Chronic Obstructive Pulmonary Disease (COPD) is characterized by airflow limitation due to chronic bronchitis and emphysema, with symptoms including cough, dyspnea, and wheezing, often leading to significant health decline and comorbidities. Patients can be classified as 'blue bloaters' (chronic bronchitis) or 'pink puffers' (emphysema) based on their symptoms and physiological responses, with a need for careful management including smoking cessation and bronchodilator therapy. Exacerbations are typically triggered by infections and require prompt intervention with short-acting bronchodilators, systemic corticosteroids, and antibiotics, along with possible hospitalization in severe cases.

1. Dr. Akram Yousuf
P.G (Med III)

2. The Global Initiative for Chronic Obstructive
Lung Disease (GOLD) guidelines define COPD is a
disease state characterized by airflow limitation
that is not fully reversible, is usually progressive,
and is associated with an abnormal
inflammatory response of the lungs to inhaled
noxious particles or gases.

8. 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.
Difference:
Airflow limitation in emphysema is due to loss of elastic recoil and
decrease in airway tethering, whereas chronic bronchitis leads to
narrowing of airway caliber and increase in airway resistance. Although
some patients predominantly display signs of one of these diseases or
the other, most fall somewhere in the middle of the spectrum between
the 2 conditions.

16. Patient with chronic
bronchitis have dec
alveolar ventilation,
with a low PaO2 and a
high PaCO2. hence
they are cyanosed and
called Blue Bloaters

22. Emphysemetic patients
have inc alveolar
ventilation, a near
normal PaO2 and a
normal or low PaCO2.
They are not Cynosed
and called Pink Puffers .

23. Blue Bloaters have dec alveolar ventilation, with a low PaO2 and
a high PaCO2. They are cyanosed but not breathless and may go
on to develop cor pulmonale. Their respiratory centres are
relatively insensitive to CO2 and they rely on hypoxic drive to
maintain respiratory effort —supplemental oxygen should be
given with care
Pink Puffers have inc alveolar ventilation, a near normal PaO2
and a normal or low PaCO2. They are breathless but are not
cyanosed. They may progress to type 1 respiratory failure
Blue Bloaters V/S Pink Puffers

30. • Occupational exposures, such as coal, silica and cadmium
• Low Birth Weight Baby
• Childhood Infections or Maternal Smoking
• Recurrent Infections
• Low socioeconomic status
• Cannabis smoking

32. • Most patients with chronic obstructive pulmonary disease
(COPD) seek medical attention late in the course of their
disease.
• Patients often ignore the symptoms because they start
gradually and progress over the course of years.
• Patients typically present with a combination of signs and
symptoms of chronic bronchitis, emphysema, and reactive
airway disease.

33. The common symptoms includes,
• Cough (The cough usually is worse in the mornings and
produces a small amount of colorless sputum)
• Worsening Dyspnea (Breathlessness is the most significant
symptom, but it usually does not occur until the 4th to 6th
decade of life. By the time the FEV1 has fallen to 50% of
predicted, the patient is usually breathless upon minimal
exertion)
• Wheezing (Wheezing may occur in some patients, particularly
during exertion and exacerbations)

34. Systemic manifestations
• Muscular weakness,
• Perpheral edema,
• weight loss due to altered fat metabolism,
• increased osteoporosis.

35. Some important clinical differences may help distinguish between
the types of COPD:
• Classic findings for patients with chronic bronchitis include
productive cough with gradual progression to intermittent
dyspnea; frequent and recurrent pulmonary infections and
progressive cardiac/respiratory failure with edema and weight
gain.
• Classic findings for patients with emphysema include a long
history of progressive dyspnea with late onset of nonproductive
cough; occasional mucopurulent relapses; and eventual
cachexia and respiratory failure.

37. • The sensitivity of a physical examination in detecting mild to
moderate COPD is relatively poor.
• Patients with severe disease experience tachypnea and
respiratory distress with simple activities.
• The respiratory rate increases in proportion to disease severity.
• Use of accessory respiratory muscles and paradoxical indrawing
of lower intercostal spaces is evident (known as the Hoover
sign).
• In advanced disease, cyanosis, elevated jugular venous pulse
(JVP), and peripheral edema can be observed.

38. On Inspection:
• The patient is dyspnoeic with pursuing of lips and resp rate of
>30 br/mins.
• The chest is barrel shaped.
• Indrawing of lower intercostal space on inspiration due to low
flat diaphragm.
• Suprasternal and Supraclavicular Excavation.
• Prominent accessory muscles of respiration may be seen.

39. On Percussion:
• Increased resonance in both lung fields.
• Obliteration of liver and cardiac dullness (liver dllness may be
lower down)
On Auscultaion:
• Breath sounds may be diminished but vesicular with prolong
expiration
• Rhonchi may be present if associated with chronic bronchitis

41. Chronic bronchitis Emphysema
• 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
• 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
• Overall appearance is more like
classic COPD exacerbation

46. • Pulmonary function tests are essential for the diagnosis and
assessment of the severity of disease, and they are helpful in
following its progress.
• If post bronchodilators shows FEV1/FVC <70% of predicted, it
may indicates the obstructive pattern of lung disease.

48. Arterial Blood Gas Analysis
• provides the best clues as to acuteness and severity of disease
exacerbation.
• Patients with mild COPD have mild to moderate hypoxemia
without hypercapnia. As the disease progresses, hypoxemia
worsens and hypercapnia may develop
Serum Electrolytes
• Patients with COPD tend to retain sodium. In addition, serum
potassium should be monitored carefully, because diuretics, beta-
adrenergic agonists, and theophylline act to lower potassium
levels.
• Chronic respiratory acidosis leads to compensatory metabolic
alkalosis. In the absence of blood gas measurements, bicarbonate
levels are useful for following disease progression

49. Sputum DR
• In persons with stable chronic bronchitis, the sputum is
mucoid and macrophages are the predominant cells.
• With an exacerbation, sputum becomes purulent because of
the presence of neutrophils
• A mixture of organisms often is visible with Gram stain.The
pathogens cultured most frequently during exacerbations are
Streptococcus pneumoniae, Haemophilus influenzae, Moraxella
catarrhalis and Pseudomonas aeruginosa.
Alpha 1 Anti Trypsin :
• Measure alpha1-antitrypsin (AAT) in all patients younger than 40
years or in those with a family history of emphysema at an early
age. The diagnosis of severe AAT deficiency is confirmed when the
serum level falls below the protective threshold value of 11
mmol/L (ie, in the range of 3-7 mmol/L)

50. Pulse Oximeter
• when combined with clinical observation, this test can be a
powerful tool for instant feedback on a patient's status
Blood C.P
• Chronic hypoxemia may lead polycythemia.
• A hematocrit greater than 52% in men or 47% in women is
indicative of polycythemia.
• Correction of hypoxemia should reduce secondary
polycythemia in patients who have quit smoking

51. Echocardiography:
• Many patients with long-standing COPD develop secondary
pulmonary hypertension from chronic hypoxemia and
vascular remodeling.
• This may result in eventual right-sided heart failure (cor
pulmonale)
right-sided heart catheterization
• may be performed to measure pulmonary artery pressures
directly and to gauge the response to vasodilators.

53. Modified British Medical Research Council (mMRC) is used to
assess the degree of Breathlessness in the patient of COPD.

54. GOLD criteria for assessing the severity of airflow obstruction
(based on the percent predicted postbronchodilator FEV1 when
the FEV1/FVC is < 70%) are as follows:
• Stage I (mild) - FEV 1 80% or greater of predicted
• Stage II (moderate) - FEV 1 50-79% of predicted
• Stage III (severe) - FEV 1 30-49% of predicted
• Stage IV (very severe) - FEV 1 less than 30% of predicted or FEV 1
less than 50% and chronic respiratory failure

63. Once the diagnosis of COPD is
established, it is important to
educate the patient about the
disease and to encourage his or
her active participation in
therapy.

70. • Smoking cessation continues
to be the most important
therapeutic intervention for
COPD

71. • Smoking cessation continues
to be the most important
therapeutic intervention for
COPD
• Studies have shown that
brief (3 mins) counseling
to urge a smoker to quit
results in smoking quit rate
of 5 – 10%.

72. • Smoking cessation continues
to be the most important
therapeutic intervention for
COPD
• Studies have shown that
brief (3 mins) counseling
to urge a smoker to quit
results in smoking quit rate
of 5 – 10%.
• Nicotine replacement
therapy (nicotine gum,
nasal spray, transdermal
patch, sublingual tablet) as
well as pharmacotherapy
with Bupropion or
nortriptyline reliably
increases long term
smoking abstinence rate.

76.  Bronchodilators (Inhalers):
• SABA: Salbutamol , Terbutaline
• SAMA: Ipratropium: 2-4 puffs 6-8 hourly
• LABA: Salmeterol: 2 puff B.D, Formoterol: 2 puff B.D, Indacaterol: 2 puff O.D,
• LAMA: Tiotropium 2 puff O.D
 Inhaled Corticosteroids: Fluticasone, Budesonide
 Bronchodilators (ORAL):
• Xanthine derivatives (ie, theophylline)
• Phosphodiesterase-4 Inhibitors (ie, roflumilast)
 Oral Corticosteroids: Prednisone

77. Other Therapy
• Mucolytics: Acetylcysteine
• Antibiotic: If Infection
• Diuretics

80. Oxygen therapy for COPD
• Oxygen is usually given via a facemask or nasal cannulae.
• Titrate the amount guided by the SaO2 (aim for 94–98% (or 88–92% if, or at
risk of hypercapnia)
• Humidification is only required for longer-term delivery of O2 at high flow
rates and tracheostomies.
 Nasal cannulae: preferred by patients, but O2 delivery is relatively imprecise
and may cause nasal soreness. The flow rate (1–4L/min) roughly defines the
concentration of O2 (24–40%). May be used to maintain SaO2 when
nebulizers need to be run using air.
 Venturi mask: provides a precise percentage of O2 (FiO2) at high flow rates.
Colour codes:
24% BLUE
28% WHITE
35% YELLOW
40% RED
60% GREEN
Start at 24–28% in COPD

81. Indication of Long term Oxygen
Therapy in COPD
When PaO2 is <55mmHg or SaO2 <88% irrespective of PaCO2.
When PaO2 is 55-60 mmHg associated with
• Pulmonary Hypertension
• Peripheral Edema suggesting CCF
• Nocturnal Hypoxemia
• Secondary Polycythemia (Hematocrit > 55%)
• Carboxyhemoglobin <3% (in patient who have stopped
smoking)

91. An exacerbation of COPD is:
“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.”

92.  The most common causes of COPD exacerbations are viral
upper respiratory tract infections and infection of the
tracheobronchial tree.
 Diagnosis relies exclusively on the clinical presentation of the
patient complaining of an acute change of symptoms that is
beyond normal day-to-day variation.
 The goal of treatment is to minimize the impact of the current
exacerbation and to prevent the development of subsequent
exacerbations.

93.  Short-acting inhaled beta2-agonists with or without short-
acting anticholinergics are usually the preferred
bronchodilators for treatment of an exacerbation.
 Systemic corticosteroids and antibiotics can 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.
 COPD exacerbations can often be prevented.

94.  Short-acting inhaled beta2-agonists with or without short-
acting anticholinergics are usually the preferred
bronchodilators for treatment of an exacerbation.
 Systemic corticosteroids and antibiotics can 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.
 COPD exacerbations can often be prevented.

97. Indications of Hospitalization
Marked increase in the symptoms.
Severe underlying COPD
Failure to respond to initial Outpatient management
Presence of serious comorbidities
Older age
Insufficient home support