alok sinha department of medicine manipal college of medical sciences pokhara , nepal
DESCRIPTION
C O P D. 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. - PowerPoint PPT PresentationTRANSCRIPT
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ALOK SINHADepartment of Medicine
Manipal College of Medical SciencesPokhara, Nepal
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DEFINATION
Chronic obstruction of lung airflow
which is permanent & progressiveover time
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COPD is comprised primarily of
EmphysemaChronic bronchitis
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.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)
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Emphysema and Ch.Bronchitis are two ends of spectrum of COPD with various shades in between
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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
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Ch.
Bro
nchi
tisE
mph
ysem
a
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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
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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.
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Pulmonary capillary bed relatively undamaged
Centrilobular Emphysema present to a variable degree
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Centrilobular emphysema
Pulmonary vessels in between alveoli are undamaged
Normal
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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
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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
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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
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• 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
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Panacinar emphysema
Destruction of the alveoli – blood vessels obstrcted/destroyed
reduced diffusing capacity of the lung for carbon monoxide (DLCO)
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Now identify them
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Normal lung
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Emphysematous lung
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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
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• 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
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• 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
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Causes for cachexia in emphysema
• Increased work of breathing• Low cardiac out put • Increase in TNF alpha and other mediators of
inflammation
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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
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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
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Etiology
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• 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
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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
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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
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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.
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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
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Clinical features of COPDClinical features of COPD
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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
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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
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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
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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
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Haemoptysis may complicate exacerbations of COPD but should not be attributed to COPD without thorough investigation
Exclude
Infection
malignancy &
other causes
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Barrel shaped cheststernum more archedspine unduly concaveAP diam > Trans diamt (5 : 7)horizontal ribs
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Emphysema
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NormalCompare it with
Previous one
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Movement of chest wall diminished & reduced expansion < 2 cm (from neutral to maximum inspiration)
FRC
IC
IRV
VT
ERV
RV
TLC
TLC
Normal
COPD
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Laboured breathing – pursed lip breathingIncreased hollow in supraclavicular &
suprasternal spaceIndrawing of intercostal spacesAccessory muscles of inspiration /
expiration active
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Tracheal span reduced - < 2 c.m.Tracheal tug – may be present
Indicates the severity of disease
Apical impulse/Apex beat – not visible/palpable
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• 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
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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
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Increase in A-P dimension by upper ribs; Pump- Handle Motion
mywebpages.comcast.net/wnor/respap.gif
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Increase in transverse dimension by lower ribs; Bucket-handle motion
mywebpages.comcast.net/wnor/respap.gif
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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
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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
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Features of CO2 narcosisheadacheFlapping tremorsfull & bounding pulseWarm & moist extrimitesDetoriation of consciousnessPapilloedema
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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.
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Finger clubbing
is not consistent with COPD and should alert the physician to potentially more serious pathology.
persistent crepts
raise the possibility of bronchiectasis
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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
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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
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Flow Volume Curves
25%
50%
75%
In early C.O.P.D. FEV1 may be normal but FEF25%-75% is reduced
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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
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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 ?
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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
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CBC - Polycythemia Hematocrit > 50
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Chest radiography
Chronic bronchitis is associated with increased bronchovascular markingsCardiomegalyFeatures of pulmonary hypertension
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Emphysema is associated with a small hearthyperinflation flat hemidiaphragmspossible bullous changes
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BULLAE
SUBPLEURAL BULLAE
Bleb
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.
.
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BLEBS
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Chest radiographyChronic bronchitis
associated withincreased bronchovascular markings
cardiomegaly.
Emphysema
associated withsmall hearthyperinflationflat hemidiaphrampossible bullous
changes.
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CT scan
Is useful
-detection, characterisation and quantification
-more sensitive than the chest X-ray at detecting bullae.
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.
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.
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ASSESSMENT OF SEVERITY OF COPD
GOLD CRITERIA
Global Initiative for Chronic Obstructive Lung Disease
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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
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ManagementManagement
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EMERGENCY TREATMENT
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Acute exacerbation
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Treat hypoxia
Treat bronchospasm and inflammation
Treat any underlying cause if present InfectionPneumothorax
Assess the need for intensive care
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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
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.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
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3. Bronchodilators
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.
Bronchodilator
short-acting beta-agonist short-acting anticholinergics
given initially by nebulizer therapy
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.
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
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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
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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
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.
In severe airflow obstruction
combination of Ipratropium Salbutamol/albuterol
provide better broncho dilatation than used alone
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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)
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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
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Monitoring progress
Pre- and post-nebulizer peak flows
Repeated arterial blood gases 1-2 hourly or according to response especially if SaO2 <93%
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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)
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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
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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
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.
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
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.•When every thing fails
definitive airway management via
Intubation & mechanical ventilation
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life saving
high risk of complications overall mortality of ~13%.
hypotension in ~38%
Barotrauma seen in ~14% • pneumothorax • pneumo-mediastinum• subcutaneous emphysema
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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%
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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
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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.
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Smoking cessation
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Aids for stopping smoking
Nicotine patch
Nicotine gum
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Oxygen therapy Bronchodilators Inhaled Corticosteroids (ICS) Pulmonary rehabilitation Physiotherapy Annual influenza & pneumococcal vaccine Surgical intervention
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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
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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
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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
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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
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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)
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Incentive SpirometryIncentive Spirometry
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QUIZHow much capitation fee will be charged at MCOMS if she takes admission ?
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COPDCOPDCachexia
Cor pulmonale
pneumothorax
Respiratory failure
Acute exacerbations
Secondary polycythemia
Due to Treatment
(P.T.)
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Cor pulmonale caused by pulmonary hypertension This leads to enlargement and
subsequent failure of the right side of the heart
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pneumothorax consider in all patients
with COPD with acute exacerbation
Due to rupture of subpleural bullae Blebs
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Acute exacerbations due toAcute infections – preventive role of
pneumococcal and influenza vaccineRecent increase in size of bullae
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Secondary polycythemia due to hypoxiaIncreases blood viscosity
Pulmonary hypertensionthrombosis
Hematocrit > 60 then phlebotomy is done
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• 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
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CachexiaIncreased work of respirationReduced appetite and absorbtionRelease of inflammatory mediators (TNF alfa)
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Bronchial Asthma Vs COPD
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• 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
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• 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
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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