Cause Of Hypoxemia Research Articles

The effects of obesity on lung volumes and oxygenation

IntroductionObesity can cause hypoxemia by decreasing lung volumes to where there is closure of lung units during normal breathing. Studies describing this phenomenon are difficult to translate into clinical practice. We wanted to determine the lung volume measurements that are associated with hypoxemia in obese patients, and explore how we could use these measurements to identify them. MethodsWe collected pulmonary function test results and arterial blood gas data on 118 patients without obstruction on pulmonary function testing. We included only patients with normal chest imaging and cardiac testing within one year of the pulmonary function test, to exclude other causes of hypoxemia. ResultsWe found that as BMI increases, the mean paO2, ERV % predicted, and ERV/TLC decrease (BMI 20-30 kg/m2: paO2=90±8 mmHg, ERV% predicted 112±50, ERV/TLC (%) 19.7±6.5; BMI 30-40 kg/m2: paO2=84±10 mmHg, ERV% predicted 84±40 ERV/TLC(%) 13.6±7.6; BMI>40 kg/m2: paO2 78 ±12 mmHg, ERV% predicted 64±27 ERV/TLC(%) 11.4±5.8, ANOVA p<0.001). The A-a gradient increases as BMI increases (r=0.42, p<0.001). This correlation was stronger in men (r=0.54) than in women (r=0.35). The paO2 is lower in patients with a low ERV than in those with a normal ERV (p<0.001). In a multivariate linear regression, only the ERV/TLC predicted (%), age, and BMI were associated with oxygenation (r2 for A-a gradient =0.28, p=0.036). ConclusionsIn obese patients without cardiopulmonary disease, oxygen levels decrease as BMI increases. This effect is associated with the obesity-related reduction in ERV and is independent of hypoventilation.

Hepato-Pulmonary syndrome and Porto-Pulmonary Hypertension: Rare combination cause of Hypoxemia in patient with end-stage renal failure on Hemodialysis and hepatitis C Induced Decompensated Cirrhosis

Hepato-Pulmonary syndrome and Porto-Pulmonary Hypertension: Rare combination cause of Hypoxemia in patient with end-stage renal failure on Hemodialysis and hepatitis C Induced Decompensated Cirrhosis

Severe acute respiratory failure (SARF) secondary to concurrent pulmonary‐only anti‐GBM syndrome and thrombo‐embolic disease

SummaryWe report the case of a 20‐year‐old male patient presenting to the Emergency Department with severe type 1 respiratory failure due to diffuse alveolar haemorrhage secondary to pulmonary‐only anti‐glomerular basement membrane (anti‐GBM) disease, a rare presentation of this reno‐pulmonary syndrome. The patient had developed multiple pulmonary venous emboli and an intracerebral arterial thrombus. There are limited reports of pulmonary emboli coinciding with anti‐GBM disease and no other reports of concomitant arterial thrombus. We describe the presentation and consider the management of this rare, serious cause of hypoxaemia and the possible role of extra‐corporeal membrane oxygenation in this patient group. We review the pathophysiology of anti‐GBM disease and the reported cases of accompanying venous or arterial thrombo‐emboli in related conditions.

Platypnea-Orthodeoxia Syndrome: A Case of Chronic Paroxysmal Hypoxemia

A 75-year-old man with chronic (30-year) unexplained paroxysmal hypoxemia presented with postural hypoxemia and desaturation consistent with a clinical manifestation of platypnea-orthodeoxia syndrome. His history included a lack of significant past pulmonary disease, yet with intermittent need for oxygen supplementation. On admission he was found to have an interatrial shunt through a patent foramen ovale. Device closure by percutaneous catheterization led to sustained resolution of symptoms. Platypnea-orthodeoxia syndrome is a rare but important consideration in the differential diagnosis of hypoxemia, as it represents a potentially curable cause of hypoxemia, with missed diagnosis leading to possible patient morbidity if untreated. Even more importantly, an astute and careful history and physical examination are integral to the diagnosis of this rare but likely under-recognized syndrome.

Neuroendocrine cell hyperplasia of infancy: an unusual cause of hypoxemia in children

BackgroundChildhood interstitial lung disease (chILD) is a heterogeneous group of rare disorders characterized by abnormal imaging findings, impaired gas exchange; and is associated with substantial morbidity and mortality. Neuroendocrine cell hyperplasia (NEHI) is a unique sub-group, which is more prevalent in infants and children younger than 2 years of age, and typically manifests with chronic tachypnea, retractions, hypoxemia and failure to thrive. NEHI insidiously appears in the first year of life, subtly masquerading as one of the more common lung diseases of childhood. Therefore, the diagnosis of NEHI is challenging and requires a systematic approach.Case presentationWe report a case of an infant, with a history of recurrent respiratory infections and wheezing, who presented with persistent hypoxemia (PaO2 88 mmHg) and chronic respiratory symptoms, that prompted an extensive diagnostic work up for chILD; eventually a diagnosis of NEHI was made.ConclusionNEHI is a rare chILD disorder presenting in the first 2 years of life with common but challenging key clinical features. Increased awareness among pediatricians and prompt recognition of the clinical presentation may enable timely diagnosis and improve disease management and prognosis.

Prone position in the Acute Respiratory Distress Syndrome, physiology to clinical practice

El síndrome de diicultad respiratoria aguda incluye una compleja serie de acontecimientos que conducen a daño alveolar, edema pulmonar por aumento de la permeabilidad vascular e insuiciencia respiratoria; muchos procesos están relacionados con su aparición, la característica común es la activación de los neutróilos en la circulación pulmonar o sistémica. Las manifestaciones clínicas aparecen generalmente 6 a 72 horas posterior al inicio del evento y empeoran rápidamente. El tratamiento se basa en un manejo interdisciplinario por parte del personal de la unidad de cuidados intensivos, se debe realizar un reconocimiento precoz de los pacientes descartando otras causas de hipoxemia, identiicar y tratar la causa subyacente, y emplear la ventilación mecánica para asegurar correcta oxigenación, intentando siempre proteger los pulmones de la lesión pulmonar inducida por la técnica. La ventilación en decúbito prono favorece el aumento de la oxigenación en pacientes con este síndrome, los mecanismos que producen este incremento son probablemente múltiples e interdependientes y no han sido dilucidados en su totalidad. Es un procedimiento de bajo costo, recomendado implementar en pacientes categoría grave, y preferentemente en etapa tempana de la enfermedad, aunque es necesario realizar estudios futuros que puedan establecer el verdadero impacto en la mortalidad para evaluar su uso sistemático en todos los pacientes con Síndrome de Diicultad Respiratoria Aguda. MÉD.UIS. 2016;29(2):81-101.

Ventilation/perfusion distributions revisited.

A major cause of hypoxemia in anesthesia is ventilation-perfusion (VA/Q) mismatch. With more advanced surgery and an aging population, monitoring of VA/Q is of increasing importance. The classic multiple inert gas elimination technique has been simplified with a new approach based on mass spectrometry. VA/Q distributions can also be measured, at the bedside, by varying inspired oxygen concentration. MRI, 3-dimensional single photon emission computed tomography, positron emission tomography, and electrical impedance tomography enable imaging of perfusion and ventilation, and in some of the techniques also the distribution of inflammation. One-lung ventilation with thoracoscopy and capnothorax require careful monitoring of VA/Q, made possible bedside by electrical impedance tomography. Carbon dioxide, but not air, for pneumoperitoneum enhances shift of perfusion to ventilated regions. Ventilatory support during cardiopulmonary resuscitation causes less VA/Q mismatch when inspired oxygen concentrations are lower. Mechanisms of redistribution of lung blood flow by inhaled nitric oxide include endothelin-mediated vasoconstriction in collapsed lung regions. Methods are continuously developing to simplify measurement of VA/Q and also to relate VA/Q to inflammation. The recording of VA/Q has helped to explain important aspects of gas exchange in thoracic anesthesiology and in intensive care medicine.

Monitoring Oxygen Status.

Although part of a common "blood gas" test panel with pH and pCO2, the pO2, %O2Hb, and related parameters are independently used to detect and monitor oxygen deficits from a variety of causes. Measurement of blood gases and cooximetry may be done by laboratory analyzers, point of care testing, noninvasive pulse oximetry, and transcutaneous blood gases. The specimen type and mode of monitoring oxygenation that are chosen may be based on a combination of urgency, practicality, clinical need, and therapeutic objectives. Because oxygen concentrations in blood are extremely labile, there are several highly important preanalytical practices necessary to prevent errors in oxygen and cooximetry results. Effective utilization of oxygen requires binding by hemoglobin in the lungs, transport in the blood, and release to tissues, where cellular respiration occurs. Hydrogen ion (pH), CO2, temperature, and 2,3-DPG all play important roles in these processes. Additional measurements and calculations are often used to interpret and locate the cause and source of an oxygen deficit. These include the Hb concentration, Alveolar-arterial pO2 gradient, pO2:FIO2 ratio, oxygenation index, O2 content and O2 delivery, and pulmonary dead space and intrapulmonary shunting. The causes of hypoxemia will be covered and, to illustrate how the oxygen parameters are used clinically in the diagnosis and management of patients with abnormal oxygenation, two clinical cases will be presented and described.

Methemoglobinemia After Isolated Lidocain Spray: A Rare Phenomenon

AbstractMethemoglobinemia is a state recognized by the increased production of met-hemoglobin, which is a form of oxidized hemoglobin, which is unable to bind oxygen. As a result the patient has a functional anemia, in which the remaining oxyhemoglobin has increased oxygen affinity, shifting the oxygen curve to left and perpetuating the impairment of oxygen delivery to tissues. Methemoglobinemia is a rare, but serious cause of hypoxemia, which can be difficult to recognize. It has been traditionally associated with the use of benzocaine class of anesthetic agents and FDA has issued warning for the use of benzocaine class of anesthetic agents for the same reason. It has been very seldom reported with the use of lidocaine class of agents alone. Through this case report we want to emphasize development of methemoglobinemia through the isolated use of lidocaine.

Platypnoea-orthodeoxia syndrome, an underdiagnosed cause of hypoxaemia: four cases and the possible underlying mechanisms.

Cardiac platypnoea-orthodeoxia syndrome (POS) is a position-dependent condition of dyspnoea and hypoxaemia due to right-to-left shunting. It often remains unrecognised in clinical practice, possibly because of its complex underlying pathophysiology. We present four consecutive patients with POS and patent foramen ovale (PFO) who underwent a successful percutaneous PFO closure, describe the mechanism of their POS and provide a review of the literature.

CFTR and sphingolipids mediate hypoxic pulmonary vasoconstriction

Hypoxic pulmonary vasoconstriction (HPV) optimizes pulmonary ventilation-perfusion matching in regional hypoxia, but promotes pulmonary hypertension in global hypoxia. Ventilation-perfusion mismatch is a major cause of hypoxemia in cystic fibrosis. We hypothesized that cystic fibrosis transmembrane conductance regulator (CFTR) may be critical in HPV, potentially by modulating the response to sphingolipids as mediators of HPV. HPV and ventilation-perfusion mismatch were analyzed in isolated mouse lungs or in vivo. Ca(2+) mobilization and transient receptor potential canonical 6 (TRPC6) translocation were studied in human pulmonary (PASMCs) or coronary (CASMCs) artery smooth muscle cells. CFTR inhibition or deficiency diminished HPV and aggravated ventilation-perfusion mismatch. In PASMCs, hypoxia caused CFTR to interact with TRPC6, whereas CFTR inhibition attenuated hypoxia-induced TRPC6 translocation to caveolae and Ca(2+) mobilization. Ca(2+) mobilization by sphingosine-1-phosphate (S1P) was also attenuated by CFTR inhibition in PASMCs, but amplified in CASMCs. Inhibition of neutral sphingomyelinase (nSMase) blocked HPV, whereas exogenous nSMase caused TRPC6 translocation and vasoconstriction that were blocked by CFTR inhibition. nSMase- and hypoxia-induced vasoconstriction, yet not TRPC6 translocation, were blocked by inhibition or deficiency of sphingosine kinase 1 (SphK1) or antagonism of S1P receptors 2 and 4 (S1P2/4). S1P and nSMase had synergistic effects on pulmonary vasoconstriction that involved TRPC6, phospholipase C, and rho kinase. Our findings demonstrate a central role of CFTR and sphingolipids in HPV. Upon hypoxia, nSMase triggers TRPC6 translocation, which requires its interaction with CFTR. Concomitant SphK1-dependent formation of S1P and activation of S1P2/4 result in phospholipase C-mediated TRPC6 and rho kinase activation, which conjointly trigger vasoconstriction.

Unusual Cause of Hypoxemia

Unusual cause of hypoxemia is presented in a 12 year old boy of Iraqi national. *Corresponding author: Sushil Upadhyay, Asistant Professor, Rama Medical College and Hospital, Pulmonary Medicine, H 104 Swarn Residency, 132 GT Road, Sahibabad, Ghaziabad, Uttar Pradesh 201005, India, Tel: 919899393006; Fax: 911222327311; E-mail: skupadhyay2002@rediffmail.com Received June 11, 2015; Accepted July 15, 2015; Published July 20, 2015 Citation: Upadhyay S (2015) Unusual Cause of Hypoxemia. J Pulm Respir Med 5: 279. doi:10.4172/2161-105X.1000279 Copyright: © 2015 Upadhyay S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

English

INTRODUCTION: Pulmonary abnormalities and symptoms are common in patients with chronic liver disease. Hepatopulmonary syndrome is an important cause in a patient with hypoxemia and chronic liver disease. Hepatopulmonary syndrome consists of a triad of hepatic dysfunction and/or portal hypertension, intrapulmonary vascular dilatations and hypoxemia/ widened alveolar- arterial gradient. The present study evaluated the arterial blood gas levels and correlated these with 2D contrast echocardiographic findings in patients of liver cirrhosis. METHODS: 40 patients of liver cirrhosis were included in the study. All patients underwent ultrasonography, LFTs, biochemical tests and upper gastrointestinal endoscopy, chest X-ray, 2-D contrast enhanced transthoracic echocardiogram, viral markers and arterial blood gas analysis. The patients in whom arterial hypoxemia/ widened alveolar-arterial gradient was detected with a positive contrast echocardiogram were considered to have hepatopulmonary syndrome. Patients with intrinsic heart disease like patent foramen ovale, atrial septal defect, ventricular septal defect, haemoglobin less than 7gm% and history of COPD were excluded from the study. RESULTS: 4 patients of liver cirrhosis with hypoxemia had intrapulmonary vascular dilatations were labelled as hepatopulmonary syndrome. 2 additional patients with IPVDs had widened alveolar arterial gradient without hypoxemia and were also labelled as HPS. Dyspnoea (p=0.001), platypnea (p<0.001), clubbing (p=0.002) and cyanosis (p=0.001) were significantly commoner in the six patients of hepatopulmonary syndrome. Patients with cyanosis had poor prognosis. CONCLUSION: Hepatopulmonary syndrome is an important cause of hypoxemia in patients of liver cirrhosis. It is not uncommon in patients of liver cirrhosis. Platypnea is both sensitive as well as specific marker of the disease. Transthoracic contrast enhanced echocardiogram is a safe and accurate bedside tool for the detection of IPVDs.

The physiological basis of pulmonary gas exchange: implications for clinical interpretation of arterial blood gases

The field of pulmonary gas exchange is mature, with the basic principles developed more than 60 years ago. Arterial blood gas measurements (tensions and concentrations of O₂ and CO₂) constitute a mainstay of clinical care to assess the degree of pulmonary gas exchange abnormality. However, the factors that dictate arterial blood gas values are often multifactorial and complex, with six different causes of hypoxaemia (inspiratory hypoxia, hypoventilation, ventilation/perfusion inequality, diffusion limitation, shunting and reduced mixed venous oxygenation) contributing variably to the arterial O₂ and CO₂ tension in any given patient. Blood gas values are then usually further affected by the body's abilities to compensate for gas exchange disturbances by three tactics (greater O₂ extraction, increasing ventilation and increasing cardiac output). This article explains the basic principles of gas exchange in health, mechanisms of altered gas exchange in disease, how the body compensates for abnormal gas exchange, and based on these principles, the tools available to interpret blood gas data and, quantitatively, to best understand the physiological state of each patient. This understanding is important because therapeutic intervention to improve abnormal gas exchange in any given patient needs to be based on the particular physiological mechanisms affecting gas exchange in that patient.

Study of pulmonary dysfunctions in liver cirrhosis

IntroductionEnd-stage liver disease and its complications are a leading cause of death among adults. The liver plays a central role in health and homeostasis and thus the diseased liver leads to many deleterious effects on multiple organ systems, including the pulmonary system Julie et al. (2007) [1]. A variety of causes for pulmonary dysfunction in liver disease have been identified and include intrinsic cardiopulmonary disorders not specifically related to liver disease as well as unique problems associated with the presence of liver disease and/or portal hypertension Michael et al. (2000) [2]. Liver disease and portal hypertension can be associated with pulmonary vascular complications, including portopulmonary hypertension (POPH), and hepatopulmonary syndrome (HPS) Mateo et al. (2012) [3]. AimThis study aimed to evaluate the pulmonary dysfunctions complicating liver cirrhosis. Patients and methodsFifty patients with liver cirrhosis without intrinsic cardiopulmonary disease were enrolled in this study. All were subjected to complete clinical examination, laboratory investigations, radiological investigations including abdominal ultrasound, chest x ray and CT chest, ECG, contrast enhanced echocardiography with colored Doppler study, gastroscopy, ventilatory function tests, measurement of SaO2 using portable pulse oximetry and arterial blood gas analysis. ResultsThe prevalence of arterial hypoxemia in cirrhotic patients was 14.6%. The presence of hypoxemia is increased in patients with advanced liver disease and the severity of hypoxemia was positively correlated with the severity of liver disease assessed by the Child Pugh score. HPS represents 64.1% of causes of hypoxemia. Pulse oximetry is a simple non-invasive method for detection of arterial hypoxemia as an initial screening test for HPS. Contrast enhanced echocardiography (CEE) is the gold standard method for the diagnosis of HPS by detection of intrapulmonary vasodilatation (IPV) characteristic of HPS, while CT chest assists in diagnosis by exclusion of intrinsic pulmonary disease. ConclusionLiver cirrhosis is associated with unique pulmonary complications. The early identification of pulmonary dysfunctions in cirrhotic patients is crucial as it affects the prognosis and guides the future management by speeding up orthotopic liver transplantation (OLT) recommendations.

Nitric oxide therapy for post-laparoscopic surgery associated patent foramen ovale: Incidence, mechanisms, diagnosis and therapy

ObjectivePostoperative hypoxemia is a common clinical challenge. The diagnosis of an underlying cause of hypoxemia may not immediately be apparent. Clinically silent and non-functional intracardiac shunt may become apparent and pose significant management problems in the postoperative period. Data sourceWe describe a case where clinically significant hypoxemia resulted from a patent foramen ovale (PFO) after laparoscopic surgery due to changes in the intra-abdominal and intrathoracic pressures. ConclusionThis condition was effectively diagnosed by bedside echocardiography, and was effectively treated with nitric oxide.

Unusual cause of hypoxemia in myocardial infarction: Interventional management

Unusual cause of hypoxemia in myocardial infarction: Interventional management

Cardiac Compression of Lung Lower Lobes after Coronary Artery Bypass Graft with Cardiopulmonary Bypass

BackgroundAtelectasis is a major cause of hypoxemia after coronary artery bypass grafting (CABG) and is commonly ascribed to general anesthesia, high inspiratory oxygen concentration and cardiopulmonary bypass (CPB). The objective of this study was to evaluate the role of heart-induced pulmonary compression after CABG with CPB.MethodsSeventeen patients without pre-operative cardiac failure who were scheduled for coronary artery bypass graft underwent pre- and postoperative thoracic computed tomography. The cardiac mass, the pressure exerted on the lungs by the right and left heart and the fraction of collapsed lower lobe segments below and outside of the heart limits were evaluated on a computed tomography section 1 cm above the diaphragmatic cupola.ResultsIn the postoperative period, cardiac mass increased by 32% (117±31 g versus 155±35 g, p<0.001), leading to an increase in the pressure that was exerted on the lungs by the right (2.2±0.6 g.cm−2 versus 3.2±1.2 g.cm−2, p<0.05) and left heart (2.4±0.7 g.cm−2 versus 4.2±1.8 g.cm−2, p<0.001). The proportion of collapsed lung segments beneath the heart markedly increased [from 6.7% to 32.9% on the right side (p<0.001) and from 6.2% to 29% on the left side (p<0.001)], whereas the proportion of collapsed lung segments outside of the heart limits slightly increased [from 0.7% to 10.8% on the right side (p<0.001) and from 1.5% to 12.6% on the left side (p<0.001)].ConclusionThe pressure that is exerted by the heart on the lungs increased postoperatively and contributed to the collapse of subjacent pulmonary segments.

Platypnea–orthodeoxia syndrome in the elderly treated by percutaneous patent foramen ovale closure: A case series and literature review

BackgroundPlatypnea–orthodeoxia syndrome (POS) is a rare clinical phenomenon, associating normal oxygen saturation in a supine position and arterial hypoxemia in an upright position. This pathology can be secondary to an intracardiac shunt, a pulmonary vascular shunt or a ventilation–perfusion mismatch. Cardiac POS occurs in the presence of a right-to-left cardiac shunt, most commonly through a patent foramen ovale (PFO). Methods and resultsFrom our single-center prospective database of percutaneous PFO closure we identified five patients (4 females, mean age: 77±11years) out of 224 (2.2%) patients with a PFO who presented with a POS of cardiac origin. Transthoracic and transoesophageal echocardiographic examinations revealed the underlying mechanisms of POS and the diagnosis was confirmed by right-and-left cardiac catheterization (RLC) and by measuring serial blood oxygen saturation in the pulmonary veins and left atrium in supine and upright positions. PFO was associated with atrial septal aneurysm and a persistent prominent Eustachian valve in 3 patients.All patients underwent a successful percutaneous PFO closure without any immediate or subsequent complications (mean follow-up of 24±18months). Immediately after the procedure, mean arterial oxygen saturation improved from 83%±3 to 93%±2 in an upright position and symptoms disappeared. ConclusionPOS is a rare and under-diagnosed pathology that must be actively investigated in the presence of position-dependent hypoxemia. The diagnostic work-up must exclude other causes of hypoxemia and confirm the intracardiac shunt using either contrast echocardiography or RLC. For cardiac POS, percutaneous PFO closure is a safe and effective technique that immediately relieves orthodeoxia and patient symptoms.

Preliminary evaluation of the utility of comparing SpO2/FiO2and PaO2/FiO2ratios in dogs

AbstractObjectiveTo determine whether the ratio of pulse oximetry saturation/fraction of inspired oxygen (SpO2/FiO2, [SF]) correlates with the ratio of partial pressure of oxygen in arterial blood/FiO2(PaO2/FiO2, [PF]) in dogs.DesignProspective, observational pilot study.SettingUrban tertiary veterinary referral center.AnimalsThirty‐eight client‐owned dogs requiring assessment of oxygenation.InterventionsNone.Measurements and Main ResultsArterial blood gas analysis with co‐oximetry was performed on samples obtained from the dorsal pedal artery. Median SpO2was 91.5% (range 80–97%) and median PaO2was 70.1 mmHg (range 44.5–103.8 mmHg). Hypoventilation was uncommon and venous admixture was the predominant cause of hypoxemia in this population. Median SF was 435.7 (range 381.0–461.9) and median PF was 334.0 (range 211.9–494.3). Nine dogs (23.6%) had PF &lt;300; no dogs had PF below 200. SF and PF were correlated (ρ = 0.618,P&lt; 0.01).ConclusionsSF and PF in dogs spontaneously breathing room air have good correlation, suggesting that SF may be a useful, noninvasive surrogate for PF when assessing oxygenation in canine patients. Further studies are warranted to confirm and validate this relationship in spontaneously breathing and mechanically ventilated dogs on varying levels of FiO2and to assess the ability of SF to predict outcome.