Transcript CHRONIC OBSTRUCTIVE PULMONARY DISEASE

ALOK SINHA
Department of Medicine
Manipal College of Medical Sciences
Pokhara, Nepal
.
DEFINATION
Chronic obstruction of lung airflow
which is permanent & progressive
over time
.
COPD is comprised primarily of
Chronic bronchitis
Emphysema
 Asthma
also is a pulmonary disease
in which there is obstruction to the
flow of air out of the lungs
 obstruction
.
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
CHR. BRONCHITIS
a result of a loss of
increase in resistance of the
elastic recoil due to
conducting airways due to
lung tissue destruction • accumulation of inflammatory
mucous exudates in the lumens
of small airways
• Thickening of their walls
Pathology
Pathology confined
starts beyond terminal
up to terminal bronchioles
bronchioles
Emphysema
Ch. Bronchitis
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
Normal
Pulmonary vessels in between
alveoli are undamaged
 Compared
to Emphysema
 Air
way narrowing is more
 Pulmonary circulation is less affected
 Body
responds by decreasing ventilation
and increasing cardiac output.
V/Q mismatch due to rapid circulation in a poorly
ventilated lung – increase in physiological shunt
leading to
 Hypoxemia
 Polycythemia
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
Expiration
Inspiration
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
• 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)
• V/Q mismatch 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
• Normally expiration is passive processeffortless
– 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
EMPHYSEMA
Pulmonary capillary bed
relatively damaged
V/Q mismatch - relatively limited
blood flow through a fairly well
oxygenated lung with normal
blood gases & pressures in the
Lung -
Dead Space
Body compensates with
lowered cardiac output and
Hyperventilation
.
CHR. BRONCHITIS
Pulmonary capillary bed
relatively undamaged
V/Q mismatch – rapid
circulation in a poorly ventilated
lung, leading to hypoxemia and
Polycythemia
Shunt
Body responds by
increasing cardiac output
& decreasing ventilation
Chronic Asthma
Obstruction to the flow of air is due to
inflammation 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 symptoms
 coughing,
 shortness of breath
passive smoking – equally harmful
MECHANISM
 Irritation
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 deficiency
.

Genetic 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 COPD
Patients with COPD present with a combination
of signs and symptoms of
chronic bronchitis
emphysema
.
Symptoms
Worsening dyspnea
Progressive exercise intolerance
Alteration in mental status
Common
symptoms
 In addition, some important clinical and historical differences
exist between the types of COPD
Chronic bronchitis
Emphysema
.
• Productive cough, with
• A long history of
progression over time to
progressive dyspnea
intermittent dyspnoea
with late onset of
• Cough and sputum on most days nonproductive cough
-at least 3 consecutive months
for at least 2 successive years • Occasional
mucopurulent relapses
• Morning headache – CO2 retention
• Hemoptysis – usually small
• Eventual cachexia
• Frequent & recurrent pulmonary
and respiratory
infections
failure
• Progressive cardiac/respiratory
failure over time, with oedema
and weight gain
19.29 MODIFIED MRC DYSPNOEA
SCALE
.
Grade 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 chest
sternum more arched
 spine unduly concave
 AP diam > Trans diamt (5 : 7)
 horizontal ribs

Emphysema
Normal
Compare it with
Previous one

Movement of chest wall diminished & reduced
expansion < 2 cm (from neutral to maximum
inspiration)
COPD
Normal
IRV
TLC
IC
VT
ERV
FRC
RV
TLC
breathing – pursed lip breathing
 Increased hollow in supraclavicular &
suprasternal space
 Indrawing of intercostal spaces
 Accessory muscles of inspiration /
expiration active
 Laboured
Tracheal span reduced - < 2 c.m.
 Tracheal tug – may be present


Indicates the severity of disease
impulse/Apex beat – not
visible/palpable
 Apical
• 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
 Diaphragm
 External

pump handle action of the upper 8 ribs


increases the AP diameter of the chest
bucket handle action of the lower 4 ribs


intercoastals
increases the transverse diameter of the chest
resulting in costal elevation & lateral expansion
Increase in A-P
dimension by
upper ribs; PumpHandle Motion
mywebpages.comcast.net/wnor/respap.gif
Increase in
transverse
dimension by lower
ribs; Bucket-handle
motion
mywebpages.comcast.net/wnor/respap.gif
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 drawingin 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 sign
refers to the inspiratory retraction of the lower
intercostal spaces
 results 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 narcosis
 headache
 Flapping
tremors
 full & bounding pulse
 Warm & moist extrimites
 Detoriation of consciousness
 Papilloedema
Chronic bronchitis
• Patients may be obese.
• Frequent cough and
expectoration are typical.
Emphysema
• Patients may be very thin
with a barrel chest.
• Typically have little or no
cough or expectoration.
• Use of accessory muscles of • Breathing may be assisted by
pursed lips & use of
respiration not so prominent
accessory respiratory musls.
• chest hyper resonant
• Coarse rhonchi and wheezing • wheezing may be heard;
heart sounds very distant
may be heard on auscultation.
• Patients may have signs of
right heart failure - edema &
cyanosis.
.
• Overall appearance is more
like classic COPD exacerbation.
Rt H.F. usually not seen till
late
Finger clubbing
is not consistent with COPD and should alert
the physician to potentially more serious
pathology.
persistent crepts
raise the possibility of bronchiectasis
.
PFT
Obstructive pattern
Reduced FEV1 to <80% predicted (FEV1 is the
measurement of choice to assess progression
of COPD)
 FEV1/FVC < 0.7
 Minimal 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
TLCO=CO transfer factor for whole lung KCO=gas
transfer coefficient
PEFR diary – less than 20% variation
 No change in FEV1: FVC with exercise
(absence of exercise induced bronchospasm)

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 markings
Cardiomegaly
Features of pulmonary hypertension

Emphysema is associated with a
small heart
hyperinflation
flat hemidiaphragms
possible bullous changes
SUBPLEURAL
BULLAE
Bleb
BULLAE
.

.
BLEBS
Chest radiography
Chronic bronchitis
associated with
increased broncho
vascular markings
cardiomegaly.
Emphysema
associated with
small heart
hyperinflation
flat hemidiaphram
possible 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
0: at risk
cough, sputum Normal spirometry
production
I : mild COPD
FEV1/FVC < 70%
(With or without) FEV1 ≥ 80% predicted
FEV1/FVC < 70%
,,
FEV1 = 50 – 80%
IIA: moderate
COPD
IIB: Potential for
severe exacerb.
severe COPD
Characteristics
,,
,,
,,
FEV1/FVC < 70%
FEV1 = 30 – 50%
FEV1/FVC < 70%
FEV1 < 30% predicted
Or < 50% with signs of
resp.failure or CCF
Management
EMERGENCY TREATMENT
.
Acute exacerbation
Treat hypoxia
Treat bronchospasm and inflammation
Treat any underlying cause if present
 Infection
 Pneumothorax
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 choice
Add 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 a
fluroquinolone or
Co Amoxyclav 650 m.g.X 3 or
Doxycyclline 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




Oxygen therapy
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 polycythaemia
 peripheral oedema
 pulmonary hypertension present

FEV1 < 1.5 liters
use for a minimum of 15 hours per day (including
Sleep)

LONG-TERM DOMICILIARY
OXYGEN THERAPY (LTOT)
 improves
survival,
 reduces secondary polycythaemia
 prevents 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
Bronchodilators
Ipratropium bromide
by M.D.I. – 2 puffs (36-72 mcg) X 6h
Nebul.
Long acting beta2 agonist
Salmeterol
Bambuterol
less expensive than above
rapid onset
more 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 Spirometry
QUIZ
How much
capitation fee will
be charged at
MCOMS if she
takes admission ?
Due to
Treatment
(P.T.)
Cachexia
Cor pulmonale
pneumothorax
COPD
Acute
exacerbations
Respiratory
failure
Secondary
polycythemia
 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
 Blebs
bullae
 Acute
exacerbations due to
Acute infections – preventive role of
pneumococcal and influenza vaccine
 Recent increase in size of bullae


Secondary polycythemia due to hypoxia

Increases blood viscosity
 Pulmonary
hypertension
 thrombosis

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

Cachexia
Increased work of respiration
 Reduced appetite and absorbtion
 Release of inflammatory mediators (TNF alfa)

 Bronchial
Asthma Vs COPD
• airflow obstruction due to • Chronic obstruction of
inflammation & increased lung airflow which is
airway hyper-responsive
permanent & progressive
ness & bronchospasm
over time
which is
• variable over short
periods of time
• reversible with treatment
cause
• Mostly by allergens in atopic • Due to the chemical
irritation of the airways
persons
caused by smoke(ing)
Age group
• Mostly affects the young
people
• Disease of middle aged &
elderly
Pathogenesis
• Airway obstruction due to
• Due to
– Smooth muscle spasm
– oedema
– Loss of elastic recoil: Emphysema
– Remodeling of the air way: Ch
Bronchitis
Clinical features
• Chest normal in between
the attacks
• Features of air way
obstruction always seen
Complications
• Emphysematous changes • Seen after some years
do not occur
• Does not progress to cor
• Many cases develop
pulmonale or type II
these complication
respiratory failure
Pulmonary Function Test
Obstructive 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
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
No change in FEV1: FVC with
exercise (absence of exercise
induced bronchospasm)
3.
X ray chest
•
Normal in between attacks. Hyper •
inflated lungs at the time of acute
attack
Shows
–
–
Emphysematous changes with
bullae
Features of pulmonary
hypertension