COPD

1. COPD AND MANAGEMENT
Dr Devawrat Buche ,MD
FNB Fellow

2. Definition
• As per GOLD guidelines ( Jan. 2015 ), it is defined
as :
• “COPD is a common preventable and treatable
disease, characterized by persistant airflow
limitation, that is usually progressive,
• and associated with chronic inflammatory
response in the airways and lungs to noxious
particles and gases “
• Exacerbations and comorbity contribute to the
overall severity in the individual.

3. • COPD is said to be an independent entity and previously
included conditions like emphysema and chronic broncitis are
not included in the current definition.
• However the basic pathophysioloic mechanism may have
features of both the diseases ,i.e., chronic inflammation (
chronic bronchitis) or parenchyma destruction ( emphysema ).

4. Burden of COPD
• Leading cause of morbidity and moratlity
worldwide – economic and social burden
• The prevalence related primarily to tobacco
smoking , also biomass fuel, indoor and outdoor
pollution.
• The global burden of disesase study projected
that COPD may become 3rd leading cause of
death by the year 2030
• It is a major economic burden and healthcare
costs.

5. Risk factors for COPD
• Genes – α1 AT deficiency
• Exposure to particles - Tobacco smoke, Occupational
Indoor and Outdoor air pollution
• Lung growth and development : factors affecting normal
lung growth can increase individual risk.
• Gender – M >F, but prevalence changing.
• Age – association unclear. Indicates cumulative exposure.
• Respiratory infections – severe childhood respiratory
infection, TB, HIV : Independent risk factors
• Socioeconomic status – poverty is a risk factor
• Asthma/Bronchial hyperreactivity - a risk factor. 12 – 20%
asthmatics may progress on to chronic airflow limitation
• Chronic Bronchitis – increased likelihood in people with
mucus hypersecretion, reduced FEV 1 and those who
continue to smoke

6. Pathology
• Changes found in :
Parenchyma
Vasculature
And airways
The salient changes are :
• Chronic inflammation
• Parenchymal / airspace destruction

7. Pathogenesis
• Oxidative stress
 Oxidents generated in cigarrette smoke and inflammatory cells
 Reduced endogenous oxidents : reduction in transcription factor
nrf2
 Biomarkers found in exhaled breath : hydrogen peroxide, 8-
isoprostane
• Protease-antiprotease imbalance
 Protease mediated destruction of elastin- major cause of
emphysema
• Inflammatory cells
 Increase in CD8+ T lymphocytes
 Increased macrophages and neutrophils
• Inflammatory mediators
• Chemotactic factors – recruit inflammatory cells
• Proinflammatory chemokines – amplify inflammation
• Growth factors – amplify remodelling

8. Pathophysiology
• Airflow limitation and air trapping
 Progressive hyperinflation and air trapping – reduction in
FEV1/FVC and FEV1
 Hyperinflation – dyspnea and effort limitation
 Up regulation of pro- inflammatory cytokines ( IL 8, TNF α )
• Gas exchange abnormalities
 Gas exchange worsens as disease progresses
 Reduced ventilatory drive – reduced ventilation
 V : Q mismatch
• Mucus hypersecretion
 Increase in Goblet cells and submucosal glands – increased
mucus production

9. • Pulmonary hypertension
 Develops late in course
 Chronic hypoxic vasoconstriction and vascular remodelling
 May lead to right heart hypertrophy and failure
• Exacerbations
 Triggered by pollutants, infections or unknown factors
 Increased hyperinflation and gas trapping, expiratory flow limitation
 V:Q mismatch is worsened
• Systemic features
 Inflammatory mediators – cachexia, muscle wasting
 IHD, heart failure
 Osteoporosis
 Anemia of chronic disease,
 DM, metabolic syndrome
 Major depression

10. Assessment
The goals are to :
• Determine the severity of the disease,
• its impact on the patient’s health status
• and the risk of future events ( exacerbations)
• to guide therapy.
Assess :
 symptoms
 degree of airflow limitation using spirometry
 risk of exacerbations
comorbidities

11. Assessment : History taking
• Exposure to risk factors : cigarette smoke, biomass
fuels, occupational exposure
• Medical history – bronchial asthma, allergy , sinusitis,
nasal polyps, childhood resp. infection
• Family history of COPD
• History of exacerbations or previous hospitalizations
• Presence of comorbidities
• Social and family support available
• Possibilities of reducing risk factors : smoking cessation

12. Assessment : Symptoms
• The characteristic symptoms of COPD are chronic
and progressive dyspnea, cough, and sputum
production that can be variable from day-to-day.
• Dyspnea: Progressive, persistent and
characteristically worse with exercise.
• Chronic cough: May be intermittent and may be
unproductive.
• Chronic sputum production: COPD patients
commonly cough up sputum.

13. • Quantitative measurement of symptoms:
• COPD Assessment Test (CAT): An 8-item
measure of health status impairment in
COPD(http://catestonline.org).
• Clinical COPD Questionnaire (CCQ): Self-
administered questionnaire developed to
measure clinical control in patients with COPD
(http://www.ccq.nl).
• Breathlessness Measurement using the
Modified British Medical Research Council
(mMRC) Questionnaire: relates well to other
measures of health status and predicts future
mortality risk.

14. Assessment : degree of airflow limitation
• Spirometry should be performed after the
administration of an adequate dose of a short-
acting inhaled bronchodilator to minimize
variability.
• A post-bronchodilator FEV1/FVC < 0.70
confirms the presence of airflow limitation.
• Where possible, values should be compared to
age-related normal values to avoid over
diagnosis of COPD in the elderly.

17. Classification of severity
There is however a weak correlation between FEV1, symptoms and patient’s QOL.
WITHIN ANY CATEGORY PATIENT MAY HAVE QOL VARYING FROM WELL PRESERVED
TO POOR HEALTH STATUS.
Thus, formal symptomatic assessment is also required.

18. Assessment : risk of exacerbations
To assess risk of exacerbations use history of
exacerbations and spirometry:
• 2 or more exacerbations within the last year
or an FEV1 < 50 % of predicted value are
indicators of high risk.
• 1 or more hospitalizations for COPD
exacerbation should be considered high risk.

20. Assessment : comorbidities
COPD patients are at increased risk for:
• Cardiovascular diseases
• Osteoporosis
• Respiratory infections
• Anxiety and Depression
• Diabetes
• Lung cancer
• Bronchiectasis
These comorbid conditions may influence mortality
and hospitalizations and should be looked for
routinely, and treated appropriately

21. Other investigations
• Chest X-ray: Seldom diagnostic but valuable to exclude alternative
diagnoses and establish presence of significant comorbidities.
• CT chest : not routinely recommended. Done only when there is
doubt in diagnosing COPD or to rule out other D.D.
• Lung Volumes and Diffusing Capacity: Help to characterize severity,
but not essential to patient management.
 Typically there is decresed FEV1, FEV1/FVC ; increased RV , RV/TLC ;
DlCo may reduce in emphysema
• Oximetry and Arterial Blood Gases: Pulse oximetry can be used to
evaluate a patient’s oxygen saturation and need for supplemental
oxygen therapy.
SpO2 < 92% warrants ABG analysis.
• Alpha-1 Antitrypsin Deficiency Screening: Perform when COPD
develops in patients of Caucasian descent under 45 years or with a
strong family history of COPD and /or lower lobe emphysema.
 Values 15 -20% of normal suggest homozygous deficiency

22. • Exercise Testing: Objectively measured exercise
impairment, is a powerful indicator of health
status impairment and predictor of prognosis.
6MWT
Ergometry ( cycle / treadmill )
CPET
• Composite Scores: Several variables (FEV1,
exercise tolerance assessed by walking distance
or peak oxygen consumption, weight loss and
reduction in the arterial oxygen tension) identify
patients at increased risk for mortality.

23. BODE index
It is a composite tool for predicting severity. Its utility is still under
investigation.

24. Differential diagnosis

25. Treatment
• Management of stable COPD
• Management of acute exacerbation

26. Key points ( stable COPD )
• Smoking cessation has the greatest capacity to influence the natural
history of COPD. Health care providers should encourage all
patients who smoke to quit.
• Pharmacotherapy and nicotine replacement : reliably increase long-
term smoking abstinence rates.
• regular physical activity and should repeatedly be encouraged to
remain active
• Appropriate pharmacologic therapy : can reduce COPD symptoms,
reduce the frequency and severity of exacerbations, and improve
health status and exercise tolerance.
• None of the existing medications for COPD has been shown
conclusively to modify the long-term decline in lung function.
• Influenza and pneumococcal vaccination should be offered
depending on local guidelines.

27. Therapeutic options ( stable COPD )

28. Overview of treatment of stable COPD
• Identification and reduction of exposure to risk
factors are important steps in prevention and
treatment.
• Individualized assessment of symptoms, airflow
limitation, and future risk of exacerbations should
be incorporated into the management strategy.
• rehabilitation and maintenance of physical
activity.
• Pharmacologic therapy is used to reduce
symptoms, reduce frequency and severity of
exacerbations, and improve health status and
exercise tolerance

29. • Long-acting formulations of beta2-agonists and
anticholinergics are preferred over short-acting
formulations.
• inhaled bronchodilators are preferred over oral
bronchodilators.
• Long-term treatment with inhaled corticosteroids
added to long-acting bronchodilators is recommended
for patients with high risk of exacerbations
• Long-term monotherapy with oral or inhaled
corticosteroids is not recommended in COPD.
• The phospodiesterase-4 inhibitor roflumilast may be
useful to reduce exacerbations for patients with FEV1 <
50% of predicted, chronic bronchitis, and frequent
exacerbations

30. MANAGEMENT OF ACUTE EXACERBATION
• DEFINITION ( GOLD, jan 2015)
“an acute event characterized by a worsening of the
patient’s respiratory symptoms that is beyond normal
day-to-day variations and leads to a change in
medication.”
There is notable change in :
• Baseline dyspnea
• Cough
• Sputum production

31. Consequences of AE
EXACERBATIONS
Negative
impact on
quality of life
Accelerated
lung function
decline
Increased
Mortality
Increased
economic
costs
Impact on
symptoms
and lung
function

32. ASSESSMENT OF AE
• SIGNS OF SEVERITY ARE :
Use of accessory muscles of respiration
Paradoxical chest wall movements
Worsening or new onset central cyanosis
Development of peripheral edema
Hemodynamic instability
Deterioration of mental status

33. Investigations to be sent
• Arterial blood gas measurements (in hospital): PaO2 < 8.0 kPa with
or without PaCO2 > 6.7 kPa when breathing room air indicates
respiratory failure.
• Chest radiographs: useful to exclude alternative diagnoses.
• ECG: may aid in the diagnosis of coexisting cardiac problems.
• Whole blood count: identify polycythemia, anemia or bleeding.
• Purulent sputum during an exacerbation: indication to begin
empirical antibiotic treatment.
• Biochemical tests: detect electrolyte disturbances, diabetes, and
poor nutrition.
• Spirometric tests: not recommended during an exacerbation

34. Criteria for hospital admission

35. Criteria for ICU admission

36. TREATMENT OPTIONS
• OXYGEN THERAPY
• PHARMACOTHERAPY
Bronchodilators
Corticosteroids
Antibiotics
Adjunctive therapy
• VENTILATION :
NIV
INVASIVE VENTILATION

37. Oxygen therapy
• low-flow intranasal cannulae / 24–35% Venturi mask - titrated to SpO2 of
88–92% .
• Excessive oxygen therapy is the cause of increased hypercapnia
• ABGs should be repeated 1 hour
• If the rise in PaCO2 is excessive (>10¯mmHg ), then FiO2 should be
reduced, titrating SpO2 to 2–3% below the previous value, and arterial
blood gases should be repeated.
• If no PaCO2 rise occurs with oxygen therapy, then a higher SpO2 may be
targeted with repeat ABG.
• Inadequate reversal of hypoxia (e.g. SpO2 < 85%) is suggestive of an
additional problem such as pneumonia, pulmonary oedema or embolus,
or a pneumothorax.
• Although high levels of O2 should be avoided, reversal of hypoxia is
important and O2 should not be withheld in the presence of hypercapnia,
or withdrawn if it worsens.

38. PHARMACOTHERAPY
• Bronchodilators:
 Short-acting inhaled beta2-agonists with or without short-acting
anticholinergics are preferred ( no controlled trials).
 No significant difference between MDI vs nebulizers
 No studies done to evaluate long acting bronchodilators ( beta 2
agonists/ anticholinergics ) with or without inhaled steroids in AE.
 IV methylxanthines ( amino, theophylline) : considered 2nd line
therapy. Used in selected patients when insufficient response to
short acting bronchodilators.
NEBULIZED MAGNESIUM AS AN ADJUVANT TO SALBUTAMOL HAS NO
EFFECT ON IMPROVING FEV1

39. • Systemic Corticosteroids:
 Shorten recovery time,
 improve lung function (FEV1) and arterial hypoxemia
(PaO2), and
 reduce the risk of early relapse, treatment failure, and
length of hospital stay.
• A dose of 40 mg prednisone per day for 5 days is
recommended
• Methylprednisolone 0.5 mg/kg every 6 hrly for 72 hrs. also
has been tried
• Nebulized budesonide may be alternative to oral steroids.
• LONG TERM ORAL OR NEBULIZED STEROIDS ARE NOT
RECOMMENDED.

40. • Antibiotics should be given to patients with 3 cardinal
symptoms:
 increased dyspnea,
 increased sputum volume,
 and increased sputum purulence,
 Who require mechanical ventilation
• Recommended duration : 5 -10 days
• Drug choice based on local resistance pattern. Usually
empirical treatment is with aminopenicillin with or
without BLI, macrolide or tetracycline.
• Improvement in dyspnea and sputum purulence
indicates clinical success.

41. Treatment : ventilation strategies

42. • The goal of NIV is:
 to unload respiratory muscles and augment
ventilation and oxygenation
 reduce CO2 and correct acidosis until the
underlying problem can be reversed
 when applied intermittently, to offset the
adverse effects of sleep- or position-induced
adverse changes to ventilation, increased upper
airway resistance and lung volume.
Reduce VAP
Reduce ICU LOS

43. INVASIVE VENTILATION

44. • The goals of IMV in COPD are:
 to support ventilation while reversible
components improve,
to allow respiratory muscle to rest and recover
whilst preventing wasting from total inactivity
 to minimise dynamic hyperinflation.

45. INVASIVE VENTILATION TECHNIQUE
• MODE : Volume A/C
• INITIAL Tv : 5 -8 ml/kg IBW
• TARGET PEAK PRESSURE : below 40 – 45
cmH2O
• RR : < 14/ min
• I : E RATIO – 1:3 to 1:4
• FiO2 : < 0.5 ( depending on PaO2 )

46. PEEP
• e PEEP is beneficial as :
It reduces gas trapping
Stents open the airways
Reduces work of breathing to trigger
inspiratory flow.
• As e PEEP is applied , the Tv will increase
without an increase in airway pressure until :
e PEEP exceeds i PEEP.

47. Weaning
• The simple criterion of patient respiration rate/tidal volume <100
breaths/min per litre had the best predictive value for weaning
• Other indications to extubate include :
• FiO2<40%;
• PaO2/FiO2>200,
• PEEP 5cmH2O,
• Cardiovascular stability,
• afebrile,
• pH > 7.35, PaCO2<50mmHg
• GCS >10 and,
• static compliance >25mL/cmH2O.
• Some patients unable to achieve these criteria may require weaning with
PaCO2 50–65mmHg with a bicarbonate level of >30¯mmol/L allowed or
encouraged to reduce the work of breathing and achieve a less abnormal
pH.
• Following extubation, weaning can be continued with immediate
placement upon NIV

48. Adjunctive therapy
1. ANTICOAGULANTS
• Subcutaneous heparin (e.g. 5000 units b.d.) is recommended as a prophylactic measure
against venous thromboembolism. There is no evidence for warfarinisation in COPD patients
with pulmonary hypertension.
2. ELECTROLYTE CORRECTION
• Electrolyte correction is important. Hypophosphataemia,hypomagnesaemia,hypocalcaemia
and hypokalaemia may impair respiratory muscle function.
• Hyponatraemia may occur with inappropriate antidiuretic hormone release or with excess
use of diuretics and inappropriate intravenous fluids.
3. NUTRITION
• Nutrition is important, as patients with severe COPD are often undernourished – a subnormal
BMI is a risk factor for mortality in COPD.
• Excessive carbohydrate calories should be avoided as this increases CO2 production (by
>15%) and may worsen respiratory failure.
• Low-carbohydrate/high-fat combinations are preferred in ARF during spontaneous
ventilation.

49. 4. CHEST PHYSIOTHERAPY
• Chest physiotherapy should be initiated and regularly
repeated as both a curative and preventive measure.
• Encouragement of coughing and deep breathing are the
two most important factors.
• ‘Bubble positive expiratory pressure (PEP)’ is an
inexpensive method of assisting sputum clearance in
patients with retained secretions or those having difficulty
expectorating.
5. NEBULISED MUCOLYTIC AGENTS
• Nebulised mucolytic agents, such as N-acetylcysteine,
continue to be proposed, although their benefit hasnever
been established in acute exacerbations of COPD.
• Oral mucolytics have been shown to reduce cough
frequency and severity in stable COPD

50. THANK YOU !!!