Presentation on theme: "Department of Medicine Manipal College of Medical Sciences"— Presentation transcript:
1 Department of Medicine Manipal College of Medical Sciences C O P DALOK SINHADepartment of MedicineManipal College of Medical SciencesPokhara, Nepal
2 Chronic obstruction of lung airflow .DEFINATIONChronic obstruction of lung airflowwhich is permanent & progressiveover time
3 COPD is comprised primarily of .COPD is comprised primarily ofChronic bronchitisEmphysema
4 .Asthma also is a pulmonary disease in which there is obstruction to the flow of air out of the lungsobstruction in asthma usually is reversibleBetween "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 COPD with various shades in betweenEmphysema and Ch.Bronchitis.
6 Defining feature of COPD is irreversible airflow limitation during forced expiration FEV1(<80%) & FEV1/FVC (<70%) are reducedEMPHYSEMAa result of a loss ofelastic recoil due tolung tissue destructionPathologystarts beyond terminalbronchiolesCHR. BRONCHITISincrease in resistance of theconducting airways due toaccumulation of inflammatorymucous exudates in the lumensof small airwaysThickening of their wallsPathology confinedup to terminal bronchioles
8 Chronic Bronchitis Inflammation & swelling of the airways lining narrowing and obstruction of airways due toHyperplasia of mucus-producing glandsOver production of mucous - further obstruction of the airways - increaseslikelihood of bacterial lung infections
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 0.4is increased in chronic bronchitis.
11 Pulmonary capillary bed relatively undamaged .Pulmonary capillary bed relatively undamagedCentrilobular Emphysema present to a variable degree
12 Centrilobular emphysema NormalPulmonary vessels in between alveoli are undamaged
13 Body responds by decreasing ventilation and increasing cardiac output. Compared to EmphysemaAir way narrowing is morePulmonary circulation is less affectedBody responds by decreasing ventilation and increasing cardiac output.due to rapid circulation in a poorly ventilated lung – increase in physiological shunt leading toHypoxemiaPolycythemiaV/Q mismatch
14 Eventually, hypercapnia and respiratory acidosis develop Leading to pulmonary artery vasoconstriction and pulmonary hypertension with cor pulmonalePatients have signs of right heart failure and are known as“Blue bloaters"
15 Emphysema Permanent enlargement of the air spaces distal to the terminal bronchioles, with destruction of theirwallsreduces the elasticity of the lungcollapse of the bronchiolesobstructing airflow out of the alveoliInspirationExpiration
16 Air trapping in the alveoli Inability of the lung to shrink during exhalationAmount of air inhaled is reducedLess air for the exchange of gasses in lungsTrapped air compress adjacent less damagedlung tissue compromising their function.
17 Panacinar emphysemaDestruction of the alveoli – blood vessels obstrcted/destroyedreduced diffusing capacity of the lung for carbon monoxide (DLCO)
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 withlowered cardiac outputhyperventilation.V/Q mismatch
22 Normally expiration is passive process- effortless extra effort required to exhale due to collapse of airwaysLungs are already inflated due to air trapping so more effort required to inhale furtherWork of breathing is increasedReduced gaseous exchange increase theBreathing 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“Pink puffers"
24 Causes for cachexia in emphysema Increased work of breathingLow cardiac out putIncrease in TNF alpha and other mediators of inflammation
25 Pulmonary capillary bed relatively damaged EMPHYSEMAPulmonary capillary bedrelatively damagedV/Q mismatch - relatively limitedblood flow through a fairly welloxygenated lung with normalblood gases & pressures in theLung - Dead SpaceBody compensates withlowered cardiac output andHyperventilationCHR. BRONCHITISPulmonary capillary bedrelatively undamagedV/Q mismatch – rapidcirculation in a poorly ventilatedlung, leading to hypoxemia andPolycythemiaShuntBody responds byincreasing cardiac output& decreasing ventilation.
26 Chronic Asthma Obstruction to the flow of air is due to inflammation of the airways -thickening of theairway walls lead to scarring and fixed airwayobstructionspasm of smooth muscles - bronchospasm reversiblesubsides spontaneously orwith the use of bronchodilators
28 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 ratesthan non smokers with COPDHave more frequent respiratory symptomscoughing,shortness of breathpassive smoking – equally harmful
29 MECHANISMIrritation of cigarette smoke attracts cells to the lungs that promote inflammation.They release elastase -breaks down the elastic fibers in lung tissueIncreases mucus productionDecreases ciliary motility
30 2. Air pollution Role of outdoor air pollution – unclear most common cause of COPD in nonindustrialized world is indoor air pollution due toindoor stoves used for cooking – biomass fuel3. Occupational pollutants:Cadmium & Silica - increase the risk of COPD
31 Alpha-1 antitrypsin deficiency Genetic disorderAccounts for less than 1% of the COPDEnzyme elastase is found normally in lungs.It canbreak down the elastin and damage the airwaysand alveoliAlpha-1 antitrypsin produced by liver block thedamaging effects of elastase on elastin..
32 Alpha-1 antitrypsin deficiency causes 1. Early on set of emphysema- homozygos2. Accelerated emphysema in smokers- hetrozygos3. Chronic liver disease leading to cirrhosis due totheir defective release leading to intra hepaticaccumulation.
34 Progressive exercise intolerance Alteration in mental status Patients with COPD present with a combination of signs and symptoms ofchronic bronchitisemphysemaSymptomsWorsening dyspneaProgressive exercise intoleranceAlteration in mental statusIn addition, some important clinical and historical differences exist between the types of COPD.Commonsymptoms
35 Chronic bronchitis Emphysema Productive cough, with progression over time to intermittent dyspnoeaCough and sputum on most days -at least 3 consecutive months for at least 2 successive yearsMorning headache – CO2 retentionHemoptysis – usually smallFrequent & recurrent pulmonary infectionsProgressive cardiac/respiratory failure over time, with oedema and weight gainEmphysemaA long history of progressive dyspnea with late onset of nonproductive coughOccasional mucopurulent relapsesEventual cachexia and respiratory failure.
36 0 No breathlessness except with strenuous exercise 19.29 MODIFIED MRC DYSPNOEA SCALEGrade Degree of breathlessness0 No breathlessness except with strenuous exercise1 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 pace3 Stops for breath after walking about 100 m or after a few minutes on level ground4 Too breathless to leave the house, or breathless when dressing or undressing
38 Exclude Infection malignancy & other causes Haemoptysis may complicate exacerbations of COPD but should not be attributed to COPD without thorough investigationExcludeInfectionmalignancy &other causes
43 Movement of chest wall diminished & reduced expansion < 2 cm (from neutral to maximum inspiration)COPDNormalTLCIRVTLCICVTERVFRCRV
44 Laboured breathing – pursed lip breathing Increased hollow in supraclavicular & suprasternal spaceIndrawing of intercostal spacesAccessory muscles of inspiration / expiration active
45 Apical impulse/Apex beat – not visible/palpable Tracheal span reduced - < 2 c.m.Tracheal tug – may be presentIndicates the severity of diseaseApical impulse/Apex beat – not visible/palpable
46 Hyper resonant note, liver & cardiac dullness diminished or obliterated Breath sounds –diminished, vesicular with prolonged expirationRonchi or wheeze during expirationCrepitations may be present more during inspiration
47 pump handle action of the upper 8 ribs Inspiration:result of active contractionDiaphragmExternal intercoastalspump handle action of the upper 8 ribsincreases the AP diameter of the chestbucket handle action of the lower 4 ribsincreases the transverse diameter of the chestresulting in costal elevation & lateral expansion
48 dimension by upper ribs; Pump- Handle Motion Increase in A-Pdimension by upper ribs; Pump- Handle Motionmywebpages.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
51 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 diaphragmSeen in up to 70% of patients with severe obstruction can be an excellent marker for severe airway obstruction
54 Features of CO2 narcosis headacheFlapping tremorsfull & bounding pulseWarm & moist extrimitesDetoriation of consciousnessPapilloedema
55 Chronic bronchitis Emphysema Patients may be obese. Frequent cough and expectoration are typical.Use of accessory muscles of respiration not so prominentCoarse rhonchi and wheezing may be heard on auscultation.Patients may have signs of right heart failure - edema & cyanosis.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 resonantwheezing may be heard; heart sounds very distantOverall appearance is more like classic COPD exacerbation. Rt H.F. usually not seen till late.
56 Finger clubbingis not consistent with COPD and should alert the physician to potentially more serious pathology.persistent creptsraise the possibility of bronchiectasis
58 PFT Obstructive 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
59 PEFR diary – less than 20% variation Decreased TLCO and kCO because presence of emphysema decreases surface area available for gas diffusionPEFR 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
60 Flow Volume Curves25%50%75%In early C.O.P.D. FEV1 may be normal but FEF25%-75% is reduced
61 Pulmonary function tests (Summary)Decreased forced expiratory volume in 1 second (FEV1) with concomitant reduction in FEV1/forced vital capacity (FVC) ratioPoor/absent reversibility with bronchodilatorsFVC normal or reducedNormal or increased total lung capacity (TLC)Increased residual volume (RV)Normal or reduced diffusing capacity.
62 Arterial blood gas Arterial blood gas (ABG) analysis provides the best clues as to acuteness and severitypH usually is near normal due to renal compensation in chronic diseaseGenerally, consider any pH below 7.3 a sign of acute respiratory compromise ?.
63 These patients tend to retain sodium. 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.
82 Treat bronchospasm and inflammation Treat hypoxiaTreat bronchospasm and inflammationTreat any underlying cause if presentInfectionPneumothoraxAssess the need for intensive care
83 Initial treatment 1. Sit the patient up in bed 2. Oxygen: Adequate oxygen should be given to relieve hypoxiaWith 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 deteriorationIf the patient's condition is that tenuous, intubation most likely is needed anyway.
87 stimulation of receptors relaxes airway smooth muscles It help in COPD by-stimulation of receptors relaxes airway smooth musclesincreases mucociliary clearancedecreases mucous productionDelivered by-NebulizerM D I with space halers – if nebulizer not availableParentral in refractory cases.
88 Nebulization with short acting bronchodilators Salbutamol 5mg orTerbutaline 10mgadministered with O2repeat up to every minutes if requiredcontinuous nebulization of salbutamol 10mg/h if inadequate response to initial treatmentMonitor Serum K+ regularly to prevent hypokalemia as a side effect
89 Anticholinergicsact via inhibition of cyclic guanosine monophosphate (GMP)–mediated bronchoconstriction.decrease mucus productionimprove mucociliary clearanceIpratropium bromide -agent of choiceAdd ipratropium bromide 0.5mg 6 hourly if initial response to –Beta-2 agonists is poor
90 In severe airflow obstruction combination of .In severe airflow obstructioncombination ofIpratropiumSalbutamol/albuterolprovide better broncho dilatation than used alone
91 Obtain iv access4. Start Steroids:Hydrocortisone - 200mg intravenouslyRepeat 6 – 8 hourlyOr Methylprednisolone: 1-2 mg/kg IV q6h; not to exceed 125 mgFollow 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 Prefferably a purulent sputum/ or feverabnormal CXRraised WBCshould provide coverage againstPneumococcusH influenzaeLegionella speciesGram-negative entericsPrefferably afluroquinolone orCo Amoxyclav 650 m.g.X 3 orDoxycyclline 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 minutes7. magnesium sulphate iv single dose1.2-2g infused over 20 minutes8. iv Aminophylline infusionLoading dose: 250mg (4-5mg/kg) iv in 20 minMaintenance 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 minutesMaintenance infusion: 5 -20µg/min (5mg in 500ml saline at 1- 3ml/min)Side Effects:tremortachycardiahypokalaemiahyperglycaemiaSummon 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 comaRespiratory arrestFailure to improve despite adequate therapy
97 Heliox (ie, mixture of helium and oxygen) inhalation may be tried NON INVASIVE POSITIVE PRESSURE VENTILATIONcontinuous positive airway pressure(CPAP)biphasic positive airway pressure (BiPAP)prevents airways collapse & air trappingreduces the need for endotracheal intubationHeliox (ie, mixture of helium and oxygen) inhalation may be tried.
98 definitive airway management via Intubation & mechanical ventilation .When every thing failsdefinitive airway management viaIntubation & mechanical ventilation
99 high risk of complications overall mortality of ~13%. life savinghigh risk of complications overall mortality of ~13%.hypotension in ~38%Barotrauma seen in ~14%pneumothoraxpneumo-mediastinumsubcutaneous emphysema
100 On-going therapycontinue nebulized beta2-agonist, reducing to 4-hourly and withdraw after hoursPeak flow rate should be measured before and after each nebulizerMaintain 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 daysMonitor serum K+ daily and supplement as necessary
102 DischargePEF should be 75% of best without significant morning dippingshould be established on inhalers with no requirement for nebulizers for hours prior to discharge.
108 Oxygen therapyLTOT via an oxygen concentrator for patients in respiratory failure, withPaO2 < 55 mm / Hg (7.3 kPa) with any PCO2PaO2 of 7.3 – 8 kPa (55 – 60 mm) with any of:secondary polycythaemiaperipheral oedemapulmonary hypertension presentFEV1 < 1.5 litersuse for a minimum of 15 hours per day (includingSleep)
109 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 PaCO2MUST STOP SMOKING
110 a. N O TPaO2 < 55 mm SaO2 < 88%- while awakeDecrease in PaO2 > 10 mm & SaO2 > 5%while asleepc. Supplementation during exercisewhen 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 agonistSalmeterolBambuterolless expensive than aboverapid onsetmore side effectsTheophylline -have other effects on diaphragm, resp centre etc
112 Inhaled corticosteroids (ICS) reduce the frequency & severity of exacerbationsrecommended in patients with severe disease 1.FEV1 < 50%2.two or more exacerbations requiring antibiotics or oral steroids per year.previuos response to steroidsduring acute exacerbationconcomitent asthmaHas 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)
123 airflow obstruction due to inflammation & increased airway hyper-responsive ness & bronchospasm which isvariable over short periods of timereversible with treatmentMostly by allergens in atopic personsMostly affects the young peopleChronic obstruction of lung airflow which is permanent & progressive over timeDue to the chemicalirritation of the airwayscaused by smoke(ing)Disease of middle aged & elderlycauseAge group
124 Chest normal in between the attacks Airway obstruction due toSmooth muscle spasmoedemaChest normal in between the attacksEmphysematous changes do not occurDoes not progress to cor pulmonale or type II respiratory failurePathogenesisDue toLoss of elastic recoil: EmphysemaRemodeling of the air way: Ch BronchitisFeatures of air way obstruction always seenSeen after some yearsMany cases develop these complicationClinical featuresComplications
125 Pulmonary Function Test Obstructive picture +FEV1 ≥ 15% (and 200 ml) increase following administration of a bronchodilator/trial of corticosteroids> 20% diurnal variation on ≥ 3 days in a week for 2 weeks on PEF diaryFEV1 ≥ 15% decrease after 6 mins of exerciseNormal in between attacks. Hyper inflated lungs at the time of acute attackObstructive pattern +Minimal bronchodilator reversibility (<15%, usually <10%)< 20% diurnal variation on ≥ 3 days in a week for 2 weeks on PEF diaryNo change in FEV1: FVC with exercise (absence of exercise induced bronchospasm)ShowsEmphysematous changes with bullaeFeatures of pulmonary hypertensionX ray chest