Chronic Hypoxemia Research Articles

Prevalence and phenotypic trajectories of hypoxaemia among hospitalised adults in Kenya: a single-centre, prospective cohort study

ObjectiveGlobal medical oxygen security is limited by knowledge gaps in hypoxaemia burden and oxygen access in low-income and middle-income countries. We examined the prevalence and phenotypic trajectories of hypoxaemia among...

No impact of a high-fat meal coupled with intermittent hypoxemia on acute kidney injury biomarkers in adults with and without obstructive sleep apnea.

Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxemia, which is associated with progressive loss of kidney function, where postprandial fluctuations in renal physiology may further compromise oxygen supply and kidney function. Therefore, we measured biomarkers of acute kidney injury (AKI) following a high-fat meal with and without intermittent hypoxemia. Eighteen healthy young men (mean age [SD]: 22.7 years [3.1]) and seven middle-aged to older individuals with OSA (54.4 years [6.4]) consumed a high-fat meal during normoxia or intermittent hypoxemia (~15 hypoxic cycles per hour, ~85% oxyhemoglobin saturation) for 6 h. We observed no changes in estimated glomerular filtration rate and plasma concentrations of creatinine, neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1) at any measured time points. In both groups, plasma concentrations of interleukin-18 (IL-18) increased after 6 h during normoxia only (p = 0.033, ηp 2 = 0.122), and plasma concentrations of liver-type fatty acid-binding protein (L-FABP) transiently decreased after 3 h in both conditions (p = 0.008, ηp 2 = 0.152). These findings indicate that AKI biomarkers are not acutely elevated during the postprandial state with or without intermittent hypoxemia, suggesting that other mechanisms may play more important roles in the progression of kidney disease in OSA.

The upper airway in obstructive sleep apnea patients is pathological even when awake

Obstructive sleep apnea (OSA) is characterized by partial or complete obstruction of the pharyngeal airway. Anatomical factors can be distinguished from non-anatomical factors. Age and obesity are the main risk factors for OSA; however, approximately 50% of patients are not obese. In older patients (>60 years), the importance of obesity decreases. There is an increased prevalence of OSA among patients with normal weight. The effects of chronic intermittent hypoxemia, low-grade inflammation, increased sympathetic tone and mechanical stress contribute to a transformation of muscle fibers in the upper airway, resulting in reduced muscle mass and strength. Less frequently encountered non-anatomical factors include decreased muscle tone, increased arousal threshold, and altered sensitivity of CO2 chemoreceptors.

The medullary serotonergic centres involved in cardiorespiratory control are disrupted by fetal growth restriction.

Fetal growth restriction (FGR) is associated with cardiovascular and respiratory complications after birth and beyond. Despite research showing a range of neurological changes following FGR, little is known about how FGR affects the brainstem cardiorespiratory control centres. The primary neurons that release serotonin reside in the brainstem cardiorespiratory control centres and may be affected by FGR. At two time points in the last trimester of sheep brain development, 110 and 127days of gestation (0.74 and 0.86 of gestation), we assessed histopathological alterations in the brainstem cardiorespiratory control centres of the pons and medulla in early-onset FGR versus control fetal sheep. The FGR cohort were hypoxaemic and asymmetrically growth restricted. Compared to the controls, the brainstem of FGR fetuses exhibited signs of neuropathology, including elevated cell death and reduced cell proliferation, grey and white matter deficits, and evidence of oxidative stress and neuroinflammation. FGR brainstem pathology was predominantly observed in the medullary raphé nuclei, hypoglossal nucleus, nucleus ambiguous, solitary tract and nucleus of the solitary tract. The FGR groups showed imbalanced brainstem serotonin and serotonin 1A receptor abundance in the medullary raphé nuclei, despite evidence of increased serotonin staining within vascular regions of placentomes collected from FGR fetuses. Our findings demonstrate both early and adaptive brainstem neuropathology in response to placental insufficiency. KEY POINTS: Early-onset fetal growth restriction (FGR) was induced in fetal sheep, resulting in chronic fetal hypoxaemia. Growth-restricted fetuses exhibit persistent neuropathology in brainstem nuclei, characterised by disrupted cell proliferation and reduced neuronal cell number within critical centres responsible for the regulation of cardiovascular and respiratory functions. Elevated brainstem inflammation and oxidative stress suggest potential mechanisms contributing to the observed neuropathological changes. Both placental and brainstem levels of 5-HT were found to be impaired following FGR.

Biomarkers of the L-Arginine/Dimethylarginine/Nitric Oxide Pathway in People with Chronic Airflow Obstruction and Obstructive Sleep Apnoea.

Chronic obstructive pulmonary disease (COPD) and obstructive sleep apnoea (OSA) are common chronic diseases that are associated with chronic and intermittent hypoxemia, respectively. Patients affected by the overlap of COPD and OSA have a particularly unfavourable prognosis. The L-arginine/nitric oxide (NO) pathway plays an important role in regulating pulmonary vascular function. Asymmetric (ADMA) and symmetric dimethylarginine (SDMA) interfere with NO production. We analysed the serum concentrations of ADMA, SDMA, L-arginine, L-citrulline, and L-ornithine in a large sample of the Icelandic general population together with chronic airflow obstruction (CAO), a key physiological marker of COPD that was assessed by post-bronchodilator spirometry (FEV1/FVC < LLN). OSA risk was determined by the multivariable apnoea prediction (MAP) index. 713 individuals were analysed, of whom 78 (10.9%) showed CAO and 215 (30%) had MAP > 0.5. SDMA was significantly higher in individuals with CAO (0.518 [0.461-0.616] vs. 0.494 [0.441-0.565] µmol/L; p = 0.005), but ADMA was not. However, ADMA was significantly associated with decreasing FEV1 percent predicted among those with CAO (p = 0.002). ADMA was 0.50 (0.44-0.56) µmol/L in MAP ≤ 0.5 versus 0.52 (0.46-0.58) µmol/L in MAP > 0.5 (p = 0.008). SDMA was 0.49 (0.44-0.56) µmol/L versus 0.51 (0.46-0.60) µmol/L, respectively (p = 0.004). The highest values for ADMA and SDMA were observed in individuals with overlap of CAO and MAP > 0.5, which was accompanied by lower L-citrulline levels. The plasma concentrations of ADMA and SDMA are elevated in COPD patients with concomitant intermittent hypoxaemia. This may account for impaired pulmonary NO production, enhanced pulmonary vasoconstriction, and disease progression.

Molecular and environmental contributors to neurological complications in sickle cell disease.

Sickle cell disease (SCD) is an inherited hemoglobinopathy in which affected hemoglobin polymerizes under hypoxic conditions resulting in red cell distortion and chronic hemolytic anemia. SCD affects millions of people worldwide, primarily in Sub-Saharan Africa and the Indian subcontinent. Due to vaso-occlusion of sickled red cells within the microvasculature, SCD affects virtually every organ system and causes significant morbidity and early mortality. The neurological complications of SCD are particularly devastating and diverse, ranging from overt stroke to covert cerebral injury, including silent cerebral infarctions and blood vessel tortuosity. However, even individuals without evidence of neuroanatomical changes in brain imaging have evidence of cognitive deficits compared to matched healthy controls likely due to chronic cerebral hypoxemia and neuroinflammation. In this review, we first examined the biological contributors to SCD-related neurological complications and then discussed the equally important socioenvironmental contributors. We then discuss the evidence for neuroprotection from the two primary disease-modifying therapies, chronic monthly blood transfusions and hydroxyurea, and end with several experimental therapies designed to specifically target these complications.

MitoQ as an antenatal antioxidant treatment improves markers of lung maturation in healthy and hypoxic pregnancy.

Chronic fetal hypoxaemia is a common pregnancy complication that increases the risk of infants experiencing respiratory complications at birth. In turn, chronic fetal hypoxaemia promotes oxidative stress, and maternal antioxidant therapy in animal models of hypoxic pregnancy has proven to be protective with regards to fetal growth and cardiovascular development. However, whether antenatal antioxidant therapy confers any benefit on lung development in complicated pregnancies has not yet been investigated. Here, we tested the hypothesis that maternal antenatal treatment with MitoQ will protect the developing lung in hypoxic pregnancy in sheep, a species with similar fetal lung developmental milestones as humans. Maternal treatment with MitoQ during late gestation promoted fetal pulmonary surfactant maturation and an increase in the expression of lung mitochondrial complexes III and V independent of oxygenation. Maternal treatment with MitoQ in hypoxic pregnancy also increased the expression of genes regulating liquid reabsorption in the fetal lung. These data support the hypothesis tested and suggest that MitoQ as an antenatal targeted antioxidant treatment may improve lung maturation in the late gestation fetus. KEY POINTS: Chronic fetal hypoxaemia promotes oxidative stress, and maternal antioxidant therapy in hypoxic pregnancy has proven to be protective with regards to fetal growth and cardiovascular development. MitoQ is a targeted antioxidant that uses the cell and the mitochondrial membrane potential to accumulate within the mitochondria. Treatment of healthy or hypoxic pregnancy with MitoQ, increases the expression of key molecules involved in surfactant maturation, lung liquid reabsorption and in mitochondrial proteins driving ATP synthesis in the fetal sheep lung. There were no detrimental effects of MitoQ treatment alone on the molecular components measured in the present study, suggesting that maternal antioxidant treatment has no effect on other components of normal maturation of the surfactant system.

The effect of maternal position on placental blood flow and fetoplacental oxygenation in late gestation fetal growth restriction: a magnetic resonance imaging study.

Fetal growth restriction (FGR) and maternal supine going-to-sleep position are both risk factors for late stillbirth. This study aimed to use magnetic resonance imaging (MRI) to quantify the effect of maternal supine position on maternal-placental and fetoplacental blood flow, placental oxygen transfer and fetal oxygenation in FGR and healthy pregnancies. Twelve women with FGR and 27 women with healthy pregnancies at 34-38weeks' gestation underwent MRI in both left lateral and supine positions. Phase-contrast MRI and a functional MRI technique (DECIDE) were used to measure blood flow in the maternal internal iliac arteries (IIAs) and umbilical vein (UV), placental oxygen transfer (placental flux), fetal oxygen saturation (FO2 ), and fetal oxygen delivery (delivery flux). The presence of FGR, compared to healthy pregnancies, was associated with a 7.8% lower FO2 (P=0.02), reduced placental flux, and reduced delivery flux. Maternal supine positioning caused a 3.8% reduction in FO2 (P=0.001), and significant reductions in total IIA flow, placental flux, UV flow and delivery flux compared to maternal left lateral position. The effect of maternal supine position on fetal oxygen delivery was independent of FGR pregnancy, meaning that supine positioning has an additive effect of reducing fetal oxygenation further in women with FGR, compared to women with appropriately grown for age pregnancies. Meanwhile, the effect of maternal supine positioning on placental oxygen transfer was not independent of the effect of FGR. Therefore, growth-restricted fetuses, which are chronically hypoxaemic, experience a relatively greater decline in oxygen transfer when mothers lie supine in late gestation compared to appropriately growing fetuses. KEY POINTS: Fetal growth restriction (FGR) is the most common risk factor associated with stillbirth, and early recognition and timely delivery is vital to reduce this risk. Maternal supine going-to-sleep position is found to increase the risk of late stillbirth but when combined with having a FGR pregnancy, maternal supine position leads to 15 times greater odds of stillbirth compared to supine sleeping with appropriately grown for age (AGA) pregnancies. Using MRI, this study quantifies the chronic hypoxaemia experienced by growth-restricted fetuses due to 13.5% lower placental oxygen transfer and 26% lower fetal oxygen delivery compared to AGA fetuses. With maternal supine positioning, there is a 23% reduction in maternal-placental blood flow and a further 14% reduction in fetal oxygen delivery for both FGR and AGA pregnancies, but this effect is proportionally greater for growth-restricted fetuses. This knowledge emphasises the importance of avoiding supine positioning in late pregnancy, particularly for vulnerable FGR pregnancies.

Comparison of cognitive functions and quality of life in chronic obstructive pulmonary disease patients depending on the presence of obstructive sleep apnea syndrome

There are more and more studies that focus on cognitive decline in patients with chronic obstructive pulmonary disease (COPD). Obstructive sleep apnea syndrome (OSAS) is characterized by a repetitive cessation or decrease in airflow due to upper airway obstruction. Chronic sleep disturbance and intermittent hypoxemia lead to neurocognitive changes. Patients with comorbidity of COPD and OSAS may develop more severe nocturnal hypoxia than those with OSAS or COPD alone. At the same time, cognitive dysfunction in elderly patients with comorbidity of OSA and COPD has not been previously studied. Objective. The study the effects of OSAS on cognitive impairment and quality of life in elderly patients with COPD. Materials and methods. We examined 84 patients with COPD of moderate severity, controlled course at the age of 60–74 years (mean age – 66.3±4.1 years), of which the first group consisted of 43 patients with COPD, the second group – 41 patients with COPD and OSA of moderate severity. Results. Patients with COPD and moderate OSA had worse MMSE and EQ-5D-3L scores compared to patients with COPD alone, and were more likely to have dementia on the MMSE scale (MMSE≤24 scores), which may require an individual approach to the treatment of such patients.

Patient-Assessed Quality of Virtual Consultations as Follow-Up on Long-Term Oxygen Therapy for Patients With COPD.

Long-term oxygen therapy (LTOT) can increase survival time and relieve symptom burden in patients with COPD and chronic hypoxemia. The Department of Respiratory Medicine at Odense University Hospital invites patients with LTOT and COPD to the out-patient clinic for treatment evaluation every 6 months to regulate or terminate treatment and support patients' treatment adherence. The out-patient clinic, however, experiences many absences or cancellations from patients. For that reason, patients were offered virtual consultation as an alternative to physical attendance. This study was initiated to uncover reasons for absences and the patients' experiences of virtual consultation to promote a more patient-centered clinical practice for patients with COPD and LTOT. A qualitative study encompassing semi-structured interviews with 20 subjects was conducted in the winter of 2021. The subjects had tried or been given the opportunity of virtual consultation. Data were analyzed inspired by Kvale and Brinkmann focusing on the subject's perspectives on virtual consultation. The analysis resulted in 3 main themes: limitations and vulnerabilities, independence and quality of life, and personal strategies. Subjects expressed that everyday life with LTOT and COPD was characterized by limited resources in terms of energy, oxygen, and time. LTOT was perceived as a necessary means to maintain a sense of independence and quality of life. However, LTOT also meant additional limitations due to cumbersome equipment and feelings of isolation. Most subjects considered the virtual consultation to be oxygen-, energy-, and time-preserving, as it meant avoiding stressful transportation and handling of oxygen cylinders, COVID-19 exposure, waiting time, and not having to involve others for help. The subjects' perspective showed that follow-up on LTOT as a virtual consultation was considered a valuable offer. The chosen method was found to be relevant in uncovering subjects' attitudes toward clinical practice procedures.

High prevalence of peripheral and carotid artery disease in patients with interstitial lung diseases

Background: Interstitial lung diseases (ILD) are a heterogenous group of diseases, which have pulmonary fibrosis, restrictive lung disease, and decreased diffusion capacity as a common final path. Premature death frequently results not from ILD itself but from comorbidities. Peripheral artery disease (PAD) is a common comorbid disease in different chronic lung diseases. The focus of the present study is to clarify the prevalence of PAD in ILD. Patients and methods: A total of 97 patients with ILD and 30 controls were included in the study. Patients with ILD were subdivided into two groups according to the progression of pulmonary fibrosis: progressive fibrosing and non-progressive fibrosing ILD (PF-ILD and nPF-ILD, respectively). All participants underwent standard angiological and pneumological diagnostic procedures including six-minute walking test, measurement of ankle-brachial-index, and colour-coded duplex sonography. Results: We observed no relevant differences in the baseline characteristics except age. Both, PF-ILD and nPF-ILD patients, presented with a highly increased incidence of atherosclerotic lesions compared to the control group (p<0.001). PAD was present in all patients with PF-ILD and in 73% of patients with nPF-ILD. These results were confirmed by age-adjusted regression analyses. Conclusions: The present results indicate that ILD is an independent risk factor for atherosclerosis. Patients with PF-ILD are more severely affected than nPF-ILD patients with age as a confounding variable. Atherogenesis in ILD may be mediated by increased cardiovascular risk, systemic inflammation and chronic hypoxemia.

Fetal heart rate responses in chronic hypoxaemia with superimposed repeated hypoxaemia consistent with early labour: a controlled study in fetal sheep.

Deceleration area (DA) and capacity (DC) of the fetal heart rate can help predict risk of intrapartum fetal compromise. However, their predictive value in higher risk pregnancies is unclear. We investigated whether they can predict the onset of hypotension during brief hypoxaemia repeated at a rate consistent with early labour in fetal sheep with pre-existing hypoxaemia. Prospective, controlled study. Laboratory. Chronically instrumented, unanaesthetised near-term fetal sheep. One-minute complete umbilical cord occlusions (UCOs) were performed every 5 minutes in fetal sheep with baseline pa O2 <17 mmHg (hypoxaemic, n=8) and >17 mmHg (normoxic, n=11) for 4 hours or until arterial pressure fell <20 mmHg. DA, DC and arterial pressure. Normoxic fetuses showed effective cardiovascular adaptation without hypotension and mild acidaemia (lowest arterial pressure 40.7 ± 2.8 mmHg, pH 7.35 ± 0.03). Hypoxaemic fetuses developed hypotension (lowest arterial pressure 20.8 ± 1.9 mmHg, P < 0.001) and acidaemia (final pH 7.07 ± 0.05). In hypoxaemic fetuses, decelerations showed faster falls in FHR over the first 40 seconds of UCOs but the final deceleration depth was not different to normoxic fetuses. DC was modestly higher in hypoxaemic fetuses during the penultimate (P=0.04) and final (P=0.012) 20 minutes of UCOs. DA was not different between groups. Chronically hypoxaemic fetuses had early onset of cardiovascular compromise during labour-like brief repeated UCOs. DA was unable to identify developing hypotension in this setting, while DC only showed modest differences between groups. These findings highlight that DA and DC thresholds need to be adjusted for antenatal risk factors, potentially limiting their clinical utility.

The Role of Inverted Papilloma Surgical Removal for Sleep Apnea Treatment Success—A Case Report

In recent years, increased attention has been directed to sleep apnea syndrome due to its high prevalence and preventable severe health consequences. Besides enhancing the risk of cardiovascular, cerebrovascular, and metabolic disorders, it determines increased daytime somnolence, cognitive impairment, and delayed reaction time. These symptoms, determined by sleep fragmentation and chronic hypoxemia, can result in a decrease in professional performance and, moreover, could have tragic implications, especially in patients with high-risk professions. We present the case of a 58-year-old male-truck driver, known to suffer from uncontrolled OSA and chronic obstructive pulmonary disease, who presented to our ENT department for incapacitating daytime somnolence and severe nasal obstruction. These symptoms were caused by a voluminous sinonasal inverted papilloma, occupying the entire left cavity with extension in the nasopharynx. Following nose permeabilization, the patients' APAP compliance grew substantially, with a dramatic decrease in daytime sleepiness and improvement in polysomnographic parameters. Due to the overlap syndrome of OSA and COPD, an oxygen supplementation was added to PAP therapy by a pulmonologist, improving pulse-oximetry parameters and resulting in the best outcome for the patient. Through this case report, we aim to emphasize the importance of multimodal, personalized treatment of sleep apnea with a focus on nasal surgical permeabilization. At the same time, we sustain a multidisciplinary approach, especially in patients with sleep apnea and associated pathologies, to obtain therapeutic success. We propose increased attention to the early recognition and proper treatment of sleep apnea in patients with high-risk professions as it prevents catastrophes.

Progressive Right Ventricular Obstruction Caused by a Double-Chambered Right Ventricle Resulting in Shunt-Reversal via a Concomitant Congenital Ventricular Septal Defect and Subsequent Erythrocytosis in a Dog

A 3-year-old Chihuahua was presented because of exercise intolerance, respiratory distress, and syncopal episodes. At the age of 10 weeks, the dog was diagnosed with a congenital small left-to-right shunting ventricular septal defect and a mild right ventricular outflow tract obstruction via echocardiography. At that time, the dog was asymptomatic, but the breeder's veterinarian heard a murmur. Both cardiac defects were judged to be clinically non-relevant at that time. However, at 3 years of age, echocardiography revealed a severe right ventricular obstruction, known as a double-chambered right ventricle, along with right-to-left shunting via the ventricular septal defect. Because of chronic hypoxemia due to the right-to-left shunting, erythrocytosis developed. Flow reversal via the shunt was caused by a progressively worsening right ventricular obstruction leading to a supra-systemic right ventricular systolic pressure. Because of the poor prognosis, the dog was euthanized, and the heart was submitted for post-mortem examination. Gross pathologic findings revealed the close proximity of the right ventricular obstructive lesion to the ventricular septal defect. Histopathology revealed localized muscular hypertrophy and severe endocardial fibrosis. The suspected pathogenesis of the progressive obstruction was infiltrative myocardial fibrosis due to turbulent blood flow from the left-to-right shunting ventricular septal defect, as described in humans.

Chronic anemia complicated by cardiac failure, pulmonary hypertension, and pericardial effusion: a case report

BackgroundWorldwide, iron deficiency anaemia (IDA) is the most common cause of anaemia. Iron deficiency alone has an association with heart failure and pulmonary hypertension. Chronic iron deficiency anemia triggers various physiologic adjustments, leading to hyperdynamic circulation and enhanced hypoxic pulmonary vasoconstriction. Those mechanisms may result in the development of high output cardiac failure and pulmonary hypertension; however, pericardial effusion remains a rare association.Case presentationA 44-year-old Nepalese man presented with fatigability and swollen ankles. Except for a hemorrhoidectomy 4 years ago, he had no comorbidities. Labs confirmed severe iron deficiency anemia (hemoglobin 1.8 grams per deciliter) likely secondary to hemorrhoids. An echocardiogram revealed high output cardiac failure, pericardial effusion, and severe pulmonary hypertension. He responded well to the correction of anemia and diuretics with the resolution of vascular complications.ConclusionWe report a unique presentation of chronic severe iron deficiency anemia complicated by heart failure, pulmonary hypertension, and pericardial effusion. We believe it to be the first-ever such case reported in the literature. These cardiovascular complications seem to result from internal homeostatic mechanisms against the chronic tissue hypoxemia observed in severe anemia. Furthermore, iron deficiency alone has an association with heart failure and pulmonary hypertension. After excluding other potential causes, we confirmed iron deficiency anaemia as the cause of those complications. The correction of anemia led to an excellent recovery without any sequelae. Our case report highlights the fact that management of such a case should be focused on underlying etiology rather than the complications.

Embolização percutânea de fístulas arteriovenosas pulmonares

Pulmonary arteriovenous malformation is an abnormal communication between an artery and a vein, causing clinical manifestations, such as chronic hypoxemia and embolic events. Arteriovenous malformations were treated surgically, with a significant rate of complications. In the 1970 ́s, the first percutaneous catheter embolization was performed with coils. We describe three cases in which percutaneous embolization techniques were effective to prevent embolic, hemorrhagic, and hypoxemic events in the follow-up of patients.

Assessment of Diaphragmatic Mobility by Transthoracic Ultrasound in Patients with Interstitial Lung Diseases

Background: As interstitial lung diseases may promote respiratory muscles dysfunction due to increased lung elastic recoil, chronic hypoxemia, systemic inflammation, physical inactivity, malnutrition and corticosteroids therapy. Therefore, measuring diaphragmatic function is quite helpful when assessing patients with interstitial lung disorders. Aim of the work: was to compare the diaphragmatic mobility which assessed by ultrasonography between healthy individuals and patients with interstitial lung diseases. Patients and Methods: this case-control trial, whereas Thirty patients with clinically stable interstitial lung diseases and twenty healthy persons as a control. Whereas age, sex and body mass index matched apparently in control group. Pulmonary functions tests: as six-minute walk test, ultrasonographic measurement of both diaphragmatic excursion and thicknesses at residual functional capacity and total lung capacity, with calculation of the diaphragmatic thickening fraction were done for all participants. Results: Diaphragmatic kinetics are greatly impaired in interstitial lung diseases patients at total lung capacity, but almost not affected at functional residual capacity. Diaphragmatic excursion and thickness at total lung capacity, as well as diaphragmatic thickening fraction showed considerable positive correlations with forced vital capacity and 6-minute walk distance, whereas they exhibited considerable negative correlations with modified Medical Research Council dyspnea scale. Conclusion: Diaphragmatic kinetics measured at total lung capacity and thickening fraction have good correlations with degree of dyspnea, forced vital capacity and exercise tolerance.

PREVALENCE, PREDICTORS AND PROFILE OF MALNUTRITION IN CHILDREN WITH CONGENITAL HEART DEFECTS

Background: Malnutrition in children with congenital heart defects [CHDs] has been linked to increased morbidity and mortality as indicated by frequent hospitalisation, poor surgical outcomes, persistent impairment of somatic growth and increased death. All types of malnutrition, and severe forms in particular, contribute to mortality in childhood. There is strong evidence that poor growth [ malnutrition] is associated with delayed mental development and poor school performance.The mechanisms for growth deficiency in CHD are multifactorialand include associated chromosomal anomalies/ genetic syndromes, inadequate nutritional intake due to feeding difficulties, and poor absorption of nutrients from digestive tract in chronic congestive heart failure. Also increased calories are required to sustain the increased myocardial, respiratory and neuro-humoral functions in CHD-related heart failure. Chronic CHF and chronic hypoxemia in CHD impair cellular metabolism and cell growth. Other mechanisms of growth deficiency in CHD have been reported.The WHO recommends the WHO/National Center for Health Statistics [NCHS] growth standards for nutrition surveys.The present study aims to describe the prevalence, profile and predictors of malnutrition using recommended case definitions.The findings of present study could be applied to current and future paediatric cardiac care practice. Aims And Objectives: To investigate the prevalence, profile, predictors and epidemiological pattern of malnutrition in children with congenital heart defects. Materials And Methods: This was a Case-control, observational study which was conducted in post graduate department of paediatrics GB Pant Children Hospital on all patients above 6 months of age admitted in the hospital as cases of congenital heart defects and controls will include the patients with minor ailments admitted for short stay. Study was conducted between December 2020-November 2022 Stastical Analysis: Data was entered in a Microsoft Excel spreadsheet. Categorical variables were summarized as frequency and percentage. Continuous variables were summarized as mean and SD. Results: The study was conducted on two hundred and fifty cases of CHD. The detected cardiac anomalies were classified as acyanotic heart diseases (n=163 65%) and cyanotic heart diseases (n=87 35%). The prevalence of CHD-related malnutrition was 90% as compared to 21.2% in the control patients with 63.3% of cases having severe malnutrition. Among cases, the relative proportions of wasting, stunting and underweight were 40.8%, 28.8% and 20.8%, respectively. Wasting was proportionately higher (58.3%) in acyanotic CHD, while stunting was predominant (67.8%) in cyanotic CHD (p=0.0001).

Rearrangement of cell types in the rat carotid body neurogenic niche induced by chronic intermittent hypoxia.

The carotid body (CB) is a prototypical acute oxygen (O2 )-sensing organ that mediates reflex hyperventilation and increased cardiac output in response to hypoxaemia. CB overactivation, secondary to the repeated stimulation produced by the recurrent episodes of intermittent hypoxia, is believed to contribute to the pathogenesis of sympathetic hyperactivity present in sleep apnoea patients. Although CB functional plasticity induced by chronic intermittent hypoxia (CIH) has been demonstrated, the underlying mechanisms are not fully elucidated. Here, we show that CIH induces a small increase in CB volume and rearrangement of cell types in the CB, characterized by a mobilization of immature quiescent neuroblasts, which enter a process of differentiation into mature, O2 -sensing and neuron-like, chemoreceptor glomus cells. Prospective isolation of individual cell classes has allowed us to show that maturation of CB neuroblasts is paralleled by an upregulation in the expression of specific glomus cell genes involved in acute O2 -sensing. CIH enhances mitochondrial responsiveness to hypoxia in maturing neuroblasts as well as in glomus cells. These data provide novel perspectives on the pathogenesis of CB-mediated sympathetic overflow that may lead to the development of new pharmacological strategies of potential applicability in sleep apnoea patients. KEY POINTS: Obstructive sleep apnoea is a frequent condition in the human population that predisposes to severe cardiovascular and metabolic alterations. Activation of the carotid body, the main arterial oxygen-sensing chemoreceptor, by repeated episodes of hypoxaemia induces exacerbation of the carotid body-mediated chemoreflex and contributes to sympathetic overflow characteristic of sleep apnoea patients. In rats, chronic intermittent hypoxaemia induces fast neurogenesis in the carotid body with rapid activation of neuroblasts, which enter a process of proliferation and maturation into O2 -sensing chemoreceptor glomus cells. Maturing carotid body neuroblasts and glomus cells exposed to chronic intermittent hypoxia upregulate genes involved in acute O2 sensing and enhance mitochondrial responsiveness to hypoxia. These findings provide novel perspectives on the pathogenesis of carotid body-mediated sympathetic hyperactivation. Pharmacological modulation of carotid body fast neurogenesis could help to ameliorate the deleterious effects of chronic intermittent hypoxaemia in sleep apnoea patients.

Экономическая эффективность длительной кислородотерапии у больных бронхолегочными заболеваниями с тяжелой хронической артериальной гипоксемией

Background: long-term oxygen therapy (LTOT) for chronic lung diseases associated with chronic hy-poxemia is effective in terms of increasing life expectancy. However, by now, the costs of LTOT are not reimbursed by the healthcare system of the Russian Federation. Aim: to evaluate the economic efficiency of respiratory therapy centers in providing pa-tients with chronic lung diseases and severe chronic hypoxemia with LTOT at home. Patients and Methods: direct medical and nonmedical costs associated with the introduc-tion of LTOT into clinical practice were identified and calculated. Costs of LTOT, outpatient management of patients without exacerbations, treatment for exacerbations, and disability-related payments were considered. Clinical and economic modeling was performed. A cost-effectiveness analysis was performed and the budget impact was assessed. Published data and the experience of St. Petersburg Regional Respiratory Support Center were used to evaluate LTOT efficacy. Results: additional costs for LTOT per patient for 5 years are 229,759 RUB. LTOT signif-icantly (by 74%) reduce the costs of treating patients with exacerbations of chronic obstructive pulmonary disease, mainly due to a reduction in exacerbation rate, including those requiring ad- mission to hospital. Analysis of budget impact over 5 years demonstrates a decrease in direct medical costs per 100 oxygen concentrators by 32% (from 181,666,728.90 RUB to 123,247,630.82 RUB). Given mortality, the estimated number of patients opting for LTOT using 100 oxygen concentrators over 5 years is 150. Conclusions: reimbursement for LTOT costs in Russian healthcare is economically reason-able. KEYWORDS: long-term oxygen therapy, economic efficiency, respiratory therapy center, cost-effectiveness analysis, chronic hypoxemia. FOR CITATION: Gomon Yu.M., Titova O.N., Kolbin A.S., Kuzubova N.A., Balykina Yu.E. Economic efficiency of long-term oxygen therapy in patients with chronic lung diseases and severe chronic hypoxemia. Russian Medical Inquiry. 2023;7(8):475–481 (in Russ.). DOI: 10.32364/2587-6821-2023-7-8-1.