Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because of its low density, the He/O2 mixture markedly affects the dynamics of gas-flow, increasing inspiratory and expiratory flows, reducing WOB and respiratory acidosis, and relieving dyspnea in various clinical situations associated with obstructive airway disease. The magnitude of these changes varies according to the proportion of turbulent, transitional, and laminar flow conditions. These effects, however, last only as long as the patient breathes the He/O2 mixture, because it has no curative effect on the cause of airway obstruction. Thus, He/O2 ventilation is mostly useful while awaiting the effects of more definitive treatment. Evidence shows that He/O2 ventilation can improve pathophysiologic and clinical parameters in spontaneously breathing patients with upper airway obstruction, asthma. COPD, bronchopulmonary dysplasia. and bronchiolitis. Furthermore. He/O2 ventilation may prove to be a valuable adjunct in decompensated COPD patients, during both NIV and conventional mechanical ventilation. Despite promising results, however, there are two primary pitfalls to He/O2 ventilation. First, the consequences of the physical properties of the He/O2 mixture on various ventilator functions, the major differences between machines, and the correction factors to apply (if necessary) should be known. Second, in this age of cost control, particular attention should be paid to the cost-benefit ratio of He/O2 ventilation. Indeed, despite clinical evidence that the pathophysiologic principles on which He/O2 ventilation rests can be translated into favorable short-term physiologic and subjective effects, there is presently no evidence of a significant effect on patient outcome. Hence, before He/O2 ventilation can be recommended for widespread use, prospective outcome studies should be conducted in patients who suffer from the conditions discussed in this article to identify which, if any, are most likely to receive a benefit. Meanwhile, the authors recommend that He/O2 ventilation be reserved for patients who have a severe condition and who do not respond to the classic validated treatment modalities.
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PMID:Helium-oxygen ventilation. 1248 21

The density of helium is markedly lower than that of air or any of its components, leading to a substantial decrease in airway resistance to flow when it is inhaled. In mechanically ventilated patients with obstructive airway disease, replacing the usual air-oxygen mixture with helium-oxygen has been shown to reduce dynamic hyperinflation and intrinsic positive end-expiratory pressure; to decrease lung inflation pressures, respiratory acidosis, and work of breathing; and to improve arterial blood gases. Aerosol delivery to distal airways is enhanced with helium-oxygen. Preliminary data also suggest that the use of helium-oxygen could be a valuable approach to decrease postextubation respiratory distress. However, interference with ventilator function and added costs are two major disadvantages of helium-oxygen. Hence, before its widespread use in mechanically ventilated patients can be recommended, studies are needed to determine whether these favorable short-term effects can influence patient outcome.
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PMID:Usefulness of helium-oxygen mixtures in the treatment of mechanically ventilated patients. 1254 29

We previously showed that severe inspiratory resistive loads cause acute (<1 h) cardiorespiratory failure characterized by arterial hypotension, multifocal myocardial infarcts, and diaphragmatic fatigue. The mechanisms responsible for cardiovascular failure are unknown, but one factor may be the increased ventricular afterload caused by the large negative intrathoracic pressures generated when breathing against an inspiratory load. Because expiratory threshold loads increase intrathoracic pressure and decrease left ventricular afterload, we hypothesized that anesthetized rats forced to breathe against such a load would experience only diaphragmatic failure. Loading approximately doubled end-expiratory lung volume, halved respiratory frequency, and caused arterial hypoxemia and hypercapnia, respiratory acidosis, and increased inspiratory drive. Although hyperinflation immediately reduced the diaphragm's mechanical advantage, fatigue did not occur until near load termination. Mean arterial pressure progressively fell, becoming significant (cardiovascular failure) midway through loading despite tachycardia. Loading was terminated (endurance 125 +/- 43 min; range 82-206 min) when mean arterial pressure dropped below 50 mmHg. Blood samples taken immediately after load termination revealed hypoglycemia, hyperkalemia, and cardiac troponin T, the last indicating myocardial injury that was, according to histology, mainly in the right ventricle. This damage probably reflects a combination of decreased O(2) delivery (decreased venous return and arterial hypoxemia) and greater afterload due to hyperinflation-induced increase in pulmonary vascular resistance. Thus, in rats breathing at an increased end-expiratory lung volume, cardiorespiratory, not just respiratory, failure still occurred. Right heart injury and dysfunction may contribute to the increased morbidity and mortality associated with acute exacerbations of obstructive airway disease.
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PMID:Hyperinflation-induced cardiorespiratory failure in rats. 1940 48