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COPD

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Suboptimally Due to Angle and Length. COPD. Classic Description: Barrel Chest ... Active smoker (within 4 months) Unstable angina or cardiac arrhythmia ... – PowerPoint PPT presentation

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Title: COPD


1
COPD
  • (Bonus Lecture)Jim Pierce
  • January 19, 2009

2
COPD
  • Chronic Obstructive Pulmonary Disease
  • A group of diseases
  • Intrathoracic Obstruction

3
COPD
Asthma
Emphysema
Chronic Bronchitis
4
COPD
  • Clinical Diagnosis
  • History
  • Physical
  • Physiologic Diagnosis
  • Physiologic Testing
  • Pathologic Diagnosis
  • Anatomic Changes
  • Pathologic (Histology) Changes

5
COPD
Asthma
Emphysema
Physiologic Diagnosis
PathologicDiagnosis
Chronic Bronchitis
Clinical Diagnosis
6
COPD
  • Why are they grouped together?
  • Intrathoracic Obstruction

7
COPD
  • Intrathoracic Obstruction
  • Inspiration
  • Transthoracic Pressure Gradient
  • Airways Pulled Open
  • Expiration
  • Recoil or Transthoracic Gradient
  • Airways Pushed Closed

8
COPD
  • Inspiration
  • Relatively Normal Mechanics
  • Expiration
  • Abnormal Mechanics(Prolonged Expiratory Time)

9
Hysteresis
10
COPD
  • Early
  • Enough Expiratory Reserve
  • Middle
  • Expiratory Reserve Depleted
  • Air Trapping
  • Shift of Hysteresis Curve

11
COPD
12
COPD
  • Late
  • Expiratory Reserve Depleted
  • Air Trapping causes Inefficiency
  • Inefficiency so severe Active Exhalenecessary
    just to allow inhalation
  • Increase in Work of Breathing

13
COPD
  • Very Late
  • Air Trapping causes Inefficiency
  • Air Trapping changes Diaphragmand Chest
    Dimensions
  • Inefficiency so severe Active Exhalenecessary
    just to allow inhalation
  • Dimensions Make Muscles functionSuboptimally Due
    to Angle and Length

14
COPD
  • Classic Description
  • Barrel Chest
  • Pursed Lip Breathing
  • Shortness of Breath

15
Barrel Chest
16
Pursed Lip Breathing
17
COPD
  • Why does pursed lip breathing work?
  • Fixed airway obstructioncauses air trapping
  • Air trapping causesAirways to stay open

18
COPD
Asthma
Emphysema
Physiologic Diagnosis
PathologicDiagnosis
Chronic Bronchitis
Clinical Diagnosis
19
Chronic Bronchitis
  • Clinical Diagnosis
  • History
  • Cough that leads to Sputum
  • Almost Daily
  • At least 3 months of year
  • At least 2 years

20
Asthma
  • Physiologic Diagnosis
  • Obstructive Physiologyon Pulmonary Function
    Tests
  • Gets better with Smooth MuscleRelaxant
    (beta-adrenergic agonist)

21
Asthma
22
Emphysema
  • Pathologic Diagnosis
  • A Biopsy (or Autopsy)demonstrates destruction of
    alveoli and airway wallsleading to decreased
    elasticity

23
Normal Lung versus Emphysema
24
Normal Lung versus Emphysema
25
COPD
  • USA
  • 14.2 Million People have COPD
  • 12.5 Million Chronic Bronchitis
  • 1.7 Million Emphysema
  • Globally
  • 9-10 of people 40 and older

26
COPD
  • Yearly Mortality, USA
  • Males 50-80 200 per 100,000
  • Females 50-80 80 per 100,000

27
COPD
  • The Truth
  • No one has just one disease.
  • There are components of
  • Sputum Production and SOB
  • Physiologic reversible obstruction
  • Destruction of Lung Parenchyma

28
COPD
  • History
  • Generally starts 40-50 yrs
  • More frequently male
  • Chronic Cough, worse in morning
  • Sputum Clear or Carbonaceous
  • 20 cigarettes a day for 20 years
  • Shortness of breath, esp. on exertion

29
COPD
  • History
  • Initially presents with either cough or acute
    illness (bronchitis/pneumonia)
  • Over years, more frequent acute exacerbations /
    attacks
  • By 60s, usually breathless on minimal exertion

30
COPD
  • Physical Exam
  • Not very good at mild/moderatestage of illness
  • VERY sensitive for severe illness
  • Barrel Chest
  • Weight loss
  • Coughing
  • Pursed Lip Breathing

31
COPD
  • Causes
  • Smoking
  • Air Pollution
  • Airway Hyper-responsiveness
  • Alpha1-Anti-Trypsin Deficiency

32
Pathogenesis
  • Inflammation
  • Case 1
  • Stimulus leads to local inflammatorymediators in
    airway
  • Smooth Muscle responds to cytokines by increase
    in tone and reactivity
  • This leads to chronic secretion stasis
  • This leads to frequent acute attacks

33
Pathogenesis
  • Inflammation
  • Case 2
  • Stimulus leads to local inflammatorymediators in
    airway
  • Smooth Muscle responds by hypertrophy and
    Connective tissue responds by Scar
  • This leads to chronic secretion stasis
  • This leads to frequent acute attacks

34
Pathogenesis
  • Inflammation
  • Case 3
  • Inflammatory mediators lead to mucus gland
    hypertrophy and increase in sputum
  • This leads to sputum trapping and stasis, leading
    to more acute exacerbations

35
Pathogenesis
  • Inflammation
  • Case 4
  • Inflammatory mediators lead to an imbalance of
    proteinases (specifically MMP/TIMP imbalance)
  • This leads to destruction of airway walls and
    pathophysiology of COPD

36
Pathogenesis
  • In all cases
  • Chronic Inflammation withAcute Exacerbations
  • Leads to some combination
  • Secretions (Clinical)
  • Airway Reactivity (Physiologic)
  • Parenchymal Destruction (Pathologic)

37
Diagnosis
  • Threshold of DiagnosisMUST be related to therapy
  • Examples
  • Smoking Cessation
  • Surgery

38
Diagnosis
  • History
  • Physical
  • Chest XRay / CT scan
  • Arterial Blood Gas
  • Pulmonary Function Tests
  • Autopsy

39
CXR
40
CT Scan
41
Pulmonary Function Tests
42
Therapy
  • Smoking Cessation
  • Pulmonary Rehabilitation
  • Medication
  • Surgery

43
Therapy
  • Oxygen
  • Bronchodilators (Beta-Agonist)
  • Anticholinergic
  • Anti-inflammatory
  • Topical Steriod
  • Oral/IV Steroid
  • Anti-Leukotrienes
  • Mucolytic
  • Anti-Allergy
  • Antibiotics

44
Surgery
  • Lung Volume Reduction Surgery
  • NETT Trial

45
NETT
  • National Emphysema Treatment Trial
  • 1996 Participating Centers announced
  • 1997 Screening for entry begins
  • July 2002 Recruitment Ends

46
NETT
  • After recruitment, patients
  • Underwent exercise testing, pulmonary function
    testing, and radiography.
  • Met with a Pulmonologist, Cardiologist, and
    Thoracic Surgeon
  • Completed a 6-10 week courseof lung mechanical
    physiotherapy
  • Exercise Protocol and Classes
  • Oxygen and Medication Adjustment
  • Perioperative Teaching
  • Randomized to Bilateral LVRSversus continuing
    physiotherapy

47
NETT
  • Inclusion Criteria
  • Diagnosis of Emphysema
  • Met Radiologic and PFT criteria
  • Accepted by all Physicians
  • Severe Impact on Function

48
NETT
  • Exclusion Criteria
  • Active smoker (within 4 months)
  • Unstable angina or cardiac arrhythmia
  • Heart attack within 6 months
  • Had certain thoracic or cardiac surgeries or had
    another disease that was likely to interfere with
    participation in the trial or to reduce survival.

49
NETT
  • Medical Arm
  • Continued Physiotherapy andOxygen/Medication
    managementby Center Pulmonologists
  • Surgical Arm
  • Bilateral LVRS
  • Open (median sternotomy)and Thoracoscopic both
    allowed

50
NETT
  • 3777 people evaluated
  • 1218 individuals selected
  • 608 assigned surgery
  • 610 assigned medical therapy only
  • 95 received treatment as directed
  • 99 surviving participants followup

51
NETT
  • Interim Outcomes
  • May 2001
  • Homogenous Disease identifiedas having less post
    operative benefit
  • Severe Emphysema with Homogenous Disease noted to
    have increased risk of death
  • Interim results published in NEJM
  • Inclusion criteria adjusted

52
NETT
  • Final Outcomes
  • Overall Long-term Mortality identical between
    Surgical and Medical arms
  • 3 month Mortality 7.9 in surgery arm
  • 3 month Mortality 1.3 in medical arm

53
NETT
  • Mostly upper-lobe emphysema
  • With low exercise capacity
  • More likely to live longer after LVRS
  • More likely to function better after LVRS than
    after medical treatment
  • With high exercise capacity
  • No difference in survival between the LVRS and
    Medical participants
  • Surgical group more likely to function better
    than medical group

54
NETT
  • Mostly non upper-lobe emphysema
  • With low exercise capacity
  • Similar survival and exercise ability after LVRS
    as after medical treatment
  • Had less shortness of breath.
  • With high exercise capacity
  • Had poorer survival after LVRS than after medical
    treatment
  • Both LVRS and Medical participants had similar
    low chance of functioning better

55
NETT
  • Identified and supported viaLevel One evidence
  • Subset of Patients benefiting from surgery
  • Subset of Patients harmed by surgery
  • Efficacy of Medical Therapy

56
Thanks!
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