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Chronic Obstructive
Pulmonary Disease
Josh Solomon, MD
COPD
• Definition
• Epidemiology
• Clinical Disease and Diagnosis
• Exacerbations
– Definition
– Treatment
• Ventilation
• Outpatient Treatment
Definition
• A clinical syndrome characterized by:
– Partially reversible airflow limitation
– Slow clinical progression
– Minimal airway hyperresponsiveness vs.
asthma
• Strongly linked to chronic exposure to
tobacco smoke
• An inflammatory airway disease
Epidemiology
• Fourth leading cause of death in the
United States
• Seen in 10% of adults over the age of
40 globally
– Higher in smokers
– Higher in men
Clinical Disease
• Slow onset of progressive shortness
of breath
• Inability to tolerate physical activity
• Increasing frequency of
exacerbations
• Cough and sputum production
Diagnosis
Airflow obstruction
TIME
1 2 3 4 5 6
V
O
L
U
M
E
FVC
FEV1
FEV1 FEV1/FVC >70%
Spirometric Criteria for COPD
• Forced expiratory volume in one
second (FEV1) < 80% predicted
• FEV1/FVC ratio < 70%
• Airflow does not improve ≥ 12% and
200mL with albuterol
Pauwels RA, et al. AJRCCM 2001; 163.
Fabbri LM and Hurd SS. Eur Respir J 2003; 22.
0
20
40
60
80
100
20 30 40 50 60 70 80 90
FEV1
(%)
Age (years)
Death
Disability
Symptoms
Fletcher C, Peto R. Br Med J. 1977; 1.
Natural History: FEV1 Decline
Never-smoker
Smoker
COPD - Pathology
• Irreversible changes:
– Airway fibrosis and narrowing
– Loss of airways elastic recoil
– Alveoli destruction
• Reversible changes:
– Smooth muscle contraction/hypertrophy
– Airway accumulation of cells, mucus
COPD
Toxic Inhaled Agent
(tobacco smoke, air pollution, occupational)
Occupation
Respiratory infection
Airway responsiveness
Socioeconomics
COPD
Susceptibility
Genetics
Patient X
• 65 years old
• Smoke 1 pack/day for 30 years
• Complains of morning cough
with a lot of sputum and
worsening shortness of breath
over last 5 years
Chest X-ray
Chest X-ray
Chest CT
Spirometry
• FEV1 45%
• FEV1/FVC 50%
V
O
L
U
M
E
TIME
PATIENT X
Exacerbation
Definition
• Abrupt increase in symptoms
• Shortness of breath
• Amount of sputum
• Color of sputum
• Requires change in medication
• Increase in frequency as disease
gets more severe
Exacerbation
•infection account for 80% of
exacerbations
•Strep Pneumonia, Hemophilus influenza,
Moraxella catarrhalis most common
•Other causes include pulmonary
embolism, heart failure, pneumothorax
Sethi et al. CHEST 2001; 115.
Workup
• History/physical exam
• Chest Xray - 20% abnormal
• Arterial Blood Gas
– Degree of hypoxemia (O2) and hypercarbia
(CO2)
Treatment
•Oxygen
•keep SaO2 > 90% but avoid high SaO2
(>97%)
•B agonists(albuterol/terbutaline/salbuterol)
•Nebulized or MDI have same delivery
•inhaled better than intravenous (FEV1)
Mcrory et at. CHEST 2001; 119.
•anticholinergics (ipratropium)
•use with beta agonists in inhaled form
Treatment
•Methylxanthines (aminophylline)
•No good data that they work in COPD
•Minimal if any improvement in FEV1
•Only use if no access to B- agonists or
anticholinergics
Barr et al. Cochrane Review 2001
Treatment
•Antibiotics
•All ICU and ventilated patients
Saint et al. JAMA 1995, 273.
•Inpatient – mild
•macrolide, fluoroquinolone, 3rd generation
cephalosporin, antipseudomonal penicillin
•Inpatient – sick (ICU)
•3rd generation ceph/antipseudomonal PCN
+ fluoroquinolone or aminoglycoside
Treatment
•Steroids
•studies show shorter hospital stay and faster
improvement in FEV1
Niewoehner et al. NEJM 1999, 340.
•Severe disease
•methylprednisolone 0.5 to 1 mg/kg every 6
hrs for 3 days, then prednisone 40 mg for 2
weeks
•slow taper in severe disease
COPD and respiratory failure
•Non-invasive ventilation
•studied in COPD – prevents intubation and
improves outcome in respiratory failure
Brochard et al. NEJM 1995, 333.
•Contraindications : altered mental status,
increased secretions, CV instability
COPD and respiratory failure
•Ventilation Goals
•rest muscles of breathing
•allow time for exhalation
•prevent hyperinflation
COPD and respiratory failure
•Ventilation
•Volume Control
•Vt – 8 – 10 cc/kg body weight
•RR – use to target normal or patients CO2
•PEEP 5 mm H2O
•I:E 1:3 to 1:5 (**important long expiratory
time)
•#1 risk is HYPERINFLATION
Hyperinflation
• Increased volume of lung at end -
expiration
• Causes - expiratory airflow obstruction +
inadequate expiratory time
• Signs - hypotension, high airway
pressures, hypoxemia, pneumothorax
Hyperinflation
• Measure - breath hold at end expiration
(iPEEP, autoPEEP)
Hyperinflation Treatment
• Increase expiratory time
– Decrease respiratory rate
– Decrease tidal volume
– Increased flow rate/change I:E ratio
– Tolerate higher CO2 levels
• Decrease airflow obstruction
– Aggressive use of bronchodilators
– Sedation/paralysis if necessary
COPD and respiratory failure
•Ventilation
•Extubate as soon as patient tolerates a 30
minute wean
•Target patients baseline CO2
•Can extubate early to noninvasive
Ferrer et al. AJRCCM 2006; 173.
Discharge
•Smoking cessation #1
•inhaled albuterol/salbuterol + ipratropium
•slow prednisone taper(2 weeks
minimum)
•oxygen if SaO2 <88% on room air
(improves survival)
NOTT. Ann Int Med 1980; 93(3).
Summary
•patients admitted for COPD get antibiotics,
steroids, inhaled albuterol/ipratropium and O2
•if intubated, careful to avoid hyperinflation by
altering RR, I:E time
•at discharge, all go home with prednisone taper,
inhaled albuterol/ipratropium and follow-up
References
• www.goldcopd.com
• www.copd-international.com
• Evidence Based Review of COPD management
Soto et al. Curr Opin Pulm Med 2003, 9: 117-124.
5  copd

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5 copd

  • 2. COPD • Definition • Epidemiology • Clinical Disease and Diagnosis • Exacerbations – Definition – Treatment • Ventilation • Outpatient Treatment
  • 3. Definition • A clinical syndrome characterized by: – Partially reversible airflow limitation – Slow clinical progression – Minimal airway hyperresponsiveness vs. asthma • Strongly linked to chronic exposure to tobacco smoke • An inflammatory airway disease
  • 4. Epidemiology • Fourth leading cause of death in the United States • Seen in 10% of adults over the age of 40 globally – Higher in smokers – Higher in men
  • 5. Clinical Disease • Slow onset of progressive shortness of breath • Inability to tolerate physical activity • Increasing frequency of exacerbations • Cough and sputum production
  • 7.
  • 8. TIME 1 2 3 4 5 6 V O L U M E FVC FEV1 FEV1 FEV1/FVC >70%
  • 9. Spirometric Criteria for COPD • Forced expiratory volume in one second (FEV1) < 80% predicted • FEV1/FVC ratio < 70% • Airflow does not improve ≥ 12% and 200mL with albuterol Pauwels RA, et al. AJRCCM 2001; 163. Fabbri LM and Hurd SS. Eur Respir J 2003; 22.
  • 10. 0 20 40 60 80 100 20 30 40 50 60 70 80 90 FEV1 (%) Age (years) Death Disability Symptoms Fletcher C, Peto R. Br Med J. 1977; 1. Natural History: FEV1 Decline Never-smoker Smoker
  • 11. COPD - Pathology • Irreversible changes: – Airway fibrosis and narrowing – Loss of airways elastic recoil – Alveoli destruction • Reversible changes: – Smooth muscle contraction/hypertrophy – Airway accumulation of cells, mucus
  • 12.
  • 13.
  • 14. COPD Toxic Inhaled Agent (tobacco smoke, air pollution, occupational) Occupation Respiratory infection Airway responsiveness Socioeconomics COPD Susceptibility Genetics
  • 15. Patient X • 65 years old • Smoke 1 pack/day for 30 years • Complains of morning cough with a lot of sputum and worsening shortness of breath over last 5 years
  • 19. Spirometry • FEV1 45% • FEV1/FVC 50% V O L U M E TIME PATIENT X
  • 21. Definition • Abrupt increase in symptoms • Shortness of breath • Amount of sputum • Color of sputum • Requires change in medication • Increase in frequency as disease gets more severe
  • 22. Exacerbation •infection account for 80% of exacerbations •Strep Pneumonia, Hemophilus influenza, Moraxella catarrhalis most common •Other causes include pulmonary embolism, heart failure, pneumothorax Sethi et al. CHEST 2001; 115.
  • 23. Workup • History/physical exam • Chest Xray - 20% abnormal • Arterial Blood Gas – Degree of hypoxemia (O2) and hypercarbia (CO2)
  • 24. Treatment •Oxygen •keep SaO2 > 90% but avoid high SaO2 (>97%) •B agonists(albuterol/terbutaline/salbuterol) •Nebulized or MDI have same delivery •inhaled better than intravenous (FEV1) Mcrory et at. CHEST 2001; 119. •anticholinergics (ipratropium) •use with beta agonists in inhaled form
  • 25. Treatment •Methylxanthines (aminophylline) •No good data that they work in COPD •Minimal if any improvement in FEV1 •Only use if no access to B- agonists or anticholinergics Barr et al. Cochrane Review 2001
  • 26. Treatment •Antibiotics •All ICU and ventilated patients Saint et al. JAMA 1995, 273. •Inpatient – mild •macrolide, fluoroquinolone, 3rd generation cephalosporin, antipseudomonal penicillin •Inpatient – sick (ICU) •3rd generation ceph/antipseudomonal PCN + fluoroquinolone or aminoglycoside
  • 27. Treatment •Steroids •studies show shorter hospital stay and faster improvement in FEV1 Niewoehner et al. NEJM 1999, 340. •Severe disease •methylprednisolone 0.5 to 1 mg/kg every 6 hrs for 3 days, then prednisone 40 mg for 2 weeks •slow taper in severe disease
  • 28. COPD and respiratory failure •Non-invasive ventilation •studied in COPD – prevents intubation and improves outcome in respiratory failure Brochard et al. NEJM 1995, 333. •Contraindications : altered mental status, increased secretions, CV instability
  • 29. COPD and respiratory failure •Ventilation Goals •rest muscles of breathing •allow time for exhalation •prevent hyperinflation
  • 30. COPD and respiratory failure •Ventilation •Volume Control •Vt – 8 – 10 cc/kg body weight •RR – use to target normal or patients CO2 •PEEP 5 mm H2O •I:E 1:3 to 1:5 (**important long expiratory time) •#1 risk is HYPERINFLATION
  • 31. Hyperinflation • Increased volume of lung at end - expiration • Causes - expiratory airflow obstruction + inadequate expiratory time • Signs - hypotension, high airway pressures, hypoxemia, pneumothorax
  • 32. Hyperinflation • Measure - breath hold at end expiration (iPEEP, autoPEEP)
  • 33. Hyperinflation Treatment • Increase expiratory time – Decrease respiratory rate – Decrease tidal volume – Increased flow rate/change I:E ratio – Tolerate higher CO2 levels • Decrease airflow obstruction – Aggressive use of bronchodilators – Sedation/paralysis if necessary
  • 34. COPD and respiratory failure •Ventilation •Extubate as soon as patient tolerates a 30 minute wean •Target patients baseline CO2 •Can extubate early to noninvasive Ferrer et al. AJRCCM 2006; 173.
  • 35. Discharge •Smoking cessation #1 •inhaled albuterol/salbuterol + ipratropium •slow prednisone taper(2 weeks minimum) •oxygen if SaO2 <88% on room air (improves survival) NOTT. Ann Int Med 1980; 93(3).
  • 36. Summary •patients admitted for COPD get antibiotics, steroids, inhaled albuterol/ipratropium and O2 •if intubated, careful to avoid hyperinflation by altering RR, I:E time •at discharge, all go home with prednisone taper, inhaled albuterol/ipratropium and follow-up
  • 37. References • www.goldcopd.com • www.copd-international.com • Evidence Based Review of COPD management Soto et al. Curr Opin Pulm Med 2003, 9: 117-124.