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ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara, Nepal.

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Presentation on theme: "ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara, Nepal."— Presentation transcript:

1 ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara, Nepal

2 . DEFINATION Chronic obstruction of lung airflow which is permanent & progressive over time

3 . COPD is comprised primarily of Emphysema Chronic bronchitis

4 . Asthma also is a pulmonary disease in which there is obstruction to the flow of air out of the lungs 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 obstruction in asthma usually is reversible Between "attacks" of asthma the flow of air through the airways usually is good Between "attacks" of asthma the flow of air through the airways usually is good ( With execptions)

5 . Emphysema and Ch.Bronchitis are two ends of spectrum of COPDwith various shades in between

6 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

7 Ch. Bronchitis Emphysema

8 Chronic Bronchitis Inflammation & swelling of the airways lining narrowing and obstruction of airways due to narrowing and obstruction of airways due to Hyperplasia of mucus-producing glands Hyperplasia of mucus-producing glands Over production of mucous - further obstruction of the airways - increases Over production of mucous - further obstruction of the airways - increases likelihood of bacterial lung infections likelihood of bacterial lung infections

9

10 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.

11 . Pulmonary capillary bed relatively undamaged Pulmonary capillary bed relatively undamaged Centrilobular Emphysema present to a variable degree Centrilobular Emphysema present to a variable degree

12 Centrilobular emphysema Pulmonary vessels in between alveoli are undamaged Normal

13 Compared to Emphysema Compared to Emphysema Air way narrowing is more Air way narrowing is more Pulmonary circulation is less affected Pulmonary circulation is less affected Body responds by decreasing ventilation and increasing cardiac output. Body responds by decreasing ventilation and increasing cardiac output. due to rapid circulation in a poorly ventilated lung – increase in physiological shunt leading to due to rapid circulation in a poorly ventilated lung – increase in physiological shunt leading to Hypoxemia Hypoxemia Polycythemia Polycythemia V/Q mismatch

14 Eventually, hypercapnia and respiratory acidosis develop Eventually, hypercapnia and respiratory acidosis develop Leading to pulmonary artery vasoconstriction and pulmonary hypertension with cor pulmonale Leading to pulmonary artery vasoconstriction and pulmonary hypertension with cor pulmonale Patients have signs of right heart failure and are known as Patients have signs of right heart failure and are known as

15 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 Inspiration Expiration

16 . 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

17 Panacinar emphysema Destruction of the alveoli – blood vessels obstrcted/destroyed reduced diffusing capacity of the lung for carbon monoxide (DLCO)

18 Now identify them

19 Normal lung

20 Emphysematous lung

21 . 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

22 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

23 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

24 Causes for cachexia in emphysema Increased work of breathing Low cardiac out put Increase in TNF alpha and other mediators of inflammation

25 . 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

26 Chronic Asthma Obstruction to the flow of air is due to inflammation of the airways -thickening of the inflammation of the airways -thickening of the airway walls lead to scarring and fixed airway obstruction spasm of smooth muscles - bronchospasm reversible spasm of smooth muscles - bronchospasm reversible subsides spontaneously or subsides spontaneously or with the use of bronchodilators with the use of bronchodilators

27 Etiology

28 Smoking responsible for 90% of COPD Smoking responsible for 90% of COPD not all cigarette smokers develop COPD-15% will (don’t tell this to smokers) not all cigarette smokers develop COPD-15% will (don’t tell this to smokers) Smokers with COPD have higher death rates Smokers with COPD have higher death rates than non smokers with COPD Have more frequent respiratory symptoms Have more frequent respiratory symptoms coughing, coughing, shortness of breath shortness of breath passive smoking – equally harmful

29 MECHANISM Irritation of cigarette smoke attracts cells to the lungs that promote inflammation. 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 Increases mucus production Decreases ciliary motility Decreases ciliary motility

30 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

31 . Alpha-1 antitrypsin deficiency Genetic disorder Genetic disorder Accounts for less than 1% of the COPD 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.

32 . 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

33 Clinical features of COPD

34 . Patients with COPD present with a combination of signs and symptoms of chronic bronchitis emphysemaSymptoms Worsening dyspnea Worsening dyspnea Progressive exercise intolerance Progressive exercise intolerance Alteration in mental status Alteration in mental status In addition, some important clinical and historical differences exist between the types of COPD In addition, some important clinical and historical differences exist between the types of COPD Common symptoms

35 . 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 gainEmphysema A long history of progressive dyspnea with late onset of nonproductive cough Occasional mucopurulent relapses Eventual cachexia and respiratory failure

36 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

37 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

38 Haemoptysis may complicate exacerbations of COPD but should not be attributed to COPD without thorough investigation ExcludeInfection malignancy & other causes

39

40 Barrel shaped chest Barrel shaped chest sternum more arched sternum more arched spine unduly concave spine unduly concave AP diam > Trans diamt (5 : 7) AP diam > Trans diamt (5 : 7) horizontal ribs horizontal ribs

41 Emphysema

42 Normal Compare it with Previous one

43 Movement of chest wall diminished & reduced expansion < 2 cm (from neutral to maximum inspiration) Movement of chest wall diminished & reduced expansion < 2 cm (from neutral to maximum inspiration) FRC IC IRV VT ERV RV TLC Normal COPD

44 Laboured breathing – pursed lip breathing Laboured breathing – pursed lip breathing Increased hollow in supraclavicular & suprasternal space Increased hollow in supraclavicular & suprasternal space Indrawing of intercostal spaces Indrawing of intercostal spaces Accessory muscles of inspiration / expiration active Accessory muscles of inspiration / expiration active

45 Tracheal span reduced - < 2 c.m. Tracheal span reduced - < 2 c.m. Tracheal tug – may be present Tracheal tug – may be present Indicates the severity of disease Indicates the severity of disease Apical impulse/Apex beat – not visible/palpable Apical impulse/Apex beat – not visible/palpable

46 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

47 Inspiration: Inspiration: result of active contraction result of active contraction Diaphragm Diaphragm External intercoastals External intercoastals pump handle action of the upper 8 ribs pump handle action of the upper 8 ribs increases the AP diameter of the chest increases the AP diameter of the chest bucket handle action of the lower 4 ribs bucket handle action of the lower 4 ribs increases the transverse diameter of the chest increases the transverse diameter of the chest resulting in costal elevation & lateral expansion resulting in costal elevation & lateral expansion

48 Increase in A-P dimension by upper ribs; Pump- Handle Motion mywebpages.comcast.net/wnor/respap.gif

49 Increase in transverse dimension by lower ribs; Bucket-handle motion mywebpages.comcast.net/wnor/respap.gif

50 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 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

51 Hoover's sign refers to the inspiratory retraction of the lower intercostal spaces 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 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 Seen in up to 70% of patients with severe obstruction can be an excellent marker for severe airway obstruction

52

53

54 Features of CO2 narcosis headache headache Flapping tremors Flapping tremors full & bounding pulse full & bounding pulse Warm & moist extrimites Warm & moist extrimites Detoriation of consciousness Detoriation of consciousness Papilloedema Papilloedema

55 . Emphysema Emphysema Patients may be very thin with a barrel chest.Patients may be very thin with a barrel chest. Typically have little or no cough or expectoration.Typically have little or no cough or expectoration. Breathing may be assisted by pursed lips & use of accessory respiratory musls.Breathing may be assisted by pursed lips & use of accessory respiratory musls. chest hyper resonantchest hyper resonant wheezing may be heard; heart sounds very distantwheezing may be heard; heart sounds very distant Overall appearance is more like classic COPD exacerbation. Rt H.F. usually not seen till lateOverall 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.

56 Finger clubbing is not consistent with COPD and should alert the physician to potentially more serious pathology. persistent crepts raise the possibility of bronchiectasis

57 .

58 PFT Obstructive pattern Reduced FEV1 to <80% predicted (FEV1 is the measurement of choice to assess progression of COPD) Reduced FEV1 to <80% predicted (FEV1 is the measurement of choice to assess progression of COPD) FEV1/FVC < 0.7 FEV1/FVC < 0.7 Minimal bronchodilator reversibility (<15%, usually <10%) Minimal bronchodilator reversibility (<15%, usually <10%) Raised total lung volume, FRC, and residual volume because of emphysema, air trapping, and loss of elastic recoil Raised total lung volume, FRC, and residual volume because of emphysema, air trapping, and loss of elastic recoil

59 Decreased TLCO and kCO because presence of emphysema decreases surface area available for gas diffusion Decreased TLCO and kCO because presence of emphysema decreases surface area available for gas diffusion PEFR diary – less than 20% variation PEFR diary – less than 20% variation No change in FEV1: FVC with exercise (absence of exercise induced bronchospasm) No change in FEV1: FVC with exercise (absence of exercise induced bronchospasm) TLCO=CO transfer factor for whole lung KCO=gas transfer coefficient

60 Flow Volume Curves 25% 50% 75% In early C.O.P.D. FEV1 may be normal but FEF25%-75% is reduced

61 . Pulmonary function tests Pulmonary function tests (Summary) Decreased forced expiratory volume in 1 second (FEV1) with concomitant reduction in FEV1/forced vital capacity (FVC) ratio Decreased forced expiratory volume in 1 second (FEV1) with concomitant reduction in FEV1/forced vital capacity (FVC) ratio Poor/absent reversibility with bronchodilators Poor/absent reversibility with bronchodilators FVC normal or reduced FVC normal or reduced Normal or increased total lung capacity (TLC) Normal or increased total lung capacity (TLC) Increased residual volume (RV) Increased residual volume (RV) Normal or reduced diffusing capacity Normal or reduced diffusing capacity

62 . Arterial blood gas Arterial blood gas Arterial blood gas (ABG) analysis provides the best clues as to acuteness and severity 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 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 ? Generally, consider any pH below 7.3 a sign of acute respiratory compromise ?

63 . Serum chemistry Serum chemistry These patients tend to retain sodium. These patients tend to retain sodium. Diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels serum potassium should be monitored carefully. 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 Beta-adrenergic agonists also increase renal excretion of serum calcium and magnesium, which may be important in the presence of hypokalemia

64 CBC - Polycythemia Hematocrit > 50

65 . Chest radiography Chest radiography Chronic bronchitis is associated with Chronic bronchitis is associated with increased bronchovascular markings increased bronchovascular markings Cardiomegaly Cardiomegaly Features of pulmonary hypertension Features of pulmonary hypertension

66

67

68 Emphysema is associated with a Emphysema is associated with a small heart small heart hyperinflation hyperinflation flat hemidiaphragms flat hemidiaphragms possible bullous changes possible bullous changes

69 BULLAE SUBPLEURAL BULLAE Bleb

70 ..

71

72 BLEBS

73 Chest radiography Chronic bronchitis associated with increased broncho increased broncho vascular markings vascular markings cardiomegaly. cardiomegaly.Emphysema associated with small heart small heart hyperinflation hyperinflation flat hemidiaphram flat hemidiaphram possible bullous changes. possible bullous changes.

74 CT scan Is useful -detection, characterisation and quantification -detection, characterisation and quantification -more sensitive than the chest X-ray at detecting bullae. -more sensitive than the chest X-ray at detecting bullae.

75

76 . Pulse oximetry Pulse oximetry Pulse oximetry does not offer as much information as ABG analysis. 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. When combined with clinical observation, this test can be a powerful tool for instant feedback on the patient's status.

77 ASSESSMENT OF SEVERITY OF COPD GOLD CRITERIA Global Initiative for Chronic Obstructive Lung Disease

78 StageSymptomsCharacteristics 0: at riskcough, 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% predicted Or < 50% with signs of resp.failure or CCF

79 ManagementManagement

80 . EMERGENCY TREATMENT

81 Acute exacerbation

82 Treat hypoxia Treat bronchospasm and inflammation Treat any underlying cause if present  Infection  Pneumothorax Assess the need for intensive care

83 Initial treatment 1. Sit the patient up in bed 2. Oxygen: 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

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

85 3. Bronchodilators

86 .Bronchodilator  short-acting beta-agonist  short-acting anticholinergics given initially by nebulizer therapy given initially by nebulizer therapy

87 . 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

88 Nebulization with short acting bronchodilators Salbutamol 5mg or Terbutaline 10mg administered with O2 administered with O2 repeat up to every minutes if required repeat up to every minutes if required continuous nebulization of salbutamol 10mg/h if inadequate response to initial treatment continuous nebulization of salbutamol 10mg/h if inadequate response to initial treatment Monitor Serum K + regularly to prevent hypokalemia as a side effect

89 Anticholinergics act via inhibition of cyclic guanosine monophosphate (GMP)–mediated bronchoconstriction. decrease mucus production decrease mucus production improve mucociliary clearance improve mucociliary clearance Ipratropium bromide -agent of choice Add ipratropium bromide 0.5mg 6 hourly if initial response to –Beta-2 agonists is poor

90 . In severe airflow obstruction combination of Ipratropium Ipratropium Salbutamol/albuterol Salbutamol/albuterol provide better broncho dilatation than used alone

91 Obtain iv access 4. Start Steroids : Hydrocortisone - 200mg intravenously Hydrocortisone - 200mg intravenously Repeat 6 – 8 hourly Repeat 6 – 8 hourly Or Methylprednisolone: 1-2 mg/kg IV q6h; not to exceed 125 mg 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 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)

92 5. Antibiotics Antibiotics in chest infection purulent sputum/ or fever purulent sputum/ or fever abnormal CXR abnormal CXR raised WBC raised WBC should provide coverage against P neumococcus P neumococcus H influenzae H influenzae Legionella species Legionella species Gram-negative enterics Gram-negative enterics Prefferably a Prefferably a fluroquinolone or fluroquinolone or Co Amoxyclav 650 m.g.X 3 or Co Amoxyclav 650 m.g.X 3 or Doxycyclline 100 m.g. X 2 Doxycyclline 100 m.g. X 2

93 Monitoring progress Pre- and post-nebulizer peak flows Repeated arterial blood gases 1-2 hourly or according to response especially if SaO2 <93%

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

95 Consider iv salbutamol infusion Loading dose: µg over 10 minutes Loading dose: µg over 10 minutes Maintenance infusion: 5 -20µg/min (5mg in 500ml saline at 1- 3ml/min) Maintenance infusion: 5 -20µg/min (5mg in 500ml saline at 1- 3ml/min) Side Effects: Side Effects: tremor tremor tachycardia tachycardia hypokalaemia hypokalaemia hyperglycaemia hyperglycaemia Summon anaesthetic help

96 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

97 . NON INVASIVE POSITIVE PRESSURE VENTILATION continuous positive airway pressure continuous positive airway pressure(CPAP) biphasic positive airway pressure (BiPAP) 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

98 . When every thing fails definitive airway management via Intubation & mechanical ventilation

99 life saving high risk of complications overall mortality of ~13%.  hypotension in ~38%  Barotrauma seen in ~14% pneumothoraxpneumothorax pneumo-mediastinumpneumo-mediastinum subcutaneous emphysemasubcutaneous emphysema

100 On-going therapy continue nebulized beta2-agonist, reducing to 4-hourly and withdraw after hours Peak flow rate should be measured before and after each nebulizer Maintain O2 sats >92%

101 Continue nebulized ipratropium bromide 6-hourly until the condition is improving Continue steroids, hydrocortisone 100mg q6h iv switching to mg o d oral prednisolone when able to swallow, and continue for days Monitor serum K+ daily and supplement as necessary

102 Discharge PEF should be 75% of best without significant morning dipping should be established on inhalers with no requirement for nebulizers for hours prior to discharge.

103

104  Smoking cessation

105

106 Aids for stopping smoking Nicotine patch Nicotine gum

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

108 LTOT via an oxygen concentrator for patients in respiratory failure, with LTOT via an oxygen concentrator for patients in respiratory failure, with PaO 2 < 55 mm / Hg (7.3 kPa) with any PCO 2 PaO 2 < 55 mm / Hg (7.3 kPa) with any PCO 2 PaO 2 of 7.3 – 8 kPa (55 – 60 mm) with any of: PaO 2 of 7.3 – 8 kPa (55 – 60 mm) with any of: secondary polycythaemia secondary polycythaemia peripheral oedema peripheral oedema pulmonary hypertension present pulmonary hypertension present FEV1 < 1.5 liters FEV1 < 1.5 liters use for a minimum of 15 hours per day (including Sleep) Oxygen therapy

109 LONG-TERM DOMICILIARY OXYGEN THERAPY (LTOT) improves survival, improves survival, reduces secondary polycythaemia reduces secondary polycythaemia prevents progression of primary pulmonary hypertension. 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 MUST STOP SMOKING

110 a. N O T PaO2 < 55 mm SaO2 < 88%- while awake Decrease in PaO2 > 10 mm & SaO2 > 5% Decrease in PaO2 > 10 mm & SaO2 > 5% while asleep while asleep c. Supplementation during exercise when after exercise the gas saturation comes down when after exercise the gas saturation comes down

111 Bronchodilators Ipratropium bromide by M.D.I. – 2 puffs (36-72 mcg) X 6h Nebul. Long acting beta2 agonist SalmeterolBambuterol less expensive than above rapid onset more side effects Theophylline -have other effects on diaphragm, resp centre etc

112 Inhaled corticosteroids (ICS) reduce the frequency & severity of exacerbations recommended in patients with severe disease 1.FEV1 < 50% 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 previuos response to steroids during acute exacerbation during acute exacerbation concomitent asthma concomitent asthma Has no role in modifying the disease as opposed to bronchial asthma (no need to give early in disease) 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) (Role of oral CS)

113 Incentive Spirometry

114 QUIZ How much capitation fee will be charged at MCOMS if she takes admission ?

115 COPD Cachexia Cor pulmonale pneumothorax Respiratory failure failure Acuteexacerbations Secondarypolycythemia Due to Treatment(P.T.)

116 Cor pulmonale Cor pulmonale caused by pulmonary hypertension caused by pulmonary hypertension This leads to enlargement and subsequent failure of the right side of the heart This leads to enlargement and subsequent failure of the right side of the heart

117 pneumothorax pneumothorax consider in all patients with COPD with acute exacerbation consider in all patients with COPD with acute exacerbation Due to rupture of Due to rupture of subpleural bullae subpleural bullae Blebs Blebs

118 Acute exacerbations due to Acute exacerbations due to Acute infections – preventive role of pneumococcal and influenza vaccine Acute infections – preventive role of pneumococcal and influenza vaccine Recent increase in size of bullae Recent increase in size of bullae

119 Secondary polycythemia due to hypoxia Secondary polycythemia due to hypoxia Increases blood viscosity Increases blood viscosity Pulmonary hypertension Pulmonary hypertension thrombosis thrombosis Hematocrit > 60 then phlebotomy is done Hematocrit > 60 then phlebotomy is done

120 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

121 Cachexia Cachexia Increased work of respiration Increased work of respiration Reduced appetite and absorbtion Reduced appetite and absorbtion Release of inflammatory mediators (TNF alfa) Release of inflammatory mediators (TNF alfa)

122 Bronchial Asthma Vs COPD Bronchial Asthma Vs COPD

123 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

124 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

125 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 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


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