1. Attila Somfay Dept.Pulmonology, University of Szeged, Deszk, Hungary
COPD
Attila Somfay
Dept.Pulmonology,
University of Szeged, Deszk,
Hungary

2. Chronic obstructive bronchitis and emphysema
chronic obstructive airway disease
(COAD, COLD)
( chronic obstructive pulmonary disease )
COPD

3. COPD
emphysema bronchitis
„pink puffer” „blue bloater”

4. CIBA Guest Symposium: Terminology, definitions and classifications of chronic pulmonary emphysema and related conditions (1959)
1./ Obstructive emphysema: abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of the alveolar walls and without obvious fibrosis.
2./ Chronic bronchitis: the presence of chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes (heart failure, tbc, bronchiectasis, tumor, lung abscess) of chronic cough have been excluded. 1

5. 1. COPD, a common preventable and treatable disease, is characterized by persistent airflow limitation.
2. The airway obstruction is usually progessive and associated with an enhanced chronic ionflammatory response in the airways and the parenchyma to noxius particles and gases.
3. Exacerbations and comorbidities contribute to the overall severity in an individual patient.
GOLD 2011

10. Percent Change in Age-Adjusted Death Rates, U.S.
Proportion of 1965 Rate
3.0
Coronary
Heart
Disease
Stroke
Other CVD
COPD
All Other
Causes
2.5
2.0
1.5
1.0
0.5
–59%
–64%
–35%
+163%
–7%

11. „Global burden of disease”
(Science 1996; 274: )

12. Mortality (Global Burden of Disease Study) 1990 2010
Lozano, Lancet 2012
COPD death/
inhabitant
1990
2010

13. Epidemiology 4-7% of adult population, 9-10 % for those over 40
Prevalence expected to rise 3x in 10 years.
By 2020, it becomes the 3rd most frequent cause of death

14. COPD morbidity in Hungary
PREVALENCE
INCIDENCE
12 853
Korányi Bulletin, 2018

15. Etiology: host factors

17. Etiology: acquired risk

18. Effect of smoking on annual decline in lung function Fletcher C, Peto R: BMJ 1977:i: 1645

20. Pathology
1. chronic bronchitis – increased mucus production, chronic cough

21. 2. obstructiv bronchiolitis – small airway obstruction with inflammation and fibrosis of bronchioles

22. 3. Emphysema – alveolar destruction, hiperinflation, loss of elastic recoil, gázcserezavar, bronchiális obstrukció

23. Small airways in COPD
Barnes, NEJM,2004

24. Loss of alveolar attachments in smokers
Saetta M, Ghezzo H, Kim WDM, et al. Loss of alveolar attachments in smokers. A morphometric correlate of lung function impairment. Am Rev Respir Dis 1985; 132:
Normal
Smoker
Saetta et al. ARRD 1985

25. Airway muscle thickness increases in COPD
Non-smoker
COPD
© M Saetta
Saetta. 1998

26. Causes of Airflow Limitation
Irreversible
Fibrosis and narrowing of the airways
Loss of elastic recoil due to alveolar destruction
Destruction of alveolar support that maintains patency of small airways

27. Causes of Airflow Limitation
Reversible
Accumulation of inflammatory cells, mucus, and plasma exudate in bronchi
Smooth muscle contraction in peripheral and central airways
Dynamic hyperinflation during exercise

28. Airflow limitation Driving pressure (parenchyma) =
Resistance (small airways)

29. Pathology and gas exchange in COPD
Stockley, Rennard, Rabe, Celli, 2007

30. Differential diagnosis of airway obstruction
Chronic bronchitis
Emphysema
COPD
Airflow obstruction
Adapted from Snider GL. American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease
Am J Respir Crit Care Med. 1995; 152: S77–S121
Asthma
Adapted from Snider 1995

31. Differencial diagnostics
Asthma
CHF
Bronchiectasis
Bronchiolitis obliterans (young, non-smoker, RA, smoke exposition, HRCT:hypodens area)
Diffuse panbronchiolitis (non-smoker malei, sinusitis, HRCT:centrilobular foci and hyperinflation)

32. Inflammation and lung function
In asthma and COPD
Barnes, 2009
Overlap ~ %

33. COPD
asthma
neutrophils
mild AHR*
no(poor) bronchodilation
no corticosteroid
effect
eosinophils
AHR*
good bronchodilator effect
good corticosteroid
effect
10 –
40 %
“ Wheezy bronchitis ”
reversibility threshold: 12 –15% (>200ml) FEV1- increase
*AHR= airway hyperreactivity

34. Characteristics of phenotypes
bronchitis emphysema
Dynamic lung volumes decreased decreased
( FEV1 , FEV1/FVC)
Static lung volumes
TLC normal or mild increase increased
RV moderate increase increasd
Diffusion capacity normal or mild decreased
decrease
Blood gas hypoxaemia, hypercapnia hypoxaemia in end-stage
exercise hypoxaemia: no change, improves hypoxaemia
or deteriorates deteriorates
Cor pulmonale frequent rare

35. FEV1 (ref %) symptoms Diagnosis: postbronchodilator FEV1/FVC<70%
Classification
FEV1 (ref %) symptoms
cough, sputum
mild  80 % morning sputum,
minimal breathing dyscomfort
moderate % dyspnea on moderate exertion with or without wheezing,
discolored sputum
severe – 50 % acute worsening with infection, with
significant erosion of QoL
very severe < 30% n cough, wheezing,
breathlessness on minimal exertion
signs of RHF,
significantly impaired QoL

36. Pharm.spir.
Beta-2 agonist
Parasympatho-
lytics
Xantin derivate

37. Systemic consequences/comorbidities in COPD
Expiratory flow limitation
Air trapping
Exacerbation
Hyperinflation
Dyspnea
Reduced exercise
tolerance
Quality of life
Inactivity
In patients with COPD, there is a cycle of airflow limitation, dyspnea, and reduced exercise endurance.
The physiological impairment in COPD is characterized by airflow limitation, air trapping, and hyperinflation.
These physiologic abnormalities lead to dyspnea (or breathlessness).
Dyspnea in itself is unpleasant, and it also severely limits the amount of activity a patient can undertake. Often patients will avoid situations that demand physical activity.
Avoiding exercise leads to deconditioning and worsening of the disease and, ultimately, the patient’s health-related quality of life suffers.
COPD is often associated with acute exacerbations of symptoms.
Exacerbations are periodic worsenings of disease that are often triggered by respiratory tract infections.
As COPD worsens, patients are more likely to experience exacerbations, which become more severe.
Exacerbations may have a long-term impact on the disease and can contribute to premature mortality.
Deconditioning
Systemic consequences
e.g. Muscle atropgy/wasting, atherosclerosis, depression, osteoporosis, anaemia, diabetes

38. Airway inflammation and systemic consequences in COPD (theory)
Tüdő
Inzulin resistance,
II. type diabetes
Muscle wasting/atrophy
TNFa
IL-6 ?
Local
inflammation
Osteoporosis
Cardiovascular
events
CRP
Liver

40. GOLD Workshop Report Four components of COPD Management
Asses and monitor disease
Reduce risk factors
Manage stabil COPD
Education
PharmacologicGyógyszeres
Non-pharmacologic
Manage exacerbations

42. Smoking: early and late quit
Doll, BMJ 2004
British male physicians,

44. Combined assessment in COPD
GOLD 2011
GOLD stages by FEV1
Risk
(Exacerbation history in the previous year)
≥ 2 or
> 1 with hospital admission
1 (without
hospitalization)
Symptoms
(C)
(D)
(A)
(B)
CAT < 10 4 3 2 1
CAT > 10
Dspnoe
mMRC 0–1
mMRC > 2 46

45. Dyspnea questionnaire (mMRC)
Grade
Level of physical activity
Only strenous exercise provokes dyspnea 1
When hurry or walk uphill 2
While walking on the level, slower than people with same age 3
Shoud stop after 100 m walk 4
Dressing provokes dyspnea, unable to leave home because of dyspnea 47

46. CAT
COPD
Assessment
Test

47. Pneumococcus vaccination
Global Strategy for Diagnosis, Management and Prevention of COPD Treatment of stable COPD: Non-pharmacological
Patient
Intervention
Suggestion
Local guidelines A
Smoking cessation
Physical activity
Influenza/
Pneumococcus vaccination
B, C, D
Rehabilitation

48. 1.. 2.. 3.. Treatment of COPD Short , fast acting bronchodilator
SAMA – anticholinergics, ipratropium bromid spray, MDI, 4 x daily,
Short , fast acting
bronchodilator
1..
SABA - β2 agonist, salbutamol spray, MDI, 4 x daily
+ LAMA - DPI (tiotropium, glycopyrronium, umeclidinium o.d., aclidinium b.i.d.)
LABA - DPI (salmeterol, formoterol b.i.d.), (indacaterol, olodaterol napi 1x)
2..
Long acting
bronchodilator
+ ICS/LABA (frequent AE, asthma in medical history)
flutikazon/salmeterol, budezonid/formoterol,
beklometazon/formoterol, b.i.d.
3..
Antiinflammatory
drugs
oral corticosteroid ± antibiotics
32 mg methylprednisolon for days
Exacerbation =

49. The new ABCD
GOLD 2017
Consider two patients - both patients with FEV1 < 30% of predicted, CAT scores of 18 and one with no exacerbations in the past year and the other with three exacerbations in the past year. Both would have been labelled GOLD D in the prior classification scheme. However, with the new proposed scheme, the subject with 3 exacerbations in the past year would be labelled GOLD grade 4, group D.

50. Terápiás javaslat GOLD 2017
Ha a tünetek és a PFT között nagy az eltérés, további vizsgálatok szükségesek

51. Longterm oxygen in COPD
NOTT: Ann Intern Med, 1980
BMC: Lancet, 1981
the only treatment which prolongs life in hypoxic COPD
Indication: resting
PaO2 < 55 mmHg or SAT < 88%
55 Hgmm < PaO2 < 60 mmHg, and pulmonary hypertension, polyglobulia or heart failure
Target: PaO2 ≈ 60 mmHg or SAT ≈ 90 %
Pa CO2 increase < mmHg
Dose: > 15 h/day, 1-2 L/min through nasal prong

52. Respiratory insufficiency in COPD
acute exacerbation
pink puffer blue bloater
partial global
(hypoxaemic/transfer failure) (pump-, ventilatory failure)

53. wheezing, chest tightness, increased cough and sputum purulence
Main symptomps in acute exacerbation of COPD
increased dyspnea
wheezing, chest tightness, increased cough and sputum purulence
+/-
reduced exercise tolerance, fever , change in chest x-ray, leukocytosis
malice, disturbed sleep, daytime sleepiness, depression, confusion (CO2 retention)

54. Antibacterial treatment of AECOPD (CRP, procalcitonin)
pathogens treatment
1./ acute tracheobronchitis atipical agent ? macrolide ?
2./ Chronic bronchitis H. influenzae aminopenicillin/cv
without comorbidity M. catarrhalis cefalo. II, III
( FEV1 > 50% ) res. S. pneumoniae ? makrolide
3./ Chronic bronchitis with „ „
comorbidity ( FEV1 < 50% ) res. Pneumococcus ! respiratory kinolon
4./ Chronic bronchial infection „ respiratory kinolon
Gram-neg enterobact Ps. aeruginosa
= ciprofloxacin 11

55. Non-invasive mechanical ventilation in
acute respiratory insufficiency (BiPAP)
ABG: pH < 7,35 and PaCO2 > 50 Hgmm