Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite advances in neonatal care including prenatal diagnosis, conventional ventilation, surfactant, high frequency oscillation, nitric oxide and extracorporeal membrane oxygenation (ECMO) the diagnosis of CDH is reported to carry a high mortality rate. Pulmonary hypoplasia and persistent pulmonary hypertension are major factors that contribute to death. In an effort to improve the survival of these infants a protocolized approach was adopted. In summary, this involves antenatal use of steroids if CDH antenatally diagnosed, sedation and muscle relaxation following tracheal intubation, administration of surfactant, gentle ventilation with permissive hypercapnia, trial of nitric oxide, preoperative ECMO for those infants failing therapy and delayed repair of the CDH. With the use of this protocolized approach the survival of infants with isolated CDH was 96 % for inborn and 81 % for outborn infants.
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PMID:Improving survival of neonates with isolated congenital diaphragmatic hernia. 1559 64

The pathophysiology of upper-airway obstruction (UAO) is complex. Possible causes of UAO that may lead to acute respiratory failure, are as follows: infections like acute epiglottitis and croup, obstructing tumors in the base of the tongue, larynx or hypopharynx, aspirated food or liquid contents, obesity and anatomical variations. Management changes according to the pathogenesis of the disorder. In patients with severe carbon dioxide retention or apnea, emergency endotracheal intubation must be carried out. Hereby, we describe a 23-year-old patient with susceptible upper-airway anatomy and UAO occurred following an upper respiratory infection and complicated with pulmonary hypertension and pulmonary edema. Our patient seems to be one of the complicated UAO cases, with an unusual but critical clinical presentation, evaluated in a wide spectrum and nicely returned to life.
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PMID:Pulmonary hypertension and acute pulmonary edema in a 23-year-old male with a history of an upper respiratory tract infection. 1576 90

The authors report the results of a study on patients with chronic cor pulmonale hospitalized in the Departement of Cardiology (Dakar), from 1990 to 1998. The hospital prevalence is 0.9% with a male predominance (73.5%). The clinical signs were dominated by dyspnea and cough. The right heart failure is noted in 85.29% of cases. As far as the biological factor is concerned, it exists an polycythemia about 75% of cases, hypoxia (88.8%), hypercapnia (55.5%) and a respiratory acidoses (55.5%). The spirometry showed in 66% of cases, a mixed syndrom with obstructive predominance. The echocardiography showed in all cases right heart dilatation with pulmonary hypertension. The etiological factors are dominated by tobacco (21 cases). The hospital evolution has been favorable in 19 cases underoxygentherapy, lowdosediuretic, expectorant, bronchodilatators and salt restriction. However, 14 patients have died.
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PMID:[Chronic cor pulmonale: a study of 34 cases in the Dakar University Hospital Center Cardiology Department]. 1577 62

John T. (Jack) Reeves' science is reviewed across the 37 years of his research career at the University of Colorado Health Sciences Center, a period which occupied approximately half his remarkable life. His contributions centered on understanding the inter-relatedness as well as the underlying mechanisms controlling the various components of the O(2) transport system. We review here his studies on exercise performance; these encompassed about half his scientific output with the other half being devoted to the study of hypoxic pulmonary hypertension. Early studies concerned cardiac output, showing how it was a balance between O(2) uptake and O(2) extraction, and that cardiac output during exercise at high altitude was reduced, most likely because of decreased plasma volume and left ventricular filling. Jack's many studies addressed virtually every aspect of the O(2) transport system -- adding significantly to our understanding of the syndromes of altitude illness, the mechanisms by which ventilatory sensitivity to hypoxia and hypercapnia influenced ventilatory acclimatization, and the contributions of the various limbs of the autonomic nervous system on systemic blood pressure, vascular resistance and substrate utilization. His scientific career ended abruptly in 2004 when struck by a car while biking to work, but his legacy remains in his more than 385+ research articles or chapters, the 40+ fellows he trained, and the countless number of younger (and older) scientists for whom he served as a role model for learning how to scrutinize their data and present their findings in clear and sometimes bold prose. An integral man, he is sorely missed.
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PMID:Jack Reeves and his science. 1638 71

Induction of hypercapnia by breathing high concentrations of carbon dioxide (CO(2)) may have beneficial effects on the pulmonary circulation. We tested the hypothesis that exposure to CO(2) would protect against chronic pulmonary hypertension in newborn rats. Atmospheric CO(2) was maintained at <0.5% (normocapnia), 5.5%, or 10% during exposure from birth for 14 days to normoxia (21% O(2)) or moderate hypoxia (13% O(2)). Pulmonary vascular and hemodynamic abnormalities in animals exposed to chronic hypoxia included increased pulmonary arterial resistance, right ventricular hypertrophy and dysfunction, medial thickening of pulmonary resistance arteries, and distal arterial muscularization. Exposure to 10% CO(2) (but not to 5.5% CO(2)) significantly attenuated pulmonary vascular remodeling and increased pulmonary arterial resistance in hypoxia-exposed animals (P < 0.05), whereas both concentrations of CO(2) normalized right ventricular performance. Exposure to 10% CO(2) attenuated increased oxidant stress induced by hypoxia, as quantified by 8-isoprostane content in the lung, and prevented upregulation of endothelin-1, a critical mediator of pulmonary vascular remodeling. We conclude that hypercapnic acidosis has beneficial effects on pulmonary hypertension and vascular remodeling induced by chronic hypoxia, which we speculate derives from antioxidant properties of CO(2) on the lung and consequent modulating effects on the endothelin pathway.
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PMID:Therapeutic hypercapnia prevents chronic hypoxia-induced pulmonary hypertension in the newborn rat. 1682 30

A 52-year-old obese woman was admitted to our institution for evaluation of dyspnea and pulmonary hypertension (PH). Polysomnography revealed severe obstructive sleep apnea (OSA) with an apnea hypopnea index of 99.8. Treatment with nocturnal continuous positive airway pressure (CPAP) resulted in correction of daytime hypoxemia, hypercapnia, and near-normalization of pulmonary artery pressure. To our knowledge, this is the most severe case of OSA-associated PH (approximately70 mmHg) reported to date, and it was successfully treated with nocturnal CPAP. This case demonstrates that OSA should be considered and polysomnography performed in all patients with PH, irrespective of severity, and that nocturnal CPAP has therapeutic effects on both OSA and daytime PH.
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PMID:Continuous positive airway pressure ameliorated severe pulmonary hypertension associated with obstructive sleep apnea. 1683 48

Patients with obesity hypoventilation syndrome (OHS) have a lower quality of life, more healthcare expenses, a greater risk of pulmonary hypertension, and a higher mortality compared to eucapnic patients with obstructive sleep apnea (OSA). Despite significant morbidity and mortality associated with OHS, it is often unrecognized and treatment is frequently delayed. The objective of this observational study was to determine the prevalence of OHS in patients with OSA seen at the sleep disorders clinic of a large public urban hospital serving predominantly minority population and to identify clinical--not mechanistic--predictors that should prompt clinicians to measure arterial blood gases. In the first stage, we randomly selected 180 patients referred to our sleep disorders clinic between 2000 and 2004 for suspicion of OSA. From this retrospective random sample we calculated the prevalence of OHS in patients with OSA and identified independent clinical predictors using logistic regression. In the second stage, we prospectively validated these predictors in a sample of 410 consecutive patients referred to the sleep disorders clinic for suspicion of OSA between 2005 and 2006. The prevalence of OHS in patients with OSA was 30% in the retrospective random sample and 20% in the prospective sample. Three variables independently predicted OHS in both samples: serum bicarbonate level (p < 0.001), apnea-hypopnea index (p = 0.006), and lowest oxygen saturation during sleep (p < 0.001). Due to the serious morbidity associated with OHS, we selected a highly sensitive threshold of serum bicarbonate level. A threshold of 27 mEq/l had a sensitivity of 92% and a specificity of 50%. Only 3% of patients with a serum bicarbonate level <27 mEq/l had hypercapnia compared to 50% with a serum bicarbonate > or =27 mEq/l. In conclusion, OHS is common in severe OSA. A normal serum bicarbonate level excludes hypercapnia and an elevated serum bicarbonate level should prompt clinicians to measure arterial blood gases.
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PMID:Obesity hypoventilation syndrome: prevalence and predictors in patients with obstructive sleep apnea. 1765 82

Obstructive sleep apnea (OSA) affects approximately 5% of women and 15% of men in the middle-aged adults, and associated with adverse health outcomes. Cardiovascular disturbances are the most serious complications of OSA. These complications include heart failure, left/right ventricular dysfunction, acute myocardial infarction, arrhythmias, stroke, systemic and pulmonary hypertension. All these cardiovascular complications increase morbidity and mortality of OSA. Several epidemiologic studies have demonstrated that sleep related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic activity, and altered baroreflex control during sleep. Arterial hypertension, obesity, diabetes mellitus and coronary artery disease (CAD) which are independent predictors of left ventricular dysfunction, often have co-existence with OSA. Especially severe OSA patients having diastolic dysfunction might have an increased risk of heart failure, since diastolic dysfunction might be combined with systolic dysfunction. Early recognition and appropriate therapy of ventricular dysfunction is advisable to prevent further progression to heart failure and death. Patients with acute myocardial infarction, especially if they had apneas and hypoxemia without evident heart failure should be evaluated for sleep disorders. So, patients with CAD should be evaluated for OSA and vice versa. Early recognition and treatment of OSA may improve cardiovascular functions. Continuous positive airway pressure (CPAP) applied by nasal mask, is still the gold standard method for treatment of the disease and prevention of complications.
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PMID:Cardiovascular diseases in obstructive sleep apnea. 1720 27

Broilers are susceptible to pulmonary hypertension syndrome (PHS; ascites syndrome) when their pulmonary vascular capacity is anatomically or functionally inadequate to accommodate the requisite cardiac output without an excessive elevation in pulmonary arterial pressure. The consequences of an inadequate pulmonary vascular capacity have been demonstrated experimentally and include elevated pulmonary vascular resistance (PVR) attributable to noncompliant, fully engorged vascular channels; sustained pulmonary arterial hypertension (PAH); systemic hypoxemia and hypercapnia; specific right ventricular hypertrophy, and right atrioventricular valve failure (regurgitation), leading to central venous hypertension and hepatic cirrhosis. Pulmonary vascular capacity is broadly defined to encompass anatomical constraints related to the compliance and effective volume of blood vessels, as well as functional limitations related to the tone (degree of constriction) maintained by the primary resistance vessels (arterioles) within the lungs. Surgical occlusion of 1 pulmonary artery halves the anatomical pulmonary vascular capacity, doubles the PVR, triggers PAH, eliminates PHS-susceptible broilers, and reveals PHS-resistant survivors whose lungs are innately capable of handling sustained increases in pulmonary arterial pressure and cardiac output. We currently are using i.v. microparticle injections to increase the PVR and trigger PAH sufficient in magnitude to eliminate PHS-susceptible individuals while allowing PHS-resistant individuals to survive as progenitors of robust broiler lines. The microparticles obstruct pulmonary arterioles and cause local tissues and responding leukocytes to release vasoactive substances, including the vasodilator NO and the highly effective vasoconstrictors thromboxane A(2) and serotonin [5-hydroxytryptamine (5-HT)]. Nitric oxide is the principal vasodilator responsible for modulating (attenuating) the PAH response and ensuing mortality triggered by i.v. microparticle injections, whereas microparticle-induced increases in PVR can be attributed principally to 5-HT. Our observations support the hypothesis that susceptibility to PHS is a consequence of anatomically inadequate pulmonary vascular capacity combined with the functional predominance of the vasoconstrictor 5-HT over the vasodilator NO. The contribution of TxA(2) remains to be determined. Selecting broiler lines for resistance to PHS depends upon improving both anatomical and functional components of pulmonary vascular capacity.
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PMID:An inadequate pulmonary vascular capacity and susceptibility to pulmonary arterial hypertension in broilers. 1743 37

Pulmonary artery hypertension is defined as persistent elevation of mean pulmonary artery pressure > 25 mm Hg with pulmonary capillary wedge pressure < 15 mm Hg or elevation of exercise mean pulmonary artery pressure > 35 mm Hg. Although mild pulmonary hypertension rarely impacts anesthetic management, severe pulmonary hypertension and exacerbation of moderate hypertension can lead to acute right ventricular failure and cardiogenic shock. Knowledge of anesthetic drug effects on the pulmonary circulation is essential for anesthesiologists. Intraoperative management should include prevention of exacerbating factors such as hypoxemia, hypercarbia, acidosis, hypothermia, hypervolemia, and increased intrathoracic pressure; monitoring and optimizing right ventricular function; and treatment with selective pulmonary vasodilators. Recent advances in pharmacology provide anesthesiologists with a wide variety of options for selective pulmonary vasodilatation. Pulmonary hypertension is a major determinant of perioperative morbidity and mortality in special situations such as heart and lung transplantation, pneumonectomy, and ventricular assist device placement.
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PMID:Management of pulmonary hypertension in the operating room. 1753 16


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