High Concentration Oxygen Therapy Research Articles

Research progress on high-concentration oxygen therapy after cerebral hemorrhage.

Recently, the role of high-concentration oxygen therapy in cerebral hemorrhage has been extensively discussed. This review describes the research progress in high-concentration oxygen therapy after cerebral hemorrhage. High-concentration oxygen therapy can be classified into two treatment methods: hyperbaric and normobaric high-concentration oxygen therapy. Several studies have reported that high-concentration oxygen therapy uses the pathological mechanisms of secondary ischemia and hypoxia after cerebral hemorrhage as an entry point to improve cerebral oxygenation, metabolic rate, cerebral edema, intracranial pressure, and oxidative stress. We also elucidate the mechanisms by which molecules such as Hypoxia-inducible factor 1-alpha (HIF-1α), vascular endothelial growth factor, and erythropoietin (EPO) may play a role in oxygen therapy. Although people are concerned about the toxicity of hyperoxia, combined with relevant literature, the evidence discussed in this article suggests that as long as the duration, concentration, pressure, and treatment interval of patients with cerebral hemorrhage are properly understood and oxygen is administered within the treatment window, it can be effective to avoid hyperoxic oxygen toxicity. Combined with the latest research, we believe that high-concentration oxygen therapy plays an important positive role in injuries and outcomes after cerebral hemorrhage, and we recommend expanding the use of normal-pressure high-concentration oxygen therapy for cerebral hemorrhage.

Endoscopic fenestration treatment for pneumatosis cystoides intestinalis in patient with recurrent colonic intussusception.

Pneumatosis cystoides intestinalis (PCI) is a rare disease characterized by intestinal mural pneumatized cysts that appear most commonly in the colon [1] [2]. Although primarily asymptomatic, PCI occasionally causes intussusception that usually requires surgical treatment [3] [4]. Hyperbaric or high-concentration oxygen therapy is reportedly effective, though complete remission is uncertain [5]. We present the first report of an endoscopic fenestration procedure used for successful treatment of PCI with recurrent intussusception.

The Progress of Diagnosis and Management in Inhalation Injury

Inhalation injury is one of the important causes of death in critically burned patients, and rich experiences have been accumulated in the diagnosis and treatment. However, the understanding of some new biomarkers, evidence-based evidences, and diagnosis and treatment measures is still very limited. In this review, on the basis of our team’s experiences in clinical treatment, we discuss the new diagnostic principles (such as dynamic diagnosis, airway depth grading theory, biomarkers, etc.) and the new treatments (such as chest physical therapy, artificial nose and high flow respiratory humidification therapeutic apparatus in airway management, atmospheric pressure high concentration oxygen therapy, extracorporeal membrane oxygenation (ECMO) support, etc.). New comprehensive protocols and evidence-based evidences for the diagnosis and treatment of inhalation injury are summarized. The treatment of inhalation injury is a multi-faceted and multi-disciplinary comprehensive diagnosis and treatment. It is of great clinical significance to explore new measures to improve the early diagnosis and management.

Association between timing of intubation and mortality in patients with idiopathic pulmonary fibrosis.

Delayed intubation is associated with poor prognosis in patients with respiratory failure. However, the effect of delayed intubation in patients with idiopathic pulmonary fibrosis (IPF) remains unknown. This study aimed to analyze whether timing of intubation after high-concentration oxygen therapy was associated with worse clinical outcomes in IPF patients. This retrospective propensity score-matched study enrolled adult patients with IPF who underwent mechanical ventilation between January 2011 and July 2021. Patients were divided into early and delayed intubation groups. Delayed intubation was defined as use of high-concentration oxygen therapy for at least 48 hours before tracheal intubation. The primary outcome was intensive care unit (ICU) mortality, and a conditional logistic regression model was used to evaluate the association between timing of intubation and clinical outcomes. The median duration of high-concentration oxygen therapy before intubation was 0.5 days in the early intubation group (n=60) and 5.1 days in the delayed intubation group (n=36). The ICU mortality rate was 56.7% and 75% in the early and delayed intubation groups, respectively, before propensity matching (P=0.075). After matching for demographic and clinical covariates, 33 matched pairs were selected. In the propensity-matched cohort, delayed intubation significantly increased the risk of ICU mortality (adjusted odds ratio, 3.99; 95% confidence interval, 1.02-15.63; P=0.046). However, in-hospital mortality did not differ significantly between the groups. In patients with IPF, delayed intubation after initiation of high-concentration oxygen therapy was significantly associated with increased risk of ICU mortality compared to early intubation.

ETS1 Ameliorates Hyperoxia-Induced Alveolar Epithelial Cell Injury by Regulating the TGM2-Mediated Wnt/β-Catenin Pathway.

Bronchopulmonary dysplasia (BPD) is a chronic lung disease that affects newborns who need oxygen therapy, and high-concentration oxygen therapy may cause neonatal morbidity and mortality in newborns. E26 oncogene homologue 1 (ETS1) and transglutaminase 2 (TGM2) have been reported to be associated with lung cell injury. However, the mechanism of ETS1 in regulating BPD is still unclear. Hyperoxia-induced A549 cells to simulate hyperoxia-induced alveolar epithelial cell injury. MTT assays and colony formation assays were performed to investigate the proliferation of A549 cells. Flow cytometry was carried out to quantify the apoptosis of A549 cells. The expression levels of ETS1 and TGM2 were quantified by qRT-PCR. The protein expression levels of ETS1, TGM2, β-catenin, c-Jun and MET were measured by western blot. Overexpression of ETS1, overexpression of TGM2, overexpression of ETS1 with downregulation of TGM2 and overexpression of TGM2 with inhibition of Wnt/β-catenin pathway were performed to investigate the role of ETS1, TGM2 and Wnt/β-catenin pathways in hyperoxia-induced alveolar epithelial cell injury. Hyperoxia decreased the proliferation and promoted the apoptosis of cells in a time-dependent manner. Moreover, overexpression of ETS1 rescued the effect of hyperoxia on proliferation and apoptosis. In addition, overexpression of TGM2 participated in the regulation of hyperoxia-induced proliferation and apoptosis. ETS1 regulated hyperoxia-induced alveolar epithelial cell injury through the Wnt/β-catenin pathway via TGM2. ETS1 ameliorates hyperoxia-induced alveolar epithelial cell injury through the TGM2-mediated Wnt/β-catenin pathway.

Evaluation of inpatient oxygen therapy in hypercapnic chronic obstructive pulmonary disease.

High concentration oxygen therapy in hypercapnic chronic obstructive pulmonary disease (COPD) is associated with increased mortality. In ward-based patients with acute exacerbation of COPD and hypercapnia, this study examines oxygen prescription and the association between high concentration oxygen therapy and adverse outcome. To investigate the association between over-oxygenation and in-hospital adverse events. Inpatients with acute exacerbation of hypercapnic COPD at a tertiary Australian hospital over a 1-year period were retrospectively identified. Oxygen prescription and therapy was determined based on chart review. Over-oxygenation was defined as ≥10% of nursing chart observations recording oxygen delivery with oxygen saturation above 92%. A composite adverse outcome was defined as medical emergency team response, recommencement of non-invasive ventilation or death. The association between over-oxygenation and adverse outcome was assessed using survival analysis and conditional logistic regression modelling. The study cohort comprised 106 unique patients and 157 admissions. Oxygen prescription was recorded in 132 (84%) and over-oxygenation occurred in 97 (62%) admissions. Over-oxygenation was higher in non-respiratory ward admissions (76% vs 57%, P = 0.03) and those without any form of oxygen prescription (84% vs 58%, P = 0.01). During follow up, 23 (22%) patients experienced an adverse event. Cox proportional hazards modelling found weak evidence for increased risk of an adverse event in over-oxygenated patients (hazard ratio 2.5; 95% confidence interval 0.8-7.3, P = 0.10). Conditional logistic regression, after matching on age, Charlson comorbidity category and length of follow up, found a similar estimate of association (hazard ratio 2.6; 95% confidence interval 0.8-8.7, P = 0.12). Over-oxygenation to hypercapnic COPD inpatients is common and rates of oxygen prescription are suboptimal. We found weak evidence of association between over-oxygenation and adverse events, likely due to low statistical power. Larger prospective studies are needed.

The effect of 50% oxygen on PtCO2 in patients with stable COPD, bronchiectasis, and neuromuscular disease or kyphoscoliosis: randomised cross-over trials

BackgroundHigh-concentration oxygen therapy causes increased arterial partial pressure of carbon dioxide (PaCO2) in patients with COPD, asthma, pneumonia, obesity and acute lung injury. The objective of these studies was to investigate whether this physiological response to oxygen therapy occurs in stable patients with neuromuscular disease or kyphoscoliosis, and bronchiectasis.MethodsThree randomised cross-over trials recruited stable patients with neuromuscular disease or kyphoscoliosis (n = 20), bronchiectasis (n = 24), and COPD (n = 24). Participants were randomised to receive 50% oxygen and 21% oxygen (air), each for 30 min, in randomly assigned order. The primary outcome was transcutaneous partial pressure of carbon dioxide (PtCO2) at 30 min. The primary analysis was a mixed linear model.ResultsSixty six of the 68 participants had baseline PtCO2 values < 45 mmHg. The intervention baseline adjusted PtCO2 difference (95% CI) between oxygen and room air after 30 min was 0.2 mmHg (− 0.4 to 0.9), P = 0.40; 0.5 mmHg (− 0.2 to 1.2), P = 0.18; and 1.3 mmHg (0.7 to 1.8), P < 0.001, in the neuromuscular/kyphoscoliosis, bronchiectasis and COPD participants respectively.ConclusionsThe small increase in PtCO2 in the stable COPD patients with high-concentration oxygen therapy contrasts with the marked increases in PaCO2 seen in the setting of acute exacerbations of COPD. This suggests that the model of studying the effects of high-concentration oxygen therapy in patients with stable respiratory disease is not generalisable to the use of oxygen therapy in the acute clinical setting. Appropriate studies of high-concentration compared to titrated oxygen in acute clinical settings are needed to determine if there is a risk of oxygen-induced hypercapnia in patients with neuromuscular disease, kyphoscoliosis or bronchiectasis.Trial registrationAustralian New Zealand Clinical Trials Registry ACTRN12615000970549 Registered 16/9/15, ACTRN12615000971538 Registered 16/9/15 and ACTRN12615001056583 Registered 7/10/15.

INVASIVE MECHANICAL VENTILATION WITH HIGH CONCENTRATION OXYGEN THERAPY FOR AECOPD PATIENTS WITH ACUTE MYOCARDIAL INFARCTION

SESSION TITLE: Topics in Obstructive Lung Disease SESSION TYPE: Original Investigations PRESENTED ON: 10/23/2019 02:15 PM - 03:15 PM PURPOSE: To evaluate the efficacy of invasive ventilation with high concentration oxygen for AECOPD patients with acute myocardial infarction（AMI）. METHODS: It was a randomized and prospective controlled trial,87 elderly AECOPD patients were included, who complicated with AMI,who could not accept PCI,80 cases (92%)with congestive heart failure), the shock and malignant arrhythmia were excluded. All subjects were divided into(1:1:1) three groups depending on therapy. Conventional oxygen therapy group (3-7L/min, via nasal catheter);high concentration oxygen group: invasive ventilation with PRVC mode, management of FiO2 included two steps: Step 1:FiO2:50%-70% within 48 hours; Step 2: FiO2 from 50% to 40% gradually after the 48th hour, moderate concentration oxygen group: invasive ventilation with PRVC mode, FiO2:30%-50%.All groups were received Heparin Sodium continuous venous pump(100IU/kg/d), anti-anxiety and expansion of coronary therapy, etc. RESULTS: 14-day mortality rate and occurrence of malignant arrhythmia in high concentration oxygen group were lower than other groups <0.01). Compared with moderate-concentration oxygen, there was a higher extubation rate (75.9% vs. 44.8%, p=0.016). Recurrence rate of myocardial Infarction were 31.0% (n=9) and 6.9% (n=2) in moderate and high concentration oxygen group respectively (p=0.019). There was no difference in occurrence of hyperoxia among groups (p>0.05). CONCLUSIONS: There was significant improvement in mortality rate and extubation for AECOPD patients with AMI who accepted invasive ventilation with high concentration oxygen therapy than in moderate-concentration oxygen group. CLINICAL IMPLICATIONS: AECOPD patients with AMI maybe benefit from invasive ventilation with high concentration oxygen therapy, and seems to be an appropriate therapy for these patients who could not undergo PCI, but which potential impacts need further study. DISCLOSURES: no disclosure on file for Boxue Han; No relevant relationships by Jiao Jun, source=Web Response no disclosure on file for Fuzhou Liu; no disclosure on file for Lei Sun; no disclosure on file for Ying Wang; no disclosure on file for Guoru Yang

The Role of Oxygen Therapy in Normoxemic Acute Coronary Syndrome: A Systematic Review of Randomized Controlled Trials.

Supplemental oxygen has been commonly used in the cases of acute coronary syndrome (ACS); however, recent evidence suggests that high-concentration oxygen supplementation and hyperbaric oxygen in ACS patients are associated with adverse cardiovascular effects. The purpose of this article is to systematically review the role of supplemental oxygen therapy in normoxemic patients with ACS. A search for randomized controlled trials before November 2017 in biomedical databases was performed, and a total of 6 eligible studies with 7508 participants were identified. Four studies reported all-cause mortality after randomization, whereas 3 studies measured myocardial infarct size using cardiac enzyme levels and magnetic resonance imaging. The effect size of our primary end point was the odds ratio for all-cause mortality. The mean difference was calculated as a secondary outcome for myocardial infarct size. Compared with ambient air or titrated oxygen, high-concentration oxygen therapy did not significantly decrease all-cause mortality (odds ratio, 1.01; 95% confidence interval [CI], 0.81-1.25; P = .95) within 1 year nor infarct size detected by peak cardiac troponin (mean difference, -0.53 ng/mL; 95% CI, -1.20 to 0.14; P = .12) and magnetic resonance imaging (mean difference, 1.45 g; 95% CI, -1.82 to 4.73; P = .39). These outcomes were listed through a fixed-effects model because of low statistical heterogeneity across the studies. Oxygen therapy did not significantly reduce clinical all-cause mortality and myocardial infarct size in ACS patients with normoxemia. Further large-scale randomized clinical trials are warranted to evaluate the cardiovascular effects in this field.

WISP-3/CCN6 inhibits apoptosis by regulating caspase pathway after hyperoxia in lung epithelial cells

Cell death is a normal phenomenon in the course of biological development, moreover, which is also a prominent feature in lung exposed to hyperoxia. Severe hypoxia occurs in ALI/ARDS patients, who generally require high concentration oxygen therapy assisted by mechanical ventilation. Nevertheless, high oxygen can cause excessive reactive oxygen species (ROS), leading to apoptosis in lung epithelial cells, which has been reported in our previous study. Herein, the correlation between increments of ROS and CCN6 expression was negative in CCN6-mediated the mitochondria dependent, intrinsic apoptotic pathway. Our latest research explained that CCN6 can inhibit caspase-8 mediated extrinsic apoptotic pathway to protect cells from hyperoxia-induced apoptosis. As demonstrated by Western Blot Analysis, Caspase 8 cleavage and Caspase 3 cleavage in CCN6-depleted cells exceeded the control group treated with high oxygen (48 h). And deletion of CCN6 enhanced caspase-8 activation after hyperoxia shown by Flow Cytometry. Although, it is unclear how CCN6 participated in the regulation of apoptotic pathways, the future targeted therapy drugs inhibiting CCN6 may be useful in the treatment of ALI/ARDS.

Effect of Oxygen Therapy by Venturi Mask versus Non Invasive Ventillation on the Outcome of Patients Who Devolope Hypoxia after Open Heart Surgery

Background: Cardiothoracic surgery is a common cause of acute respiratory failure and is associated with increased morbidity and mortality. We aimed to compare the outcomes of open heart surgery patients treated using oxygen delivery devices with patients who receive NIV as a first-line therapy for hypoxemic respiratory failure. Materials and Methods: 40 patients who developed acute hypoxemic respiratory failure after open heart surgery and admitted to cardiothoracic ICU 20 patients received NIV and 20 patient received oxygen by venture mask. For all patients the following measurements were performed before and after CPAP AND Venture use: CBC, blood urea, serum creatinine body temperature, chest X-ray, Arterial blood gases (arterial pH, sodium bicarbonate, pcO2, SpO2 and PaO2-to-FiO2 ratio). Results: Mean PO2 and SO2 have increased after using of both venture and Cpap, increase in both PCO2 and HCO3 levels after using Venturi mask, CPAP mask was superior to venturi mask in avoiding the need of intubation, decreasing The ICU stay median length and also median length of hospitalization, all were lower in CPAP group than venture group. Also the mortality rate was lower in CPAP group than the venturi group. Conclusion: Using CPAP mask in severe AHRF following open heart surgery can avoid intubation, decreases the levels of tachypnea and arterial hypoxemia, decreases ICU stay, the length of hospitalization and also decreases the mortality rate compared with patients receiving high-concentration oxygen therapy with venture mask.

High flow or titrated oxygen for obese medical inpatients: a randomised crossover trial.

To compare the effects on transcutaneous carbon dioxide tension (Ptco2) of high concentration and titrated oxygen therapy in medical inpatients with morbid obesity who were not selected for a pre-existing diagnosis of obesity hypoventilation syndrome. A randomised, crossover trial undertaken between February and September 2015. Internal medicine service, Wellington Regional Hospital, New Zealand. 22 adult inpatients, aged 16 years or more, with a body mass index exceeding 40 kg/m2. Participants received in random order two 60-minute interventions, with a minimum 30-minute washout period between treatments: titrated oxygen therapy (oxygen delivered, if required, via nasal prongs to achieve peripheral oxygen saturation [Spo2] of 88-92%), and high concentration oxygen therapy (delivered via Hudson mask at 8 L/min, without regard to Spo2). Ptco2 and Spo2 were recorded at 10-minute intervals. Ptco2 at 60 minutes, adjusted for baseline. Baseline Ptco2 was 45 mmHg or lower for 16 participants with full data (73%). The mean difference in Ptco2 between high concentration and titrated oxygen therapy at 60 minutes was 3.2 mmHg (95% CI, 1.3-5.2 mmHg; P = 0.002). High concentration oxygen therapy increases Ptco2 in morbidly obese patients. Our findings support guidelines that advocate oxygen therapy, if required in patients with morbid obesity, be titrated to achieve a target Spo2 of 88-92%. Australian New Zealand Clinical Trials Registry, ACTRN12610000522011.

The clinical value of urinary antigen detection of Legionella pneumonia

To investigate the clinical value of urinary antigen detection of Legionella, and to describe the clinical characteristics of Legionella pneumonia. Patients with suspected Legionella pneumonia were enrolled from the Respiratory departments of 3 tertiary hospitals in Shenyang during May 2011 to November 2013. Urinary Legionella antigen was detected for all the enrolled patients. Bacterial culture, polymerase chain reaction (PCR) for Legionella, and double Legionella antibody detection in sera were performed for each patient whose urinary antigen was positive. Patients confirmed to have Legionella pneumonia were pooled and analyzed. Totally 13 cases presenting with pneumonia were positive for Legionella by the urinary antigen method, and in one of them Legionella strain was isolated from the secretion of lower respiratory tract. PCR detection was performed in 8 patients, and 4 of them were positive. Legionella antibody detection was performed in 12 patients, and 7 of them were positive. Nine patients had a history of exposure to Legionella high-risk environments. The characteristics of the cases with Legionella pneumonia were as follows: characteristic orange sputum in 4 patients, digestive symptoms in 6, neurologic disorders in 8, hyponatremia in 10, hypoxia with oxygenation index < 300 mmHg (1 mmHg = 0.133 kPa) in 11, and severe pneumonia with PSI of grade V (PSI score > 130) in 8 patients . Chest CT scan showed bilateral involvement in 6, ground-glass opacity combined with consolidation in 11, and moderate pleural effusion in 11 patients. Cavity and reversed halo sign were found in one case, respectively. All of the patients received fluoroquinolone treatment, and 11 patients recovered completely while 2 died of multiple organ dysfunction syndrome, one of them was complicated with secondary infection. Detection of urinary antigen of Legionella is very useful in the diagnosis of Legionella pneumonia. Attention should be paid to exposure history to the high-risk environments and multiple organ impairment when Legionella infection is suspected. Orange sputum may be characteristic for Legionella pneumonia and therefore a clue for diagnosis. In critical cases, secondary infection and additional lung injuries induced by high concentration oxygen therapy may occur.

Outcomes of acute exacerbations in COPD in relation to pre-hospital oxygen therapy

BackgroundPre-hospital, high-concentration oxygen therapy during acute exacerbation of chronic obstructive pulmonary disease (AECOPD) has been associated with increased mortality. Recent COPD guidelines have encouraged titrated oxygen therapy with a target saturation range of 88–92%. Oxygen therapy leading to saturation above 92% is defined as ‘inappropriate oxygen therapy’.ObjectivesTo examine the frequency of inappropriate oxygen therapy and whether inappropriate oxygen therapy in the ambulance in an urban area with short transit time to hospital was associated with poor outcome.MethodsIn an audit of 405 consecutive patients with AECOPD arriving by ambulance to Hvidovre Hospital, details of transit time, oxygen administration, saturation, and arterial blood gases were registered. Outcomes were respiratory acidosis, need of supported ventilation, length of hospitalisation, and in-hospital mortality.ResultsOnly 15 patients were not treated with oxygen and information on oxygen flow was missing in seven patients and on saturation on one patient. Altogether, 352 (88.7%) of 397 patients received inappropriate oxygen therapy. Patients on ‘inappropriate oxygen therapy’ (saturation ≥92%) had a high frequency of respiratory acidosis at hospital admission, 108 (33.5%) of 324 patients, length of stay was on average 5.1 days, 12.5% of the patients needed ventilatory support, and in-hospital mortality was 3.4%.ConclusionThe majority of patients with AECOPD received inappropriate oxygen therapy in the ambulance, but their need of ventilatory support, length of stay, and mortality were low. Randomised studies are needed to clarify the optimal pre-hospital oxygen therapy.

Comparative audit of oxygen use in the prehospital setting in acute COPD exacerbation over 5 years

BackgroundIn 2009 the Wellington Free Ambulance implemented an education programme to reduce high concentration oxygen delivery to patients with an acute exacerbation of chronic obstructive pulmonary disease (AECOPD). The aim...

Human lung on a chip: innovative approach for understanding disease processes and effective drug testing

Human lung on a chip: innovative approach for understanding disease processes and effective drug testing

The risk of serious adverse outcomes associated with hypoxaemia and hyperoxaemia in acute exacerbations of COPD

BackgroundPrehospital high concentration oxygen therapy leads to worse clinical outcomes in patients presenting with acute exacerbations of chronic obstructive pulmonary disease (AECOPD). Less is known about the risks of hypoxaemia...

Randomized controlled trial of high concentration oxygen in suspected community-acquired pneumonia

To determine whether high concentration oxygen increases the PaCO(2) in the treatment of community-acquired pneumonia. Randomized controlled clinical trial in which patients received high concentration oxygen (8 L/min via medium concentration mask) or titrated oxygen (to achieve oxygen saturations between 93 and 95%) for 60 minutes. Transcutaneous CO(2) (PtCO(2)) was measured at 0, 20, 40 and 60 minutes. The Emergency Departments at Wellington, Hutt and Kenepuru Hospitals. 150 patients with suspected community-acquired pneumonia presenting to the Emergency Department. Patients with chronic obstructive pulmonary disease (COPD) or disorders associated with hypercapnic respiratory failure were excluded. The primary outcome variable was the proportion of patients with a rise in PtCO(2) ≥4 mmHg at 60 minutes. Secondary outcome variables included the proportion of patients with a rise in PtCO(2) ≥8 mmHg at 60 minutes. The proportion of patients with a rise in PtCO(2) ≥4 mmHg at 60 minutes was greater in the high concentration oxygen group, 36/72 (50.0%) vs 11/75 (14.7%), relative risk (RR) 3.4 (95% CI 1.9 to 6.2), P < 0.001. The high concentration group had a greater proportion of patients with a rise in PtCO(2) ≥8 mmHg, 11/72 (15.3%) vs 2/75 (2.7%), RR 5.7 (95% CI 1.3 to 25.0), P = 0.007. Amongst the 74 patients with radiological confirmation of pneumonia, the high concentration group had a greater proportion with a rise in PtCO(2) ≥4 mmHg, 20/35 (57.1%) vs 5/39 (12.8%), RR 4.5 (95% CI 1.9 to 10.6) P < 0.001. We conclude that high concentration oxygen therapy increases the PtCO(2) in patients presenting with suspected community-acquired pneumonia. This suggests that the potential increase in PaCO(2) with high concentration oxygen therapy is not limited to COPD, but may also occur in other respiratory disorders with abnormal gas exchange.

Randomized Controlled Trial of High Concentration versus Titrated Oxygen Therapy in Severe Exacerbations of Asthma: Perrin K, Wijesinghe M, Healy B, et al. Thorax 2011;66:937–41.

In patients with chronic obstructive pulmonary disease (COPD) exacerbations, high concentrations of oxygen therapy can lead to subsequent retention of carbon dioxide (CO2). This study sought to evaluate whether a similar effect occurs in patients presenting to the emergency department with acute exacerbations of asthma. In this randomized controlled trial, 106 patients presenting with acute asthma exacerbations were randomized into two treatment groups: a high oxygen concentration group and a titrated oxygen group. Patients between the ages of 18 and 65 years were included if they had a previous diagnosis of asthma, a history consistent with asthma exacerbation, and a 1-s forced expiratory volume (FEV1)<50% of predicted. Patients placed in the high concentration group received 8 L/min of oxygen through a concentration mask. Those in the titration group were given oxygen only if their saturations were<92% on room air. If patients had oxygen saturations<92%, oxygen flow was then titrated every 5 min until saturations were between 93% and 95%. All patients with an FEV1 between 30% and 50% predicted, also received nebulized salbutamol and oral prednisone. Those patients with FEV1<30% received salbutamol, intravenous hydrocortisone, and magnesium sulfate. The primary outcome for this study was the proportion of patients with a transcutaneous partial pressure of carbon dioxide (PtCO2) increase>4 mm Hg at 60 min. The secondary outcome was those with both a PtCO2 increase>4 mm Hg and a PtCO2≥38 mm Hg at 60 min. Twenty-two patients (44%) in the high concentration group had a change in PtCO2>4 mm Hg, whereas only 10 (19%) in the titrated oxygen group had the same result, yielding a significant difference (p=0.006). The proportion of patients with a PtCO2 increase>4 mm Hg and a PtCO2>38 mm Hg at 60 min was also significantly larger in those patients treated with high oxygen concentrations (p=0.001). Also of note, the mean change in PtCO2 from baseline was significantly larger in the high oxygen concentration group, with a mean difference of 2.6 mm Hg (p<0.003). From these data, the authors concluded that high-concentration oxygen therapy increases the risk of hypercapnia in patients with severe asthma exacerbations. They postulated that the mechanism is similar to that in COPD related to worsening ventilation-perfusion mismatching from pulmonary vascular dilatation in response to high oxygen concentrations.

Early use of noninvasive positive pressure ventilation for acute lung injury

Noninvasive positive pressure ventilation is beneficial for patients with acute respiratory failure. However, its possible benefit for patients with acute lung injury (200 mm Hg < PaO(2)/FIO(2) ≤300 mm Hg) remains unclear. Our aim was to assess the safety and efficacy of noninvasive positive pressure ventilation for patients with acute lung injury and compare this with high-concentration oxygen therapy. A multicentered randomized controlled trial. Ten multipurpose intensive care units. Forty patients who fulfilled the criteria for acute lung injury were included in this study. Patients were randomly allocated to receive either noninvasive positive pressure ventilation (noninvasive positive pressure ventilation group) or high-concentration oxygen therapy through a Venturi mask (control group). Twenty-one patients were assigned to the noninvasive positive pressure ventilation group and 19 were in the control group. At study entry, the patients' characteristics in the two groups were similar. Noninvasive positive pressure ventilation application decreased the respiratory rate and improved PaO(2)/FIO(2) with time. The proportion of patients requiring intubation and the actual number of intubations in the noninvasive positive pressure ventilation group were significantly less than in the control group (one of 21 vs. seven of 19; p = .02, and one of 21 vs. four of 19; p = .04, respectively). Noninvasive positive pressure ventilation showed a trend for reducing inhospital mortality (one of 21 vs. five of 19; p = .09). The total number of organ failures in the noninvasive positive pressure ventilation group was significantly lower than in the control group (three vs. 14; p < .001). Noninvasive positive pressure ventilation is safe for selected patients with acute lung injury. However, a larger randomized trial with need for intubation and mortality as the outcomes of interest is required.