3 Chronic Obstructive Pulmonary Disease Definition: Disease state characterised by airflow limitation that is not fully reversible The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking.In patients with COPD either of these conditions may be present but the relative contribution of each is different.
4 Chronic Obstructive Pulmonary Disease Definition: Disease state characterised by airflow limitation that is not fully reversible The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking.In patients with COPD either of these conditions may be present but the relative contribution of each is different.
5 COPD: Chronic Bronchitis Includes: Peripheral Airways disease EmphysemaDoesn’t includeAsthma, Asthmatic BronchitisCystic FibrosisBronchiactesisPulmonary fibrosis due to othercauses
6 COPD Chronic Bronchitis: (Clinical Definition) Chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of productive chronic cough have been excluded.Emphysema: (Pathological Definition)The presence of permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis
7 Comparative features of COPD Chronic BronchitisEmpysemaMech of Airway ObstructionDecreased Lumen d/t mucus & inflammationLoss of elastic recoilDysnoeaModerateSevereFEV1DecreasedPaO2Marked Decrease (Blue Bloater)Modest Decrease (Pink Puffer)PaCO2IncreasedNormal or DecreasedDiffusing capacityNormalHematocritCor PulmonaleMarkedMildPrognosisPoorGood
8 COPD: Risk factors Host factos: Genetic factors: Eg. α1 Antitrypsin DeficiencySex : Prevalence more in males.?Females more susceptibleAirway hyperactivity,Immunoglobulin E and asthmaExposures:Smoking: Most Important Risk FactorSocioeconomic statusOccupationEnvironmental pollutionPerinatal events and childhood illnessRecurrent bronchopulmonary infectionsDiet
9 Natural History:It is increasingly apparent that COPD often has its roots decades before the onset of symptoms. Impaired growth of lung function during childhood and adolescence, caused by recurrentinfections or tobacco smoking, may lead to lower maximally attained lung function in earlyadulthood . This abnormal growth will, often combined with a shortened plateau phase inteenage smokers, increase the risk of COPD. This is visualised in figure 1 .Fig The normal course of forced expiratory volume in one second (FEV1) over time (–––)is compared with the result of impaired growth of lung function (––– ) an accelerated decline(–––) and a shortened plateau phase (–––). All three abnormalities can be combined(Kerstjens HAM, Rijcken B, Schouten JP, Postma DS. Decline of FEV1 by age andsmoking status: facts, figures, and fallacies. Thorax 1997; 52: 820–827.)
10 Pathophysiology:Pathological changes are seen in 4 major compartments of lungs:central airwaysPeripheral airwayslung parenchymapulmonary vasculature.
11 Airflow limitation and hyperinflation Pathophysiology:Excessive Mucus productionCentral Airways: (cartilaginous airways >2mm of internal diameter)Bronchial glands hypertrophyGoblet cell metaplasiaAirway Wall Changes:Inflammatory CellsLoss of cilia and ciliary dysfunctionSquamous metaplasia of the airway epitheliumIncreased smooth muscle and connective tissuePeripheral airways (noncartilaginous airways<2mm internal diameter)BronchiolitisPathological extension of goblet cells and squamous metaplasiaInflammatory cellsFibrosis and increased deposition of collagen in the airway wallsAirflow limitation and hyperinflation
12 Airflow limitation and hyperinflation Pathophysiology:Lung parenchyma (respiratory bronchioles, alveoli and capillaries)Emphysema (abnormal englagement of air spaces distal to terminal bronchioles)occurs in the parenchyma:2 Types: Centrilobular and PanlobularEarly microscopic lesion progress to Bullae over time.Results in significant loss of alveolar attachments, which contributesto peripheral airway collapseInflammatory cellsAirflow limitation and hyperinflationPulmonary HTNRV dysfunction (cor Pulmonale)Pulmonary Vasculature:Thickening of the vessel wall and endothelial dysfunctionIncreased vascular smooth muscle & inflammatory infiltration of the vessel wallCollagen deposition and emphysematous destruction of the capillary bed
13 Pathogenesis: Tobacco smoke & other noxious gases Alpha 1 antitrypsin def.Increased Neutrophils, Lymphocytes & MacrophagesProteinase & Antiproteinase imbalanceInflammatory response in airwaysOxidative StressTissue DestructionImpaired defense against tissue destructionImpaired repair mechanisms
14 Physiological Effects: Mucous hypersecretion and cilliary dysfunctionGoblet cell hyperplasia & squamous metaplasiaAirflow limitation and hyperinflationAirway remodellingLoss of eleastic recoilDestruction of alveolar supportsAccumulation of mucus, inflammatory cells & exudateGas exchange abnormalities: (Hypoxemia +/- Hypercapnia)Abnormal V/Q ratiosAbnormal DLCOPulmonary hypertensionHypoxic Vasoconstrictoin,Endothelial dysfunctionRemodelling of arteries & capillary destructionSystemic effects
15 Diagnosis Clinical Features: Symptoms: Physical Examination: Cough: Initially intermittentPresent throughout the daySputum:Tenacious & mucoidPurulent InfectionDyspnoea: Progressively worsensPersistantPhysical Examination:Respiratory SignsBarrel ChestPursed lip breathingAdventitious Ronchi/WheezeSystemic SignsCyanosisNeck vein enlargementPeripheral edemaLiver enlargementLoss of muscle massExposure: Smoking, in pack years
16 Diagnosis Investigations: Spirometry Assessment of severityFollowing progressChest Radiograph: To exclude other diseasesEmphysematous changesBronchodilator ReversibilityExclude Bronchial Asthma<20%Alpha-1 Antitrypsin levelsYoung COPD with Family History
18 Treatment Modifying natural history of Disease: Symptomatic: Smoking cessationLong term oxygen therapySymptomatic:BronchodilatorsAntibioticsOthersPulmonary RehabilitationNutrition
19 Treatment: Smoking Cessation Need:Most important cause of COPDMajor risk factor for atherosclerotic vascular disease, cancer, peptic ulcer and osteoporosis.Quitting smoking slows progressive loss of lung function & reduces symptomsMotivation, Counselling & behavioural supportNicotine replacementPatcheschewing gumInhalernasal spraylozengesBupriopionIt approximately doubles quit rates compared to placebo.• Treatment is usually initiated at 150 mg daily and increased to 150 mg twice daily after3 days, if tolerated.• The quit day should be after 1 week of treatment.• Treatment is generally continued for 7–12 weeks.• Bupropion may be more effective than nicotine replacement therapy for individualswith a past history of depression.Contraindications include increased seizure risk, bulimia, concurrent use of monoamineoxidase inhibitors or a bupropion preparation for depression.
20 Effect of smoking and smoking cessation on Lung Function: Loss of lung function over 11 yrs in the Lung Health Study for continuous smokers(–––), intermittent quitters (–––) and sustained quitters (–––). FEV1: forced expiratoryvolume in one second(Anthonisen NR et al,Lung Health Study Research Group.Smoking and lung function of Lung Health Study participants after 11 years. Am J Respir CritCare Med 2002; 166: 675–679.
21 Treatment: Oxygen Therapy Long Term Oxygen Therapy(LTOT):Improves survival, exercise, sleep and cognitive performance.Oxygen delivery methods include nasal continuous flow, reservoir cannulas and transtracheal catheter.Physiological indications for oxygen include an arterial oxygen tension (PaO2) <7.3 kPa (55 mmHg). The therapeutic goal is to maintain SpO2 >90% during rest, sleep and exertion.
22 Physiological indications for long-term oxygen therapy (LTOT) PaO2 mmHg SaO2 % LTOT indication Qualifying condition ≤55 ≤88 Absolute None 55–59 89 Relative with qualifier “P” Pulmonale, polycythemia >55% History of edema ≥60 ≥90 None except with qualifier Exercise desaturation Sleep desaturation not corrected by CPAP Lung disease with severe dyspnea responding to O2
23 Treatment: Symptomatic Measures Bronchodilators:AnticholinergicsBeta AgonistsMethylxanthinesCorticosteroidsN-Acetyl Cysteineα1 Antitrypsin augmentationVaccinationOthers: No proven effectLeukotriene receptor antagonists/cromonesMaintenance antibiotic therapyImmunoregulatorsVasodilators: NO, CCB
24 Surgical Treatment Bullectomy Lung Volume Reduction Surgery short-term improvements inairflow obstructionlung volumeshypoxaemia and hypercapniaexercise capacitydyspnoeaLung Volume Reduction Surgerypotentially long-term improvement in survivalSpirometryexercise toleranceLung Transplantation
25 COPD: Exacerbations Definition: An exacerbation of COPD is an event in the natural course of the disease characterised by a change in the patient’s baseline dyspnoea, cough and/or sputum beyond day-to-day variability sufficient to warrant a change in management.Precipitating Causes:Infections: Bacterial, ViralAir pollution exposureNon compliance with LTOTInfectious process [7, 8]: viral (Rhinovirus spp., influenza); bacteria (Haemophilus influenzae,Streptococcus pneumoniae, Moraxella catarrhalis, Enterobacteriaceae spp., Pseudomonasspp.).
26 COPD: Exacerbations Indication for Hospitalisation: The presence of high-risk comorbid conditionspneumonia,cardiac arrhythmia,congestive heart failure,diabetes mellitus,renal or liver failureInadequate response to outpatient managementMarked increase in dyspnoea, orthopnoeaWorsening hypoxaemia & hypercapniaChanges in mental statusUncertain diagnosis.
27 COPD: Exacerbations Indication for ICU admission: Impending or actual respiratory failurePresence of other end-organ dysfunctionshockrenal failureliver failureneurological disturbanceHaemodynamic instability
28 Treatment Supplemental Oxygen (if SPO2 < 90%) Bronchodilators: Nebulised Beta Agonists,Ipratropium with spacer/MDICorticosteroidsInhaled, OralAntibiotics:If change in sputum characteristicsBased on local antibiotic resistanceAmoxycillin/Clavulamate, Respiratory FlouroquinolonesVentillatory support: NIV, Invasive ventillation
29 In a nutshellOptimal disease management entails redesigning standard medical care to integrate rehabilitative elementsinto a system of patient self-management and regular exercise
31 Anaesthetic Considerations in patients with COPD undergoing surgery: Patient Factors:Advanced agePoor general condition, nutritional statusCo morbid conditionsHTNDiabetesHeart DiseaseObesitySleep ApneaWeak HPV, blunted Ventilatory responses to hypoxia and CO2 retention
32 Age Related Pulmonary Changes: Pathological changesEffectImplicationsDecreased efficiency of lung parenchymaDecreased VCIncreased RVRespiratory FailureDecreased Muscle strengthDecreased Compliance, FEV1Poor coughInfectionAlveolar septal destructionDecreased alveolar areaDecreased gas exchangeBrohchiolar damageIncreased closing volumeAir trappingDecreased PaO2Dilated upper airwaysIncreased VDDecreased reactivityDecreased laryngeal reflexesDecreased vent response to hypoxia, hypercarbiaIncreased AspirationIncreased resp. failure
33 Anaesthetic Considerations in patients with COPD undergoing surgery: Problems due to DiseaseExacerbation of Bronchial inflammationd/t Airway instrumentationpreoperative airway infectionsurgery induced immunosuppressionincreased WOBIncreased post operative pulmonary complications
34 Anaesthetic Considerations in patients with COPD undergoing surgery: Problems due to Anaesthesia:GA decreases lung volumes, promotes V/Q mismatchFRC reduced during anaesthesia, CC parallels FRCAnaesthetic drugs blunt Ventilatory responses to hypoxia & CO2Postoperative Atelectasis & hypoxemiaPostoperative pain limits coughing & lung expansionProblems due to Surgery:Site : most important predictor of Post op complicationsDuration: > 3 hoursPosition
35 Pre-operative assessment: History:SmokingCough: Type, Progression, Recent RTISputum: Quantity, color, bloodDyspneaExercise intoleranceOccupation, AllergiesSymptoms of cardiac or respiratory failure
36 Pre-operative assessment: Examination Physical Examination: Better at assessing chance of post op complicationsAirway obstructionhyperinflation of chest, Barrel chestDecreased breath soundsExpiratory ronchiProlonged expiration: Watch & Stethoscope test, >4 sec↑WOB↑ RR, ↑HRAccessory muscles usedTracheal tugIntercostal indrawingTripod sitting posture
37 Pre-operative assessment: Examination Respiratory failureHypercapniaHypoxiaCyanosisCor Pulmonale and Right heart failureDependant edematender enlarged liverPulmonary hypertensionLoud P2Right Parasternal heaveTricuspid regurgitationBody HabitusObesity/ MalnourishedActive infectionSputum- change in quantity, natureFeverCrepitations
38 Preoperative Assessment: Investigations Complete Blood countSerum ElectrolytesBlood SugarUrinalysisECGArterial Blood GasesDiagnostic RadiologyChest X RaySpiral CTPreoperative Pulmonary Function TestsTool for optimisation of pre-op lung functionNot to assess risk of post op pulmonary complications
39 Investigations: Chest X-Ray OverinflationDepression or flattening of diaphragmIncrease in length of lung↑ size of retrosternal airspace↑ lung markings- dirty lungBullae +/-Vertical Cardiac silhouette↑ transverse diameter of chest, ribs horizontal, square chestEnlarged pulmonary artery with rapid tapering in MZ
40 Pulmonary Function Tests: MeasurementNormalObstructiveRestrictiveFVC (L)80% of TLC (4800) FEV1 (L)80% of FVCFEV1/FVC(%)75- 85%N to N to FEV25%-75%(L/sec)4-5 L/ secPEF(L/sec)L/minSlope of FV curveMVV(L/min)L/minTLC6000 mlRV1500 mLRV/TLC(%)0.25N
41 Spirometric tracing in COPD patients FEV1FVCseconds21345LitresCOPDNORMAL60%3900235080%52004150NormalFEV1/FVC
42 Maximum inspiratory and expiratory flow-volume curves (i. e Maximum inspiratory and expiratory flow-volume curves (i.e., flow-volume loops) in four types of airway obstruction.
43 Preoperative Assessment: Investigations ECGSigns of RVH:RADp Pulmonale in Lead IIPredominant R wave in V1-3RS pattern in precordial leadsArterial Blood Gases:In moderate-severe diseaseNocturnal sample in cor PulmonaleIncreased PaCO2 is prognostic markerStrong predictor of potential intra op respiratory failure & post op Ventilatory failureAlso, increased d/t post op pain, shivering, fever,respiratory depressants
44 Pre-operative preparation Cessation of smokingDilation of airwaysLoosening & Removal of secretionsEradication of infectionRecognition of Cor Pulmonale and treatmentImprove strength of skeletal muscles – nutrition, exerciseCorrect electrolyte imbalanceFamiliarization with respiratory therapy, education, motivation & facilitation of patient care
45 Effects of smoking: Cardiac Effects: Respiratory Effects: Risk factor for development of cardiovascular diseaseCO decreases Oxygen delivery & increases myocardial workCatecholamine release, coronary vasoconstrictionDecreased exercise capacityRespiratory Effects:Major risk factor for COPDDecreased Mucociliary activityHyperreactive airwaysDecreased Pulmonary immune functionOther SystemsImpairs wound healing
46 Smoking cessation and time course of beneficial Effects Time after smokingPhysiological Effects12-24 HrsFall in CO & Nicotine levels48-72 HrsCOHb levels normaliseAirway function improves1-2 WeeksDecreased sputum production4-6 WeeksPFTs improve6-8 WeeksNormalisation of Immune function8-12 WeeksDecreased overall post operative morbidity
47 Dilatation of Airways: Bronchodilators:Only small increase in FEV1Alleviate symptoms by decreasing hyperinflation & dyspnoeaImprove exercise toleranceAnticholinergicsBeta AgonistsMethylxanthines
48 Anticholinergics: Block muscarinic receptors Onset of action within 30 MinIpratropium –40-80 μg by inhalation20 μg/ puff – 2 puffs X 3-4 times250 μg / ml respirator soln ml X 4 times dailyTiotropium - long lastingSide Effects:Dry Mouth, metallic tasteCaution in Prostatism & GlaucomaBetter in COPD then asthmaS/E – Dryness of mouth, Scratching of trachea, Cough, nervousness
50 Bronchodilators: methylxathines Mode of Action– inhibition of phospodiesterase,↑ cAMP, cGMP – BronchodilatationAdenosine receptor antagonism↑ Ca release from SROral(Theophyllin) & Intravenous (Aminophylline, Theophyllin)loading – 5-6 mg/kgPrevious use – 3 mg/kgMaintenace –1.0mg/kg h for smokers0.5mg/kg/h for nonsmokers0.3 mg/kg/h for severely ill patients.
51 Inhaled Corticosteroids: Anti-inflammatoryRestore responsiveness to β2 agonistReduce severity and frequency of exacerbationsDo not alter rate of decline of FEV1Beclomethasone, Budesonide, FluticasoneDose: 200 μg BD ↑ upto 400 μg QID> 1600 μg / day- suppression of HPA axisNot bronchodilators.↓ bronchial reactivity and edema↓ inflammatory response
53 Anaesthetic Technique COPD is not a limitation on the choice of anaesthesia. Type of Anaesthesia doesn’t predictably influence Post op pulmonary complications.
54 Concerns in RA Neuraxial Techniques: No significant effect on Resp function: Level above T6 notrecommendedNo interference with airway Avoids bronchospasmNo swings in intrathoracic pressureNo danger of pneumothorax from N2OSedation reqd. May compromise expiratory fn.Peripheral Nerve Blocks:Suitable for peripheral limb surgeriesMinimal respiratory effectsSupraclavicular techniques contraindicated in severePulmonary disease
55 Concerns in RA Improved Surgical outcome: Better pain control Attenuation of neuroedocrine respones to surgeryImprovement of tissue oxygenationMaintenance of immune functionFewer episodes of DVT, PE, stroke, blood TxTechnique of choice in perineal, pelvic extraperitoneal& lower extremitiesNo benefit over GA in Intraperitoneal surgery,or when high levels are needed
56 Concerns in GA Airway instrumentation & bronchospasm Residual NMB Nitrous OxideAttenuation of HPVRespiratory depression with opioids, BZDsAirway humidification
57 Premedication ↑ Sensitivity to the effect of respiratory depressants Opioids & Benzodiazepines - ↓ response to hypoxia, hypercarbiaBronchodilator puff / nebulisation, inhaled steroidsAtropine ?: Should be individualisedDecreases airway resistanceDecreases secretion-induced airway reactivityDecreases bronchospasm from reflex vagal stimulationCause drying of secretions, mucus plugging
58 General Anaesthesia: Induction Opioids:Fentanyl(DoC)Morphine ,PethidineRespiratory Depression, Histamine release, Chest tightnessPropofol (DoC)Better suppression of laryngeal reflexesHemodynamic compromiseAgent of choice in stable patientKetamineBronchodilator Catecholamine release, neural inhibitionTachycardia and HT, may increase PVR
59 Intubation NMB : Attenuation of Intubation Response: Succinyl Choline (1-2mg/kg)Vecuronium( mg/kg)Rocuronium ( mg/kg )Attenuation of Intubation Response:IV lignocaine ( mg/kg) 90s prior to laryngoscopyFentanyl 1-5 microgram/KgEsmolol mg bolusAdequate plane of anaesthesia prior to intubationLMA Vs Endotracheal TubeAvoids tracheal stimulationP-LMA also allows for suctioning
60 Maintenance Muscle relaxant Prefer Vecuronium, Rocuronium, CisatracuriumAvoid Atracurium, Mivacurium, Doxacurium ( histamine release)Volatile anaestheticNO Caution in pulmonary bullae, dilution of delivered O2Inhalational agents attenuate HPVSevoflurane: non pungent, bronchodilatorHalothane: Non pungent, bronchodilator.Slower onset & elimination, Sensitises to catecholamines
61 Maintenance Ventialatory Strategy: Aim: Maximise alveolar gas emptying Minismise dynamic hyperinflation, iPEEPSettings:Decrease minute vent Low frequencyAdequate Exp time, Low I:E ratio, minimal exp pauseReduce exp flow resistanceRecruitment maneuversAcceptance of mild hypercapnia & acidemiaHumidification of gasesPressure Cycled mode with decelerating flow.Reduce exp low res by bronchodilators, coriticosteroids, low res tubings, helioxThe pressure ventilatory mode (PV) with a decelerating flow has the potential advantage of decreasing the peak airway pressure and providing more homogenous distribution of inspiratory airflow at a lower or similar mean distending pressure
62 Maintenance Monitoring Intraoperative IV Fluids ECG, NIBP Pulse OximetryCapnographyNeuromuscular MonitoringDepth of AnaesthesiaIntraoperative IV FluidsExcessive IV volume Water accumulation & tissue edema Respiratory/heart failureHaemodynamic goal directed fluid loadingRestrictive fluid administration
63 Intraoperative Increased PIP BronchospasmLight anaesthesia, coughing, buckingObstruction in the circuitBlocked / kinked tubeEndobronchial intubationPneumothoraxPulmonary embolismMajor AtelectasisPulmonary edemaAspiration pneumoniaHead down position, bowel packing
64 Management of intraoperative bronchospasm Increase FiO2Deepen anaesthesiaCommonest cause is surgical stimulation under light anaesthesiaIncremental dose of Ketamine or PropofolRelieve mechanical stimulationendotracheal suctionStop surgeryβ2 agonists – Nebulisation or MDIs/c Terbutaline, iv Adrenalineintravenous AminophylineIntravenous corticosteroid indicated if severe bronchospasm
65 Reversal/ Recovery: Neostigmine - may provoke bronchospasm Atropine mg or Glycopyrrolate 0.6mg before NeostigmineTracheal toiletingExtubation : deep or awake?Deep extubation may reduce chance of bronchospasmDeepNOYESGood airway - accessibleEasy intubationNo Residual NMBNormothermicNot at increased risk of aspirationDifficult airwayDifficult intubationResidual NMBFull stomach
66 Post operative care ↑ Risk of Post op pulmonary complications Postoperative analgesia –Parenteral NSAIDSNeuraxial drugsNerve blocksPCAPostoperative respiratory therapy –Chest physiotherapy & postural drainageVoluntary Deep BreathingIncentive Spirometry
67 Post operative care Mechanical Ventilation: Continue Bronchodilators Indications:Severe COPD undergoing major surgeryFEV1/FVC<70%Preop PaCO2 > 50mm HgFiO2 & Ventillator settings adjusted to maintain PaO mm Hg & PaCO2 in range that maintains pH atContinue BronchodilatorsOxygen therapyLung Expansion maneuvers
68 Post Operative Pulmonary Complications: Incidence: 6.8% (Range 2-19%)(Sementa et al, Annals of internal Medicine, 2006,144:581–95)Include:AtelectasisBronchopneumoniaHypoxemiaRespiratory FailureBronchopleural fistulaPleural effusionGrade I complication entails any deviation from the normal postoperative course with no need for medical interventions, except antiemetics, antipyretics, analgesics, electrolytes, diuretics. Grades II and III involve complications requiring pharmacological treatment, blood transfusions or endoscopic, surgical or radiological interventions. Grade IV includes lifethreatening complications as well as single or multiple organ failure requiring ICU admission. Ultimately, perioperative death corresponds to a grade V.
69 Post Operative Pulmonary Complications: Patient Related:Age > 70 yrsASA Class II or aboveCHFPre-existing Pulmonary DiseaseFunctionally DependentCigarette smokingHypoalbuimnemia , 3.5g/dLPredictors ofPPCs:Procedure Related:Emergency SurgeryDuration > 3 HrsGAAbd, Thoracic, Head & Neck,Nuero, Vascular Surgery
70 Post Operative Pulmonary Complications: Specific Risk Factors:COPDBronchial AsthmaGAOSAAdvanced ageMorbid Obesity(BMI > 40)Functional limitationSmoking > 20 Pack yearAlcohol consumption (>60ml ethanol/day)he incidence of PPCs (except atelectasis) most often parallels the severity of respiratory impairment (moderate,if FEV1 50%–80%; severe, if FEV1 50%), particularly in patients with abnormal clinical findings (decreased breath sounds, wheezes, ronchi, prolonged expiration) and/or marked alterations of gas exchange (PaCO2 7 kPa, hypoxemia requiring supplemental oxygen).Br Asthma; Recent asthma symptoms, current use of anti-asthma drugs and history of tracheal intubation for asthma have all been associated with the development of PPCs.
72 Post Operative Pulmonary Complications: Post Operative Analgesia:OpioidsParavertebral/Intercostal N BlocksEpidural AnalgesiaLANSAIDS Bronchospasm
73 Post Operative Pulmonary Complications: Lung Expansion maneuvers:Incentive spirometryDeep breathing exercisesChest Physiotherapy & postural drainageIntermittant Positive Pressure VentilationCPAP, BiPAPEarly AmbulationOf proven benefit in decreasing PPCs. Decrease atelectasis by increasing lung volume All are equally efficaciosIncentive spirometry: Simple. Inexpensive. Objective goal given to the patient provides sustained lung expansion & helps in opening closed alveoli. But needs patient coorperation.Positive pressure breathing tech not cost effective.
74 Summary:COPD is a progressive disease with increasing irreversible airway obstruction.Cigarette smoking is the most important causative factor for COPDSmoking cessation & LTOT are the only measures capable of altering the natural history of COPD.COPD is not a contraindication for any particular anaesthsia technique if patients have been appropriately stabilised.COPD patients are prone to develop intraoperative and postoperative pulmonary complications.Preoperative optimisation should include control of infection and wheezing.Postoperative lung expansion maneuvers and adequate post op analgesia have been proven to decrease incidence of post op complications.
75 References: Stoelting’s Anaesthesia & Coexisting Disease, 5th Ed. Standards for Diagnosis & Management of COPD Patients, American Thoracic Society & European Respiratory SocietyGlobal Initiative for COPDRefresher course lectures, 57th National Conference of ISACOPD: Perioperative management, M.E.J. Anesth (6)Post Operative Pulmonary Complications, IJA April 2006Periop Management of patients with COPD: Review, IJ COPD 2007:2(4) 493:515Harrison’s Principles of Medicine, 16th EdPrinciples of respiratory Care, Egan’s, 9th EdMiller’s Anaesthsia, 7th EdIrwin & Rippe’s Intensive care medicine, 6th Ed.Clinical Application of Mechanical Ventilation, David W Chang, 3rd Ed