g m c f i n a l

41
MECHANICAL VENTILATION MECHANICAL VENTILATION IN COPD IN COPD SPEAKER :DR.GOOLAPPA SPEAKER :DR.GOOLAPPA MODERATOR: DR.HARISH MODERATOR: DR.HARISH R.D.T HOSPITAL, BTP. R.D.T HOSPITAL, BTP.

Upload: goolappa

Post on 11-May-2015

1.088 views

Category:

Health & Medicine


0 download

TRANSCRIPT

Page 1: G M C  F I N A L

MECHANICAL VENTILATION MECHANICAL VENTILATION IN COPDIN COPD

SPEAKER :DR.GOOLAPPASPEAKER :DR.GOOLAPPA

MODERATOR: DR.HARISHMODERATOR: DR.HARISH

R.D.T HOSPITAL, BTP.R.D.T HOSPITAL, BTP.

Page 2: G M C  F I N A L

DEFINITION OF COPDDEFINITION OF COPD1. It is chronic

2. It is progressive

3. Mostly fixed airway obstruction

4. Non reversible by bronchodilators

5. Exposure to noxious agent is a must

6. Chronic obstructive lung disease (COLD)

7. Chronic obstructive airways disease (COAD)

8. Two entities in COPD – namely

1. Chronic Bronchitis 2. Emphysema

Page 3: G M C  F I N A L

22. . CHRONIC BRONCHITISCHRONIC BRONCHITIS1. EMPHYSEMA

1. Productive cough

2. For a period of 3 months

3. In each of 2 consecutive years

4. Absence of any other identifiable cause of excessive sputum production

5. Airflow limitation that is not fully reversible

6. Abnormal inflammatory response to noxious agent - like smoking

1. Alveolar wall destruction

2. Irreversible enlargement of the air spaces

3. Distal to the terminal bronchioles

4. Without evidence of fibrosis

Page 4: G M C  F I N A L

SMOKING - SMOKING - THE CULPRITTHE CULPRITSMOKING - SMOKING -

THE CULPRITTHE CULPRIT

Page 5: G M C  F I N A L

RISK FACTORS FOR COPD RISK FACTORS FOR COPD MOST IMP

RISK

Host FactorsHost Factors– Genes (alphaGenes (alpha11- anti-trypsin- anti-trypsin↓↓))– Hyper responsivenessHyper responsiveness– Lung growth, low BW, AgeLung growth, low BW, Age

ExposureExposure– Tobacco smokeTobacco smoke, , – Bio mass fuel smoke, open firesBio mass fuel smoke, open fires– Occupational dusts and chemicalsOccupational dusts and chemicals– Chronic Chronic uncontrolled asthmauncontrolled asthma– Infections, overcrowding, dampInfections, overcrowding, damp– Low socioeconomic statusLow socioeconomic status– Low dietary vegetable and fruit intakeLow dietary vegetable and fruit intake

Page 6: G M C  F I N A L

CLINICAL CLINICAL FEATURESFEATURESCLINICAL CLINICAL

FEATURESFEATURES

Page 7: G M C  F I N A L

CHRONIC BRONCHITISCHRONIC BRONCHITIS EMPHYSEMA

1.1. Mild dyspneaMild dyspnea2.2. Cough before dyspnea startsCough before dyspnea starts3.3. Copious, purulent sputumCopious, purulent sputum4.4. More frequent infectionsMore frequent infections5.5. RepeatedRepeated resp. insufficiency resp. insufficiency6.6. PaCOPaCO22 50-60 mmHg 50-60 mmHg

7.7. PaOPaO22 45-60 mmHg 45-60 mmHg

8.8. Hematocrit 50-60%Hematocrit 50-60%9.9. DLCO is not that much DLCO is not that much ↓↓10.10. Cor pulmonale commonCor pulmonale common

1. Severe dyspnea2. Cough after dyspnea 3. Scanty sputum4. Less frequent infections5. Terminal RF

6. PaCO2 35-40 mmHg

7. PaO2 65-75 mmHg

8. Hematocrit 35-45%9. DLCO is decreased10. Cor pulmonale rare.

Page 8: G M C  F I N A L

CHRONIC BRONCHITISCHRONIC BRONCHITIS EMPHYSEMA

BLUE BLOTTERBLUE BLOTTER PINK PUFFERPINK PUFFER

Page 9: G M C  F I N A L

ALPHAALPHA11 ANTITRYPSIN ANTITRYPSIN ↓↓ EMPHYSEMA

Specific circumstances of Alpha 1- ATSpecific circumstances of Alpha 1- AT↓include↓include. .

Emphysema in a young individual (< 35)Emphysema in a young individual (< 35)

Without obvious risk factors (smoking etc) Without obvious risk factors (smoking etc)

Necrotizing panniculitis, Systemic vasculitis Necrotizing panniculitis, Systemic vasculitis

Anti-neutrophil cytoplasmic antibody (ANCA)Anti-neutrophil cytoplasmic antibody (ANCA)

Cirrhosis of liver, Hepatocellular carcinomaCirrhosis of liver, Hepatocellular carcinoma

Bronchiectasis of undetermined etiologyBronchiectasis of undetermined etiology

Otherwise unexplained liver disease, or a Otherwise unexplained liver disease, or a

Family history of any one of these conditionsFamily history of any one of these conditions

Especially siblings of PI*ZZ individuals.Especially siblings of PI*ZZ individuals.

Only 2% of COPD is alpha 1- AT ↓ Only 2% of COPD is alpha 1- AT ↓

Page 10: G M C  F I N A L

1. Decreased FEV1

2. Decreased FVC

3. FEV1 < 80%

4. FEV1 ÷ FVC < 70%

5. Post bronchodilator –

no change in FEV1

6. PEF is decreased

7. FET – is prolonged

8. V Max - decreased

CLINICAL SIGNSCLINICAL SIGNS SPIROMETRY

1.1. Physical exam may be Physical exam may be negativenegative 2.2. Hyper-inflated chest, Barrel chestHyper-inflated chest, Barrel chest3.3. Wheeze or quite breathingWheeze or quite breathing4.4. Pursed lip / accessory muscles resp.Pursed lip / accessory muscles resp.5.5. Peripheral edemaPeripheral edema6.6. Cyanosis, Cyanosis, ↑↑ JVP JVP7.7. CachexiaCachexia8.8. Cough, wheeze, dyspnea, sputumCough, wheeze, dyspnea, sputum

Page 11: G M C  F I N A L

MRC DYSPNOEA SCALEMRC DYSPNOEA SCALE GradeGrade Degree of breathlessness - related activityDegree of breathlessness - related activity

00 No breathlessness except on strenuous exerciseNo breathlessness except on strenuous exercise

11 Short of breath when walking uphill or while hurrying to catch a bus or Short of breath when walking uphill or while hurrying to catch a bus or train train

22 Walks slower than contemporaries or has to stop for breath while Walks slower than contemporaries or has to stop for breath while walking alonewalking alone

33 Stops for breath on walking 100 m or after 2 or 3 minutes continuouslyStops for breath on walking 100 m or after 2 or 3 minutes continuously

44 Too breathless to leave house or breathless while dressingToo breathless to leave house or breathless while dressing

Page 12: G M C  F I N A L

DIFF. Dx. of COPD & ASTHMADIFF. Dx. of COPD & ASTHMA ClinicalClinical COPDCOPD ASTHMAASTHMA

SmokerSmoker Nearly allNearly all May or may not beMay or may not be

Age < 35Age < 35 RareRare Nearly allNearly all

SputumSputum ProductiveProductive Mucoid or noneMucoid or none

DyspneaDyspnea PersistentPersistent EpisodicEpisodic

CourseCourse ProgressiveProgressive Variable, staticVariable, static

SpirometrySpirometry ObstructiveObstructive Normal or Obstru.Normal or Obstru.

ReversibilityReversibility Change < 15%Change < 15% Change > 15%Change > 15%

Most IMP Rx.Most IMP Rx. IBD (Ipa+Salm)IBD (Ipa+Salm) ICSICS

Anti leukotrn.Anti leukotrn. Not usefulNot useful Useful ad on Rx.Useful ad on Rx.

Page 13: G M C  F I N A L

CHEST SKIAGRAMS OF CHEST SKIAGRAMS OF EMPHYSEMAEMPHYSEMA

Page 14: G M C  F I N A L

CHEST SKIAGRAM OF CHRONIC CHEST SKIAGRAM OF CHRONIC BRONCHITISBRONCHITIS

Page 15: G M C  F I N A L

CHEST LATERAL VIEW CHEST LATERAL VIEW CHRONIC CHRONIC

BRONCHITISBRONCHITIS

Page 16: G M C  F I N A L

ASSESSMENT OF COPDASSESSMENT OF COPD Diagnosis of COPDDiagnosis of COPD• Spirometry is the Gold StandardSpirometry is the Gold Standard• Every COPD suspect must get spirometry test Every COPD suspect must get spirometry test

donedone• Like ECG, Like ECG, Spirometry is essentialSpirometry is essential• Arterial blood gas tensions are needed if the Arterial blood gas tensions are needed if the

FEVFEV11 < 40% < 40%

• Respiratory failure, CorpulmonaleRespiratory failure, Corpulmonale

Page 17: G M C  F I N A L

NORMAL AND COPDNORMAL AND COPD SPIROMETRY

0

5

1

4

2

3

Lit

er

1 65432

FVC

FVC

FEV1

FEV1

Normal

COPD

3.900

5.200

2.350

4.150 80 %

60 %NormalCOPD

FVCFEV1 FVCFEV1/

Seconds

Page 18: G M C  F I N A L

IBD are the main stayIBD are the main stay

As when needed basisAs when needed basis

The main drugs areThe main drugs are

– ββ22 - Agonists (Salbutamol group) - Agonists (Salbutamol group)

– Anticholinergics (Ipatropium group)Anticholinergics (Ipatropium group)

– Their combination Their combination

– ?? Theophylline?? Theophylline

MANAGEMENT - IBDMANAGEMENT - IBD

Page 19: G M C  F I N A L

Pledge to stop smokingPledge to stop smoking

Page 20: G M C  F I N A L

Why use ventilatory assistance ?

• patients with COPD are prone to exacerbations of respiratory failure

• mechanical ventilatory assistance is useful in patients with respiratory failure

• in COPD, 16-35% of acute exacerbations are intubated

• overall mortality is high (19-29%)

Page 21: G M C  F I N A L

Limitations of invasive ventilation

• requirement for sedation (& paralysis)

• nosocomial infection

• laryngeal/tracheal injury

• weaning difficulties

• progression to tracheostomy

• prolonged stay in ICU (cost)

Page 22: G M C  F I N A L

Advantages of NPPV• avoids intubation & potential complications

• better patient comfort

• coughing, speech & swallowing preserved

• little or no sedation required

• can be used where intubation inappropriate

• can be used away from ICU & potentially ↓ costs

Page 23: G M C  F I N A L

Limitations of NPPV

• need patient co-operation

• patient must protect upper airway

• no direct access to airway (secretion clearance)

• risk of mask dislodgment

⇒ inadequate ventilation

• not all patients tolerate NPPV (up to 20% fail)

• appropriately skilled staff required

Page 24: G M C  F I N A L

Current Recommendations - NPPV in ARF

• Strong Evidence – Level A (multiple controlled trials)• Acute hypercapnic COPD• Acute cardiogenic Pulmonary Oedema – most evidence for CPAP• Immunocompromised patients• Less strong – Level B (single controlled trials, multiple case series)• Asthma• Community Acquired Pneumonia in COPD patients• Facilitation of weaning in COPD• Avoidance of extubation failure• Post Operative Respiratory Failure• Do not intubate patients

Page 25: G M C  F I N A L

NPPV in COPD

Mechanism of action

• multifactorial, controversial and poorly understood

• ↓ work of breathing

• ‘rest’ respiratory muscles

• ↓ respiratory muscle fatigue

• ↓ dyspnoea

• counter intrinsic PEEP

• reverses acidosis

• allows time for conventional therapy to work

• avoid death by intubation

Page 26: G M C  F I N A L

NPPV in acute COPD – results

• reduction in mortality - 48%

• reduction in intubation rates – 59%

• significant improvements in pH, PaCO2, & PaO2 &

respiratory rate

• reduction in hospital length of stay > 3 days

• only 1 negative study – here less sick, & delay ~12

hours to commencement of NPPV

Page 27: G M C  F I N A L

NPPV – How to Make it work in ARF

• Patient factors• diagnosis• clinical characteristics• lower APACHE score• no pneumonia• pH > 7.10, PaCO2 < 92mmHg• better neurological state• good initial response to NPPV

Page 28: G M C  F I N A L

• Staff

need adequate training

Site for NPPV

need to be able to monitor patient properly

need expertise in intubation – especially with

conditions where failure more likely e.g. asthma

Page 29: G M C  F I N A L

Contraindications

• patients requiring >50% oxygen• thoracic / gastric surgery / pneumothorax• patients unable to maintain patent airway / clear secretions• significant hypotension induced by NPPV therapy• fractured base skull / facial fractures / ↑ Intracranial pres• respiratory arrest

Page 30: G M C  F I N A L

Interfaces:-Nasal & Full Face masks

Page 31: G M C  F I N A L

Implementation - Hypercapnoeic RF

• sit patient upright & explain procedure

• commence and titrate up to maximum tolerated level

• full face masks get better control of leaks

• apply chin strap if required / instruct patient to close mouth

• apply oxygen to machine end of tubing if required

Page 32: G M C  F I N A L

Monitoring

• Observations• BP, RR, HR & rhythm, O2 saturation, conscious state• Treatment tolerance, complications• Initially, 15 minutely for 1 hour, 30 minutely for 2hours, Hourly for 2 hours, then 4 hourly• ABGs – measured prior to commencement, at 1 hour,within 1 hour of setting changed, then as clinically needed

Page 33: G M C  F I N A L

Weaning in Acute COPD Exacerbation

• Aim to remove NPPV within 48hours• weaning is commenced• once reversal of acute factors & improved ABGs• after consultation with medical team• weaning carried out during day initially and then night• ↑ing time off ventilation rather than ↓ing pressures• monitor clinically and with ABGs as required

Page 34: G M C  F I N A L

The Decision To IntubateThe Decision To Intubate

Initiation of mechanical ventilation in COPD Initiation of mechanical ventilation in COPD patients is associated with high patient mortality patients is associated with high patient mortality and poor potential for weaningand poor potential for weaning

Indications: (E.B.M. vs. clinical Indications: (E.B.M. vs. clinical gestaltgestalt))– Patient failed conservative managementPatient failed conservative management– Severe, persistent acidosisSevere, persistent acidosis– Continued arterial hypoxemia despite initial therapyContinued arterial hypoxemia despite initial therapy– Patient fatiguePatient fatigue– Altered mental statusAltered mental status– Additional major illness (pulmonary embolism, AMI)Additional major illness (pulmonary embolism, AMI)

Page 35: G M C  F I N A L

Goals for COPD patientsGoals for COPD patients

Adequate patient monitoringAdequate patient monitoring

Optimize ventilator settings to minimize Optimize ventilator settings to minimize excessive work of breathingexcessive work of breathing

Assure SynchronyAssure Synchrony

Detect auto-PEEP and prevent barotraumaDetect auto-PEEP and prevent barotrauma

Prevent further respiratory muscle atrophyPrevent further respiratory muscle atrophy

Intubate using the widest diameter ET tube Intubate using the widest diameter ET tube possible (R = 8nl / possible (R = 8nl / ππr r 44))

Page 36: G M C  F I N A L

Vent GuidelinesVent Guidelines

Emphasis on assisted modes of ventilation Emphasis on assisted modes of ventilation (patient initiated), institution preference for (patient initiated), institution preference for A/CA/C vs. IMV with PSV (to overcome ET vs. IMV with PSV (to overcome ET tube)tube)

SIMV: probably causes excess work, b/c SIMV: probably causes excess work, b/c of high resistance circuit but debatable; of high resistance circuit but debatable; requires close patient monitoringrequires close patient monitoring

Page 37: G M C  F I N A L

Vent GuidelinesVent Guidelines

Tidal Volume: 5-7 ml/kgTidal Volume: 5-7 ml/kg

Set Rate: 4 less than spontaneous rateSet Rate: 4 less than spontaneous rate

FiO2: adjust to PaO2 of at least 60 mmHgFiO2: adjust to PaO2 of at least 60 mmHg

Triggering: -1 to -2 cm H2OTriggering: -1 to -2 cm H2O

Prevent Auto-PEEP with sufficient PEEPPrevent Auto-PEEP with sufficient PEEP

Flow rate: Increase to provide increased Flow rate: Increase to provide increased expiratory expiratory time (70-90 lpm)time (70-90 lpm)

Continue inhaled medications: requires sufficient Continue inhaled medications: requires sufficient tidal volume and inspiratory timetidal volume and inspiratory time

Page 38: G M C  F I N A L

SummarySummaryThe need to initiate mechanical ventilation in patients with The need to initiate mechanical ventilation in patients with obstructive lung disease in the emergency department is obstructive lung disease in the emergency department is associated with a higher inpatient mortalityassociated with a higher inpatient mortality

Patients with obstructive lung disease require close Patients with obstructive lung disease require close monitoring of all physiologic parameters to prevent monitoring of all physiologic parameters to prevent complications associated with positive pressure ventilationcomplications associated with positive pressure ventilation

Assessing a distressed ventilator dependent patient requires Assessing a distressed ventilator dependent patient requires an organized approachan organized approach

In general: low tidal volumes, higher flow rates and application In general: low tidal volumes, higher flow rates and application of a conservative amount of PEEP are appropriate initial of a conservative amount of PEEP are appropriate initial settings for patients with obstructive lung disease settings for patients with obstructive lung disease

Page 39: G M C  F I N A L

ReferencesReferences

““The ICU Book” Marino PL, 2The ICU Book” Marino PL, 2ndnd Edition Edition““Respiratory Physiology” West JB, 5Respiratory Physiology” West JB, 5thth EditionEdition““Pulmonary Pathophysiology” Grippi MAPulmonary Pathophysiology” Grippi MA““Textbook of Medical Physiology” Guyton Textbook of Medical Physiology” Guyton and Hall 9and Hall 9thth Edition Edition““Chest Radiology Companion” Stern EJ, Chest Radiology Companion” Stern EJ, White CSWhite CSHarrison’s Principles of Internal Medicine Harrison’s Principles of Internal Medicine 1616thth Edition Edition

Page 40: G M C  F I N A L
Page 41: G M C  F I N A L