Copd And The Gold Guidelines 02 21 2005[2]
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Transcript of Copd And The Gold Guidelines 02 21 2005[2]
COPD and the GOLD Guidelines
Fiona R. Prabhu, MD
Assistant Professor, Family & Community Medicine
February 21, 2005
Prevalence
12.1 million adults aged 25 and over were diagnosed with COPD in 2001
24 million adults have evidence of impaired lung function → underdiagnosis
Mortality
4th leading cause of death in the United States currently
Projected to be the 3rd leading cause of death for both males and females by 2020
119,000 adults age 25 and over died from COPD in 2000
Costs
1.5 million emergency room visits in 2000 726,000 hospitalizations in 2000 Total estimated cost of COPD in 2002 was
$32.1 billion $18 billion in direct costs $14.1 billion in indirect costs
Definition
Airflow limitation that is NOT fully reversible Progressive Associated with an abnormal inflammatory
response of the lungs to noxious particles or gases
Pathogenesis
Three processes: Chronic inflammation Imbalance of proteinases and anti-proteinases Oxidative stress
Chronic Inflammation
Chronic inflammation in airways, parenchyma, pulmonary vasculature
Inflammatory cells involved are: Macrophages
leukotriene B4 T-lymphocytes (CD8) interleukin 8 Neutrophils TNF-α
Pathology
Central Airways: Enlarged mucus secreting
glands Increase in goblet cells
Mucus hypersecretion Peripheral Airways
Repeated cycles of injury and repair
Increased collagen/scarring in airway wall
Pathology
Pulmonary vascular changes
Thickening of vessel wall (intima)
Increase in smooth muscle
Infiltration of vessel wall by inflammatory cells As COPD worsens, more smooth muscle, proteoglycans and
collagen further thicken the vessel wall
Pathophysiology
Mucus hypersecretion
Ciliary dysfunction
Airflow limitation
Pulmonary hyperinflation
Gas exchange abnormalities
Pulmonary hypertension
Cor pulmonale
Mucus hyperserection & ciliary dysfunction → cough, sputum production
Diagnosis of COPD
History of Present Illness
Chronic Cough Intermittently or every day Present throughout the day;
seldom only nocturnal Chronic sputum production
Any pattern Repeated episodes of acute
bronchitis
Chronic cough and sputum production often precede development of airflow limitation by many years
Not all patients with these symptoms develop COPD
Dyspnea on exertion Progressive Persistent Worse with exercise Worse during respiratory
infections History of exposure to risk
factors Tobacco smoke Occupational dusts and
chemicals Smoke from home cooking and
heating fuels
Medical History
Exposure to risk factors, incl. intensity/duration
History of exacerbations or previous hospitalizations for respiratory disorder
Past medical history Asthma, allergies, sinusitis/nasal
polyps, respiratory infections in childhood
Presence of co-morbid conditions Heart disease Rheumatic disease
Family History COPD Other chronic respiratory diseases
Social History Impact of disease on patient’s life,
inc. activity, missed work and economic impact
Effect on family routines Depression/anxiety Social and family support available
to the patient Other:
Appropriateness of current medical treatments
Possibilities for reducing risk factors, esp. smoking cessation
Risk Factors
Tobacco Smoke Cigarettes, Pipes, cigars – lower rates than
cigarette smokers but higher than non-smokers
Occupational dusts and chemicals
Vapors, irritants, fumes Need sufficiently intense or
prolonged exposure Indoor air pollution
Biomass fuel used for cooking and heating in poorly vented dwellings
Outdoor air pollution Minor risk factor Passive
cigarette smoke exposure Respiratory infections in early
childhood Lower socioeconomic status
association with COPD May be secondary to crowding,
poor nutrition, etc.
Physical Examination
Thorax: Barrel chest
Lungs Decreased breath sounds Wheezing
Cardiac Right-sided heart failure
Edema, tender liver, distended abdomen
Physical signs are rarely apparent until significant impairment of lung
function has occurred
Diagnostic Tests
Chest X-ray Flattened diaphragms Use to exclude other diagnoses
High resolution CT Not routinely recommended If in doubt about diagnosis of
COPD If considering bullectomy or lung
volume reduction surgery CBC
May see increased hemoglobin/hematocrit secondary to hemoconcentration
ABG Spirometry
Spirometry
Measure of FVC and FEV1 FVC = forced vital capacity
Maximum volume of air forcibly exhaled from the point of maximal inhalation
FEV1 = forced expiratory volume in 1 second Volume of air exhaled in the 1st second of the FVC maneuver
Calculate the FVC/FEV1 ratio Normal ratio = 70/80% COPD ratio = <70% pre-bronchodilator FVC & FEV are COPD ratio = <80% post-bronchodilator both decreased
Essential to making the diagnosis of COPD
Spirometry
Best performed with the patient seated Optimal results:
Patient breathes in fully Patient must seal their lips around the mouthpiece Have the patient force the air out of their chest as hard and fast as
they can until their lungs are completely “empty” Exhalation must be at least 6 seconds and can take up to 15 seconds
Breathe in again and relax Need 3 technically satisfactory curves
Vary no more than 5% (or 100 mL) Ratio is calculated from the maximum FVC and FEV1 from any of
these curves.
Spirometry
Bronchodilator Reversibility Testing Perform in the initial assessment of COPD in
order to:Exclude asthmaEstablish best attainable lung functionGauge patient prognosisGuide treatment decisions
Arterial Blood Gas (ABG)
Obtain in patients with FEV1 < 40% predicted OR Clinical signs of respiratory or right heart failure
Central cyanosis, ankle swelling, increase in jugular venous pressure (JVP) OR
Respiratory Failure: PaO2 < 60 mm Hg with or without PaCO2 > 45 mm Hg
while breathing air at sea level Technique:
Obtain by arterial puncture; DO NOT USE finger or ear oximeters
Other Tests
Alpha-1 antitrypsin Consider in patients with COPD < age 45 Strong family hx of early COPD or with alpha-1
antitrypsin deficiency
Differential Diagnosis of COPD
Asthma Reversible airflow limitation Early onset (childhood) Symptoms vary day to day
Congestive heart failure Volume restriction, NOT airflow
limitation CXR with dilated heart, pulmonary
edema Bronchiectasis
Large volumes of purulent sputum Commonly associated with bacterial
infection Bronchial dilation and bronchial
wall thickening on CXR or CT
Tuberculosis Onset at all ages Chest x-ray with infiltrate or
nodular lesions Obliterative bronchiolitis
Younger patients/non-smokers May have a hx of rheumatoid
arthritis or fume exposure CT shows hypodense areas with
expiration Diffuse panbronchiolitis
Male/non-smokers Chronic sinusitis CXR and high resolution CT show
diffuse small centrilobular nodular opacities and hyperinflation
COPD Management Program
GOLD (Global Initiative for Chronic Obstructive Lung Disease)
Guidelines
Goals
Prevent disease progression Relieve symptoms Improve exercise tolerance Improve health status Prevent and treat complications Prevent and treat exacerbations Reduce mortality Prevent or minimize side effects from treatment Cessation of cigarette smoking
Components
Assess and monitor disease Reduce risk factors Manage stable COPD Manage acute exacerbations
Assess and Monitor Disease
Initial Visit
Pattern of symptom development Exposure to risk factors History of exacerbations or previous hospitalizations for respiratory
disorder Past medical history Family history Social history
Impact of disease on patient’s life Effect on family routines Feelings of depression or anxiety Social and family support available to the patient
Possibilities for reducing risk factors, especially smoking cessation
Testing
Spirometry Initially and yearly
ABG Obtain if FEV1 < 40% predicted OR Clinical signs of respiratory or right heart failure Respiratory Failure
Alpha-1 antitrypsin If patient <45 years old or strong family history of COPD
Follow-Up Visits
Discuss new or worsening symptoms Perform spirometry if there is a substantial increase in symptoms
OR if a complication occurs ABG
Patients with an FEV1 <40% predicted Early signs of respiratory failure or CHF
Monitor pharmacotherapy Dosages Adherence Inhaler technique Effectiveness of current regimen at controlling symptoms Side effects of treatment
Follow-up Visits
Monitor co-morbid conditions Bronchial carcinoma Tuberculosis Sleep apnea Left heart failure
Obtain appropriate information through CXR, ECG whenever symptoms suggest one of these conditions
Reduce Risk Factors
Risk Factors
Tobacco smoke Occupational dusts and chemicals Indoor and outdoor air pollutants
Smoking Cessation
The single MOST effective and cost-effective intervention to reduce the risk of developing COPD and to stop its progression
Brief tobacco dependence treatment is effective Offer this at EVERY visit to the health care provider
Brief 3 minute period of counseling Three types of counseling are esp. effective:
Practical counseling Social support as part of the treatment Social support arranged outside of the treatment
Several effective medications are available and at least one of these medications should be added to counseling if necessary and if there are no contraindications
Nicotine gum, inhaler, nasal spray, trasndermal patch, sublingual tablet, lozenges Bupropion nortriptyline
Treating Tobacco Use and Dependence. Quick Reference Guide for Clinicians.
Smoking Cessation Strategy
Ask Systematically identify all tobacco users at every visit
Advise Strongly urge all tobacco users to quit, in a clear, strong, and personalized manner
Assess Determine willingness to make a quit attempt.
e.g. within the next 3 days, how willing is this person to make a quit attempt
Assist Aid the patient in quitting
e.g. quit plan, counseling, intra-treatment social support, extra-treatment social support, approved pharmacotherapy, supplementary materials
Arrange Schedule a follow-up contact, either in person or via telephone
Treating Tobacco Use and Dependence. Quick Reference Guide for Clinicians.
Smoking Prevention – What you can do as a provider:
Encourage comprehensive tobacco-control policies and programs
Work with government officials to pass legislation to establish smoke-free schools, public facilities, and work environments
Encourage patients to keep smoke-free homes
Treating Tobacco Use and Dependence. Quick Reference Guide for Clinicians.
Occupational Exposures
Primary prevention Eliminate or reduce exposures to various
substances in the workplace
Secondary prevention Surveillance and early detection
Indoor and Outdoor Air Pollution
Implement measures to reduce or avoid indoor air pollution from biomass fuel burned for cooking and heating in poorly ventilated dwellings
Advise patients to monitor public announcements of air quality
Avoid vigorous exercise outdoors or stay indoors during pollution episodes, depending on COPD severity
Manage Stable COPD
General Principles
Determine disease severity Implement step-wise
treatment plan Educate the patient
Improve skills Improve ability to cope with
illness Improve health status
Prescribe Treatment Pharmacologic Non-pharmacologic
Rehabilitation Exercise training Nutrition counseling education Oxygen therapy
Surgical interventions
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Stage Characteristics
0:
At Risk
Normal spirometry
Chronic symptoms (cough, sputum)
I:
Mild
FEV1/FVC < 70%
FEV1 >= 80% predicted
Usu. Chronic cough and sputum production
II: Moderate 50% <= FEV1 < 80% predicted
Progression of symptoms; dyspnea on exertion
III:
Severe
30%<= FEV1 < 50% predicted
↑ dyspnea; repeated exacerbations which have an impact on patients’ quality of life
IV
Very severe
FEV1< 30% predicted OR
FEV1<50% predicted + chronic respiratory failureQuality of life is appreciably impairedExacerbations may be life-threatening
COPD Severity
Patient Education
Smoking cessation Basic information about COPD and pathophysiology of the
disease General approach to therapy and specific aspects of medical
treatment Self-management skills Strategies to help minimize dyspnea Advice about when to seek help Self-management and decision-making in exacerbations Advance directives and end-of-life issues
Medications
Goals Prevent and control symptoms Reduce frequency and severity of exacerbations Improve health status Improve exercise tolerance
No existing medications can modify the long-term decline in lung function
Reduction of therapy once symptom control occurs is not normally possible
COPD is progressive and over time will require progressive introduction of more treatments to attempt to limit the impact of these changes
Bronchodilators
Central to symptom management Used in all stages of COPD severity
Inhaled forms are preferred Can be prescribed as needed OR regularly to prevent or reduce
symptoms Long-acting inhaled bronchodilators are more effective and convenient
(but are more expensive) Combining drugs with different mechanisms and durations of action
may increase the degree of bronchodilation for equivalent or lesser side effects
All categories of bronchodilators have been show to increase exercise capacity without necessarily producing significant changes in FEV1
Bronchodilators
Beta2-agonists Short-acting: albuterol Long-acting: salmeterol (Serevent™), formoterol (Foradil™)
Anticholinergics Short acting: ipratropium bromide (Atrovent™) Long acting: tiotropium bromide (Spiriva™)
Methylxanthines (Theophylline™) Combination bronchodilators
Fenoterol/ipratropium (Duovent™) Salbutamol/ipratropium (Combivent™)
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Glucocorticosteroids
Use if FEV1 < 50% predicted and repeated exacerbations, e.g. three in the last three years
Severe COPD and Very Severe COPD Does not modify the long-term decline in FEV1 BUT does reduce the
frequency of excacerbations and improves health status The combination of a long-acting beta2-agonist and an inhaled
glucocorticosteroid is more effective than the individual components Long-term treatment with oral glucocorticoids is NOT recommended Glucocorticosteroid (inhaled) reversibility testing
Treatment trial of inhaled glucocorticosteroids for 6 to 12 weeks then repeat spirometry with and without bronchodilators
Patients most likely to respond to inhaled steroids have an FEV1 increase of 200 mL and 15% above baseline post-bronchodilator
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Inhaled Glucocorticoids
Beclomethasone (Vanceril™) Budesonide (Pulmicort™) Fluticasone (Flovent™) Triamcinolone (Azmacort™)
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Immunizations
Vaccines Influenza yearly
Reduces serious illness and death in COPD patients by approximately 50%
Give once yearly: autumn OR twice yearly: autumn and winter
Pneumovax Sufficient data to support its general use in COPD is
lacking, but it is commonly used
Other Medications?
Alpha-1 Antitrypsin Augmentation Therapy Only if this deficiency is present in an individual should they undergo
treatment Antibiotics
Prophylactic use is NOT recommended Can be used in the treatment of infectious exacerbations of COPD
Mucolytic agents Overall benefits are small, so currently not recommended for widespread
use Types:
Ambroxol Erdosteine (Erdostin, Mucotec) Carbocysteine (Mucodyne) Iodinated gylerol (Expigen)
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Other Medications?
Antioxidant agents N-acetylcysteine (Bronkyl, Fluimucil, Mucomyst) Have been shown to reduce the frequency of exacerbations and could have a role in
the treatment of patients with recurrent exacerbations More studies are needed
Immunoregulators Not recommended at this time No reproducible studies are available
Antitussives Regular use is contraindicated in stable COPD since cough has a significant protective
role Vasodilators
Inhaled nitric oxide Can worsen gas exchange because of altered hypoxic regulation of ventilation-perfusion
balance and is contraindicated in stable COPD
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Other Medications?
Respiratory stimulants Doxapram (IV) Almitrine bismesylate
Not recommended in stable COPD Narcotics
Oral and parenteral opioids are effective for treating dyspnea in patients with advanced COPD
Use this with caution; benefits may be limited to a few sensitive subjects nebulized opioids: insufficient evidence re: efficacy
Miscellaenous: Nedocromil Leukotriene modifiers Alternative healing methods
None have been adequately studied in COPD patients at this time
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Stage 0: At Risk
Avoid risk factors Offer influenza vaccination
Stage I: Mild COPD
Avoid risk factors Offer vaccination Use short-acting
bronchodilators as needed
I:
Mild
FEV1/FVC < 70%
FEV1 >= 80% predicted
Usu. Chronic cough and sputum production
Stage II: Moderate COPD
Avoid risk factors Offer influenza vaccine Add short-acting
bronchodilators when needed
Add regular treatment with 1 or more long-acting bronchodilators
Add rehabilitation
II: Moderate
50% <= FEV1 < 80% predicted
Progression of symptoms; dyspnea on exertion
Stage III: Severe COPD
Avoid risk factors Offer influenza vaccine Add short-acting
bronchodilators when needed Add regular treatment with 1 or
more long-acting bronchodilators
Add rehabilitation Add inhaled glucocorticoids if
repeated exacerbations
III:
Severe
30%<= FEV1 < 50% predicted
↑ dyspnea; repeated exacerbations which have an impact on patients’ quality of life
Stage IV: Very Severe COPD
Avoid risk factors Offer influenza vaccination Add short-acting
bronchodilators as needed Add rehabilitation Add inhaled glucocorticoids if
repeated exacerbations Add long-term oxygen if chronic
respiratory failure Consider surgical treatments
IV
Very severe
FEV1< 30% predicted OR
FEV1<50% predicted + chronic respiratory failureQuality of life is appreciably impairedExacerbations may be life-threatening
Non-Pharmacologic Therapy
Rehabilitation
COPD patients at all stages of severity benefit from exercise training programs Improves both exercise tolerance and symptoms of dyspnea and fatigue
Goals Reduce symptoms Improve quality of life Increase physical and emotional participation in everyday activities
Comprehensive program should include several types of health professionals: Exercise training Nutrition counseling Education
Minimum effective length of time = 2 months Setting: inpatient OR outpatient OR home Baseline and outcome assessments of each participant should be made to quantify
individual gains and target areas for improvement Measurement of spirometry before and after a bronchodilator drug Assessment of exercise capacity Assessment of inspiratory and expiratory muscle strength and lower limb strength
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Oxygen Therapy
Stage IV - Severe COPD PaO2 at or below 55 mm Hg or SaO2 at or below 88% with or without
hypercapnia OR PaO2 between 55-60 mm Hg or SaO2 89% IF pulmonary hypertension,
peripheral edema suggesting congestive heart failure, or polycythemia (Hct > 55%)
Based on awake PaO2 values GOAL
Increase baseline PaO2 to at least 60 mm Hg at sea level and rest and/or produce SaO2 at least 89%
Need to use at least 15 hours per day in patients with chronic respiratory failure to improve survival
Can have a beneficial impact on hemodynamics, hematologic characteristics, exercise capacity, lung mechanics and mental state
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Surgical Treatment
Bullectomy Effective in reducing dyspnea and improving lung function in
appropriately selected patient Lung volume reduction surgery
Parts of the lung are resected to reduce hyperinflation Does not improve life expectancy Does improve exercise capacity in patients with predominantly
upper lobe emphysema and a low post-rehabilitation exercise capacity
May improve global health status in patients with heterogeneous emphysema
High hospital costs; still experimental/palliative
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Surgical Treatment
Lung transplantation Improves quality of life and functional capacity
in appropriately selected patient Criteria for referral:
FEV1 < 35% predicted all fourPaO2 < 55-60 mm Hg criteria
PaCO2 > 50 mm Hg must beSecondary pulmonary hypertension present
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
COPD Patients and Surgery
Increased risk of post-operative pulmonary complications
Risk of complications increases as the incision approaches the diaphragm
Epidural and spinal anesthesia have a lower risk than general anesthesia
Postpone surgery if the patient has a COPD exacerbation
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Manage Exacerbations
General Points
Most common causes of exacerbations are: Infection of the tracheobronchial tree Air pollution In 1/3 of severe exacerbations a cause cannot be identified
Inhaled bronchodilators, theophylline, and systemic (preferably oral) glucocorticosteroids are effective treatments
Patients with clinical signs of airway infection may benefit from antibiotic treatment Increased volume of sputum Change in color of sputum Fever
Non-invasive intermittent positive pressure ventilation (NIPPV) in exacerbations is helpful:
Improves blood gases and pH Reduces in-hospital mortality Decreases the need for invasive mechanical ventilation and intubation Decreases the length of hospital stay
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Diagnosis and Assessment of Severity
History Increased breathlessness Chest tightness Increased cough and sputum Change of color and/or tenacity of
sputum Fever Non-specific:
Malaise, insomnia, sleepiness, fatigue, depression, or confusion
Assessment of Severity
Lung Function Tests PEF < 100 L/min. or FEV1 < 1
L = severe exacerbation Arterial Blood Gas
PaO2 < 60 mmHg and/or SaO2 < 90% with or without PaCO2 < 50 mmHg when breathing room air = respiratory failure
PaO2 < 50 mmHg, PaCO2 < 70 mmHg and ph < 7.3 = life-threatening episode
Chest x-ray Look for complications
Pneumonia Alternative diagnoses
ECG Right ventricular hypertrophy Arrhythmias Ischemia
Sputum Culture/sensitivity
Comprehensive Metabolic Profile
Assess for electrolyte disturbances, diabetes
Albumin to assess nutrition
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Home? Hospital admission?
Floor? ICU?
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Indications for Hospital Admission
Marked increase in intensity of symptoms such as sudden development of resting dyspnea
Severe background COPD Onset of new physical signs
Cyanosis, peripheral edema Failure of exacerbation to respond to initial medical management Significant co-morbidities Newly occurring arrhythmias Diagnostic uncertainty Older age Insufficient home support
Indications for ICU Admission
Severe dyspnea that responds inadequately to initial emergency therapy
Confusion, lethargy, coma Persistent or worsening hypoxemia (PaO2 < 50 mm Hg)
and/or Severe/worsening hypercapnia (PaCO2 > 70 mm Hg) and/or Severe/worsening respiratory acidosis (pH < 7.30) despite
supplemental oxygen and NIPPV
NIPPV = non-invasive positive pressure ventilation
Management of Exacerbations
Risk of dying from an exacerbation is closely related to: Development of respiratory acidosis Presence of significant co-morbidities Need for ventilatory support
Severe Exacerbation, Non Life Threatening
Assess severity of symptoms Obtain arterial blood gas and chest x-ray Administer controlled oxygen therapy
Repeat ABG after 30 minutes Bronchodilators Glucocorticosteroids Consider antibiotics Consider non-invasive mechanical ventilation Monitor fluid balance and nutrition Consider subcutaneous heparin therapy Identify and treat associated conditions (CHF, arrhythmias)
Management of COPD Exacerbations
Controlled oxygen therapy Administer enough to maintain PaO2 > 60 mmHG or
SaO2 > 90% Monitor patient closely for CO2 retention or acidosis
Bronchodilators (inhaled) Increase doses or frequency Combine ß2 agonists and anticholinergics Use spacers or air-driven nebulizers Consider adding IV methylxanthine (aminophylline) if
needed
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Management of COPD Exacerbations
Glucocorticosteroids (oral or IV) Recommended as an addition to bronchodilator therapy If baseline FEV1 < 50% predicted
30-40 mg oral prednisolone x 10 days OR nebulized budesonide (Pulmicort™)
Antibiotics IF breathlessness and cough are increased AND sputum is purulent
and increased in volume Choice of antibiotics should reflect local antibiotic sensitivity for the
following microbes: S. pneumoniae H. influenzae M. catarrhalis
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Management of COPD Exacerbations
Manual or mechanical chest percussion and postural drainage may be beneficial in patients producing > 25 mL sputum per day OR with lobar atelectasis.
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
Management of COPD Exacerbations
Ventilatory Support Decrease mortality and morbidity Relieve symptoms Used most commonly in Stage IV, Very Severe COPD Forms:
Non-invasive using negative or positive pressure devices invasive/mechanical with oro- or naso-tracheal tube OR
tracheostomy
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention
NIPPV
Success rates of 80-85% Increases pH, reduces PaCO2, reduces
severity of breathlessness in the first 4 hours of treatment
Decreases length of hospital stay Decreases mortality/intubation rate
NIPPV (C-PAP, Bi-PAP)
Selection criteria Moderate to severe dyspnea with use of
accessory muscles and paradoxical abdominal motion
Moderate to severe acidosis (pH < 7.35) and hypercapnia (PaCO2 > 45 mmHg)
Respiratory frequency > 25 breaths/minute
NIPPV
Exclusion criteria Respiratory arrest Cardiovascular instability
Hypotension Arrhythmias Myocardial infarction
Somnolence, impaired mental status, lack of cooperation High aspiration risk – viscous/copius secretions Recent facial or gastroesophageal surgery Cranio-facial trauma, fixed nasopharyngeal abnormalities Extreme obesity
Indications for Invasive Mechanical Ventilation
Severe dyspnea with use of accessory muscles and paradoxical abdominal motion
Respiratory rate > 35 breaths/minute Life-threatening hypoxemia: PaO2 < 40 mm Hg Severe acidosis (pH < 7.25) and hypercapnia (PaCO2 > 60 mm Hg) Respiratory arrest Somnolence, impaired mental status Cardiovascular complications
Hypotension/shock/heart failure Other complications
Metabolic abnormalities/sepsis/pneumonia/pulmonary embolism/barotrauma/massive pleural effusion
NIPPV failure
Use of Invasive Ventilation in End-Stage COPD
Hazards: Ventilator-acquired pneumonia
Increased prevalence of multi-resistant organisms Barotrauma Failure to wean to spontaneous ventilation
Mortality among COPD patients with respiratory failure is no greater than mortality among patients ventilated for non-COPD reasons
Weaning from Ventilator
Methods still debated Whatever clinical protocol is adopted, weaning is
shorted as long as a protocol is used! NIPPV used during the weaning process has
shortened weaning time, reduced stay in the ICU, decreased the incidence of nosocomial pneumonia, and improved 60-day survival rates
Discharge Criteria
Inhaled Beta2-agonist use is at most every 4 hours Patient is able to walk across the room Patient is able to eat and sleep without frequent awakening Patient has been clinically stable for 12-24 hours ABGs are stable for 12-24 hours Patient/home caregiver fully understands correct use of
medications Follow-up and home care arrangements have been
completed Patient, family, and physician are confident that patient can
manage successfully
Follow-Up Assessment after Hospital Discharge
4-6 weeks after discharge Assess:
Ability to cope in usual environment Inhaler technique Understanding of recommended treatment regimen
Measure FEV1 Determine need for long-term oxygen therapy and/or home
nebulizer (for patients with very severe COPD, Stage IV)
Follow-up after this is the same as for Stable COPD monitoring
REFERENCES
National Heart, Lung, and Blood Institute Data Fact Sheet for Chronic Obstructive Pulmonary Disease
GOLD (Global Initiative for Chronic Obstructive Lung Disease) Executive Summary, April 2001
GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention. A Guide for Health Care Professionals. Updated July 2005. www.goldcopd.org – Accessed August 21, 2006.
Fiore MC, Bailey WC, Cohen SJ, et. al. Treating Tobacco Use and Dependence. Quick Reference Guide for Clinicians. Rockville, MD: U.S. Department of Health and Human Services. Public Health Service. October 2000.