Chronic Hypoxemia Research Articles

Enchanced preoperative rehabilitation as part of the complex perioperative rehabilitation of patients with super-obesity and obstructive sleep apnea syndrome (clinical outlook)

Obesity is a global social and economic problem. The bariatric surgery is a most effective treatment for obesity. The presented clinical case demonstrates the usage of principles of enchanced perioperative rehabilitation for the preoperative preparation of a patient with super obesity and with severe obstructive sleep apnea and alveolar hypoventilation syndrome.A 54-year-old patient was hospitalized with complaints of obesity, impossibility of persistent weight loss conservatively, severe daytime sleepiness, frequent nocturnal awakenings (up to 8 times per night). The patient’s weight was 230 kg with a height of 157 cm (BMI 93.5 kg / m2). The examination revealed a syndrome of sleep apnea of mixed genesis of extremely severe degree, chronic night hypoxemia of an extremely severe degree. Preoperative preparation was performed in accordance with the program of enchanced perioperative rehabilitation. The duration of preoperative preparation was 19 days; weight loss — 40 kg (%WL -17,4), compensation of comorbidities was achieved as well. After that the patient underwent a laparoscopic sleeve gastrectomy. There were no complications in the postoperative period. Length of postoperative hospital stay was 6 days. At follow-up examination one year after surgery, body weight dropped from 230 to 153 kg (% WL-33.5), a significant improvement of the quality of life was achieved.The enchanced perioperative rehabilitation program can be successfully used as an effective method for preoperartive preparation of the patients with morbid obesity in combination with severe obstructive sleep apnea syndrome.and obesity hypoventilation. It can be a reasonable alternative to the standard program with preoperative intragastric balloon treatment. The use of this technique allows to increase the effectiveness of treatment of these high-risk patients, as well as to reduce the risk of perioperative complications.

An Erythropoietin-Independent Mechanism of Erythrocytic Precursor Proliferation Underlies Hypoxia Tolerance in Sea Nomads.

The Bajau Sea Nomads were recently demonstrated to have evolved larger spleens as an adaptation to millennia of a marine foraging lifestyle. The large-spleen phenotype appears to derive from increases in thyroid hormone (TH) production as a result of reduced expression of phosphodiesterase 10A (PDE10A), though the exact mechanism remains unknown. Through pharmacological inhibition of PDE10A using the selective inhibitor MP-10 in mice, we were able to mimic the Bajau adaptation and show that treated mice had significantly larger spleens than control animals. This difference appears connected to an excess of early stage erythrocytes and an apparent increase in red blood cell (RBC) precursor proliferation in response to increased TH. However, we determined that the stimulation of RBC production in the mouse model via TH is Erythropoietin (EPO)-independent, unlike in the altitude (chronic hypoxemia) response. We confirmed this using human GWAS data; although the Bajau PDE10A variants are significantly associated with increased TH levels and RBC count, they are not associated with EPO levels, nor are other strongly thyroid-associated SNPs. We therefore suggest that an EPO-independent mechanism of stimulating RBC precursor proliferation via TH upregulation underlies the increase in spleen size observed in Sea Nomad populations.

Tachyarrhythmias in Congenital Heart Diseases: From Ion Channels to Catheter Ablation.

Major advances in pediatric cardiology in recent decades, especially surgical techniques, have resulted in an increasing number of patients with congenital heart disease (CHD) surviving to adulthood. This has generated new challenges, particularly with regards to the late onset of complex arrhythmias. Abnormal anatomy, surgical scarring, chronic hypoxemia, hemodynamic compromise, neuro-hormonal abnormalities, and genetic factors can all contribute to creating a unique substrate for arrhythmia development. This review attempts to synthesize the current state of knowledge spanning the spectrum from underlying mechanisms of arrhythmias in patients with congenital heart disease to current ablative strategies. We discuss existing knowledge gaps and highlight important areas for future research.

Resting Oxygen Saturations are Associated With Altered Brain White Matter Microstructure in Adolescents and Adults With a Fontan Circulation; A Diffusion Brain MRI Study

Long-term cognitive dysfunction is common in people with a Fontan circulation, however underlying brain alterations associated with worse outcomes are poorly characterised. Chronic hypoxaemia is also common and is associated with long-term morbidity and mortality. This study investigated brain white matter (WM) microstructure in adolescents and adults with a Fontan circulation and associations with resting oxygen saturations (SaO2) and cognitive functioning.

Multi‐disciplinary collaborative consensus guidance statement on the assessment and treatment of breathing discomfort and respiratory sequelae in patients with post‐acute sequelae of SARS‐CoV‐2 infection (PASC)

<scp>Multi‐disciplinary</scp> collaborative consensus guidance statement on the assessment and treatment of breathing discomfort and respiratory sequelae in patients with <scp>post‐acute</scp> sequelae of <scp>SARS‐CoV</scp>‐2 infection (<scp>PASC</scp>)

Melatonin as a Cardioprotective Treatment for Fetal Growth Restriction

Offspring born following fetal growth restriction (FGR) have an increased risk of cardiovascular disease. Chronic fetal hypoxaemia caused by placental insufficiency is the primary cause of FGR. Hypoxaemia is associated with increased oxidative stress in the fetus and subsequently reduces nitric oxide (NO) bioavailability. Antenatal melatonin therapy may prevent damage to the cardiovascular system, via antioxidant actions, and improve NO bioavailability.

Intermittent maternofetal oxygenation during late gestation improved birthweight, neonatal growth, body symmetry, and muscle metabolism in intrauterine growth-restricted lambs.

In humans and animals, intrauterine growth restriction (IUGR) results from fetal programming responses to poor intrauterine conditions. Chronic fetal hypoxemia elevates circulating catecholamines, which reduces skeletal muscle β2 adrenoceptor content and contributes to growth and metabolic pathologies in IUGR-born offspring. Our objective was to determine whether intermittent maternofetal oxygenation during late gestation would improve neonatal growth and glucose metabolism in IUGR-born lambs. Pregnant ewes were housed at 40 °C from the 40th to 95th day of gestational age (dGA) to produce IUGR-born lambs (n = 9). A second group of IUGR-born lambs received prenatal O2 supplementation via maternal O2 insufflation (100% humidified O2, 10 L/min) for 8 h/d from dGA 130 to parturition (IUGR+O2, n = 10). Control lambs (n = 15) were from pair-fed thermoneutral ewes. All lambs were weaned at birth, hand-reared, and fitted with hindlimb catheters at day 25. Glucose-stimulated insulin secretion (GSIS) and hindlimb hyperinsulinemic-euglycemic clamp (HEC) studies were performed at days 28 and 29, respectively. At day 30, lambs were euthanized and ex vivo HEC studies were performed on isolated muscle. Without maternofetal oxygenation, IUGR lambs were 40% lighter (P < 0.05) at birth and maintained slower (P < 0.05) growth rates throughout the neonatal period compared with controls. At 30 d of age, IUGR lambs had lighter (P < 0.05) hindlimbs and flexor digitorum superficialis (FDS) muscles. IUGR+O2 lambs exhibited improved (P < 0.05) birthweight, neonatal growth, hindlimb mass, and FDS mass compared with IUGR lambs. Hindlimb insulin-stimulated glucose utilization and oxidation rates were reduced (P < 0.05) in IUGR but not IUGR+O2 lambs. Ex vivo glucose oxidation rates were less (P < 0.05) in muscle from IUGR but not IUGR+O2 lambs. Surprisingly, β2 adrenoceptor content and insulin responsiveness were reduced (P < 0.05) in muscle from IUGR and IUGR+O2 lambs compared with controls. In addition, GSIS was reduced (P < 0.05) in IUGR lambs and only modestly improved (P < 0.05) in IUGR+O2. Insufflation of O2 also increased (P < 0.05) acidosis and hypercapnia in dams, perhaps due to the use of 100% O2 rather than a gas mixture with a lesser O2 percentage. Nevertheless, these findings show that intermittent maternofetal oxygenation during late gestation improved postnatal growth and metabolic outcomes in IUGR lambs without improving muscle β2 adrenoceptor content.

Can Erythropoietin Reduce Hypoxemic Neurological Damages in Neonates With Congenital Heart Defects?

Congenital heart defects (CHD), the most common cause of birth defects with increasing birth prevalence, affect nearly 1% of live births worldwide. Cyanotic CHD are characterized by hypoxemia, with subsequent reduced oxygen delivery to the brain, especially critical during brain development, beginning in the fetus and continuing through the neonatal period. Therefore, neonates with CHD carry a high risk for neurological comorbidities, even more frequently when there are associated underlying genetic disorders. We review the currently available knowledge on potential prevention strategies to reduce brain damage induced by hypoxemia during fetal development and immediately after birth, and the role of erythropoietin (EPO) as a potential adjunctive treatment. Maternal hyper-oxygenation had been studied as a potential therapeutic to improve fetal oxygenation. Despite demonstrating some effectiveness, maternal hyper-oxygenation has proven to be impractical for extensive clinical application, thus prompting the investigation of specific pathways for pharmacological intervention. Among those, the role of antioxidant pathways and Hypoxia Inducible Factors (HIF) have been studied for their involvement in the protective response to hypoxic injury. One of the proteins induced by HIF, EPO, has properties of being anti-apoptotic, antioxidant, and protective for neurons, astrocytes, and oligodendrocytes. In human trials, EPO administration in neonates with hypoxic ischemic encephalopathy (HIE) significantly reduced the neurological hypoxemic damages in several reported studies. Currently, it is unknown if the mechanisms of pathophysiology of cyanotic CHD are like HIE. Neonates with cyanotic CHD are exposed to both chronic hypoxemia and episodes of acute ischemia-reperfusion injury when undergo cardiopulmonary bypass surgery requiring aortic cross-clamp and general anesthesia. Our review supports future trials to evaluate the potential efficiency of EPO in reducing the hypoxemic neurologic damages in neonates with CHD. Furthermore, it suggests the need to identify early biomarkers of hypoxia-induced neurological damage, which must be sensitive to the neuroprotective effects of EPO.

Lack of Medical Criteria for Long-Term Oxygen Therapy Usage According to International Guidance in Outpatients With Chronic Hypoxemia.

BackgroundBenefits of long-term oxygen therapy (LTOT) have been observed in hypoxemic respiratory patients. Reports have shown the lack of observance among healthcare professionals of LTOT. Thus, this study aimed to determine the demographic characteristics and observance of the medical indication of LTOT according to the international guidelines.MethodologyA cross-sectional study was conducted on patients who attended the Medical Unit in Aguascalientes, Mexico to re-evaluate the need for LTOT. Data are presented as mean ± standard deviation. Statistical analyses were performed using the chi-square test or unpaired t-tests. P-values of <0.05 were considered statistically significant.ResultsFrom 813 outpatients attended to re-evaluate whether they met the medical criteria to use LTOT, 93 outpatients were excluded, and the remaining 714 outpatients were enrolled. The mean age of the patients was 70.0 ± 15.1 years, with a female gender predominance (59.1 %). The mean PaO2 level in room air was 7.9 ± 2.3 kPa. Hemoglobin and hematocrit levels were 14.9 ± 4.1 g/dL and 44.7 ± 8.4%, respectively. The mean levels of PaO2 were higher in female patients (8.1 ± 2.5 kPa vs. 7.6 ± 1.9 kPa; p = 0.01). The most common diagnosis was chronic obstructive pulmonary disorder (60.5%). Moreover, the specialty that most indicated the use of LTOT was pulmonology (57.8%); however, 36.8% of patients who used LTOT did not have any criteria according to international guidelines.ConclusionsAlthough a significant percentage of patients do not use LTOT correctly, the most important finding is that the medical indication of LTOT by physicians is not always correct, leading to an excessive prescription of oxygen.

Cardiovascular and Respiratory Interactions in Idiopathic Pulmonary Fibrosis by Extended Partial Directed Coherence: Short-term Effects of Supplemental Oxygen.

Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease that can lead to chronic arterial hypoxemia, hypercapnia, and dyspnea. To improve clinical symptoms in IPF patients, supplemental oxygen (SupplO2) has been prescribed with the aim to maintain SpO2 level, and consequently to relieve dyspnea, increase physical activity and improve quality of life. In this study, we investigated the effect of disease and short-term SupplO2 on cardiovascular and respiratory autonomic regulation. Linear and nonlinear indices were extracted from the beat-to-beat variability of heart rate (HR), systolic (SYS) blood pressure and respiration (RESP) in IPF patients and healthy subjects spontaneously breathing ambient air (AA) and during SupplO2 at 3 L/min. It was found that the effects on autonomic nervous systems (ANS) regulation were better demonstrated by the Granger causality (GC) method. GC was significantly higher (p<0.01) in patients compared to controls for the interactions RESP→SYS and BBI→SYS.Clinical Relevance-Short-term SupplO2 in IPF could adversely affect systolic blood pressure variability in particular. This study may help in the management of SupplO2 administration.

Cyanosis in a Previously Well Child.

Cyanosis in a Previously Well Child.

AMIKACIN-INDUCED HYPERSENSITIVITY PNEUMONITIS IN A PATIENT WITH PULMONARY MYCOBACTERIUM AVIUM COMPLEX INFECTION

TOPIC: Diffuse Lung Disease TYPE: Fellow Case Reports INTRODUCTION: Inhaled amikacin is FDA approved in the treatment of pulmonary Mycobacterium avium complex (MAC). Here we present a case of acute hypersensitivity pneumonitis after initiating therapy with inhaled amikacin. CASE PRESENTATION: An 82 year old male with a history of pulmonary MAC infection and chronic hypoxemia on 2L oxygen presented with progressive non-productive cough and dyspnea. He had been diagnosed with pulmonary MAC three years prior to presentation and had been treated with azithromycin, rifampin, and ethambutol. CT chest imaging demonstrated multifocal bronchiectasis, tree in bud nodules, and cavitary lesions. Respiratory AFB cultures were positive for MAC. He was prescribed oral rifampin and azithromycin. Intravenous amikacin was considered given cavitary disease but deferred in light of age and comorbidities. Inhaled amikacin was prescribed but unable to be started as an outpatient. One week later, he was admitted with new fevers, progressive dry cough, dyspnea, and increased oxygen requirement. CT chest was negative for pulmonary embolism and showed new multifocal ground glass opacities (Image #1). He was admitted for suspected superimposed bacterial or viral pneumonia. COVID-19 and respiratory viral testing were negative. Sputum culture was unable to be obtained due to non-productive cough. Rifampin and azithromycin were continued and nebulized amikacin was initiated. Broad spectrum antibiotics were started to cover for bacterial pneumonia. He initially defervesced but on hospital day #5, his dyspnea and hypoxemia worsened. He required up to 15 liters 100% oxygen via non-rebreather mask. He was empirically diuresed and antibiotic coverage was broadened without improvement. Echocardiogram showed unchanged cardiac function. CT chest imaging on hospital day #7 demonstrated progressive multifocal ground glass opacities with intralobular and interlobular septal thickening (Image #2). Clinical picture was concerning for drug induced pneumonitis. Amikacin was discontinued and oral prednisone was started. His respiratory symptoms improved and he was weaned to 2L via nasal cannula prior to discharge. Nebulized amikacin was not restarted. DISCUSSION: In this patient, initiation of inhaled amikacin was temporally related to the development of an acute hypersensitivity pneumonitis associated with significant hypoxemia which improved promptly with the discontinuation of inhaled amikacin and initiation of corticosteroids. Trial data investigating inhaled liposomal amikacin in pulmonary MAC has reported a 3% incidence of hypersensitivity pneumonitis. CONCLUSIONS: Inhaled amikacin is a useful adjunctive therapy in the treatment of refractory pulmonary MAC infection. The development of hypersensitivity pneumonitis should prompt immediate discontinuation of the drug and consideration for corticosteroid therapy in severe cases. REFERENCE #1: Griffith DE, Eagle G, Thomson R, et al. CONVERT Study Group Amikacin liposome inhalation suspension for treatment-refractory lung disease caused by Mycobacterium avium complex (CONVERT): A prospective, open-label, randomized study. Am J Respir Crit Care Med 2018; 198:1559–69. REFERENCE #2: Swenson, C, Lapinel NC, and Ali J. Clinical Management of Respiratory Adverse Events Associated With Amikacin Liposome Inhalation Suspension: Results From a Patient Survey. Open Forum Infect Dis. 2020 Apr; 7(4): ofaa079 DISCLOSURES: No relevant relationships by Casey Graziani, source=Web Response No relevant relationships by Ali Jiwani, source=Web Response

A Man with Chronic Asymptomatic Hypoxemia.

A Man with Chronic Asymptomatic Hypoxemia.

THE DIAGNOSTIC ROLE OF FETAL HEMOGLOBIN AND BLOOD OXYGEN SATURATION IN CHRONIC LIVER DISEASES

This research aims to study levels of fetal hemoglobin and blood oxygen saturation in 264 patients with chronic diffuse liver diseases, among them 69 patients with chronic hepatitis and 195 patients with liver cirrhosis. To determine the levels of fetal hemoglobin, a patented method of rocket electrophoresis in agar gel with sodium dodecyl sulfate was used. The level of fetal hemoglobin in liver cirrhosis were significantly increased compared to chronic hepatitis, and, in both cases, compared with the control group. Oxygen saturation of the blood was reduced mainly in liver cirrhosis. In patients with liver cirrhosis a relationship between fetal hemoglobin and oxygen saturation was established. Our study helps in the early diagnosis of latent chronic hypoxia and hypoxemia in patients with liver disease. This allows to assess disease severity and adjust the treatment

Chronic foetal hypoxaemia does not cause elevation of serum markers of brain injury.

The objective of this study was to investigate changes in serum biomarkers of acute brain injury, including white matter and astrocyte injury during chronic foetal hypoxaemia. We have previously shown histopathological changes in myelination and neuronal density in fetuses with chronic foetal hypoxaemia at a level consistent with CHD. Mid-gestation foetal sheep (110 ± 3 days gestation) were cannulated and attached to a pumpless, low-resistance oxygenator circuit, and incubated in a sterile fluid environment mimicking the intrauterine environment. Fetuses were maintained with an oxygen delivery of 20-25 ml/kg/min (normoxemia) or 14-16 ml/kg/min (hypoxaemia). Myelin Basic Protein and Glial Fibrillary Acidic Protein serum levels in the two groups were assessed by ELISA at baseline and at 7, 14, and 21 days of support. Based on overlapping 95% confidence intervals, there were no statistically significant differences in either Myelin Basic Protein or Glial Fibrillary Acidic Protein serum levels between the normoxemic and hypoxemic groups, at any time point. No statistically significant correlations were observed between oxygen delivery and levels of Myelin Basic Protein and Glial Fibrillary Acidic Protein. Chronic foetal hypoxaemia during mid-gestation is not associated with elevated serum levels of acute white matter (Myelin Basic Protein) or astrocyte injury (Glial Fibrillary Acidic Protein), in this model. In conjunction with our previously reported findings, our data support the hypothesis that the brain dysmaturity with impaired myelination found in fetuses with chronic hypoxaemia is caused by disruption of normal developmental pathways rather than by direct cellular injury.

Supervivencia en pacientes con EPOC en tratamiento con oxigenoterapia continua domiciliaria

IntroductionContinuous home oxygen therapy (CHOT), along with smoking cessation, is the first treatment that has been shown to increase the survival of patients with chronic obstructive pulmonary disease (COPD) and chronic hypoxemia. ObjectiveTo determine survival in a cohort of COPD patients receiving CHOT and to analyze the main causes and risk factors associated with their mortality. MethodsProspective study of a cohort of COPD patients receiving CHOT. Numerous variables, including survival and cause of death at the end of follow-up, were collected. ResultsA total of 409 COPD patients receiving CHOT were included (85.6% men; mean age: 71.27 ± 9.74 years). Mean time of CHOT follow-up was 5.86 ± 3.24 years and median survival was 6 years (95% CI: 5.47-6.53). Mortality at the end of follow-up was 75.8%, the leading cause of death being respiratory (36.9%). Longer survival was significantly associated with lower age, correct CHOT compliance, absence of exacerbations in the previous year, use of long-acting anticholinergics (LAMA), less severe COPD, presence of sleep apnea-hypopnea syndrome/obesity hypoventilation syndrome (SAHS/SHO), absence of malignant disease, heart disease, cerebrovascular disease, and kidney disease. ConclusionsThe survival of COPD patients receiving CHOT was very long. The main causes of mortality were respiratory (36.9%). Independent predictors of mortality were age, presence of exacerbations in the previous year, previous diagnosis of cancer, and presence of cerebrovascular and renal disease.

Metabolic dysfunction in OSA: Is there something new under the sun?

The growing number of patients with obstructive sleep apnea is challenging healthcare systems worldwide. Obstructive sleep apnea is characterized by chronic intermittent hypoxaemia, episodes of apnea and hypopnea, and fragmented sleep. Cardiovascular and metabolic diseases are common in obstructive sleep apnea, also in lean patients. Further, comorbidity burden is not unambiguously linked to the severity of obstructive sleep apnea. There is a growing body of evidence revealing diverse functions beyond the conventional tasks of different organs such as carotid body and gut microbiota. Chronic intermittent hypoxia and sleep loss due to sleep fragmentation are associated with insulin resistance. Indeed, carotid body is a multi-sensor organ not sensoring only hypoxia and hypercapnia but also acting as a metabolic sensor. The emerging evidence shows that obstructive sleep apnea and particularly chronic intermittent hypoxia is associated with non-alcoholic fatty liver disease. Gut dysbiosis seems to be an important factor in the pathophysiology of obstructive sleep apnea and its consequences. The impact of sleep fragmentation and intermittent hypoxia on the development of metabolic syndrome may be mediated via altered gut microbiota. Circadian misalignment seems to have an impact on the cardiometabolic risk in obstructive sleep apnea. Dysfunction of cerebral metabolism is also related to hypoxia and sleep fragmentation. Therefore, obstructive sleep apnea may alter cerebral metabolism and predispose to neurocognitive impairment. Moreover, recent data show that obstructive sleep apnea independently predicts impaired lipid levels. This mini-review will provide novel insights into the mechanisms of metabolic dysfunction in obstructive sleep apnea combining recent evidence from basic, translational and clinical research, and discuss the impact of positive airway pressure treatment on metabolic disorders.

Recognizing chronic hypoxaemia as a risk factor for non-hereditary Paraganglioma

Recognizing chronic hypoxaemia as a risk factor for non-hereditary Paraganglioma

Abnormal pulmonary flow is associated with impaired right ventricular coupling in patients with COPD.

Cor Pulmonale or right ventricular (RV) dysfunction due to pulmonary disease is an expected complication of COPD resulting primarily from increased afterload mediated by chronic alveolar hypoxemia and resulting hypoxic pulmonary vasoconstriction. Early detection of elevated RV afterload has been previously demonstrated by visualization of abnormal flow patterns in the proximal pulmonary arteries. Prior analysis of helicity in the pulmonary arteries in pulmonary hypertension patients has demonstrated a strong association between helicity and increased RV afterload. However, these flow hemodynamics have yet to be fully explored in patients with COPD. We hypothesized that patients with COPD will have abnormal pulmonary flow as evaluated by 4D-Flow MRI and associated with RV function and pulmonary arterial stiffness. Patients with COPD (n = 15) (65 years ± 6) and controls (n = 10) (58 years ± 9) underwent 4D-Flow MRI to calculate helicity. The helicity was calculated in the main pulmonary artery (MPA) and along the RV outflow tract (RVOT)-MPA axis. Main pulmonary arterial stiffness was measured using the relative area change (RAC). We found COPD patients had decreased helicity relative to healthy controls in the MPA (19.4 ± 7.8vs 32.8 ± 15.9, P = 0.007) and reduced helicity along the RVOT-MPA axis (33.2 ± 9.0 vs 43.5 ± 8.3, P = 0.010). Our investigation indicates a strong association between helicity along the MPA-RV outflow tract axis and RV function and suggests that 4D-Flow MRI might be a sensitive tool in evaluating RV-pulmonary arterial coupling in COPD.

Clinical Markers of Chronic Hypoxemia in Respiratory Patients Residing at Moderate Altitude.

Supplemental oxygen (SO) increases survival in hypoxemic patients. In hypoxia, mammals respond by modulating O2-sensitive transducers that stabilize the transcription factor hypoxia-inducible factor-1-alpha (HIF-1α), which transactivates the genes that govern angiogenesis and metabolic pathways. Residing at high altitudes exposes millions of people to hypoxemia with potential adverse consequences on their health. We aimed to identify markers of hypoxemia that can be used in the evaluation of patients in addition to pulse oximetry and arterial blood gases, especially those that could respond after 1 month of oxygen use. We performed a prospective pilot study at 2240 m above sea level, with repeated measurements before and after (b/a) 1-month home oxygen therapy in 70 patients with lung diseases, of which 24/20 have COPD, 41/39 obstructive sleep apnea (OSA), and 5/2 with interstitial lung diseases (ILD), all of them having chronic hypoxemia, as well as 70 healthy subjects as controls. Proteins evaluated included HIF-1α, vascular endothelial growth factor (VEGF), and erythropoietin (EPO). Among the main results, we found that hypoxemic patients had normal levels of HIF-1α but increased EPO compared with healthy controls. VEGF levels were heterogeneous in the sample studied, similar to the control group in COPD, slightly increased in OSA, and decreased in fibrosis. With oxygen treatment, the HIF-1α and EPO decreased in COPD and OSA but not in fibrosis, and VEGF remained constant over time. In conclusion, erythropoietin and HIF-1α identified hypoxemia initially and responded to oxygen. In pulmonary fibrosis, HIF-1α, EPO, and VEGF increased with oxygen therapy, which is likely linked to the disease’s pathogenesis and clinical course rather than hypoxemia.