bidirectional Cavopulmonary Anastomosis.

Increased alveolar dead space fraction has been associated with prolonged mechanical ventilation and increased mortality in pediatric patients with respiratory failure. The association of alveolar dead space fraction with clinical outcomes in patients undergoing bidirectional cavopulmonary anastomosis for single ventricle congenital heart disease has not been reported. We describe an association of alveolar dead space fraction with postoperative outcomes in patients undergoing bidirectional cavopulmonary anastomosis. In a retrospective case-control study, we examined for associations between alveolar dead space fraction ([PaCO2 - end-tidal CO2]/PaCO2), arterial oxyhemoglobin saturation, and transpulmonary gradient upon postoperative ICU admission with a composite primary outcome (requirement for surgical or catheter-based intervention, death, or transplant prior to hospital discharge, defining cases) and several secondary endpoints in infants following bidirectional cavopulmonary anastomosis. Cardiac ICU in a tertiary care pediatric hospital. Patients undergoing bidirectional cavopulmonary anastomosis at our institution between 2011 and 2016. None. Of 191 patients undergoing bidirectional cavopulmonary anastomosis, 28 patients were cases and 163 were controls. Alveolar dead space fraction was significantly higher in the case (0.26 ± 0.09) versus control group (0.17 ± 0.09; p < 0.001); alveolar dead space fraction at admission was less than 0.12 in 0% of cases and was greater than 0.28 in 35% of cases. Admission arterial oxyhemoglobin saturation was significantly lower in the case (77% ± 12%) versus control group (83% ± 9%; p < 0.05). Sensitivity and specificity for future case versus control assignment was best when prebidirectional cavopulmonary anastomosis risk factors, admission alveolar dead space fraction (AUC, 0.74), and arterial oxyhemoglobin saturation (AUC, 0.65) were combined in a summarial model (AUC, 0.83). For a given arterial oxyhemoglobin saturation, the odds of becoming a case increased on average by 181% for every 0.1 unit increase in alveolar dead space fraction. Admission alveolar dead space fraction and arterial oxyhemoglobin saturation were linearly associated with prolonged ICU length of stay, hospital length of stay, duration of mechanical ventilation, and duration of thoracic drainage (p < 0.001 for all). Following bidirectional cavopulmonary anastomosis, alveolar dead space fraction in excess of 0.28 or arterial oxyhemoglobin saturation less than 78% upon ICU admission indicates an increased likelihood of requiring intervention prior to hospital discharge. Increasing alveolar dead space fraction and decreasing arterial oxyhemoglobin saturation are associated with increased lengths of stay.