Definition
Chronic obstructive pulmonary disease (COPD) is defined as a disease state characterized by airflow limitation that is not fully reversible
Suspected when age>40/50
It includes emphysema and chronic bronchitis
Emphysema((Abnormal permanent dilatation of airways distal to terminal bronchiole without obvious fibrosis)
Pink puffers(emphysema is more
predominant than chronic bronchitis)
Thin ,non cyanotic ,normal PaCO2
until end stage
Types-Centriacinal(Smoker)
,panacinar(Alpha 1 anti trypsin deficiency)
Chronic bronchitis
Blue
bloaters(Chronic bronchitis is more predominant than emphysema)
Fatty ,cyanotic ,early PaCO2 rise
Etiology
1.Cigarette smoking
2.Occupational-Silicon
,jute factory
3.Alpha 1 anti
trypsin deficiency
Pathogenesis
Dust
inhaled>Chronic irritation>Goblet hypertrophy/plasia>Increased mucous
secretion>Inflammation>Edema>Narrowing of airway>Bulla>(+Anti
trypsin)>Disrupted alveoli>Hypoxia
(If Hypoxia>Increased
erythropoietin>Increased RBC>Secondary polycythemia>Urea
production>Gout)
[COPD-Permanent narrowing
Asthma-Reversible narrowing]
Cor pulmonale
Right ventricular hypertrophy(RVH) with/without
failure due to pulmonary hypertension due to diseases of lung parenchyma or its
vasculature or (Pectus excavatum)chest wall
Mechanism-
Alveoli ruptured>Decreased capillary bed and hypoxia>Vasoconstriction>Pulmonary hypertension>RVH>Regurgitation>Right ventricular failure
When there is
RVH-Left parasternal heave,epigastric pulse ,palpable p2 is found
Clinical feature
1.Age-Middle/elderly
,usually after 50
2.Sex-M>F(Except
rangpur)
3.Onset-Gradual(Starts
as productive winter cough which
gradually increases in severity and duration on subsequent years until present
throughout the year.Initially exertional dyspnoea ,then progresses)
4.H/O
smoking(Minimum 10 pack years)
[ 1 pack year=20
sticks/day for 1 year]
Typical
presentation of COPD
Productive cough for most of the days in a month for 3 consequetive months for at least 2 successive years(Chronic bronchitis)
General physical examination
Early-Asymptomatic
Late-
Appearance-Respiratory distress ,accessory muscle are prominent
Cyanosis
Raised JVP(RVF)
Enlarged tender liver(If RVF)
Leg edema(Failure to excrete salt/water by hypoxic
hypercapnoeic kidney)
Warm hand(If respiratory failure hypercapnoea )
Full bounding pulse(If respiratory failure)
Local
examination of Respiratory system
1.Inspection-
Respiratory distress ,barrel chest ,indrawing of supraclavicular-intercostal-subcostal spaces
Hoover's
sign-In severe case paradoxical inward movement of rib cage with inspiration
2.Palpation
Vocal fremitus-Decreased
Expansibility-Decreased
Trachea-Normal
Enlarged
tender soft liver and ascitis[If Cor>RVF>Congested liver>Jaundice]
3.Percussion
Hyper resonant
(Upper border liver dullness below 5th
space and diminished superficial cardiac dullness(If emphysema) [If one is +ve
and other is -ve ,it is pneumothorax]
4.Auscultation
Breath sound-Vesicular with prolonged expiration
Added
sound-Ronchi
Pleural
rub-No
Crepitation-May
be present
Differential diagnosis
Bronchial asthma
TB
Heart failure
Bronchiectasis
Complication
1.Cor pulmonale(Check if RVH and percussion)
2.Pneumothorax
3.Secondary
polycythemia(Red dusky conjunctiva)
4.Type
2 respiratory failure(When hypoxia with hypercapnoea present , Blood gas
analysis shows PaCO2 >50mmHg ,which should be normally 35-40mmHg)
Features of hypercapnoea
Prominent eyeball , red conjunctiva ,warm extremity ,full bounding pulse ,flapping tremor
Investigation
FBC with TC DC WBC(polycythemia) , raised PCV ,reduced ESR
Chest X ray PA view
Low flat diaphragm
Horizontal rib
Tubular heart shadow
Widening of intercostal spaces
More Translucent lung with bulla
Lung function test
Decreased PEFR(500-600fm) [It is
bed side test]
Spirometry-FEV1 <70%
,FEV1/FVC ratio also reduced
Reversibility test -ve
Sputum for AFB
Arterial Blood gas analysis
ECG ,Echo
Serum Alpha 1 anti trypsin(Young ,non
smoker)
Post
bronchodilator FEV1 classification
Mild-FEV1 <80%
Moderate-FEV1 50-79%
Severe-FEV1 30-49%
Very severe-FEV1 <30%
[With FEV1/FVC ratio <70% for all the above]
Treatment
1.Avoid smoking
2.Propped up position
3.O2 in low dose & continuous(?)-[In prolonged hypercapnoea ,patient gets insensitive to PaCO2 ,only depends on hypoxia for respiration.High dose O2 corrects hypoxemia ,leaving to chemical factor to drive respiratory centre causing respiratory arrest and apnoea.Thereby further rise in CO2 leading to CO2 necrosis. So 24-28% O2 is to given by venturi mask.Correct PaO2 at <60mmHg as hypoxic drive is withdrawn if PaO2 >60mmHg]
4.Cephalosporin
5.Inhaled bronchodilator and steroid
6.Diuretics if edema
7.Breathing exercise to cough out secretions
8.LTOT/domiciliary oxygen-
2-4L O2/hr in 15 hrs in a day for
life long to prevent pulmonary hypertension ,cor pulmonale
Indication-PaO2 <7.3 kPa ,OR
,> 7.3 kPa with PTN
[1L O2 raises 4% O2 saturation]
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