DOCSLIB.ORG

Oxygen and the Airways Medical Journal], Where People Were Forced to Breathe As Deeply As They Could for 15 Minutes

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Oxygen and the Airways Medical Journal], Where People Were Forced to Breathe As Deeply As They Could for 15 Minutes Editorial Journal of Medicine [a very prestigious Thorax: first published as 10.1136/thx.2011.161497 on 18 June 2011. Downloaded from Oxygen and the airways medical journal], where people were forced to breathe as deeply as they could for 15 minutes. After 15 minutes of deep Richard Wood-Baker breathing the level of oxygen had DROPPED greatly in the blood, and the CO2 level had increased. So always The best things carried to excess are wrong oxygen use are more circumspect on use rememberdyour lungs are a gas mixing (Charles Churchill (satirist) 1731e1764) without measurement of oxygenation,3 chamber. They work best when you have stating that there is no benefit from the right mix of gases in themdjust like The use of oxygen for the management of oxygen administration in non-hypoxic the carburettor of a car’.6 Yet some patients with acute breathlessness, irre- patients and emphasising that adminis- medical practitioners did question the role spective of cause, is well established in tration should be based on, and monitored of oxygen in cases of acute severe asthma, medical practice. The perception of by, objective measures. particularly those presenting in primary benefit, even in the absence of measure- The relationship between oxygen care.7 They reported that a systematic ment of oxygenation, and concerns over concentrations and airway diseases, review was not feasible as there had never adverse outcomes from severe hypoxaemia particularly the impact on ventilatory been a randomised controlled trial of have driven the use of high-concentration responses, has been of interest for many oxygen use in acute severe asthma, so they oxygen therapy over many years with years. As early as 1979, investigations were opted to present a narrative literature little regard to possible harmful effects. being carried out on the impact of hyper- review. They went on to state that in While there have been many advocates for oxia in asthma, by measuring specific acute severe asthma, nebulisation of b the cautious use of oxygen in chronic 2 airway conductance during exercise- agonists without oxygen can cause or obstructive pulmonary disease (COPD) as induced bronchoconstriction and worsen hypoxaemia and hypothesised a result of its propensity to promote comparing patients with asthma who had that the continuing trickle of deaths from hypercarbia, liberal use in asthma appears bilateral carotid body resection with those asthma in Britain is a result of hypo- universal. This approach pervades student having intact carotid bodies. Oxygen xaemia caused by air-driven nebulisers. teaching through medical texts, even breathing during exercise markedly atten- They rationalised that the use of oxygen when there is significant respiratory input uated the post-exercise bronchospasm in before, during and after nebulised b into the publication1 and extends to 2 patients with asthma who had intact agonist therapy in primary care and in the recent evidence-based guidelines on both carotid bodies, but had no significant effect community was rational and could save asthma management and oxygen usage. in those without carotid bodies, unrelated lives, urging the BTS to review this issue The recently published British Thoracic to changes in end-tidal partial pressure of when it updated its guidelines. Society/Scottish Intercollegiate Guidelines fi carbon dioxide. The authors concluded It was not until 2003 that the rst http://thorax.bmj.com/ Network (BTS/SIGN) guidelines2 recom- that oxygen attenuates exercise-induced controlled trial to investigate the effects of mend administration of oxygen for acute bronchospasm in patients with asthma hyperoxia in patients with acute severe exacerbations of asthma, stating ‘Many through its action on the carotid bodies.4 asthma was reported.8 Seventy-four patients with acute severe asthma are Further reassurance on the safety of oxygen patients were randomised to receive 28% hypoxaemic. Supplementary oxygen should in asthma came in 1991, when bronchial or 100% oxygen for 20 min. The admin- be given urgently to hypoxaemic patients, reactivity to methacholine under normoxic istration of 100% oxygen significantly using a face mask, Venturi mask or nasal and hyperoxic conditions was studied in increased arterial carbon dioxide pressure cannulae with flow rates adjusted as a double-blind study involving nine (PaCO ) compared with 28% oxygen, on October 1, 2021 by guest. Protected copyright. necessary to maintain SpO of 94e98%’, 2 2 patients with asthma. The provocative especially in those with PaCO greater advice that is allocated a moderate to 2 concentrations that caused a 20% fall in than 40 mm Hg before oxygen treatment. low level of evidence. Furthermore, they FEV while breathing 21% and 100% Supporting these observations, in this emphasise the use of oxygen therapy even 1 oxygen were 0.18 mg/ml (range 0.06e5.73) issue of the journal, Perrin et al report on in the absence of information on oxygen- and 0.25 mg/ml (range 0.07e8.49), respec- findings that provide high-level evidence ation, recommending that the ‘Lack of tively. These were not significantly based on which recommendations have pulse oximetry should not prevent the use different, allowing the investigators to been made for oxygen administration in of oxygen’. Use of oxygen according to conclude that 100% oxygen does not affect acute asthma. They report a randomised these recommendations is likely to result bronchial reactivity in asthma.5 study comparing the effect of high- in a high fractional inspired oxygen, as These studies seem to have been concentration oxygen delivered at 8 l/min ‘In hospital, ambulance and primary accepted as evidence that hyperoxia did via a face mask with oxygen titrated to care, nebulised b agonist bronchodilators 2 not have an impact on asthma, yet achieve oxygen saturations of 93e95% in should preferably be driven by oxygen’, a number of cases were reported in the acute exacerbations of asthma presenting noting ‘A flow rate of 6 l/min is required to literature suggesting that there may be to an emergency department. Trans- drive most nebulisers’. The recently cause for concern over oxygen use in cutaneous CO pressure (PtCO ) was used published BTS guidelines on emergency 2 2 asthma under some circumstances. to measure the effect of the interventions, Although these reports did not appear to with the proportion of patients having $ alarm the medical fraternity, the broader a rise in PtCO2 4 mm Hg at 60 min Correspondence to Richard Wood-Baker, Head, asthma community seemed more being significantly greater in the high Cardiorespiratory Medicine, Royal Hobart Hospital, concerned about hypercarbia in asthma. concentration oxygen group when Honorary Member, Menzies Research Institute ‘ Tasmania, GPO Box 1061, Hobart, Tasmania, 7001, Internet postings noted A study was done compared with the titrated group. Australia; [email protected] in 1963 and written up in the New England The investigators concluded that Thorax November 2011 Vol 66 No 11 931 Editorial high-concentration oxygen therapy causes approached in the same way as any other REFERENCES Thorax: first published as 10.1136/thx.2011.161497 on 18 June 2011. Downloaded from fi 1. Souhami RL, Moxham J. Textbook of medicine. In: a clinically signi cant increase in PtCO2 drug, recognising that adverse outcomes and they recommended the use of may eventuate from either inappropri- Souhami RL, ed. Textbook of Medicine. 4th edn. Churcill Livingstone, 2002:658. a titrated oxygen regime in the treatment ately low or high concentrations. Should 2. British Guideline on the Management of Asthma; A of severe asthma. These results mirror the guidelines be revised in the light of national Clinical Guideline. British Thoracic Society those of a similar study performed this new evidence to better align recom- Scottish Intercollegiate Guidelines Network, 2011 recently in patients with COPD.9 In this mendations with the philosophy of [updated 2011; cited 2011 31.05.2011]; http://www. sign.ac.uk/pdf/sign101.pdf. randomised, controlled, prehospital study, keeping arterial oxygen saturations ‘ ’ 3. O’Driscoll BR, Howard LS, Davison AG. BTS participants allocated to titrated oxygen within the target saturation range that guideline for emergency oxygen use in adult patients. therapy were significantly less likely to aim to ‘achieve normal or near-normal Thorax 2008;63(Suppl 6):vi1e68. have respiratory acidosis (mean difference oxygen saturation’ and move away from 4. Schiffman PL, Ryan A, Whipp BJ, et al. Hyperoxic in pH 0.12; SE 0.05; p¼0.01; n¼38) or any suggestion that high-concentration attenuation of exercise-induced bronchospasm in asthmatics. J Clin Invest 1979;63:30e7. hypercapnoea (mean difference in PaCO2 oxygen should be administered in the 5. Wollner A, Ben-Dov I, Bar-Yishay E. Effect of À33.6 mm Hg; SE 16.3; p¼0.02; n¼39) absence of objective evidence of a physio- hyperoxia on bronchial response to inhaled than patients receiving high-concentration logical need? With the advent of low- methacholine. Allergy 1991;46:35e9. oxygen. Treatment with titrated oxygen cost portable oxygen saturation monitors, 6. Roy CL. Oxygen and Asthma - How To Make Asthma Worse. 2011 [updated 2011]. http://ezinearticles. was also associated with a 58% reduction surely it is time we followed the guideline e fi com/?Oxygen-and-Asthma -How-To-Make-Asthma- in mortality, the primary outcome in this exhortations to measure the fth vital Worse!&id¼313556 (accessed 31 May 2011). study. sign, as in the words of Willy Wonka 7. Inwald D, Roland M, Kuitert L, et al. Oxygen As asthma and COPD are prevalent ‘it’s the only way if you want it just treatment for acute severe asthma. BMJ e diseases in the Western world, and acute right’. 2001;323:98 100. 8. Rodrigo GJ, Rodriquez Verde M, Peregalli V, et al. exacerbations of either are associated Competing interests None. Effects of short-term 28% and 100% oxygen on with an increased risk of death, it is PaCO2 and peak expiratory flow rate in acute asthma: beholden to health professionals to ensure Provenance and peer review Commissioned; not a randomized trial.
Load more

Recommended publications
  • Maximum Expiratory Flow Rates in Induced Bronchoconstriction in Man
    Maximum expiratory flow rates in induced bronchoconstriction in man A. Bouhuys, … , B. M. Kim, A. Zapletal J Clin Invest. 1969;48(6):1159-1168. https://doi.org/10.1172/JCI106073. Research Article We evaluated changes of maximum expiratory flow-volume (MEFV) curves and of partial expiratory flow-volume (PEFV) curves caused by bronchoconstrictor drugs and dust, and compared these to the reverse changes induced by a bronchodilator drug in previously bronchoconstricted subjects. Measurements of maximum flow at constant lung inflation (i.e. liters thoracic gas volume) showed larger changes, both after constriction and after dilation, than measurements of peak expiratory flow rate, 1 sec forced expiratory volume and the slope of the effort-independent portion of MEFV curves. Changes of flow rates on PEFV curves (made after inspiration to mid-vital capacity) were usually larger than those of flow rates on MEFV curves (made after inspiration to total lung capacity). The decreased maximum flow rates after constrictor agents are not caused by changes in lung static recoil force and are attributed to narrowing of small airways, i.e., airways which are uncompressed during forced expirations. Changes of maximum expiratory flow rates at constant lung inflation (e.g. 60% of the control total lung capacity) provide an objective and sensitive measurement of changes in airway caliber which remains valid if total lung capacity is altered during treatment. Find the latest version: https://jci.me/106073/pdf Maximum Expiratory Flow Rates in Induced Bronchoconstriction in Man A. Bouiuys, V. R. HuNTr, B. M. Kim, and A. ZAPLETAL From the John B. Pierce Foundation Laboratory and the Yale University School of Medicine, New Haven, Connecticut 06510 A B S T R A C T We evaluated changes of maximum ex- rates are best studied as a function of lung volume.
    [Show full text]
  • Bronchoconstriction in Normal and Asthmatic Subjects
    Thorax: first published as 10.1136/thx.43.11.890 on 1 November 1988. Downloaded from Thorax 1988;43:890-895 The nasal response to exercise and exercise induced bronchoconstriction in normal and asthmatic subjects KINGMAN P STROHL, MICHAEL J DECKER, LESLIE G OLSON, TOD A FLAK, PETER L HOEKJE Airway Disease Center, Departments ofMedicine, University Hospitals ofCleveland; and Case Western Reserve University, Cleveland, Ohio, USA ABSTRACT Two studies were carried out to test the hypothesis that the fall and recovery of nasal resistance after exercise in asthmatic and non-asthmatic subjects are related to the development of bronchoconstriction after exercise. In study 1 nasal resistance (posterior rhinomanometry) and specific airway resistance (sRaw) were measured before challenge and one, five, 10 and 30 minutes after four minutes of exhausting legwork exercise in nine asthmatic subjects and nine age matched healthy subjects. One minute after exercise there was a reduction in nasal resistance of49% (SD 15%) from baseline in the healthy subjects and of 66% (17%) in the asthmatic subjects. This response and the subsequent return ofnasal resistance to baseline values did not differ significantly between the two groups despite a substantial difference in the change in sRaw, an increase of 74% (45%) in the asthmatic subjects 10 minutes after exercise, and no change in the non-asthmatic subjects. In study 2, nasal and specific airway resistances were monitored according to the same measurement protocolcopyright. in six subjects with increased airway reactivity. Subjects exercised on two occasions, wearing a noseclip, once while breathing cold, dry air and once while breathing warm, humid air.
    [Show full text]
  • Exercise Induced Bronchoconstriction (EIB) What Is Exercise Induced Bronchoconstriction Testing?
    Exercise Induced Bronchoconstriction (EIB) What is Exercise Induced Bronchoconstriction testing? Exercise induced bronchoconstriction or EIB, is a combined breathing and exercise test. The test can help identify what type of breathing trouble you have, if any, when you exercise. A spirometry breathing test is done before and after you exercise on a treadmill. Spirometry can show how much air you can breathe in and out. It also shows how fast you can breathe in and out. The spirometry results are compared before and after you exercise to see what changes there are in your breathing. A laryngoscopy may be scheduled after the EIB test. A laryngoscopy is often done to identify if your vocal cords may be causing you to have trouble breathing with exercise. How do you get ready for the test? Please follow these directions when getting ready for this test. These medicines will affect the results of some of these tests and may need to be stopped before the testing is done. If the medicine is not stopped, as your doctor says, before the test we will not be able to complete the test. • Stop these inhaled medicines for 48 hours before your appointment: ◦ Anora® (umeclidinium and vilanterol) ◦ Bevespi® (glycopyrrolate and formoterol) ◦ Stiolto® (olodaterol and tiotropium) ◦ Utibron® (indacaterol and glycopyrrolate) ◦ Trelegy® (fluticasone, umeclidinium and vilanterol) • Stop these inhaled medicines for 24 hours before your appointment: ◦ Incruse® (umeclidinium) ◦ Seebri® (glycopyrrolate) ◦ Spiriva® (tiotropium) ◦ Tudorza® (aclidinium) • Stop these
    [Show full text]
  • Exercise-Induced Bronchoconstriction
    American Thoracic Society Documents An Official American Thoracic Society Clinical Practice Guideline: Exercise-induced Bronchoconstriction Jonathan P. Parsons, Teal S. Hallstrand, John G. Mastronarde, David A. Kaminsky, Kenneth W. Rundell, James H. Hull, William W. Storms, John M. Weiler, Fern M. Cheek, Kevin C. Wilson, and Sandra D. Anderson; on behalf of the American Thoracic Society Subcommittee on Exercise-induced Bronchoconstriction THIS OFFICIAL CLINICAL PRACTICE GUIDELINE OF THE AMERICAN THORACIC SOCIETYWASAPPROVEDBYTHEATS BOARD OF DIRECTORS, DECEMBER 2012 CONTENTS proportion of patients with asthma experience exercise-induced respiratory symptoms. EIB has also been shown to occur in sub- Executive Summary jects without a known diagnosis of asthma. Introduction Methods Diagnosis Pathogenesis Role of the Environment d The diagnosis of EIB is established by changes in lung Diagnosis function provoked by exercise, not on the basis of Measuring and Quantifying EIB symptoms. Exercise Challenge Testing to Identify EIB d Serial lung function measurements after a specific exercise Surrogates for Exercise to Identify EIB or hyperpnea challenge are used to determine if EIB is Treatment present and to quantify the severity of the disorder. It is Questions and Recommendations preferable to assess FEV1, because this measurement has General Comments Regarding Therapy better repeatability and is more discriminating than peak Screening for EIB expiratory flow rate. Exercise, Asthma, and Doping d The airway response is expressed as the percent fall in Background: Exercise-induced bronchoconstriction (EIB) describes FEV1 from the baseline value. The difference between acute airway narrowing that occurs as a result of exercise. EIB occurs the pre-exercise FEV1 value and the lowest FEV1 value in a substantial proportion of patients with asthma, but may also recorded within 30 minutes after exercise is expressed as occur in individuals without known asthma.
    [Show full text]
  • Standardisation of Spirometry
    Eur Respir J 2005; 26: 319–338 DOI: 10.1183/09031936.05.00034805 CopyrightßERS Journals Ltd 2005 SERIES ‘‘ATS/ERS TASK FORCE: STANDARDISATION OF LUNG FUNCTION TESTING’’ Edited by V. Brusasco, R. Crapo and G. Viegi Number 2 in this Series Standardisation of spirometry M.R. Miller, J. Hankinson, V. Brusasco, F. Burgos, R. Casaburi, A. Coates, R. Crapo, P. Enright, C.P.M. van der Grinten, P. Gustafsson, R. Jensen, D.C. Johnson, N. MacIntyre, R. McKay, D. Navajas, O.F. Pedersen, R. Pellegrino, G. Viegi and J. Wanger CONTENTS AFFILIATIONS Background ............................................................... 320 For affiliations, please see Acknowledgements section FEV1 and FVC manoeuvre .................................................... 321 Definitions . 321 CORRESPONDENCE Equipment . 321 V. Brusasco Requirements . 321 Internal Medicine University of Genoa Display . 321 V.le Benedetto XV, 6 Validation . 322 I-16132 Genova Quality control . 322 Italy Quality control for volume-measuring devices . 322 Fax: 39 103537690 E-mail: [email protected] Quality control for flow-measuring devices . 323 Test procedure . 323 Received: Within-manoeuvre evaluation . 324 March 23 2005 Start of test criteria. 324 Accepted after revision: April 05 2005 End of test criteria . 324 Additional criteria . 324 Summary of acceptable blow criteria . 325 Between-manoeuvre evaluation . 325 Manoeuvre repeatability . 325 Maximum number of manoeuvres . 326 Test result selection . 326 Other derived indices . 326 FEVt .................................................................. 326 Standardisation of FEV1 for expired volume, FEV1/FVC and FEV1/VC.................... 326 FEF25–75% .............................................................. 326 PEF.................................................................. 326 Maximal expiratory flow–volume loops . 326 Definitions. 326 Equipment . 327 Test procedure . 327 Within- and between-manoeuvre evaluation . 327 Flow–volume loop examples. 327 Reversibility testing . 327 Method .
    [Show full text]
  • Airway Receptors
    Postgraduate Medical Journal (1989) 65, 532- 542 Postgrad Med J: first published as 10.1136/pgmj.65.766.532 on 1 August 1989. Downloaded from Mechanisms of Disease Airway receptors Peter J. Barnes Department of Thoracic Medicine, National Heart and Lung Institute, Dovehouse Street, London SW3 6L Y, UK. Introduction Airway smooth muscle tone is influenced by many indirect action which, in part, is due to activation of a hormones, neurotransmitters, drugs and mediators, cholinergic reflex, since the bronchoconstriction may which produce their effects by binding to specific be reduced by a cholinergic antagonist. Other surface receptors on airway smooth muscle cells. mediators may have a bronchoconstrictor effect Bronchoconstriction and bronchodilatation may which, in the case of adenosine, is due to mast cell therefore be viewed in terms of receptor activation or mediator release,2 or in the case of platelet-activating blockade and the contractile state of airway smooth factor due to platelet products.3 muscle is probably the resultant effect of interacting excitatory and inhibitory receptors. Epithelial-derived relaxantfactor It is important to recognize that airway calibre is not only the result of airway smooth muscle tone, but in Recently there has been considerable interest in the asthma it is likely that airway narrowing may also be possibility of a relaxant factor released from airway explained by oedema of the bronchial wall (resulting epithelial cells, which may be analogous to relaxant factor.4 The presence of from microvascular leakage) and to luminal plugging endothelial-derived by copyright. by viscous mucus secretions and extravasated plasma airway epithelium in bovine airways in vitro reduces proteins, which may be produced by a 'soup' of the sensitivity to and maximum contractile effect of mediators released from inflammatory cells, including spasmogens, such as histamine, acetylcholine or mast cells, macrophages and eosinophils.
    [Show full text]
  • Spirometry Nitric Oxide Exchange in a Pattern Distinct
    Exercise-induced bronchoconstriction alters airway nitric oxide exchange in a pattern distinct from spirometry Hye-Won Shin, Christina D. Schwindt, Anna S. Aledia, Christine M. Rose-Gottron, Jennifer K. Larson, Robert L. Newcomb, Dan M. Cooper and Steven C. George Am J Physiol Regulatory Integrative Comp Physiol 291:1741-1748, 2006. First published Jul 13, 2006; doi:10.1152/ajpregu.00178.2006 You might find this additional information useful... This article cites 57 articles, 35 of which you can access free at: http://ajpregu.physiology.org/cgi/content/full/291/6/R1741#BIBL Updated information and services including high-resolution figures, can be found at: http://ajpregu.physiology.org/cgi/content/full/291/6/R1741 Additional material and information about American Journal of Physiology - Regulatory, Integrative Downloaded from and Comparative Physiology can be found at: http://www.the-aps.org/publications/ajpregu This information is current as of November 29, 2006 . ajpregu.physiology.org on November 29, 2006 The American Journal of Physiology - Regulatory, Integrative and Comparative Physiology publishes original investigations that illuminate normal or abnormal regulation and integration of physiological mechanisms at all levels of biological organization, ranging from molecules to humans, including clinical investigations. It is published 12 times a year (monthly) by the American Physiological Society, 9650 Rockville Pike, Bethesda MD 20814-3991. Copyright © 2005 by the American Physiological Society. ISSN: 0363-6119, ESSN: 1522-1490. Visit our website at http://www.the-aps.org/. Am J Physiol Regul Integr Comp Physiol 291: R1741–R1748, 2006. First published July 13, 2006; doi:10.1152/ajpregu.00178.2006.
    [Show full text]
  • Keeping Children with Exercise-Induced Asthma Active
    Keeping Children With Exercise-induced Asthma Active Henry Milgrom, MD, and Lynn M. Taussig, MD ABSTRACT. Exercise-induced bronchospasm, exercise- prophylactically and do not require continuous therapy.13 induced bronchoconstriction, and exercise-induced Most asthma medications, even some unconventional asthma (EIA) are all terms used to describe the phenom- ones such as heparin, furosemide, calcium channel enon of transient airflow obstruction associated with blockers, and terfenadine, given before exercise, sup- physical exertion. It is a prominent finding in children press EIA.14,15 McFadden accounts for the efficacy of these and young adults because of their greater participation in disparate classes of drugs by their potential effect on the vigorous activities.1 The symptoms—shortness of breath, bronchial vasculature that modulates the cooling and/or cough, chest tightness, and wheezing—normally follow rewarming phases of the reaction.16 Short-acting b-ago- the brief period of bronchodilation present early in the nists provide protection in 80% to 95% of affected indi- course of exercise. Bronchospasm typically arises within viduals with insignificant side effects and have been 10 to 15 minutes of beginning exercise, peaks 8 to 15 regarded for many years as first-line therapy.17 Two long- minutes after the exertion is concluded, and resolves acting bronchodilators, salmeterol and formoterol, have 2 about 60 minutes later, but it also may appear during 18–21 3 been found effective in the prevention of EIA. A sustained exertion. EIA occurs in up to 90% of asthmat- single 50-mg dose of salmeterol protects against EIA for 9 ics and 40% of patients with allergic rhinitis; among hours; its duration appears to wane in the course of daily athletes and in the general population its prevalence is therapy.22–24 Cromolyn sodium is highly effective in 70% between 6% and 13%.4,5 to 87% of those diagnosed with EIA and has minimal EIA frequently goes undiagnosed.
    [Show full text]
  • Effect of Acute Alterations in Inspired Oxygen Tension on Methacholine
    Thorax 1997;52:453±457 453 EVect of acute alterations in inspired oxygen Thorax: first published as 10.1136/thx.52.5.453 on 1 May 1997. Downloaded from tension on methacholine induced bronchoconstriction in patients with asthma Kenneth D Dagg, Lorna J Thomson, Robert A Clayton, Scott G Ramsay, Neil C Thomson Abstract mild to moderate patients with stable Background ± Recent in vitro and in vivo asthma. studies in animals have suggested that am- (Thorax 1997;52:453±457) bient oxygen tension may in¯uence airway responsiveness to bronchoconstrictor Keywords: hyperoxia, hypoxia, bronchoconstriction, stimuli. These observations may have rel- methacholine, asthma. evance to the management of acute ex- acerbations of asthma. The present studies were designed to examine the in¯uence Little is known about the eVect of acute alter- of inspired oxygen tension (Fio2 1.0, 0.21, ations in oxygen tension on the responsiveness 0.15) on methacholine induced broncho- of the airways to bronchoconstrictor stimuli. constriction in patients with asthma. Recent in vitro and in vivo studies in animals Methods ± In a dual study two groups of suggest that hypoxia potentiates and hyperoxia asthmatic patients performed metha- attenuates the airway constrictor response to choline inhalation challenges breathing certain stimuli.12 Similar in vivo studies in man, 3±5 either air (Fio2 0.21) or a hypoxic gas mix- however, have produced con¯icting ®ndings. ture (Fio2 0.15) in study 1 and air (Fio2 If airway responsiveness is increased by a fall 0.21) or hyperoxia (Fio2 1.0) in study 2. in oxygen tension during acute exacerbations The gases were administered through a of asthma, then the administration of high closed breathing circuit in a randomised concentrations of inspired oxygen may act to http://thorax.bmj.com/ double blind fashion.
    [Show full text]
  • Respiratory Guidelines
    RESPIRATORY GUIDELINES Medicines Used in Respiratory Diseases Introduction This chapter contains brief summaries of the major drugs used in the management of respiratory disease and are recommended in these guidelines. The summaries do not contain comprehensive accounts of the pharmacology of these compounds. The reader is advised to consult standard textbooks and/or the industry product information for more details. It is important to consider the risks and benefits of drugs (particularly corticosteroids) that are used to treat respiratory diseases. As a general principle, the lowest drug doses that achieve best control should be used. For example: Patient adherence to asthma treatment is better if regimens have: fewer devices and drugs fewer adverse effects been understood and agreed between patient and health care professional. Beta2 receptor stimulating drugs (Beta2 agonists) Introduction Stimulation of beta2-receptors on airway smooth muscle relaxes the muscle resulting in bronchodilation. All beta2 agonists may also stimulate beta1-receptors; however, the effects of beta1-receptor stimulation (eg tachycardia) are more likely to occur following systemic absorption or following inhalation of relatively large doses. Under almost all circumstances, the preferred route of administration for beta2 agonists is by inhalation. Administration by inhalation causes bronchodilation with low doses thus minimising systemic adverse effects. Adverse effects: Dose-limiting adverse effects of the beta2 agonists are most commonly tachycardia (which can also lead to paroxysmal tachyarrhythmias, such as atrial fibrillation or paroxysmal supraventricular tachycardia), tremor, headaches, muscle cramps, insomnia, and a feeling of anxiety and nervousness. In high doses (eg tablets,intravenous and emergency nebulisation) all beta2 agonists can cause hypokalaemia and hyperglycaemia.
    [Show full text]
  • The Effects of a Warmed Steam Inhalation on Patients with Chronic
    ry & Re na sp o ir Kawagoshi et al., J Pulm Respir Med 2018, 8:4 m a l to u r P y : f M DOI 10.4172/2161-105X.1000471 o e Journal of l d a i n c r i n u e o J ISSN: 2161-105X Pulmonary & Respiratory Medicine Research Article Open Access The Effects of a Warmed Steam Inhalation on Patients with Chronic Obstructive Pulmonary Disease: A Cross-Sectional, Controlled Study Kawagoshi A1*, Shibata K1, Sugawara K1, Takahashi H1, Saita Y2, Oda H2 and Shioya T3 1Department of Rehabilitation, Akita City Hospital, Akita, Japan 2Development Research, Personal Health Care Products Research, Kao Corporation, Tokyo, Japan 3Department of Physical Therapy, School of Health Sciences, Akita University, Akita, Japan Abstract Background: We investigated the influence of warmed steam inhalation on the respiratory dynamics and psychological anxiety in patients with chronic obstructive pulmonary disease (COPD). Methods: This was a cross-sectional and controlled study of 16 patients with stable COPD (age: 72 ± 6 years old, % FEV1: 61.4 ± 28.2%). The patients wore a steam mask in a resting position for 15 min. Two weeks later, they wore a mask that generated no warmed steam (non-steam mask) under the same conditions. We evaluated the patients’ respiratory function, percutaneous oxygen saturation, heart rate (HR), and state anxiety based on the State-Trait Anxiety Inventory (STAI) before and after wearing the masks, and the respiratory rate was measured during the mask wearing. Results: The patients’ HR and STAI state anxiety were significantly decreased after they wore the steam mask.
    [Show full text]
  • Respiratory System.Pdf
    Respiratory System Respiratory System - Overview: Assists in the detection Protects system of odorants Respiratory (debris / pathogens / dessication) System 5 3 4 Produces sound (vocalization) Provides surface area for gas exchange (between air / blood) 1 2 For the body to survive, there must be a constant supply of Moves air to / from gas O2 and a constant exchange surface disposal of CO 2 Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Table 19.1 Respiratory System Respiratory System Functional Anatomy: Functional Anatomy: Trachea Epiglottis Naming of pathways: • > 1 mm diameter = bronchus Upper Respiratory • Conduction of air • < 1 mm diameter = bronchiole System • Gas exchange Primary • < 0.5 mm diameter = terminal bronchiole Bronchus • Filters / warms / humidifies Lower Respiratory Bronchi System incoming air bifurcation (23 orders) 1) External nares 5) Larynx 2) Nasal cavity • Provide open airway Green = Conducting zone • Resonance chamber • channel air / food Purple = Respiratory zone 3) Uvula • voice production (link) 4) Pharynx 6) Trachea 7) Bronchial tree • Nasopharynx Bronchiole 8) Alveoli • Oropharynx Terminal Bronchiole Respiratory Bronchiole • Laryngopharynx Alveolus Martini et. al. (Fundamentals of Anatomy and Physiology, 7th ed.) – Figure 23.1 Martini et. al. (Fundamentals of Anatomy and Physiology, 7th ed.) – Figure 23.9 Respiratory System Respiratory System Functional Anatomy: Functional Anatomy: Respiratory Mucosa / Submucosa: How are inhaled debris / pathogens cleared from respiratory tract? Near Near trachea alveoli Nasal Cavity: Epithelium: Particles > 10 µm Pseudostratified Simple columnar cuboidal Conducting Zone: Particles 5 – 10 µm Cilia No cilia Respiratory Zone: Mucus Escalator Particles 1 – 5 µm Mucosa: Lamina Propria (areolar tissue layer): Mucous membrane (epithelium / areolar tissue) smooth smooth muscle muscle Mucous No glands mucous glands Cartilage: Rings Plates / none Macrophages Martini et.
    [Show full text]