Chronic Obstructive Pulmonary Disease

1. CHRONIC OBSTRUCTIVE PULMONARY DISEASE
by
Dr. OGUNLADE A.F

2. OUTLINE
• Definition
• Respiratory Anatomy
• Respiratory Physiology
• Epidemiology
• Risk Factors

3. DEFINITION
• Chronic obstructive pulmonary disease (COPD) is defined as a disease
state characterized by persistent progressive respiratory symptoms
and airflow limitation that is not fully reversible
• includes emphysema
• chronic bronchitis

4. DEFINITION
• Chronic bronchitis is defined clinically as the presence of a
chronic productive cough for 3 months during each of 2 consecutive
years (other causes of cough being excluded).
• Emphysema is defined pathologically as an abnormal, permanent
enlargement of the air spaces distal to the terminal bronchioles,
accompanied by destruction of their walls and without obvious
fibrosis.

5. RESPIRATORY ANATOMY
• Upper Respiratory Tract: Nasal cavity, Pharynx. Larynx, Upper part of trachea.
• Lower Resoiratory Tract: Lower part of the trachea, Bronchial tree, Lungs
• Functionally, the respiratory system can be divided into a conducting zone and a
respiratory zone
 Conducting Zone- route for incoming and outgoing air, remove debris and
pathogens from the incoming air, and warm and humidify the incoming air
– nasal cavity, Pharynx. Larynx, trachea bronchial tree.
• bronchi have walls consisting of cartilage and smooth muscle, epithelial lining with
Cilia and goblet cells, submucosal mucus secreting glands, endocrine cells

6. RESPIRATORY ANATOMY
 Respiratory Zone- structures directly involved in gas exchange.
• begins where the terminal bronchioles join a respiratory bronchiole, the
smallest type of bronchiole, which then leads to an alveolar duct, opening
into a cluster of alveoli.

8. RESPIRATORY PHYSIOLOGY- RESPIRATORY
VOLUMES AND CAPACITIES
• Tidal volume (TV) – amount of air moving in and out of the lungs with each
breath (about 500ml on average)
• Inspiratory reserve volume (IRV) – amount of air that can be taken in forcibly
over the tidal volume
• Expiratory reserve volume (ERV) – amount of air that can be forcibly exhaled
over tidal volume
• Residual volume – amount of air that always remains in the lungs; it cannot
be exhaled.
• Vital capacity – maximum amount of air that can be forcefully exchanged; VC
= TV+IRV+ERV
• Total lung capacity = VC+RV

10. EPIDEMIOLOGY
• COPD is a disease of increasing public health importance around the
world.
• COPD is the third most common cause of death worldwide with
2.5million deaths per year(6%) and 4th most common cause of death in
low income countries (WHO)
• COPD affects >10 million persons in the United States.
• In Africa, the estimated prevalence is 13.4% (Finney et al, 2012)
• The prevalence of COPD in sub-Saharan Africa has been poorly
studied. A meta-analysis of nine crosssectional studies (5 from

11. RISK FACTORS
• Cigarette smoking (>10 packs per year)
• Passive or second-hand smoking
exposure
• Extremes of age
• Lower socio-economic group
• Male gender
• Increased airway responsiveness
• Respiratory infections
• Occupational exposures, -coal, gold,
dust, and cotton.
• Ambient air pollution
• Alpha 1 antitrypsin deficiency

12. PATHOPHYSIOLOGY
• Pathologic changes in chronic obstructive pulmonary disease (COPD)
occur in the large (central) airways, the small (peripheral)
bronchioles, and the lung parenchyma.
• Most cases of COPD are the result of exposure to noxious stimuli,
most often cigarette smoke. The normal inflammatory response is
amplified in persons prone to COPD development.
• Small airways may become narrowed by cells (hyperplasia and
accumulation), mucus, and fibrosis, and extensive small airway
destruction has been demonstrated to be a hallmark of advanced COPD.

13. EMPHYSEMA PATHOGENESIS
• comprises a series of four interrelated events:
• (1) Chronic exposure to cigarette smoke in genetically susceptible individuals
triggers inflammatory and immune cell recruitment within large and small airways
and in the terminal air spaces of the lung.
• (2) Inflammatory cells release proteinases that damage the extracellular matrix
supporting gas exchange surfaces of the lung.
• (3) Structural cell death occurs through oxidant-induced damage, loss of cellular-
matrix attachments leading to alveolar destruction.
• (4) Disordered repair of elastin and other extracellular matrix components
contributes to air space enlargement and emphysema.

14. EMPHYSEMA PATHOGENESIS

15. EMPHYSEMA PATHOGENESIS
• Furthermore, loss of alveoli leads to airflow limitation by 2
mechanisms.
• First, loss of the alveolar walls results in a decrease in
elastic recoil, which leads to airflow limitation.
• Second, loss of the alveolar supporting structure leads to airway
narrowing, which further limits airflow.

16. EMPHYSEMA PATHOGENESIS
• Emphysema has 3 morphologic patterns:
• Centriacinar
• Panacinar
• Distal acinar, or paraseptal

17. EMPHYSEMA PATHOGENESIS
• Centriacinar emphysema - focal destruction limited to the respiratory
bronchioles and the central portions of the acini. associated with
cigarette smoking and typically most severe in the upper lobes.
• Panacinar emphysema - entire alveolus distal to the terminal
bronchiole. The panacinar type is typically most severe in the lower
lung zones. generally develops in patients with homozygous alpha1-
antitrypsin (AAT) deficiency.
• Distal acinar emphysema, or paraseptal emphysema.- least common form
and involves distal airway structures, alveolar ducts, and sacs. This
form of emphysema is localized to fibrous septa or to the pleura and

18. CHRONIC BRONCHITIS PATHOGENESIS-FIXING
• Damage to the endothelium impairs the mucociliary response that clears
bacteria and mucus.
• Inflammation and secretions provide the obstructive component of chronic
bronchitis.
• Neutrophilia develops in the airway lumen, and neutrophilic infiltrates
accumulate in the submucosa.
• The respiratory bronchioles display a mononuclear inflammatory process, lumen
occlusion by mucus plugging, goblet cell metaplasia, smooth muscle
hyperplasia, and distortion due to fibrosis.
• These changes, combined with loss of supporting alveolar attachments, cause
airflow limitation by allowing airway walls to deform and narrow the airway
lumen.

19. CHRONIC BRONCHITIS PATHOGENESIS
In contrast to emphysema, chronic bronchitis is associated with a relatively
undamaged pulmonary capillary bed.
• The body responds by decreasing ventilation and increasing cardiac output.
• This V/Q mismatch results in rapid circulation in a poorly ventilated lung,
leading to hypoxemia and polycythemia.
• Eventually, hypercapnia and respiratory acidosis develop, leading to pulmonary
artery vasoconstriction and cor pulmonale.
• With the ensuing hypoxemia, polycythemia, and increased CO2 retention, these
patients have signs of right heart failure and are known as "blue bloaters."

21. SYMPTOMS
• Patients typically present with a combination of signs and symptoms
of chronic bronchitis, emphysema, and reactive airway disease.
Symptoms include the following:
• Cough, usually worse in the mornings and productive of a small
amount of colorless sputum
• Breathlessness: The most significant symptom, but usually does not
occur until the sixth decade of life
• Wheezing: May occur in some patients, particularly during exertion
and exacerbations

22. PHYSICAL EXAMINATION
Relatively poor sensitivity in mild-to-moderate COPD
• In severe COPD:
• Cyanosis, visible in the lips and nail beds
• Peripheral edema
• Tachypnea and respiratory distress with simple activities
• Use of accessory respiratory muscles and paradoxical indrawing of lower
intercostal spaces (Hoover sign)
• Sitting in the characteristic “tripod” position to facilitate the actions of the
sternocleidomastoid, scalene, and intercostal muscles for a prolonged expiratory
phase.
• Elevated jugular venous pulse (JVP)

23. PHYSICAL EXAMINATION
• Thoracic examination reveals the following:
• Hyperinflation (barrel chest)
• Wheezing – Frequently heard on forced and unforced expiration
• Diffusely decreased breath sounds
• Hyperresonance on percussion
• Prolonged expiration
• Coarse crackles beginning with inspiration in some cases

24. PHYSICAL EXAMINATION- PREDOMINANT CHRONIC BRONCHITIS (BLUE
BLOATERS)
• Patients may be obese
• Frequent cough and expectoration are typical
• Use of accessory muscles of respiration is common
• Coarse rhonchi and wheezing may be heard on auscultation
• Patients may have signs of right heart failure (ie, cor pulmonale), such as edema
and cyanosis

25. PHYSICAL EXAMINATION- PREDOMINANT EMPHYSEMA (PINK PUFFERS)
• Patients may be very thin with a barrel chest
• Patients typically have little or no cough or expectoration
• Breathing may be assisted by pursed lips and use of accessory respiratory muscles;
patients may adopt the tripod sitting position
• The chest may be hyperresonant, and wheezing may be heard
• Heart sounds are very distant

27. • current evidence demonstrates that most patients have elements of
both chronic bronchitis and emphysema and that the physical
examination does not reliably differentiate the two entities.

28. INVESTIGATIONS
• Post-bronchodilator spirometry- FEV1/FVC < 70%, with normal TLC.
• The diffusing capacity may be reduced
• Arterial blood gases and oximetry may demonstrate resting or
exertional hypoxemia.
• Elevated hematocrit suggests the presence of chronic hypoxemia,
• α1AT assay

29. INVESTIGATIONS
• Chest X Ray
–Obvious bullae, paucity of parenchymal markings, or hyperlucency on suggests
the presence of emphysema.
–Increased lung volumes and flattening of the diaphragm suggest hyperinflation
• Chest computed tomography (CT) scan
–current definitive test for establishing the presence or absence of emphysema,
the pattern of emphysema, and the presence of significant disease involving
medium and large airways
–It also enables the discovery of coexisting interstitial lung disease and
bronchiectasis,
–help determine the possible value of surgical therapy

30. INVESTIGATIONS-OTHERS
• Hematocrit – Patients with polycythemia (hematocrit greater than 52% in men or
47% in women)
• Serum potassium – Diuretics, beta-adrenergic agonists, and theophylline
• Measure AAT in all patients younger than 40 years, in those with a family history
of emphysema at an early age, or with emphysematous changes in a nonsmoker
• Sputum evaluation will show a transformation from mucoid in stable chronic
bronchitis to purulent in acute exacerbations
• Pulse oximetry.
• Electrocardiography can help establish that hypoxia is not resulting in cardiac
ischemia and that the underlying cause of respiratory difficulty is not cardiac in
nature
• Right-sided heart catheterization can confirm pulmonary artery hypertension and

31. COPD SEVERITY ASSESSMENT
• GOLD Spirometric calculation-population based method.
COPD severity categories based on respiratory symptoms.
• Modified Medical Research Council Dyspnea Scale (mMRC ) or COPD
Assessment Test (CAT) and annual frequency of COPD exacerbations.
• CAT is an 8-item COPD health status measure with Likert scale
responses for questions about cough, phlegm, chest tightness,
dyspnea on one flight of stairs, limitation in home activities,
confidence in leaving the home, sleep and energy. Range of total
score is 0–40.

35. THE REFINED ABCD ASSESSMENT TOOL

36. TREATMENT- STABLE PHASE COPD
• TREATMENT GOALS
–Provide symptomatic relief
–Reduce future risk
–Improve exercise tolerance, overall health status
–Prevent and treat exacerbation AND complications
–Reduce morbidity and mortality
• Response to therapy should be assessed, and decisions should be made
whether or not to continue or alter treatment.

37. TREATMENT- STABLE PHASE COPD
• Some interventions have been demonstrated to improve survival of
patients with COPD
 Smoking cessation.
 Oxygen therapy in chronically hypoxemic patients.
 Lung volume reduction surgery (LVRS) in selected patients with
emphysema.
 Use of triple therapy significantly lowers mortality compared with
dual bronchodilation

38. PHARMACOTHERAPY
• General management:
• smoking cessation
–nicotine replacement therapy available as gum, transdermal patch,
lozenge, inhaler, and nasal spray;
–bupropion; and
–varenicline, a nicotinic acid receptor agonist/antagonist.
• Annual influenza vaccination
• One-off pneumococcal vaccination every 5 years.

39. PHARMACOTHERAPY
• Bronchodilator therapy:
 Short-acting Beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA)
is first-line treatment.
 For patients who remain breathless or have exacerbations despite using short-
acting bronchodilators the next step is determined by the FEV1.
• FEV1 > 50% (Stage I & II):
 Long-acting beta2-agonist (LABA), for example salmeterol, or: Long-acting
muscarinic antagonist (LAMA), for example tiotropium.
• FEV1 < 50% (Stage III & IV):
 LABA + high-dose inhaled corticosteroid (ICS) in a combination inhaler, or:
LAMA.

44. LTOT
• Patients who receive LTOT should breathe supplementary oxygen for at least 15
hours a day. Oxygen concentrators are used to provide a fixed supply for LTOT.
• Assess patients for LTOT if any of the following:
• Oxygen saturations less than or equal to 92% on room air
• Very severe airflow obstruction (FEV1 < 30% predicted). Assessment should be
'considered' for patients with severe airflow obstruction (FEV1 30-49% predicted).
• Patients with a PaO2 of less than 55 mm Hg, a PaO2 of less than 59 mm Hg with
evidence of polycythemia, or cor pulmonale.
• Reevaluate these patients 1-3 months after initiating therapy.

45. OTHERS
• Theophylline
• PDE4 Inhibitors
• `A1AT Augmentation Therapy
• Mucolytics

46. NONPHARMACOLOGIC THERAPIES
• Pulmonary Rehabilitation
• Lung Volume Reduction Surgery
• Lung Transplantation

47. EXACERBATIONS OF COPD
• Exacerbations are a prominent feature of the natural history of
COPD.
• Exacerbations are episodic acute worsening of respiratory symptoms,
including increased dyspnea, cough, wheezing, and/ or change in the
amount and character of sputum.
• The three cardinal symptoms of COPD exacerbation include
–increases in dyspnea,
–Increase in sputum volume, and
–Increase in sputum purulence.

48. EXACERBATIONS OF COPD
• Though symptoms of COPD exacerbations usually last for about 7 to 10 days,
the patient may not fully recover for several weeks to months.
• Patients with severe (FEV1 <50% predicted) or very severe airflow
obstruction (FEV1 <30% predicted) on average have 1–3 episodes per year.

49. EXACERBATIONS OF COPD- RISK FACTORS
• The strongest single predictor of exacerbations is a history of a previous
exacerbation
• Duration of COPD,
• History of antibiotic or theophylline use,
• Advanced age,
• Increased ratio of pulmonary artery to aorta cross-sectional dimension,
• Comorbid conditions (e.g., chronic heart failure, diabetes mellitus, GORD
etc.).
• Patients with increased sputum production, productive cough, and an
elevated blood eosinophil count (>0.34 x 109 cells/L)

50. EXACERBATIONS OF COPD- RISK FACTORS
• Environmental pollution, temperature, and pulmonary embolism are also
known exacerbation triggers.
• Chest Infections
–Bacteria frequently implicated include Haemophilus influenzae(most
common), Streptococcus pneumoniae and Moraxella catarrhalis. In
addition, Mycoplasma pneumoniae or Chlamydia pneumoniae are found in
5–10% of exacerbations.
–Viral respiratory infections are present in approximately one-third of
COPD exacerbations. rhinovirus being the most important pathogen.
• In 20–35%, no specific precipitant can be identified.

51. SEVERITY OF EXARCEBATION
SEVERITY OF
EXARCEBATION
TYPE OF EXARCEBATION CHARACTERISTICS
SEVERE TYPE 1 Increased dyspnea, sputum
volume and sputum purulence
MODERATE TYPE 2 Any 2 of the above 3 cardinal
symptoms
MILD TYPE 3 Any 1 of the above 3 cardinal
symptoms and 1 or more of the
following minor symptoms or
signs
- Cough
- Wheezing
- Fever without an obvious
source - Upper respiratory
tract infection in the past 5 days
- Respiratory rate increase
>20% over baseline
- Heart rate increase >20% over
baseline

52. TREATMENT - COPD EXARCEBATION
• The goal of therapy when treating a COPD exacerbation are
– The recovery to baseline clinical status.
– Prevention of future exarcebations.
– Prevention of hospitalization or reduction in hospital stay,
– Prevention of acute respiratory failure and death,

53. INDICATIONS FOR ADMISSION FOR ACUTE EXARCEBATION.
• Failure of outpatient treatment
• Marked increase in dyspnea
• Altered mental status
• Increase in hypoxemia or hypercapnia
• Onset of new physical signs (eg cyanosis, periphaeral edema)
• Presence of serious comorbidities (eg heart failure or new onset
arrhythmias))
• Freque nt exarcebations
• Older age
• Inability to tolerate oral medications such as antibiotics or steroids

54. INDICATIONS FOR ICU ADMISSION
• Severe dyspnea that responds inadequately to initial emergency therapy.
• Changes in mental status.(confusion, lethargy, coma)
• Persistent or worsening hypoxemia (PaO2 <5.3Kpa, 4OmmHg) and
severe/worsening resiratory acidosis (PH <7.25) despite supplemental
oxygen and noninvasive ventilation.
• Need for invasive Mechanical ventilation.
• Hemodynamic instability-need for vasopressors.

55. TREATMENT - COPD EXARCEBATION
• Bronchodilators
Mild exacerbations- use of short-acting beta2-agonists (SABA), with or
without short-acting anticholinergics
 Moderate-to-severe exacerbations- SABA+ systemic corticosteroid.
 Continued use of long-acting bronchodilators throughout the
exacerbation or start as soon as possible before discharge.
• Controlled oxygen therapy.
 Start at 24-28%. AIM: 88-92%. Adjust according to ABG: AIM: PaO2 8kpa with rise of
PaCo2 <1.5kpa

56. TREATMENT - COPD EXARCEBATION
• Steroids
 Give prednisolone 30 mg daily for 7-14 days. Prolonged courses offer no
additional benefit.
• Antibiotics
Give antibiotics only if sputum is purulent or there are clinical signs of
pneumonia.
Improves FEV1, shortens duration of hospitalization and recovery time, reduce
the risk of early relapse.
• NIV should be considered within the first 60 minutes of hospital arrival in all
patients with an acute exacerbation of COPD in whom a respiratory acidosis

58. REFERENCES
• Adeloye D, Basquill C, Papana A, et al. An estimate of the prevalence of COPD in
Africa: a systematic analysis. COPD 2015;12:71-81. 10.3109/15412555.2014.908834
• Ozoh OB, Awokola T, Bust SA. Medical student’s knowledge about the management of COPD
in Nigeria. Int J Tuber Lung Dis 2014; 18: 117–21.
• American Journal of Respiratory and Critical Care Medicine 2012;185:A6029 Chronic
Obstructive Pulmonary Disease In Sub Saharan Africa: A Systematic Review Lydia J.
Finney , Johanna Feary , Stephen B. Gordon , Jo Leonardi Bee , Kevin Mortimer ,
https://doi.org/10.1164/ajrccm-conference.2012.185.1_MeetingAbstracts.A6029
• Oxford handbook of clinical Medicine. 10th edition P184-187; P160;P812-814
• Summarizing the 2021 Updated GOLD Guidelines for COPD, US Pharmacist. US Pharm.
2021;46(7):30-35.

59. • venturi masks
• examples of drugs and classes
• HYPOXEAMIA DEFINITION
• nasal prongs non rebreayhable
• side eefect of steroids
• NORMAL PAO2 PCO2 AND OTHERS
• COR PULMONALE SX. Cyanosis
• Polycythaemia
• Peripheral oedema
• Raised jugular venous pressure
• ASTHMA VS COPD
• RELEVANT ANATOMY
• read oxford
• when is theophylline indicated and other drugs
• respiratory failure types
• ARACHIDIONIC ACID PATHWAY FOR BROCHOCONSTRICTION

61. • Features suggesting a diagnosis of COPD
• • Persistent dyspnoea on effort with cough and wheeze
• • History of smoking or exposure to other risk factors
• • Slow progression
• • Abnormal post bronchodilator spirometry
• Features that suggest the presence of asthma
• • Young age at onset
• • Diurnal or day-to-day variability and seasonal variation
• • Presence of atopy and/or allergic rhinitis
• • Significant bronchodilator responsiveness
• Additional considerations in the diagnosis of asthma and COPD
• • Asthma and COPD may co-exist, and distinguishing them may be difficult
• • Asthmatics who smoke may have an accelerated decline in lung function
• • COPD patients may have a raised eosinophil count and bronchodilator responsiveness

62. • AIRFLOW OBSTRUCTION
• Airflow limitation, also known as airflow obstruction, is typically determined for
clinical purposes by spirometry, which involves forced expiratory maneuvers after the
subject has inhaled to total lung capacity. Key parameters obtained from spirometry
include the volume of air exhaled within the first second of the forced expiratory
maneuver (FEV1) and the total volume of air exhaled during the entire spirometric
maneuver (forced vital capacity [FVC]). Patients with airflow obstruction related to
COPD have a chronically reduced ratio of FEV1/FVC. In contrast to asthma, the reduced
FEV1 in COPD seldom shows large responses to inhaled bronchodilators, although
improvements up to 15% are common.

63. • HYPERINFLATION
• In COPD there is often “air trapping” (increased residual volume
and increased ratio of residual volume to total lung capacity) and
progressive hyperinflation (increased total lung capacity) late in
the disease

64. • hyperinflation can push the diaphragm into a flattened position with a number of
adverse effects.
– First, by decreasing the zone of apposition between the diaphragm and the abdominal
wall, positive abdominal pressure during inspiration is not applied as effectively
to the chest wall, impairing inspiration.
– Second, because the muscle fibers of the flattened diaphragm are shorter than those
of a more noRmally curved diaphragm, they are less capable of generating
inspiratory pressures than normal.
– Third, the flattened diaphragm must generate greater tension to develop the
transpulmonary pressure required to produce tidal breathing.
– Fourth, the thoracic cage is distended beyond its normal resting volume, the
inspiratory muscles must do work to further inflate as recoil function is lost.

65. GAS EXCHANGE
• The partial pressure of oxygen in arterial blood Pao2 usually
remains near normal until the FEV1 is decreased to ~50% of
predicted, and even much lower FEV1 values can be associated with a
normal Pao2, at least at rest.
• PaCO2 is usually elevated when FEV1 is <25% of predicted.
• Non-uniform ventilation and ventilation-perfusion mismatching are
characteristic of COPD, reflecting the heterogeneous nature of the
disease process within the airways and lung parenchyma.

66. • Lung volume reduction surgery in selected patients:
–If PCO2 ≥ 7.4
–Severe limitation of exercise capacity despite
maximal therapy.
–Predominant upper lobe emphysema.
– Persistent symptoms despite a period of
pulmonary rehabilitation