CHRONIC OBSTRUCTIVE

PULMONARY DISEASE

Martha Burk, MD
COPD
 Airflow obstruction caused by irreversible damage to
distal airways
 Often has partially reversible components
 Hyperreactivity of airways
 Airway secretions

 Includes
 Chronic Bronchitis
 Excessive bronchial secretions
 Daily cough for at least 3 months for at least 2 consecutive years
 Emphysema
 Destruction of airway walls causing permanent dilation of air spaces
with resulting loss of lung surface area for gaseous exchange

Martha Burk, MD
Who Is Affected?
 14 million Americans
 14 million more thought to be affected but undiagnosed
 CDC Data
Nearly 8 million diagnosed with Chronic Bronchitis 2007

 13% of Nursing Home residents had COPD as a diagnosis 2004

 NHLBI Data (National Heart, Lung and Blood Institute)

 4th leading cause of death in US
 1 American dies of COPD every 4 minutes

 American Council on Science and Health

 Odds of dying from chronic lung disease 1:2,404
 See riskometer.org

Martha Burk, MD
Leading Causes
of Death Heart Disease

Cancer

Cerebrovascular
Disease

Chronic
Lung Diabetes Mellitus
Disease
Infectious
Unintentional Diseases
Injuries

Martha Burk, MD
Adapted from American Council on Science and Health riskometer.org
Mortality Rates

Deaths due to
COPD
continue to
increase while
deaths from
other causes
decrease

Martha Burk, MD
Anatomy of the Distal Airways

Elastic fibers
provide
support to
alveoli and
bronchioles

Capillaries
surround each
alveolus for
gas exchange

Note that each

alveolus is
connected to Med.yale.edu
another
alveolus via
Pores of Kohn

Martha Burk, MD
Alveolar Structure

Electron microscopy
reveals a cork-like
structure to the alveoli

Each intact alveolus

supports other alveoli
and bronchioles

Destruction of alveoli
results in alveolar and
bronchiolar collapse,
especially during
exhalation when
intrathoracic pressures
are increased

Martha Burk, MD
Electron Microscopy Images from Imglib.lbl.gov
Anatomy of Disease

Airway collapse causes

obstruction of airflow
during exhalation

Trapped air increases

Residual Volume and
Total Lung Capacity
causing hyperinflation

Tidal Volume decreases

as a result of air
trapping

Media-2.web.britannica.com

Martha Burk, MD
Keys to Diagnosis
 History of smoking
 Still the primary cause of COPD!
 Additional risk factors include
 Inhalational drug use – cocaine, marijuana, methamphetamine
 Second hand smoke
 Occupational dusts and chemicals

 Persistent or progressive
 Dyspnea – usually worse with exercise
 Cough – may or may not be productive
 Sputum production

 Airflow limitation by pulmonary function testing

Martha Burk, MD
History
 Patients may also relate a history of
 Exercise intolerance
 Inability to catch their breath

 General fatigue or malaise

 Leg heaviness with activity

Martha Burk, MD
Exam Findings

Early Advanced Disease

 Breath sounds  Hyperinflation suggested by

 Normal to decreased
 May be localized
 Becomes diffuse with progressive
disease
 Rhonchi
 May be localized
 Diffuse with progressive disease
 Increased A-P chest diameter
 Prolonged exhalation
 Abdominal muscle use
 Jugular Venous Distention
 Pulmonary Artery Hypertension
Heart Failure

 Hepatic Failure
 Spider angiomas on face, neck
and upper chest and shoulders
 Pulmonary Artery Hypertension
 Hepatic Failure
 Cyanosis
 Chronic Hypercapneic Respiratory Failure

Martha Burk, MD
 Hypoxemia
Stages of COPD
Stage Symptoms FEV1/FVC FEV1
At Risk Asymptomatic with usual activity ≥ 70% > 80%
Increased cough
Mild Symptomatic with usual activity < 70% > 79%
Increased dyspnea or wheeze
Moderate Symptomatic with minimal activity <70% 50-79%
Increased sputum production
Severe Symptomatic at rest <70% 30-49%
Change in sputum color and quality
Very Severe <70% <30%
Global Initiative for Chronic Obstructive Lung Disease 2008

Martha Burk, MD
Timeline Estimate of Disease Progression

Symptoms Cough, Sputum Exertional Resting

dyspnea dyspnea
Severity of Normal Borderline Mild Moderate Severe
Obstruction
Based on
Spirometry
ABG Normal Hypoxemia
CXR Normal Hyperinflation
Age (Yrs) 35 40 45 50 55 60
Adapted from Interpretation of Pulmonary Function Tests A Practical Guide
Hyatt, Scanlon, Nakamura Lippincott, Williams & Wilkins 2003

Martha Burk, MD
Diagnostic Tests
 Pulmonary Function Testing
 Arterial Blood Gas Analysis
 Chest X-ray
 Computed Tomography of Chest
 Alpha-1 Antitrypsin
 Patients 45 years or less with COPD
 Patients with strong family history of COPD

Martha Burk, MD
Global Initiative for Chronic Obstructive Lung Disease 2008
Pulmonary Function Testing
FVC Forced Vital Capacity
SVC Slow Vital Capacity
FEV1 Forced Expiratory Volume in 1 second
FEF 25-75 Forced Expiratory Flow Rate (mid 50%)
MVV Maximal Voluntary Ventilation
TLC Total Lung Capacity
RV Residual Volume
DLCO Diffusion Capacity for Carbon Monoxide

Martha Burk, MD
Lung Volumes Illustrated
Inspiratory or Expiratory
Reserve Volume

Residual Volume
Lose this and your lungs collapse!

Tidal Volume
at rest

Slow Vital Capacity

Martha Burk, MD
Static Lung Volumes

Total Lung Inspiratory Reserve

Capacity Volume
Slow
Tidal Volume Vital Capacity
Expiratory Reserve
Volume Functional Residual
Capacity
Residual Volume
Adapted from Interpretation of Pulmonary Function Tests A Practical Guide
Hyatt, Scanlon, Nakamura Lippincott, Williams & Wilkins 2003

Martha Burk, MD
Flow-Volume Loop
Forced (or Slow) Vital Capacity

Flow
Exhale
Normal Tidal Volume +
Expiratory Reserve
Volume
Nothing left but . . .
Inhale Residual Volume!
Normal Tidal Volume +
Inspiratory Reserve

Unable to inhale anymore . . .

Total Lung Capacity reached!

Martha Burk, MD
Airway Obstruction on Spirometry

Airway
obstruction
decreases
airflow rates
and appears
as a “scooped
out” portion
of the flow-
volume curve
on spirometry

Martha Burk, MD bcmj.org

Forced Vital Capacity
in COPD or Bronchiectasis

Flow

Volume

Normal
Chronic Obstructive Disease

Martha Burk, MD
 Forced Vital Capacity
in Restrictive Lung Disease
(i.e., Pulmonary Fibrosis, Neuromuscular Weakness or Chest Wall Defects)

Note
Sharp peak in outflow
Flow Left shift in volume •FVC decreased
•FEV1 decreased
•Residual Volume decreased
Volume •Tidal Volume decreased
•DLCO decreased

FEV1 and FVC are decreased about the

same amount
Normal
Restrictive Lung Disease or FEV1/FVC ratio may appear “normal”!
Restrictive Chest Wall Defect

Martha Burk, MD
 Forced Vital Capacity
In Mixed Obstructive and Restrictive Defects

Note
obstructive
Flow “dipping” •FEV1 > FVC
•Residual Volume
•Tidal Volume
Volume FEV1 is reduced more than FVC, however,
FEV1/FVC ratio may still appear within normal
range!

Appearance of Flow-Volume curve is key.

Normal
Mixed Obstructive &
Restrictive Defect
Restrictive defect decreases RV and TLC
Obstructive defect increases RV and TLC
Overall effect: both may appear within the normal
range, depending on which is more severe – the
obstructive or restrictive component!

DLCO is reduced
Martha Burk, MD
Patterns of Impairment in Spirometry
Measurement Obstructive Restrictive
FVC (L)
FEV1
FEV1 /FVC Normal or Normal or
Slope of FV curve
MVV Normal or
TLC Normal or
RV
RV/TLC Normal
Adapted from
Interpretation of Pulmonary Function Tests A Practical Guide
Hyatt, Scanlon, Nakamura Lippincott Williams & Wilkins 2003

Martha Burk, MD
Measuring Oxygen and Carbon Dioxide

 Oximetry
Problems
 Noninvasively measures oxygen saturation
More costly  Co-oximetry
Invasive  Noninvasively measures oxygen & carbon dioxide
saturations
Accuracy  Arterial Blood Gas
affected by
how sample is
 Invasive measurements
obtained and  Partial pressure Oxygen
handled  Partial pressure Carbon dioxide
during  pH
transport  Can also measure
 Carbon Monoxide
 Methemoglobin

Martha Burk, MD
Arterial Blood Gas Analysis
Disorder Primary Defect Compensatory Magnitude of
Acidosis versus Response Compensation
Alkalosis
Respiratory ↑HCO3
Respiratory Acidosis
versus Acute ↑PCO2 ↑HCO3 1 per 10↑PCO2
Metabolic
Chronic ↑PCO2 ↑HCO3 3.5 per 10↑PCO2
Anion Gap Respiratory ↓HCO3 ↓HCO3
Alkalosis
Compensation
present, and Acute ↓PCO2 ↓HCO3 2 per 10 ↓PCO2
if so is it Chronic ↓PCO2 ↓HCO3 5 per 10 ↓PCO2
appropriate

Is a Mixed Metabolic ↓HCO3 ↓PCO2 ↓PCO2

disorder acidosis 1.3 per 1 ↓HCO3
present Metabolic ↑HCO3 ↑PCO2 ↑PCO2
alkalosis 0.7 per 1 ↑HCO3
Martha Burk, MD Current Medical Diagnosis & Treatment 2009
Normal Alveolar Gas Exchange

Gases move from

areas of higher Oxygen depleted blood cells
concentration to Loaded with carbon dioxide
areas of lower
concentration

Oxygen repleted

Martha Burk, MD wikimedia.org

Evaluating Oxygenation

PB = Barometric Pressure Alveolar-arterial Difference PAO2 – PaO2

Sea Level = 760 mm Hg “Normal” A-a is 10-15mm Hg
500 ft = 747 mm Hg
Increases with Exercise, Age and higher FIO2

PH2O = Water Vapor Pressure

PAO2 = [FIO2 x (PB – PH20)] – PaCO2/RQ
47 mm Hg at 37 degrees C
Assume Sea level, 37 degrees Celsius, Room Air (21%)
RQ = Respiratory Quotient (0.8)
PAO2 = [0.21x(760 – 47)] – 40/0.8
PAO2 = Alveolar Oxygen PAO2 = 150 – 50 = 100

PaO2 = Arterial Oxygen Expected A-a gradient can be estimated as

PaCO2 = Arterial Carbon dioxide 2.5 + (0.21)(Age in Years)

UpToDate
Martha Burk, MD
PaO2 to FIO2 Ratio
Arterial oxygen as percent of FIO2
300-500mm Hg = Within Normal Limits
200-300 indicates Acute Lung Injury
<201 indicates severe hypoxemia (as in ARDS)

Martha Burk, MD
A-a oxygen ratio PaO2 / PAO2
Helps predict PaO2 changes with changing FIO2
Normal lower limits of 0.77-0.82
Most accurate with FIO2 <55%

Martha Burk, MD
Normal A-a Variation Based on FiO2

FiO2 A-a
Higher than expected
values indicate one of 21% 10-15
the following
30% 89
1. V/Q mismatch
40% 160
2. Right to Left Shunt
50% 232
3. Diffusion defect 60% 303
70% 374
80% 445
90% 517
100% 588

Martha Burk, MD
Influences on A-a Gradient

Anything that
interferes with

Ventilation

Diffusion

Perfusion

will increase
the A-a
gradient.

Image from Mariemakings.blogspot.com

Martha Burk, MD
Radiographic Analysis

Hyperlucent lungs

Increased lung volume

Vascular displacement

Flattened diaphragm leaflets

Vertical mediastinal structures

Martha Burk, MD
Image from meddean.luc.edu
CT
Appearance

Panacinar
emphysema

Subpleural
blebs

Bronchiectasis
indicates
chronic
endobronchial
infection

Martha Burk, MD
Knol.google.com
Not This Emphysema

Not to be
confused with
subcutaneous
emphysema

Indicates
intrathoracic air
leak

Muscle striations
are
pathognomonic

Be sure to rule
out
Pneumothorax
paramediastinal
pneumothorax with subcutaneous emphysema

Martha Burk, MD Images from radiopaedia.org

 Treatment Options in Stable COPD
GOLD Stage Mild Moderate Mod Severe Severe
I II III IV
FEV1/FVC <70% FEV1/FVC <70% FEV1/FVC <70% FEV1/FVC <70%

FEV1 >80% FEV1 50-79% FEV1 30-49% FEV1 <30%

OR <50% with Chronic
Respiratory Failure
Investigations Screening Pre- & Post- Annual PFTs every 6 months
Spirometry Bronchodilator PFT, ABG, CXR Annual ABG, CXR
Spirometry
Treatment Options Smoking Cessation
Pneumococcal Vaccine and Annual Influenza Vaccine
Prescribe Short Acting Bronchodilator when needed
Tiotropium +/- Short Acting Bronchodilator + Pulmonary Rehab

Consider addition of inhaled corticosteroids [TORCH trial] Tiotropium + Long Acting Beta
Fewer moderate and severe exacerbations in patients taking inhaled steroids Agonist +/- Methylxanthines
compared with those taking only long acting bronchodilators Supplemental Oxygen as needed
No change in number of hospitalizations for severe exacerbations or change in
Lung Volume
mortality UpToDate
Reduction
The Role of Long Acting Bronchodilators in the Management of Stable COPD Chest 2004; 125:249-259 Surgery
Martha Burk, MD
Treatment Options Acute Exacerbations

 Supplemental oxygen
Cough
increases in  Goal 90-94%
frequency or  Short acting bronchodilators
severity  Albuterol and Ipratropium combined have a greater
effect than either individually
Sputum
 Steroids
increases in
volume or  IV administration for those intolerant of oral intake
character  Oral steroids are as effective as IV
 Dosed as 1mg/kg IBW (Ideal Body Weight)
Dyspnea  60mg orally for 7 days
increases
 Antibiotics, if appropriate
50-60% due  No Benefit
to infection  Mucolytics, methylxanthines or chest physiotherapy

Martha Burk, MD
Ventilatory Support

Precise , high  NIPPV (Noninvasive Positive Pressure Ventilation)

oxygen  Important Contraindications
concentration
 Altered Mental Status
High flow  Vomiting or High Aspiration Risk
rates  Cardiac or Respiratory Arrest
Noninvasive  Need for intubation or expecting prolonged
ventilatory support
Reduced  Inability to cooperate, protect the airway or
mortality in
handle secretions
appropriate
patient  Recent esophageal anastomosis

 When in doubt, INTUBATE

aic.cuhk.edu.hk
Martha Burk, MD
UpToDate
NIPPV Candidates Inpatient Setting

IMPORTANT  Hypercapneic respiratory failure

Evaluate  PCO2 >45
patients for
signs of  pH <7.3
improvement
within 30
 Cardiogenic pulmonary edema
minutes
 Post extubation management
Patients who
worsen in this
time should be
intubated
immediately

Martha Burk, MD
UpToDate
Nocturnal NIPPV

Improvements  Nocturnal BiPAP helps patients with

seen only with
patients with chronic hypercapnea by
chronic  Decreasing hypercapnea
hypercapnea
NOT with  Decreasing residual volume
severe but
stable COPD  Seen as decreased RV/TLC
 Increasing
 Inspiratory
Capacity
 Vital Capacity
 FEV1

Martha Burk, MD
UpToDate
Evaluating Need For Long Term Oxygen

PaO2 <55mm Hg or Sats <89%

Documentation

Need PaO2 <60 or Sats <90%

 IF Cor Pulmonale, Right Heart Failure OR Erythrocytosis
Flow rate (Hematocrit >55%) is present

Duration
SLEEP
Activity  PaO2 <55 or Sats <89%
 PaO2 falls >10mm Hg and/or Sats drop >5%
Delivery
vehicle
EXERCISE
Portable or  PaO2 <55 or Sats <89%
Ambulatory  OR in presence of significant dyspnea that may limit activity

Martha Burk, MD
UpToDate
Survival Benefit Nocturnal Oxygen Therapy Trial

Improved
survival seen
with wearing
oxygen

Survival
benefit seen
with at least
18 hours of
daily use

Martha Burk, MD
UpToDate
How Much Oxygen?

Oxygen PaO2 on Room Air FIO2 % Flow Rate (L/min)

requirements By Nasal Cannula
should include
adequate 50 24 1
levels to 45 28 2
prevent 40 32 3
desaturations
with usual 35 35 4
activity or
UpToDate
sleep

Martha Burk, MD
Oxygen Conserving Devices

Reservoir Demand Pulse Transtracheal

Mechanism Store during Early Store
exhalation inspiratory Bypass dead
delivery space
Efficacy 2:1 to 4:1 3:1 to 7:1 2:1 to 3:1
Cosmetics Obtrusive Adequate Excellent
Comfort Adequate Adequate Good
Complications Few Mechanical Mucous plug
failure Malposition
Cost Low Significant Significant
UpToDate

Martha Burk, MD
Summary
 History of chronic or progressive  Additional therapy
 Dyspnea  Pulmonary rehab
 Cough  Supplemental oxygen therapy
 Sputum  Nocturnal BiPap
 Smoking  Severe exacerbations
 Evaluate pulmonary function  Supplemental oxygen
 Diagnosis  NIPPV versus intubation
 Severity  Antibiotics
 Initiate treatment  Bronchodilators
 Bronchodilators  Steroids
 Inhaled steroids
 Annual influenza vaccine
 Pneumococcal vaccine

Martha Burk, MD