DOCSLIB.ORG

Mucus on the Move: Embed It Or Expel Itâšthe Patient, the Clinician, and Now the Ventilator

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Mucus on the Move: Embed It Or Expel Itâšthe Patient, the Clinician, and Now the Ventilator Editorials Mucus On the Move: Embed It or Expel It—The Patient, the Clinician, and Now the Ventilator Intubation and mechanical ventilation may impair muco- A “saw tooth” pattern on the expiratory flow waveform ciliary clearance and lead to sputum retention, airway occlu- and coarse expiratory sounds over the trachea are good sion, atelectasis, and ventilator-associated pneumonia.1,2 Early indicators of retained secretions in the major airways.10 work demonstrated that airway clearance can be augmented Endotracheal tube and bronchial obstruction can be de- by an expiratory flow bias generated through the 2-phase tected by a characteristic increase in the early expiratory gas-liquid transport mechanism.3,4 Higher expiratory flow than time constant9 and by acoustic reflectometry.10-12 We have inspiratory flow combined with dynamic airway compression yet to accurately diagnose secretion retention, but flow contributes to the clearance of airway secretions in intubated waveform analysis and good clinical examination may be patients,3,4 and can be achieved by physical methods, includ- useful. ing manual lung hyperinflation.5 Patent Airway SEE THE ORIGINAL STUDY ON PAGE 1287 Adequate humidification and airway suctioning are re- 6,7 Clinicians may find it challenging when repositioning quired to maintain airway patency. Closed suctioning a heavily sedated, intubated, ventilated patient who has can minimize potential adverse physiologic effects of air- poor or absent cough and secretion retention, because way suctioning but may not be as effective for secretion 13-16 repositioning may result in substantial arterial hypox- clearance. Ventilator breaths triggered by closed suc- emia, hypercarbia, and increased patient work of breath- tioning may migrate secretions away from the suction cath- 13,17 ing. The prevalence, sequelae, and optimal methods to eter tip (due to inspiratory flow bias). Open suctioning, manage or prevent these episodes are yet to be ade- higher suction pressure, a wider-bore suction catheter, or quately described in the literature. The patient’s respi- the removal of positive end-expiratory pressure (PEEP)/ ratory-muscle strength, position, volume, viscosity, and pressure support can improve secretion clearance and may location of airway secretions, depth of sedation, and be required under certain conditions, such as major airway “cough strength” (expiratory flow generated spontane- occlusion, but may compromise gas exchange in the short 13,16 ously or in response to suction) are some of the vari- term. The “pipe cleaner” effect of the suction catheter ables that may determine the impact of secretion reten- may additionally assist to ensure airway patency and needs 16 tion on ventilation, gas exchange, and patient outcome. to be further investigated. The minimum standard of airway care currently advo- Using a shorter suction catheter (to prevent contact with cates adequate humidification and suctioning.6,7 the carina) can minimize adverse physiologic effects and Below I will discuss various definitions and means to may be as effective as suctioning with a standard-length monitor secretion-retention in an intubated and ventilated catheter, in terms of duration of intubation, intensive-care- patient, and methods to maintain a patent artificial airway, unit stay, intensive-care-unit mortality, and incidence of 18 enhance secretion clearance, and prevent secretion reten- pulmonary infections. The act of disconnecting the ven- tion. tilator circuit for open suctioning may explain the equiv- alent outcomes between shorter and conventional-length Diagnosis and Monitoring catheters (simulated cough due to elastic recoil), and re- quires further investigation.16,18 Lung auscultation and chest palpation may be useful to identify the presence of airway secretions, but may be Enhanced Secretion Clearance unreliable.8 Airway secretions may also be suspected with changes in pulmonary mechanics at the bedside. However, The expiratory flow bias required to generate annular measurements of airway pressure and flow are often taken 2-phase gas-liquid flow can be created with manual lung at the proximal end of the endotracheal tube, and hence are hyperinflation.5,19 Ventilator hyperinflation can also en- mainly affected by the mechanical properties of the tube.9 hance secretion clearance,20 and hyperinflation may be 1276 RESPIRATORY CARE • OCTOBER 2008 VOL 53 NO 10 MUCUS ON THE MOVE effective up to the 10th generation of airways.4 Manual ant lung to the more compliant lung. These laboratory and ventilator hyperinflation can transiently improve air- findings cannot be directly extrapolated to clinical care but way resistance and dynamic lung/thorax compliance.20,21 should stimulate in vivo research. Gravity-assisted drainage (head-down tilt) combined with manual lung hyperinflation may further enhance secretion Overview and Recommendations clearance.22 Chest-wall vibration, with or without manual lung hy- The work by Volpe et al27 supports earlier findings that perinflation and suctioning, can improve expiratory flow, expiratory flow bias can augment secretion clearance3,4 airway resistance, and dynamic lung/thorax compliance, and demonstrates how secretions can move between lungs but has not been demonstrated to improve secretion clear- at the carina; it is unclear if this principle extends to the ance.23,24 Manual lung hyperinflation with PEEP more peripheral airway branchings. Unfortunately, airway Ͼ 10 cm H2O may retard the expiratory flow to below that suctioning, cough, and gravity were not investigated, but required for 2-phase gas-liquid flow.25 they can play an important role in mucus movement.28 In a rabbit model with pressure-controlled ventilation, Ventilator settings that have an expiratory flow bias may no PEEP, and artificial mucus instilled to create atelecta- cause “pooling” of secretions near the central or major sis, chest-wall vibration was associated with significant airways, which could lead to adverse changes in ventila- deterioration in dynamic lung/thorax compliance and gas tion and gas exchange, for example in a sedated or para- exchange. Unfortunately, those authors did not measure lyzed patient.26 Hence, adjuncts such as manual lung hy- airway resistance.26 The resultant deterioration in lung me- perinflation, chest-wall vibration, postural drainage, and chanics and gas exchange in that animal model may sup- airway suctioning could be important tools to prevent se- port the hypothesis that chest-wall vibration can mobilize cretion retention and ensure major airway patency. Newer peripheral secretions to the proximal airways.26 These ad- artificial airways, such as the “mucus slurper” and “mucus verse changes in ventilation probably occur during routine shaver,”6 combined with ventilator settings/procedures that patient care (eg, patient repositioning) but have yet to be cause an expiratory flow bias may reduce the need for studied. Adding manual lung hyperinflation, head-down conventional suctioning.5,16,27 positioning, and airway suctioning to chest-wall vibration Even though impaired mucociliary clearance may lead may be a more effective strategy to manage or prevent to pulmonary complications such as secretion retention these secretion-related adverse events. and ventilator-associated pneumonia,1,2 studies of chest physiotherapy have had mixed results,29-32 but chest phys- Mechanical Ventilator Settings iotherapy warrants further investigation.31 The current practice of manual lung hyperinflation,5 with In this issue of RESPIRATORY CARE, Volpe et al27 report a inspiratory flow of 90 L/min and expiratory flow of 196 L/ study in which they used a test-lung model connected to a min, and an inspiratory-flow-to-expiratory-flow ratio of mechanical ventilator to investigate the effects of tidal- 0.6, far exceeded the flow-magnitude threshold, expiratory ventilation airflow, airflow bias, and lung mechanics on flow bias, and minimum difference between inspiratory the movement of simulated mucus. Ventilator settings that and expiratory flow required for mucus movement during produced an expiratory flow bias moved mucus toward the tidal ventilation in test lung or animal models.3,4,27 It is ventilator, whereas settings that produced an inspiratory also conceivable that chest-wall vibration during mechan- flow bias moved mucus deeper into the lung model, away ical ventilation may move airway secretions “to and fro” from the ventilator. Thresholds for flow magnitude (min- through the alternating expiratory and inspiratory flow bias imum of 40 L/min, with a strong association between peak (negative pleural pressure on the removal of the chest flow rate and mucus movement) and phase differential compression may trigger ventilator breaths and create an would shift simulated mucus either closer to or away from inspiratory flow bias), similar to what may occur during the ventilator.27 The absolute difference between the in- closed suctioning.13 The work of Volpe et al and others spiratory flow and expiratory flow better explained the may also explain the “inexplicable” major-airway occlu- direction of mucus movement than did the ratio of expi- sion and deterioration in gas exchange and ventilation when ratory flow to inspiratory flow. Intrinsic PEEP (from in- mechanical ventilator settings favor an expiratory flow creased minute ventilation) moved mucus toward the ven- bias and the patient has highly viscous secretions, deep tilator, whereas retarding expiratory flow with an airway sedation, and/or paralysis and absent
Load more

Recommended publications
  • Ventilation Patterns Influence Airway Secretion Movement Marcia S Volpe, Alexander B Adams MPH RRT FAARC, Marcelo B P Amato MD, and John J Marini MD
    Original Contributions Ventilation Patterns Influence Airway Secretion Movement Marcia S Volpe, Alexander B Adams MPH RRT FAARC, Marcelo B P Amato MD, and John J Marini MD BACKGROUND: Retention of airway secretions is a common and serious problem in ventilated patients. Treating or avoiding secretion retention with mucus thinning, patient-positioning, airway suctioning, or chest or airway vibration or percussion may provide short-term benefit. METHODS: In a series of laboratory experiments with a test-lung system we examined the role of ventilator settings and lung-impedance on secretion retention and expulsion. Known quantities of a synthetic dye-stained mucus simulant with clinically relevant properties were injected into a transparent tube the diameter of an adult trachea and exposed to various mechanical-ventilation conditions. Mucus- simulant movement was measured with a photodensitometric technique and examined with image- analysis software. We tested 2 mucus-simulant viscosities and various peak flows, inspiratory/ expiratory flow ratios, intrinsic positive end-expiratory pressures, ventilation waveforms, and impedance values. RESULTS: Ventilator settings that produced flow bias had a major effect on mucus movement. Expiratory flow bias associated with intrinsic positive end-expiratory pressure generated by elevated minute ventilation moved mucus toward the airway opening, whereas in- trinsic positive end-expiratory pressure generated by increased airway resistance moved the mucus toward the lungs. Inter-lung transfer of mucus simulant occurred rapidly across the “carinal divider” between interconnected test lungs set to radically different compliances; the mucus moved out of the low-compliance lung and into the high-compliance lung. CONCLUSIONS: The move- ment of mucus simulant was influenced by the ventilation pattern and lung impedance.
    [Show full text]
  • COVID-19 Pneumonia: Different Respiratory Treatment for Different Phenotypes? L
    Intensive Care Medicine EDITORIAL Un-edited accepted proof COVID-19 pneumonia: different respiratory treatment for different phenotypes? L. Gattinoni1, D. Chiumello2, P. Caironi3, M. Busana1, F. Romitti1, L. Brazzi4, L. Camporota5 Affiliations: 1Department of Anesthesiology and Intensive Care, Medical University of GöttinGen 4Department of Anesthesia, Intensive Care and Emergency - 'Città della Salute e della Scienza’ Hospital - Turin 5Department of Adult Critical Care, Guy’s and St Thomas’ NHS Foundation Trust, Health Centre for Human and Applied Physiological Sciences - London Corresponding author: Luciano Gattinoni Department of Anesthesiology and Intensive Care, Medical University of Göttingen, Robert-Koch Straße 40, 37075, Göttingen, Germany Conflict of interests: The authors have no conflict of interest to disclose NOTE: This article is the pre-proof author’s accepted version. The final edited version will appear soon on the website of the journal Intensive Care Medicine with the following DOI number: DOI 10.1007/s00134-020-06033-2 1 Gattinoni L. et al. COVID-19 pneumonia: different respiratory treatment for different phenotypes? (2020) Intensive Care Medicine; DOI: 10.1007/s00134-020-06033-2 Intensive Care Medicine EDITORIAL Un-edited accepted proof The Surviving Sepsis CampaiGn panel (ahead of print, DOI: 10.1007/s00134-020-06022-5) recently recommended that “mechanically ventilated patients with COVID-19 should be managed similarly to other patients with acute respiratory failure in the ICU.” Yet, COVID-19 pneumonia [1], despite falling in most of the circumstances under the Berlin definition of ARDS [2], is a specific disease, whose distinctive features are severe hypoxemia often associated with near normal respiratory system compliance (more than 50% of the 150 patients measured by the authors and further confirmed by several colleagues in Northern Italy).
    [Show full text]
  • The Basics of Ventilator Management Overview How We Breath
    3/23/2019 The Basics of Ventilator Management What are we really trying to do here Peter Lutz, MD Pulmonary and Critical Care Medicine Pulmonary Associates, Mobile, Al Overview • Approach to the physiology of the lung and physiological goals of mechanical Ventilation • Different Modes of Mechanical Ventilation and when they are indicated • Ventilator complications • Ventilator Weaning • Some basic trouble shooting How we breath http://people.eku.edu/ritchisong/301notes6.htm 1 3/23/2019 How a Mechanical Ventilator works • The First Ventilator- the Iron Lung – Worked by creating negative atmospheric pressure around the lung, simulating the negative pressure of inspiration How a Mechanical Ventilator works • The Modern Ventilator – The invention of the demand oxygen valve for WWII pilots if the basis for the modern ventilator https://encrypted-tbn0.gstatic.com/images?q=tbn:ANd9GcRI5v-veZULMbt92bfDmUUW32SrC6ywX1vSzY1xr40aHMdsCVyg6g How a Mechanical Ventilator works • The Modern Ventilator – How it works Inspiratory Limb Flow Sensor Ventilator Pressure Sensor Expiratory Limb 2 3/23/2019 So what are the goals of Mechanical Ventilation • What are we trying to control – Oxygenation • Amount of oxygen we are getting into the blood – Ventilation • The movement of air into and out of the lungs, mainly effects the pH and level of CO 2 in the blood stream Lab Oxygenation Ventilation Pulse Ox Saturation >88-90% Arterial Blood Gas(ABG) Po 2(75-100 mmHg) pCO 2(40mmHg) pH(~7.4) Oxygenation How do we effect Oxygenation • Fraction of Inspired Oxygen (FIO 2) – Percentage of the gas mixture given to the patient that is Oxygen • Room air is 21% • On the vent ranges from 30-100% • So if the patient’s blood oxygen levels are low, we can just increase the amount of oxygen we give them 3 3/23/2019 How do we effect Oxygenation • Positive End Expiratory Pressure (PEEP) – positive pressure that will remains in the airways at the end of the respiratory cycle (end of exhalation) that is greater than the atmospheric pressure in mechanically ventilated patients.
    [Show full text]
  • Neonatal Ventilation
    Neonatal Ventilation Edward G. Shepherd History • Bourgeois, 1609: – “…give a small spoonfulof pure wine into the neonate’s mouth, …[to] help the infant to regain its spirits when being agitated by the labors, which sometimes make it so weak that it seems more dead than alive.” • Mauriceau, mid-1600’s: – “[The baby] should be rested on a warmed bed and brought near the fire, where the midwife having taken some wine into her mouth shall blow it into the infant’s mouth, which can be repeated several times if necessary … She should warm all the parts of the body to recall the blood and the spirits which retired during the weakness and endangered suffocation.” Neonatology 2008;94:144–149 History • Levret, 1766: – “There is one more means which sometimes works as by enchantment, it is to apply one’s mouth on that of the infant and to blow into it, taking care to pinch the tip of the nose simultaneously. This method is so effective that it is really rare that others are useful if it fails” Neonatology 2008;94:144–149 History • First ventilators: – Hunter, Chaussier, and Gorcy in the mid 1700’s • Bellows or gas attached to masks or tubes • 1800’s – Discovery of the breathing center – Determination of survival time in asphyxiated animals – First attempts at electrical resuscitation Neonatology 2008;94:144–149 History • By mid 1800’s ventilation fell out of favor – Fears of pnuemothorax, infection, and sudden death – Various positional techniques were developed • “Schultze swingings” • Arm extension and then chest compression – Stayed in practice
    [Show full text]
  • Respiratory Therapy Pocket Reference
    Pulmonary Physiology Volume Control Pressure Control Pressure Support Respiratory Therapy “AC” Assist Control; AC-VC, ~CMV (controlled mandatory Measure of static lung compliance. If in AC-VC, perform a.k.a. a.k.a. AC-PC; Assist Control Pressure Control; ~CMV-PC a.k.a PS (~BiPAP). Spontaneous: Pressure-present inspiratory pause (when there is no flow, there is no effect ventilation = all modes with RR and fixed Ti) PPlateau of Resistance; Pplat@Palv); or set Pause Time ~0.5s; RR, Pinsp, PEEP, FiO2, Flow Trigger, rise time, I:E (set Pocket Reference RR, Vt, PEEP, FiO2, Flow Trigger, Flow pattern, I:E (either Settings Pinsp, PEEP, FiO2, Flow Trigger, Rise time Target: < 30, Optimal: ~ 25 Settings directly or by inspiratory time Ti) Settings directly or via peak flow, Ti settings) Decreasing Ramp (potentially more physiologic) PIP: Total inspiratory work by vent; Reflects resistance & - Decreasing Ramp (potentially more physiologic) Card design by Respiratory care providers from: Square wave/constant vs Decreasing Ramp (potentially Flow Determined by: 1) PS level, 2) R, Rise Time (­ rise time ® PPeak inspiratory compliance; Normal ~20 cmH20 (@8cc/kg and adult ETT); - Peak Flow determined by 1) Pinsp level, 2) R, 3)Ti (shorter Flow more physiologic) ¯ peak flow and 3.) pt effort Resp failure 30-40 (low VT use); Concern if >40. Flow = more flow), 4) pressure rise time (¯ Rise Time ® ­ Peak v 0.9 Flow), 5) pt effort (­ effort ® ­ peak flow) Pplat-PEEP: tidal stress (lung injury & mortality risk). Target Determined by set RR, Vt, & Flow Pattern (i.e. for any set I:E Determined by patient effort & flow termination (“Esens” – PDriving peak flow, Square (¯ Ti) & Ramp (­ Ti); Normal Ti: 1-1.5s; see below “Breath Termination”) < 15 cmH2O.
    [Show full text]
  • ASV Quick Guide
    ASV Quick Guide Hamilton Medical | ASV 1 ! Warning This Quick Guide is based on evaluations by clinicians within and outside Hamilton Medical and is intended to serve as an example. This Quick Guide does not replace either the official operator’s manual of your ventilator or the clinical judgment of a physician. This Quick Guide should not - on its own - be used for clinical decision making. 2 Table of contents 1. Adaptive Support Ventilation (ASV) basics 4 2. Preparing for ventilation with ASV 6 3. Settings 8 4. ASV graph 12 5. Working principles of ASV 14 6. Monitoring ASV 16 7. Adjusting ASV 18 8. Weaning in ASV 20 Appendix 22 Lung-protective rules 22 Understanding the ASV safety box 24 Glossary 26 Hamilton Medical | ASV 3 1. Adaptive Support Ventilation (ASV) basics 1 ... 2 CO elimination ... 2 3 Oxygenation Conventional ventilation ASV 4 ASV focuses on simplification of mechanical ventilation. This means: 1 Eliminating separate modes for passive and active patients 2 Reducing controls relevant for CO2 elimination to just %MinVol 3 Adding direct access to controls relevant for oxygenation (PEEP/CPAP and Oxygen) ASV maintains an operator-preset minimum minute volume independent of the patient‘s activity. The breathing pattern (tidal volume, rate, and inspiratory time) is calculated, based on the assump- tion that the optimal breathing pattern results in: a The least work of breathing b The least amount of ventilator-applied inspiratory pressure A lung-protection strategy ensures ASV’s safety. ASV attempts to guide the patient using a favorable breathing pattern and avoids potentially detrimental patterns such as rapid shallow breathing, excessive dead space ventilation, intrinsic PEEP, barotrauma, and volutrauma.
    [Show full text]
  • 1. Ventilator Management
    1. Ventilator Management Indications for Mechanical Ventilation Apnea Ventilatory insufficiency Increase in PaCo2 and decrease in ph Refractory hypoxemia Complications Associated with Mechanical Ventilation Hypotension Increased intrathoracic pressure decreases venous return to the heart Increased risk of ventilator associated pneumonia (VAP) Keep HOB at > 30 Maintain frequent, good oral care Problems with endotracheal tube Mucous plugging Tube my become dislodged Kinking or biting of tube Cuff rupture Pneumothorax Initial Ventilator Settings—parameters to be clarified Type of ventilation Mode of ventilation Tidal volume or peak inspiratory setting Respiratory rate FiO2 PEEP (Positive End Expiratory Pressure) Types of Ventilation Volume Cycled Ventilation(VCV) A pre-selected tidal volume is delivered at the pressure required. Tidal volume guaranteed. Peak inspiratory pressure will vary depending on airway resistance and lung compliance. Pressure Control Time-Cycled Ventilation (PCV) Operator selects inspiratory pressure and inspiratory time Breath is terminated when inspiratory time is reached Inspiratory pressure is guaranteed; tidal volume is dependant on airway resistance and lung compliance Pressure Support (PSV) Requires intact respiratory drive Operator selects inspiratory pressure Patient initiates breath, pressure quickly rises to set pressure and is maintained throughout the inspiratory phase Tidal volume determined by lung compliance and inspiratory effort Modes of Ventilation Assist/Control
    [Show full text]
  • Mechanical Ventilation
    Fundamentals of MMeecchhaanniiccaall VVeennttiillaattiioonn A short course on the theory and application of mechanical ventilators Robert L. Chatburn, BS, RRT-NPS, FAARC Director Respiratory Care Department University Hospitals of Cleveland Associate Professor Department of Pediatrics Case Western Reserve University Cleveland, Ohio Mandu Press Ltd. Cleveland Heights, Ohio Published by: Mandu Press Ltd. PO Box 18284 Cleveland Heights, OH 44118-0284 All rights reserved. This book, or any parts thereof, may not be used or reproduced by any means, electronic or mechanical, including photocopying, recording or by any information storage and retrieval system, without written permission from the publisher, except for the inclusion of brief quotations in a review. First Edition Copyright 2003 by Robert L. Chatburn Library of Congress Control Number: 2003103281 ISBN, printed edition: 0-9729438-2-X ISBN, PDF edition: 0-9729438-3-8 First printing: 2003 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the author and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, express or implied, with respect to the contents of the publication. Table of Contents 1. INTRODUCTION TO VENTILATION..............................1 Self Assessment Questions.......................................................... 4 Definitions................................................................................
    [Show full text]
  • The Pathophysiology of 'Happy' Hypoxemia in COVID-19
    Dhont et al. Respiratory Research (2020) 21:198 https://doi.org/10.1186/s12931-020-01462-5 REVIEW Open Access The pathophysiology of ‘happy’ hypoxemia in COVID-19 Sebastiaan Dhont1* , Eric Derom1,2, Eva Van Braeckel1,2, Pieter Depuydt1,3 and Bart N. Lambrecht1,2,4 Abstract The novel coronavirus disease 2019 (COVID-19) pandemic is a global crisis, challenging healthcare systems worldwide. Many patients present with a remarkable disconnect in rest between profound hypoxemia yet without proportional signs of respiratory distress (i.e. happy hypoxemia) and rapid deterioration can occur. This particular clinical presentation in COVID-19 patients contrasts with the experience of physicians usually treating critically ill patients in respiratory failure and ensuring timely referral to the intensive care unit can, therefore, be challenging. A thorough understanding of the pathophysiological determinants of respiratory drive and hypoxemia may promote a more complete comprehension of a patient’sclinical presentation and management. Preserved oxygen saturation despite low partial pressure of oxygen in arterial blood samples occur, due to leftward shift of the oxyhemoglobin dissociation curve induced by hypoxemia-driven hyperventilation as well as possible direct viral interactions with hemoglobin. Ventilation-perfusion mismatch, ranging from shunts to alveolar dead space ventilation, is the central hallmark and offers various therapeutic targets. Keywords: COVID-19, SARS-CoV-2, Respiratory failure, Hypoxemia, Dyspnea, Gas exchange Take home message COVID-19, little is known about its impact on lung This review describes the pathophysiological abnormal- pathophysiology. COVID-19 has a wide spectrum of ities in COVID-19 that might explain the disconnect be- clinical severity, data classifies cases as mild (81%), se- tween the severity of hypoxemia and the relatively mild vere (14%), or critical (5%) [1–3].
    [Show full text]
  • The Roles of Bronchodilators, Supplemental Oxygen, and Ventilatory Assistance in the Pulmonary Rehabilitation of Patients with Chronic Obstructive Pulmonary Disease
    The Roles of Bronchodilators, Supplemental Oxygen, and Ventilatory Assistance in the Pulmonary Rehabilitation of Patients With Chronic Obstructive Pulmonary Disease Richard L ZuWallack MD Introduction What Pulmonary Rehabilitation Does and How It Works Enhancing the Effectiveness of Pulmonary Rehabilitation Exercise Training Bronchodilators Supplemental Oxygen Noninvasive Ventilation Summary In patients with chronic obstructive pulmonary disease, pulmonary rehabilitation significantly improves dyspnea, exercise capacity, quality of life, and health-resource utilization. These benefits result from a combination of education (especially in the promotion of collaborative self-management strategies and physical activity), exercise training, and psychosocial support. Exercise training increases exercise ca- pacity and reduces dyspnea. Positive outcomes from exercise training may be enhanced by 3 interven- tions that permit the patient to exercise train at a higher intensity: bronchodilators, supplemental oxygen (even for the nonhypoxemic patient), and noninvasive ventilatory support. Key words: broncho- dilators, oxygen, mechanical ventilation, pulmonary rehabilitation, chronic obstructive pulmonary disease, COPD, dyspnea, exercise capacity, quality of life, exercise training, exercise capacity, noninvasive ventilation. [Respir Care 2008;53(9):1190–1195. © 2008 Daedalus Enterprises] Introduction bilitation as “an evidence-based, multidisciplinary, and com- prehensive intervention for patients with chronic respiratory A recent statement from
    [Show full text]
  • Aerosol Kinetics and Bronchodilator Efficacy During Continuous Positive Airway Pressure Delivered by Face Mask
    Thorax 1997;52:171±175 171 Thorax: first published as 10.1136/thx.52.2.171 on 1 February 1997. Downloaded from Aerosol kinetics and bronchodilator eYcacy during continuous positive airway pressure delivered by face mask Scott N Parkes, Andrew D Bersten Abstract hastened recovery and prevented the need for Background ± Rates of fresh gas ¯ow intubation and mechanical ventilation.1 In a (FGF) commonly used when continuous group of patients with dynamic hyperin¯ation positive airway pressure (CPAP) is de- and intrinsic positive end expiratory pressure livered by face mask theoretically reduce (PEEP) Petrof and co-workers2 found that the the delivery and availability of therapeutic application of CPAP to intubated patients sig- aerosols. As it may be hazardous for ni®cantly reduced respiratory work. It seems patients with acute respiratory failure to likely that non-invasive CPAP will produce a interrupt mask CPAP, the eVects of CPAP similar bene®t in patients with acute severe on aerosol kinetics and bronchodilator asthma or acute exacerbations of chronic air- eYcacy were investigated. ¯ow obstruction. However, therapeutic aero- Method ± The eVect of CPAP at 10 cm H2O sols are central to the management of these at a FGF rate of 50 l/min on the delivery patients, and the concurrent administration of of technetium labelled aerosol generated CPAP may interfere with drug delivery to the from a readily available jet nebuliser was distal airway. measured using a bench model of spon- Mask CPAP is optimally applied through a taneous respiration. In a separate clinical continuous fresh gas ¯ow (FGF) circuit as this study the bronchodilator responses to in- imposes less additional work than a demand cremental doses of nebulised salbutamol valve system34 and compensates more eY- were measured in nine stable asthmatic ciently for potential gas leaks around the mask.
    [Show full text]
  • Regulation of Ventilation
    CHAPTER 1 Regulation of Ventilation © IT Stock/Polka Dot/ inkstock Chapter Objectives By studying this chapter, you should be able to do 5. Describe the chemoreceptor input to the brain the following: stem and how it modifi es the rate and depth of breathing. 1. Describe the brain stem structures that regulate 6. Explain why it is that the arterial gases and pH respiration. do not signifi cantly change during moderate 2. Defi ne central and peripheral chemoreceptors. exercise. 3. Explain what eff ect a decrease in blood pH or 7. Discuss the respiratory muscles at rest and carbon dioxide has on respiratory rate. during exercise. How are they infl uenced by 4. Describe the Hering–Breuer reflex and its endurance training? function. 8. Describe respiratory adaptations that occur in response to athletic training. Chapter Outline Passive and Active Expiration Eff ects of Blood PCO 2 and pH on Ventilation Respiratory Areas in the Brain Stem Proprioceptive Refl exes Dorsal Respiratory Group Other Factors Ventral Respiratory Group Hering–Breuer Refl ex Apneustic Center Ventilation Response During Exercise Pneumotaxic Center Ventilation Equivalent for Oxygen () V/EOV 2 Chemoreceptors Ventilation Equivalent for Carbon Dioxide Central Chemoreceptors ()V/ECV O2 Peripheral Chemoreceptors Ventilation Limitations to Exercise Eff ects of Blood PO 2 on Ventilation Energy Cost of Breathing Ventilation Control During Exercise Chemical Factors Copyright ©2014 Jones & Bartlett Learning, LLC, an Ascend Learning Company Content not final. Not for sale or distribution. 17097_CH01_Pass4.indd 3 10/12/12 2:13 PM 4 Chapter 1 Regulation of Ventilation Passive and Active Expiration Ventilation is controlled by a complex cyclic neural process within the respiratory Brain stem Th e lower part centers located in the medulla oblongata of the brain stem .
    [Show full text]