COPD Guiedline

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ERS-ATS COPD Guidelines

ERS-ATS COPDGuidelines

Copyright European Respiratory Society 2005

These slides can be used freely

for non-commercial purposes.


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Document authors

B.R. C lli W. M N

A.Anzuet A.Agusti .Austergaard W. Bailey

C. B lliger B. Berg A.S. Buist N.H. C avannes

R. Carter P. Calverley T. Dillard E.W.Ely

B. Fahy M.Estenne A. Fein M. Fi reN. Gross R. Gross an J.Heffner L.Hoffman

J.C.Hogg R.M. Kotloff S.C.Lareau N.M.Lazar

J.Lynn W.McNicholas F.J.Martinez P.M.Meek

M.Myramoto J.W.M.Muris J.B. Orens R.Pauw els

J.J. Reilly S. Rennard R. Rodriguez-Roisin A. Rossi

A.M.W.J.Schols L.Sicilian N.Siafakas G.L.Snider

B.L.Tiep J.van Noord J. Vestbo W.Weder

I.M.Weisman M.E.Wew ers E.F.M.Wouters R.D. Yusen

J. Zielinski R. ZuWallack


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Document Goals and O jectives (1)

The Standards for the Diagnosis and Treatment ofPatients withCOPD document updates the position papers on COPDpu lished y the ATS and the ERS in 1995.

Both organisations acknowledge the recent dissemination of theGlo al Initiative ofO structive Lung Disease (GOLD) as a majorcontri ution against COPD.

However, an adaptation ofGOLD was deemed necessary tomatch specific requirements of the mem ers of oth societies.

Those requirements include specific recommendations onoxygen therapy, pulmonary reha ilitation, noninvasiveventilation, surgery in and for COPD, sleep, air travel, and end-of-life.


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Document Goals and O jectives (2)

These guidelines aim at:

Improving the quality ofcare provided to patients

with COPD.

Promoting the use ofa disease-oriented approach.

aintaining a synchronous flowwith the wider

o jectives ofGOLD.

Using an electronic, we - ased format which can

e updated any time a modification is deemed

necessary.


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Definition ofCOPD

Chronic O structive Pulmonary Disease (COPD)

is a preventa le and treata le disease state

characterised y airflow limitation that is not fully

reversi le.

The airflow limitation is usually progressive and

associated with an a normal inflammatory

response of the lungs to noxious particles orgases, primarily caused y cigarette smoking.


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Epidemiology (1)

COPD is a leading cause ofmor idity and

mortality worldwide, and results in an economic

and social urden that is oth su stantial and

increasing.

Prevalence and mor idity data greatly

underestimate the total urden ofCOPD ecause

the disease is usually not diagnosed until it isclinically apparent and moderately advanced.


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Epidemiology (2)

COPD is the fourth leading cause ofdeath in the USA

and Europe, and COPD mortality in females has more

than dou led over the last 20 years.

Leading causes ofdeath in the USA, 1998 Num er

Heart disease 724,269

Cancer 538,947

Cere rovascular disease (stroke) 158,060

Respiratory diseases (COPD) 114,381

Accidents 94,828Pneumonia and influenza 93,207

Dia etes 64,574

Suicide 29,264

Nephritis 26,265

Chronic liver disease 24,936

All other causes ofdeath 469,314


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Epidemiology (3) COPD is a more costly disease than asthma and, depending on

country, 5075% ofthe costs are for services associated withexacer ations.

To acco smoke is y far the most important riskfactorfor COPD

worldwide.

Other important riskfactors are:

Host factors Exposures

Genetic factorsSex

Airway hyperreactivity,

IgE and asthma

SmokingSocio-economic status

Occupation

Environmental pollution

Perinatal events and childhood illness

Recurrent ronchopulmonary infections

Diet


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Pathogenesis and Pathophysiology

Pathogenesis To acco smoking is the main riskfactorfor COPD, although

other inhaled noxious particles and gases may contri ute.

In addition to inflammation, an im alance ofproteinases and

antiproteinases in the lungs, and oxidative stress are alsoimportant in the pathogenesis ofCOPD.

Pathophysiology The different pathogenic mechanisms produce the pathological

changes which, in turn, give rise to the physiologicala normalities in COPD:

mucous hypersecretion and ciliary dysfunction,

airflow limitation and hyperinflation,

gas exchange a normalities,

pulmonary hypertension,

systemic effects.


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Diagnosis ofCOPD (1) Diagnosis ofCOPD should e considered in any patient

who has the following: symptoms ofcough

sputum production

dyspnoea history ofexposure to riskfactors for the disease

Spirometry should e o tained in all persons with thefollowing history:

exposure to cigarettes and/or environmental or occupationalpollutants

family history ofchronic respiratory illness

presence ofcough, sputum production or dyspnoea


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Diagnosis ofCOPD (2)

Spirometry

Spirometric classification of COPD:

Post- ronchodilator E 1/forced vital capacity 0.7 u80

Mild COPD e0.7 u80

Moderate COPD e0.7 5080

Severe COPD e0.7 3050

Very severe COPD e0.7


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B I and dyspnoea Body Mass Index (BMI) and dyspnoea have proved useful in predicting

outcomes such as survival, and should thus e evaluated in all patients.

BMIvalues < 21 kgm-2 are associated with increased mortality.

Functional dyspnoea can e assessed y the Medical Research Council dyspnoeascale:

0 Not trou led with reathlessness except with strenuous exercise.

1 Trou led y shortness of reath when hurrying orwalking up aslight hill.

2 Walks slower than people ofthe same age due to reathlessnessor has to stop for reath when walking at own pace on the level.

3 Stops for reath afterwalking a out 100 m or after a few minuteson the level.

4 Too reathless to leave the house or reathless when dressing orundressing.


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Smoking cessation (1) To acco is the most important riskfactorfor COPD.

Cigarette smoking is an addiction and a chronic relapsing disorder.

Treating to acco use and dependence should e regarded as a primary andspecific intervention.

Smoking cessation activities and support for its implementation should eintegrated into the healthcare system.

The key steps in intervention are:

Ask Identify all to acco users at every visit

Advise Strongly urge all to acco users to quit

Assess Determine willingness to make a quit attempt

Assist Help the patient with a quit plan, provide practical counselling,

treatment and social support, recommend the use ofapproved

pharmacotherapy

Arrange Schedule follow-up contact


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Smoking cessation (2) Key points ofthe Treating To acco Use and Dependence

guidelines:

To acco dependence is a chronic condition that warrants repeatedtreatment until long-term or permanent a stinence is achieved.

Effective treatments for to acco dependence exist and all to acco usersshould e offered these treatments.

Clinicians and healthcare delivery systems must institutionalise theconsistent identification, documentation and treatment ofevery to accouser at every visit.

Briefto acco dependence intervention is effective and every to accouser should e offered at least rief intervention.

There is a strong dose-response relationship etween the intensity ofto acco dependence counselling and its effectiveness.


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Smoking cessation (3) Key points ofthe Treating To acco Use and Dependence guidelines

(continued):

Three types ofcounselling were found to e especially effective:practical counselling, social support as part oftreatment, and

social support arranged outside treatment.

Five first-line pharmacotherapies for to acco dependence areeffective: upropion SR, nicotine gum, nicotine inhaler, nicotinenasal spray, and nicotine patch, and at least one of thesemedications should e prescri ed in the a sence of

contraindications.

To acco-dependence treatments are cost-effective relative toother medical and disease prevention interventions.


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Management ofsta le COPD

Pharmacological therapy

Long-term oxygen therapy

Pulmonary reha ilitation

Nutrition

Surgery in and for COPD

Sleep

Air travel


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Nutrition


Sleep

Air travel


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Pharmacological therapy (1)

The medications for COPD currently availa le can reduceor a olish symptoms, increase exercise capacity, reducethe num er and severity ofexacer ations, and improvehealth status.

At present, no treatment has een shown to modify therate ofdecline in lung function.

The change in lung function after rief treatment with any

drug does not help in predicting other clinically relatedoutcomes.

The inhaled route is preferred.


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Changes in forced expiratory volume in one second

(FE 1) following ronchodilator therapy can e small ut

are often accompanied y larger changes in lung

volume, which contri ute to a reduction in perceived

reathlessness.

Com ining different agents produces a greater change in

spirometry and symptoms than single agents alone.

Three types of ronchodilators are in common clinicaluse: -agonists, anticholinergic drugs and

methylxanthines.


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Bronchodilators

LA-BD: long-acting bronchodilator; ICS: inhaled corticosteroid. Assess effectiveness by treatmentresponse criteria. If forced expiratory volume


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Bronchodilators Short-acting ronchodilators can increase exercise tolerance acutely in

COPD.

Anticholinergics given q.i.d. can improve health status over a 3-monthperiod.

Long-acting inhaled -agonists improve health status, possi ly more than

regular ipratropium. Additionally, these drugs reduce symptoms, rescuemedication use and increase the time etween exacer ations.

Com ining short-acting agents (sal utamol/ipratropium) produces a greaterchange in spirometry over 3 months than either agent alone.

Com ining long-acting inhaled -agonists and ipratropium leads to fewerexacer ations than either drug alone.

Com ining long-acting -agonists and theophylline produces a greaterspirometric change than either drug alone.

Tiotropium improves health status and reduces exacer ations andhospitalisations compared with oth place o and regular ipratropium.


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Glucocorticoids

Glucocorticoids act at multiple points within the

inflammatory cascade, although their effects in

COPD are more modest compared with

ronchial asthma.

In patients with more advanced disease (usually

classified as an FE 1


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Nutrition


Sleep

Air travel


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Long-term oxygen therapy (1)

Long-term oxygen therapy (LTOT) improves survival,

exercise, sleep and cognitive performance.

Reversal ofhypoxaemia supersedes concerns a out

car on dioxide (CO2) retention.

Arterial lood gas (ABG) is the preferred measure and

includes acid- ase information.

Oxygen sources include gas, liquid and concentrator. Oxygen delivery methods include nasal continuous flow,

pulse demand, reservoir cannulas and transtracheal

catheter.


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Physiological indications for oxygen include an arterialoxygen tension (Pa,O2) 90% during rest,sleep and exertion.

Active patients require porta le oxygen.

Ifoxygen was prescri ed during an exacer ation,recheck ABGs after 3090 days.

Withdrawal ofoxygen ecause of improved Pa,O2 inpatients with a documented need for oxygen may edetrimental.

Patient education improves compliance.


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Home treatment

Pa,O2: arterial oxygen

tension; Sa,O2: arterial

oxygen saturation; ABG:

arterial lood gases.


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Pulmonary rehabilitation

Nutrition


Sleep

Air travel


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Pulmonary reha ilitation Pulmonary reha ilitation is a multidisciplinary programme ofcare

that is individually tailored and designed to optimise physical andsocial performance and autonomy.

Pulmonary reha ilitation should e considered for patients withCOPD who have dyspnoea or other respiratory symptoms, reducedexercise tolerance, a restriction in activities ecause oftheirdisease, or impaired health status.

Pulmonary reha ilitation programmes include:

exercise training,

education,

psychosocial/ ehavioural intervention, nutritional therapy,

outcome assessment,

promotion of long-term adherence to the reha ilitationrecommendations.


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Nutrition


Sleep

Air travel


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Nutrition Weight loss and a depletion offat-free mass (FFM) may e o served in

sta le COPD patients.

Being underweight is associated with an increased mortality risk.

Criteria to define weight loss are:

Weight loss >10% in the past 6 months or >5% in the past month.

Nutritional therapy may only e effective ifcom ined with exercise or otherana olic stimuli.

Underweight BMI 50 yrs

Normal weight BMI


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Nutrition


Sleep

Air travel


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Surgery in COPD (1)

Patients with a diagnosis ofCOPD have a 2.74.7-foldincreased risk ofpost-operative pulmonarycomplications.

The further the procedure from the diaphragm, the lowerthe pulmonary complication rate.

Smoking cessation at least 48 weeks pre-operativelyand optimisation of lung function can decrease post-

operative complications. Early mo ilisation, deep reathing, intermittent positive-

pressure reathing, incentive spirometry and effectiveanalgesia may decrease postoperative complications.


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Surgery in COPD (2)

Algorithm for pre-operative testing forlung resection.DL,CO: car on dioxide

diffusing capacity of the lung; FE 1:

forced expiratory volume in one

second; ppo: predicted postoperative;

VO2,max: maximum oxygen

consumption.


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Surgery for COPD (1)

Bullectomy and lung volume reductionsurgery may result in improved spirometry, lungvolume, exercise capacity, dyspnoea, health-

related quality of life and possi ly survival inhighly selected patients.

Lung transplantation results in improvedpulmonary function, exercise capacity, quality of

life and possi ly survival in highly selectedpatients.


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Lung Volume Reduction SurgeryParameter Favourable Unfavourable

Clinical Age 7580 yrs

Clinical picture consistent with emphysema

Co-morbid illness which would increase surgical

mortality

Not actively smoking (>36 months) Clinically significant coronary artery disease

Severe dyspnea despite maximal medical treatment

including pulmonary rehabilitation

Pulmonary hypertension (PA systolic >45, PA mean

>35 mmHg)

Requiring 140 m

Low post-rehabilitation maximal achieved cycle ergometry

watts#

Radiographical

High-resolution computed tomography confirming severe

emphysema, ideally with upper lobe predominance Homogeneous emphysema and FEV1


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Lung Volume Reduction Surgery

Schematic algorithm from theNational Emphysema Therapy

Trial for Lung Volume ReductionSurgery (LVRS).FEV1:forcedexpiratory volume in one second;DLCO: car on dioxide diffusingcapacity ofthe lung.


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Nutrition


Sleep

Air travel


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Sleep Sleep in COPD is associated with oxygen desaturation, which is

predominantly due to the disease itselfrather than to sleep apnoea.The desaturation during sleep may e greater than during maximumexercise.

Sleep quality is markedly impaired in COPD, oth su jectively and

o jectively.

Clinical assessment in all patients with COPD should includequestions a out sleep quality and possi le co-existing sleep apnoeasyndrome.

Management ofsleep pro lems in COPD should particularly focus onminimising sleep distur ance y measures to limit cough anddyspnoea, and nocturnal oxygen therapy is rarely indicated forisolated nocturnal hypoxaemia.

Hypnotics should e avoided, ifpossi le, in patients with severeCOPD.


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Nutrition


Sleep

Air travel


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Exacer ation ofCOPD

Definition, evaluation and treatment

In-patient oxygen therapy

Assisted ventilation


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Exacer ation ofCOPD





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Definition, evaluation and

treatment (1)

The definition ofCOPD exacer ation is an acutechange in a patients aseline dyspnoea, coughand/or sputum eyond day-to-day varia ilitysufficient to warrant a change in therapy.

Causes ofexacer ation can e oth infectiousand non-infectious.

Medical therapy includes ronchodilators,corticosteroids, anti iotics and supplementaloxygen therapy.


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treatment (2)

Indications for hospitalisation ofpatients with a COPDexacer ation Presence ofhigh-risk co-mor id conditions, including

pneumonia, cardiac arrhythmia, congestive heart failure,dia etes mellitus, renal or liverfailure

Inadequate response ofsymptoms to outpatient management Marked increase in dyspnoea

Ina ility to eat or sleep due to symptoms

Worsening hypoxaemia

Worsening hypercapnia

Changes in mental status

Ina ility of the patient to care for her/himself

Uncertain diagnosis

Inadequate home care


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treatment (3) The Operational Classification ofSeverity is as follows: am ulatory (Level I), requiring

hospitalisation (Level II) and acute respiratory failure (Level III).

Level I Level II Level III

Clinical history

Co-mor id conditions

History offrequent exacer ationsSeverity ofCOPD

+

+

Mild/moderate

+++

+++

Moderate/severe

+++

+++

Severe

Physical findings

Haemodynamic evaluation

Use accessory respiratory muscles, tachypnoea

Persistent symptoms after initial therapy

Sta le

Not present

No

Sta le

++

++

Sta le/unsta le

+++

+++

Diagnostic procedures

Oxygen saturation

Arterial lood gases

Chest radiograph

Blood tests

Serum drug concentrations

Sputum gram stain and culture

Electrocardiogram

es

No

No

No

Ifapplica le

No

No

es

es

es

es

Ifapplica le

es

es

es

es

es

es

Ifapplica le

es

es

+: unlikely to be present; ++: likely to be present; +++: very likely to be present


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treatment (4)

Level I: outpatient treatmentPatient education

Check inhalation technique

Consider use ofspacer devices

Bronchodilators

Short-acting 2-agonist and/or ipratropium MDIwith spacer or hand-held ne uliser as neededConsider adding long-acting ronchodilator ifpatient is not using it

Corticosteroids (the actual dose may vary)

Prednisone 3040 mgper os q day for 10 days

Consider using an inhaled corticosteroid

Antibiotics

May e initiated in patients with altered sputum characteristics

Choice should e ased on local acteria resistance patterns

Amoxicillin/ampicillin, cephalosporins

Doxycycline

Macrolides

If the patient has failed prior anti iotic therapy consider:

Amoxicillin/clavulanate

Respiratory fluoroquinolones


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treatment (5)

Level II: treatment for hospitalised patient

Bronchodilators

Short acting 2-agonist (al uterol, sal utamol) and/or

Ipratropium MDIwith spacer or hand-held ne uliser as needed

Supplemental oxygen (ifsaturation


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treatment (6)

Level III: treatment in patients requiring special or intensive care unit

Supplemental oxygen

Ventilatory support

Bronchodilators

Short-acting 2-agonist (al uterol, sal utamol) and ipratropium MDIwith spacer, two puffs every 24 hIfthe patient is on the ventilator, consider MDI administration, consider long-acting -agonist

Corticosteroids

Ifpatient tolerates oral medications, prednisone 3040 mgper os q day for 10 days

Ifpatient can not tolerate, give the equivalent dose i.v.for up 14 days

Consider use inhaled corticosteroids y MDI or hand-held ne uliser

Antibiotics ( ased on local acteria resistance patterns)Choice should e ased on local acteria resistance patterns

Amoxicillin/clavulanate

Respiratory fluoroquinolones (gatifloxacin, levofloxacin, moxifloxacin)

IfPseudomonas spp. and or otherEnterobactereaces spp. are suspected consider com ination therapy


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Exacer ation ofCOPD





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In-patient oxygen therapy The goal is to prevent tissue hypoxia y maintaining arterial oxygen

saturation (Sa,O2) at >90%.

Main delivery devices include nasal cannula and venturi mask.

Alternative delivery devices include nonre reather mask, reservoir

cannula, nasal cannula or transtracheal catheter.

Arterial lood gases should e monitoredfor arterial oxygen tension(Pa,O2), arterial car on dioxide tension (Pa,CO2) and pH.

Arterial oxygen saturation as measured y pulse oximetry (Sp,O2)should e monitored for trending and adjusting oxygen settings.

Prevention of tissue hypoxia supercedes CO2 retention concerns.

IfCO2 retention occurs, monitorfor acidaemia.

Ifacidaemia occurs, consider mechanical ventilation.


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In-patient oxygen therapy (2)

Algorithm to correct hypoxaemia

in an acutely ill chronic o structivepulmonary disease patient. ABG:

arterial lood gas; Pa,O2: arterial

oxygen tension; O2: oxygen;

Sa,O2: arterial oxygen saturation;

Pa,CO2: arterial car on dioxide

tension; NPPV: noninvasivepositive pressure ventilation.


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Exacer ation ofCOPD





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Assisted ventilation (1) Noninvasive positive pressure ventilation (NPPV) should e offered

to patients with exacer ations when, after optimal medical therapyand oxygenation, respiratory acidosis (pH


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Assisted ventilation (2) Patients meeting exclusion criteria should e considered for

immediate intu ation and ICU admission.

Exclusion criteria include:

respiratory arrest,

cardiovascular insta ility, impaired mental status,

somnolence,

ina ility to cooperate,

copious and/orviscous secretions with high aspiration risk,

recent facial or gastro-oesophageal surgery; craniofacial trauma and/orfixed naso-pharyngeal a normality,

urns,

extreme o esity.

In the first hours, NPPV requires the same level ofassistance asconventional mechanical ventilation.


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Assisted ventilation (3)

Flow-chart for the use of

noninvasive positive pressureventilation (NPPV) duringexacer ation ofCOPDcomplicated y acuterespiratory failure. MV:mechanical ventilation;

Pa,CO2: arterial car on dioxidetension.


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Ethical and palliative care

issues in COPD Patients with COPD experience acute exacer ations of their

disease, which may produce respiratory failure and a possi le needfor eitherventilatory support or accepting death.

Healthcare providers should assist patients during sta le periods ofhealth to think a out their advance care planning y initiating

discussions a out end-of-life care.

End-of-life discussions and advance care planning assist decisionsregarding life-supportive care at the end of life y providinginformation on pro a le outcomes and the existence ofpalliativeinterventions, such as dyspnoea management and terminalsedation.

Patients who choose to refuse life-supportive care or have itwithdrawn require expert delivery ofpalliative care.


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Patient section


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Patient section This updated document includes

a patient section aimed at:

Providing practical information

on all aspects ofCOPD.

Promoting a healthy lifestyle to

all patients afflicted with the

disease.

This section is availa le in

English, French, German, Italian

and Spanish.

It includes printa le files whichcan e directly distri uted to

patients.


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