ALOK SINHADepartment of Medicine

Manipal College of Medical SciencesPokhara, Nepal

.

DEFINATION

Chronic obstruction of lung airflow

which is permanent & progressiveover time

.

COPD is comprised primarily of

EmphysemaChronic bronchitis

.Asthma also is a pulmonary disease in which there is obstruction to the flow of air out of the lungsobstruction in asthma usually is

reversible Between "attacks" of asthma the flow of

air through the airways usually is good

(With execptions)

.

Emphysema and Ch.Bronchitis are two ends of spectrum of COPD with various shades in between

Defining feature of COPD is irreversible airflow limitation during forced expiration

FEV1(<80%) & FEV1/FVC (<70%) are reduced

EMPHYSEMA

a result of a loss of

elastic recoil due to

lung tissue destruction

Pathology

starts beyond terminal

bronchioles

CHR. BRONCHITIS

increase in resistance of the

conducting airways due to• accumulation of inflammatory

mucous exudates in the lumens

of small airways• Thickening of their walls

Pathology confined

up to terminal bronchioles

Ch.

Bro

nchi

tisE

mph

ysem

a

Chronic Bronchitis

Inflammation & swelling of the airways lining

narrowing and obstruction of airways due to

Hyperplasia of mucus-producing glands

Over production of mucous - further

obstruction of the airways - increases

likelihood of bacterial lung infections

Reid index - chronic bronchitis

Ratio of the thickness of mucous gland layer to thickness of wall between epithelium & cartilage. Normal Reid index is less than 0.4 is increased in chronic bronchitis.

.

Pulmonary capillary bed relatively undamaged

Centrilobular Emphysema present to a variable degree

Centrilobular emphysema

Pulmonary vessels in between alveoli are undamaged

Normal

Compared to EmphysemaAir way narrowing is morePulmonary circulation is less affected

Body responds by decreasing ventilation and increasing cardiac output.

due to rapid circulation in a poorly ventilated lung – increase in physiological shunt leading to Hypoxemia Polycythemia

V/Q mismatch

Eventually, hypercapnia and respiratory acidosis develop

Leading to pulmonary artery vasoconstriction and pulmonary hypertension with cor pulmonale

Patients have signs of right heart failure and are known as

Emphysema Permanent enlargement of the air spaces distal to

the terminal bronchioles, with destruction of their

walls –reduces the elasticity of the lung –collapse of the bronchioles –obstructing airflow out of the alveoli

Insp

iratio

n

Exp

iratio

n

.

• Air trapping in the alveoli

• Inability of the lung to shrink during exhalation

• Amount of air inhaled is reduced

• Less air for the exchange of gasses in lungs

• Trapped air compress adjacent less damaged

lung tissue compromising their function

Panacinar emphysema

Destruction of the alveoli – blood vessels obstrcted/destroyed

reduced diffusing capacity of the lung for carbon monoxide (DLCO)

Now identify them

Normal lung

Emphysematous lung

.

Destruction of the alveolar walls decreases the

number of capillaries gas exchange decreases(decreased DLCO)

• due to relatively limited blood flow through a fairly well oxygenated lung – increase in physiological dead space with normal blood gases and pressures in the lung, (in contrast to the blue bloaters.)

• The body compensates with – lowered cardiac output – hyperventilation

V/Q mismatch

• Normally expiration is passive process- effortless– extra effort required to exhale due to collapse of airways

• Lungs are already inflated due to air trapping so more

effort required to inhale further

• Work of breathing is increased

• Reduced gaseous exchange increase the

Breathing rate

• Because of low cardiac output, rest of body suffers from tissue hypoxia and pulmonary cachexia. Eventually, develop muscle wasting and weight loss and are identified as

Causes for cachexia in emphysema

• Increased work of breathing• Low cardiac out put • Increase in TNF alpha and other mediators of

inflammation

.

EMPHYSEMAPulmonary capillary bedrelatively damaged

V/Q mismatch - relatively limitedblood flow through a fairly welloxygenated lung with normalblood gases & pressures in the

Lung - Dead Space

Body compensates withlowered cardiac output

andHyperventilation

CHR. BRONCHITISPulmonary capillary

bedrelatively undamaged

V/Q mismatch – rapidcirculation in a poorly ventilatedlung, leading to hypoxemia andPolycythemia

Shunt

Body responds by increasing cardiac

output& decreasing ventilation

Chronic Asthma

Obstruction to the flow of air is due toinflammation of the airways -thickening of the

airway walls lead to scarring and fixed airway

obstruction spasm of smooth muscles - bronchospasm

reversible

subsides spontaneously or with the use of bronchodilators

Etiology

• Smoking responsible for 90% of COPD • not all cigarette smokers develop COPD-15% will (don’t tell

this to smokers)

Smokers with COPD have higher death rates

than non smokers with COPD

Have more frequent respiratory symptomscoughing, shortness of breath

passive smoking – equally harmful

MECHANISMIrritation of cigarette smoke attracts cells

to the lungs that promote inflammation.

They release elastase -breaks down the elastic fibers in lung tissue

Increases mucus production

Decreases ciliary motility

2. Air pollution Role of outdoor air pollution – unclear

most common cause of COPD in non

industrialized world is indoor air pollution due to

indoor stoves used for cooking – biomass fuel

3. Occupational pollutants:

Cadmium & Silica - increase the risk of COPD

.

Alpha-1 antitrypsin deficiencyGenetic disorder

Accounts for less than 1% of the COPD

Enzyme elastase is found normally in lungs.It can

break down the elastin and damage the airways

and alveoli

Alpha-1 antitrypsin produced by liver block the

damaging effects of elastase on elastin.

.

Alpha-1 antitrypsin deficiency causes

1. Early on set of emphysema- homozygos

2. Accelerated emphysema in smokers- hetrozygos

3. Chronic liver disease leading to cirrhosis due to

their defective release leading to intra hepatic

accumulation

Clinical features of COPDClinical features of COPD

.

Patients with COPD present with a combination of signs and symptoms of

chronic bronchitis

emphysema

SymptomsWorsening dyspneaProgressive exercise intolerance Alteration in mental status

In addition, some important clinical and historical differences exist between the types of COPD

Common symptoms

.

Chronic bronchitis

• Productive cough, with progression over time to intermittent dyspnoea

• Cough and sputum on most days -at least 3 consecutive months for at least 2 successive years

• Morning headache – CO2 retention

• Hemoptysis – usually small• Frequent & recurrent

pulmonary infections • Progressive

cardiac/respiratory failure over time, with oedema and weight gain

Emphysema

• A long history of progressive dyspnea with late onset of nonproductive cough

• Occasional

mucopurulent relapses

• Eventual cachexia and respiratory failure

.

19.29 MODIFIED MRC DYSPNOEA SCALEGrade Degree of breathlessness

0 No breathlessness except with strenuous exercise

1 Breathlessness when hurrying on the level or walking up a slight hill

2 Walks slower than contemporaries on level ground because of breathlessness or has to stop for breath when walking at own pace

3 Stops for breath after walking about 100 m or after a few minutes on level ground

4 Too breathless to leave the house, or breathless when dressing or undressing

Haemoptysis may complicate exacerbations of COPD but should not be attributed to COPD without thorough investigation

Exclude

Infection

malignancy &

other causes

Barrel shaped cheststernum more archedspine unduly concaveAP diam > Trans diamt (5 : 7)horizontal ribs

Emphysema

NormalCompare it with

Previous one

Movement of chest wall diminished & reduced expansion < 2 cm (from neutral to maximum inspiration)

FRC

IC

IRV

VT

ERV

RV

TLC

TLC

Normal

COPD

Laboured breathing – pursed lip breathingIncreased hollow in supraclavicular &

suprasternal spaceIndrawing of intercostal spacesAccessory muscles of inspiration /

expiration active

Tracheal span reduced - < 2 c.m.Tracheal tug – may be present

Indicates the severity of disease

Apical impulse/Apex beat – not visible/palpable

• Hyper resonant note, liver & cardiac dullness diminished or obliterated

• Breath sounds –diminished, vesicular with prolonged expiration

• Ronchi or wheeze during expiration• Crepitations may be present more during

inspiration

Inspiration: result of active contraction

DiaphragmExternal intercoastals

pump handle action of the upper 8 ribs increases the AP diameter of the chest

bucket handle action of the lower 4 ribs increases the transverse diameter of the chest

resulting in costal elevation & lateral expansion

Increase in A-P dimension by upper ribs; Pump- Handle Motion

             

               

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Increase in transverse dimension by lower ribs; Bucket-handle motion

                            

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Hutchison's Clinical Methods (22E)page 55

Movement of the chest Body: Look at the chest movements. Are they symmetrical? If they seem to be diminished on one side, that is likely to be the side on which there is an abnormality. Intercostal recession - a drawing-in of the intercostal spaces with inspiration - may indicate severe upper

airways obstruction, as in laryngeal disease, or tumours of the trachea. In COPD the lower ribs often move inwards on inspiration instead of the normal outwards movement

Hoover's signrefers to the inspiratory retraction of the lower

intercostal spacesresults from alteration in dynamics of

diaphragmatic contraction due to hyperinflation resulting in traction on the rib margins by the flattened diaphragm

Seen in up to 70% of patients with severe obstruction can be an excellent marker for severe airway obstruction

Features of CO2 narcosisheadacheFlapping tremorsfull & bounding pulseWarm & moist extrimitesDetoriation of consciousnessPapilloedema

.

Emphysema    • Patients may be very thin

with a barrel chest. • Typically have little or no

cough or expectoration. • Breathing may be assisted by

pursed lips & use of accessory respiratory musls.

• chest hyper resonant• wheezing may be heard;

heart sounds very distant

• Overall appearance is more like classic COPD exacerbation. Rt H.F. usually not seen till late

Chronic bronchitis • Patients may be obese. • Frequent cough and

expectoration are typical.

• Use of accessory muscles of respiration not so prominent

• Coarse rhonchi and wheezing may be heard on auscultation.

• Patients may have signs of

right heart failure - edema & cyanosis.

Finger clubbing

is not consistent with COPD and should alert the physician to potentially more serious pathology.

persistent crepts

raise the possibility of bronchiectasis

.

PFTObstructive pattern

Reduced FEV1 to <80% predicted (FEV1 is the measurement of choice to assess progression of COPD)

FEV1/FVC < 0.7Minimal bronchodilator reversibility (<15%,

usually <10%)Raised total lung volume, FRC, and residual

volume because of emphysema, air trapping, and loss of elastic recoil

Decreased TLCO and kCO because presence of emphysema decreases surface area available for gas diffusion

PEFR diary – less than 20% variationNo change in FEV1: FVC with exercise

(absence of exercise induced bronchospasm)

TLCO=CO transfer factor for whole lung KCO=gas transfer coefficient

Flow Volume Curves

25%

50%

75%

In early C.O.P.D. FEV1 may be normal but FEF25%-75% is reduced

.

Pulmonary function tests (Summary)

  Decreased forced expiratory volume in 1

second (FEV1) with concomitant reduction in FEV1/forced vital capacity (FVC) ratio

Poor/absent reversibility with bronchodilators FVC normal or reduced Normal or increased total lung capacity (TLC) Increased residual volume (RV) Normal or reduced diffusing capacity

.

Arterial blood gas  

Arterial blood gas (ABG) analysis provides the best clues as to acuteness and severity

pH usually is near normal due to renal compensation in chronic disease

Generally, consider any pH below 7.3 a sign of acute respiratory compromise ?

.

Serum chemistry   These patients tend to retain sodium.

Diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels serum potassium should be monitored carefully.

Beta-adrenergic agonists also increase renal

excretion of serum calcium and magnesium, which may be important in the presence of hypokalemia

CBC - Polycythemia Hematocrit > 50

.

Chest radiography 

Chronic bronchitis is associated with increased bronchovascular markingsCardiomegalyFeatures of pulmonary hypertension

Emphysema is associated with a small hearthyperinflation flat hemidiaphragmspossible bullous changes

BULLAE

SUBPLEURAL BULLAE

Bleb

.

.

BLEBS

Chest radiographyChronic bronchitis

associated withincreased bronchovascular markings

cardiomegaly.

Emphysema

associated withsmall hearthyperinflationflat hemidiaphrampossible bullous

changes.

CT scan

Is useful

-detection, characterisation and quantification

-more sensitive than the chest X-ray at detecting bullae.

.

Pulse oximetry  

Pulse oximetry does not offer as much information as ABG analysis.

When combined with clinical observation, this test can be a powerful tool for instant feedback on the patient's status.

ASSESSMENT OF SEVERITY OF COPD

GOLD CRITERIA

Global Initiative for Chronic Obstructive Lung Disease

Stage Symptoms Characteristics

0: at risk cough, sputum production

Normal spirometry

I : mild COPD ,,(With or without)

FEV1/FVC < 70%FEV1 ≥ 80% predicted

IIA: moderate COPD

,, FEV1/FVC < 70%FEV1 = 50 – 80%

IIB: Potential for severe exacerb.

,, FEV1/FVC < 70%FEV1 = 30 – 50%

severe COPD ,, FEV1/FVC < 70%FEV1 < 30% predictedOr < 50% with signs of resp.failure or CCF

ManagementManagement

.

EMERGENCY TREATMENT

Acute exacerbation

Treat hypoxia

Treat bronchospasm and inflammation

Treat any underlying cause if present InfectionPneumothorax

Assess the need for intensive care

Initial treatment

1. Sit the patient up in bed

2. Oxygen: Adequate oxygen should be given to relieve hypoxia

With administration of oxygen, PO2 and PCO2 rise but not in proportion to the very minor changes in respiratory drive

.Supply the patient with enough oxygen to maintain a near normal saturation (above 90%)

do not be concerned about oxygen supplementation leading to clinical deterioration

If the patient's condition is that tenuous, intubation most likely is needed anyway

3. Bronchodilators

.

Bronchodilator  

short-acting beta-agonist short-acting anticholinergics

given initially by nebulizer therapy

.

It help in COPD by- stimulation of receptors relaxes airway

smooth muscles increases mucociliary clearance decreases mucous production

Delivered by-

Nebulizer M D I with space halers – if nebulizer not

available

Parentral in refractory cases

Nebulization with short acting bronchodilators Salbutamol 5mg or

Terbutaline 10mg administered with O2 repeat up to every 15-30 minutes if required

continuous nebulization of salbutamol 10mg/h if inadequate response to initial treatment

Monitor Serum K+ regularly to prevent hypokalemia as a side effect

Anticholinergics

act via inhibition of cyclic guanosine monophosphate (GMP)–mediated bronchoconstriction. decrease mucus production improve mucociliary clearance

Ipratropium bromide -agent of choiceAdd ipratropium bromide 0.5mg 6 hourly if initial response to –Beta-2 agonists is poor

.

In severe airflow obstruction

combination of Ipratropium Salbutamol/albuterol

provide better broncho dilatation than used alone

Obtain iv access

4. Start Steroids: • Hydrocortisone - 200mg intravenously

• Repeat 6 – 8 hourly• Or Methylprednisolone: 1-2 mg/kg IV q6h; not

to exceed 125 mg• Follow up with oral corticosteroid -

Prednisolone (40 to 60 mg / day) in tapering doses

(steroids should still be used in pregnant women as the risk of foetal anoxia from the asthma is high)

5. Antibiotics

Antibiotics in chest infection purulent sputum/ or fever abnormal CXR raised WBC

should provide coverage against Pneumococcus H influenzae Legionella species Gram-negative enterics

Prefferably afluroquinolone orCo Amoxyclav 650 m.g.X 3 orDoxycyclline 100 m.g. X 2

Monitoring progress

Pre- and post-nebulizer peak flows

Repeated arterial blood gases 1-2 hourly or according to response especially if SaO2 <93%

If response not brisk or patient's condition is deteriorating

Continue oxygen and nebulized beta2-agonist every 15 minutes

7. magnesium sulphate iv single dose

1.2-2g infused over 20 minutes

8. iv Aminophylline infusion

Loading dose: 250mg (4-5mg/kg) iv in 20 min

Maintenance infusion: 0.5- 0.7mg/kg/h (250mg in 1 litre N saline at 2- 4 ml/kg/h)

Consider iv salbutamol infusion Loading dose: 100- 300µg over 10 minutes Maintenance infusion: 5 -20µg/min (5mg in 500ml saline at

1- 3ml/min)

Side Effects: • tremor• tachycardia• hypokalaemia • hyperglycaemia

Summon anaesthetic help

Indications for admission to intensive care unit

Hypoxia (PaO2 <8kPa (60mmHg) despite FiO2 of 60%

Rising PaCO2 or PaCO2 >6kPa (45mmHg)

Exhaustion, drowsiness, or coma

Respiratory arrest

Failure to improve despite adequate therapy

.

NON INVASIVE POSITIVE PRESSURE VENTILATION

continuous positive airway pressure

(CPAP) biphasic positive airway pressure

(BiPAP)

prevents airways collapse & air trapping

reduces the need for endotracheal intubation

Heliox (ie, mixture of helium and oxygen) inhalation may be tried

.•When every thing fails

definitive airway management via

Intubation & mechanical ventilation

life saving

high risk of complications overall mortality of ~13%.

hypotension in ~38%

Barotrauma seen in ~14% • pneumothorax • pneumo-mediastinum• subcutaneous emphysema

On-going therapy

continue nebulized beta2-agonist, reducing to 4-hourly and withdraw after 24- 48 hours

Peak flow rate should be measured before and after each nebulizer

Maintain O2 sats >92%

Continue nebulized ipratropium bromide 6-hourly until the condition is improving

Continue steroids, hydrocortisone 100mg q6h iv switching to 30- 60mg o d oral prednisolone when able to swallow, and continue for 10-14 days

Monitor serum K+ daily and supplement as necessary

Discharge

PEF should be 75% of best without significant morning dipping

should be established on inhalers with no requirement for nebulizers for 24- 48 hours prior to discharge.

Smoking cessation

Aids for stopping smoking

Nicotine patch

Nicotine gum

Oxygen therapy Bronchodilators Inhaled Corticosteroids (ICS) Pulmonary rehabilitation Physiotherapy Annual influenza & pneumococcal vaccine Surgical intervention

LTOT via an oxygen concentrator for patients in respiratory failure, with

PaO2 < 55 mm / Hg (7.3 kPa) with any PCO2

PaO2 of 7.3 – 8 kPa (55 – 60 mm) with any of: secondary polycythaemiaperipheral oedema pulmonary hypertension present

FEV1 < 1.5 liters

use for a minimum of 15 hours per day (including

Sleep)

Oxygen therapy

LONG-TERM DOMICILIARY OXYGEN THERAPY (LTOT)

improves survival, reduces secondary polycythaemiaprevents progression of primary

pulmonary hypertension.

Use at least 15 hours/day at 2-4 litres/min to achieve a PaO2 > 8 kPa (60 mmHg) without unacceptable rise in PaCO2

MUST STOP SMOKING

a. N O T

PaO2 < 55 mm SaO2 < 88%- while awake

Decrease in PaO2 > 10 mm & SaO2 > 5%

while asleep

c. Supplementation during exercise

when after exercise the gas saturation comes down

BronchodilatorsIpratropium bromide

by M.D.I. – 2 puffs (36-72 mcg) X 6h Nebul.

Long acting beta2 agonist SalmeterolBambuterol

less expensive than aboverapid onsetmore side effects

Theophylline -have other effects on diaphragm, resp centre etc

Inhaled corticosteroids (ICS) reduce the frequency & severity of exacerbations

recommended in patients with severe disease 1.FEV1 < 50%

2.two or more exacerbations requiring antibiotics or oral steroids per year.

previuos response to steroids during acute exacerbation concomitent asthma Has no role in modifying the disease as opposed to

bronchial asthma (no need to give early in disease)

The combination of ICS with long-acting β2-agonists produces further improvement in breathlessness and reduces the frequency and severity of exacerbations.

(Role of oral CS)

Incentive SpirometryIncentive Spirometry

QUIZHow much capitation fee will be charged at MCOMS if she takes admission ?

COPDCOPDCachexia

Cor pulmonale

pneumothorax

Respiratory failure

Acute exacerbations

Secondary polycythemia

Due to Treatment

(P.T.)

Cor pulmonale caused by pulmonary hypertension This leads to enlargement and

subsequent failure of the right side of the heart

pneumothorax consider in all patients

with COPD with acute exacerbation

Due to rupture of subpleural bullae Blebs

Acute exacerbations due toAcute infections – preventive role of

pneumococcal and influenza vaccineRecent increase in size of bullae

Secondary polycythemia due to hypoxiaIncreases blood viscosity

Pulmonary hypertensionthrombosis

Hematocrit > 60 then phlebotomy is done

• Acute or chronic respiratory failure • Acute

– Due to infections– Associated with resp. acidosis

• Chronic – Type I– Type II in severe COPD when FEV1< 1 liter

• Associated with features of CO2 narcosis

CachexiaIncreased work of respirationReduced appetite and absorbtionRelease of inflammatory mediators (TNF alfa)

Bronchial Asthma Vs COPD

• airflow obstruction due to inflammation & increased airway hyper-responsive ness & bronchospasm which is

• variable over short periods of time

• reversible with treatment

• Mostly by allergens in atopic persons

• Mostly affects the young people

• Chronic obstruction of lung airflow which is permanent & progressive over time

• Due to the chemical

irritation of the airways

caused by smoke(ing)

• Disease of middle aged & elderly

cause

Age group

• Airway obstruction due to– Smooth muscle spasm– oedema

• Chest normal in between the attacks

• Emphysematous changes do not occur

• Does not progress to cor pulmonale or type II respiratory failure

• Due to– Loss of elastic recoil: Emphysema

– Remodeling of the air way: Ch Bronchitis

• Features of air way obstruction always seen

• Seen after some years

• Many cases develop these complication

Pathogenesis

Clinical features

Complications

Pulmonary Function TestObstructive picture +1. FEV1 ≥ 15% (and 200 ml)

increase following administration of a bronchodilator/trial of corticosteroids

2. > 20% diurnal variation on ≥ 3 days in a week for 2 weeks on PEF diary

3. FEV1 ≥ 15% decrease after 6 mins of exercise

• Normal in between attacks. Hyper inflated lungs at the time of acute attack

Obstructive pattern +1. Minimal bronchodilator

reversibility (<15%, usually <10%)

2. < 20% diurnal variation on ≥ 3 days in a week for 2 weeks on PEF diary

3. No change in FEV1: FVC with exercise (absence of exercise induced bronchospasm)

• Shows – Emphysematous changes with

bullae– Features of pulmonary

hypertension

X ray chest