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
Cancer Cerebrovascular Disease

Heart Disease

Chronic Lung Disease Unintentional Injuries

Diabetes Mellitus

Infectious Diseases

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 another alveolus via Pores of Kohn
Martha Burk, MD

Med.yale.edu

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 May be localized Diffuse with progressive disease

Increased A-P chest diameter Prolonged exhalation Abdominal muscle use Pulmonary Artery Hypertension Heart Failure Hepatic Failure

Jugular Venous Distention
  

Rhonchi
 

Spider angiomas on face, neck and upper chest and shoulders
 

Pulmonary Artery Hypertension Hepatic Failure Chronic Hypercapneic Respiratory Failure

Cyanosis

Martha Burk, MD

Hypoxemia

Stages of COPD
Stage At Risk Mild Moderate Severe Very Severe Symptoms Asymptomatic with usual activity Increased cough Symptomatic with usual activity Increased dyspnea or wheeze Symptomatic with minimal activity Increased sputum production Symptomatic at rest Change in sputum color and quality <70% <30%
Global Initiative for Chronic Obstructive Lung Disease 2008

FEV1/FVC ≥ 70% < 70% <70% <70%

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

Martha Burk, MD

Timeline Estimate of Disease Progression
Symptoms Severity of Obstruction ABG CXR Age (Yrs) 35 40 Normal Cough, Sputum Borderline Mild Exertional dyspnea Moderate Resting dyspnea Severe

Based on Spirometry

Normal Normal 45 50

Hypoxemia Hyperinflation 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 SVC FEV1 FEF 25-75 MVV TLC RV DLCO
Martha Burk, MD

Forced Vital Capacity Slow Vital Capacity Forced Expiratory Volume in 1 second Forced Expiratory Flow Rate (mid 50%) Maximal Voluntary Ventilation Total Lung Capacity Residual Volume Diffusion Capacity for Carbon Monoxide

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 Capacity Inspiratory Reserve Volume Tidal Volume Expiratory Reserve Volume Residual Volume Slow Vital Capacity Functional Residual Capacity

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

Inhale
Normal Tidal Volume + Inspiratory Reserve

Nothing left but . . . Residual Volume!

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 flowvolume 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)

Flow

Note Sharp peak in outflow Left shift in volume

Volume

•FVC decreased •FEV1 decreased •Residual Volume decreased •Tidal Volume decreased •DLCO decreased
FEV1 and FVC are decreased about the same amount FEV1/FVC ratio may appear “normal”!

Normal Restrictive Lung Disease or Restrictive Chest Wall Defect

Martha Burk, MD

Forced Vital Capacity
Note obstructive “dipping”

In Mixed Obstructive and Restrictive Defects

Flow

•FEV1 > FVC •Residual Volume •Tidal Volume
FEV1 is reduced more than FVC, however, FEV1/FVC ratio may still appear within normal range!

Volume

Normal Mixed Obstructive & Restrictive Defect

Appearance of Flow-Volume curve is key. 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 FVC (L) FEV1 FEV1 /FVC Slope of FV curve MVV TLC RV RV/TLC Normal Adapted from Interpretation of Pulmonary Function Tests A Practical Guide
Hyatt, Scanlon, Nakamura Lippincott Williams & Wilkins 2003

Obstructive

Restrictive

Normal or

Normal or Normal or

Normal or

Martha Burk, MD

Measuring Oxygen and Carbon Dioxide
Problems
More costly Invasive Accuracy affected by how sample is obtained and handled during transport
 

Oximetry

Noninvasively measures oxygen saturation Noninvasively measures oxygen & carbon dioxide saturations Invasive measurements
   

Co-oximetry

Arterial Blood Gas

Partial pressure Oxygen Partial pressure Carbon dioxide pH Can also measure
 

Carbon Monoxide Methemoglobin

Martha Burk, MD

Arterial Blood Gas Analysis
Acidosis versus Alkalosis Respiratory versus Metabolic Anion Gap Compensation present, and if so is it appropriate Is a Mixed disorder present
Martha Burk, MD

Disorder Respiratory Acidosis Acute Chronic Respiratory Alkalosis Acute Chronic Metabolic acidosis Metabolic alkalosis

Primary Defect

Compensatory Response

Magnitude of Compensation

↑HCO3
↑PCO2 ↑PCO2 ↑HCO3 ↑HCO3 ↓HCO3 ↓PCO2 ↓PCO2 ↓HCO3 ↑HCO3 ↓HCO3 ↓HCO3 ↓PCO2 ↑PCO2 1 per 10↑PCO2 3.5 per 10↑PCO2 ↓HCO3 2 per 10 ↓PCO2 5 per 10 ↓PCO2 ↓PCO2 1.3 per 1 ↓HCO3 ↑PCO2 0.7 per 1 ↑HCO3

Current Medical Diagnosis & Treatment 2009

Normal Alveolar Gas Exchange
Gases move from areas of higher concentration to areas of lower concentration

Oxygen depleted blood cells Loaded with carbon dioxide

Oxygen repleted

Martha Burk, MD

wikimedia.org

Evaluating Oxygenation
PB = Barometric Pressure Sea Level = 760 mm Hg 500 ft = 747 mm Hg

Alveolar-arterial Difference PAO2 – PaO2
“Normal” A-a is 10-15mm Hg Increases with Exercise, Age and higher FIO2 PAO2 = [FIO2 x (PB – PH20)] – PaCO2/RQ
Assume Sea level, 37 degrees Celsius, Room Air (21%) PAO2 = [0.21x(760 – 47)] – 40/0.8 PAO2 = 150 – 50 = 100

PH2O = Water Vapor Pressure 47 mm Hg at 37 degrees C RQ = Respiratory Quotient (0.8) PAO2 = Alveolar Oxygen PaO2 = Arterial Oxygen PaCO2 = Arterial Carbon dioxide

Expected A-a gradient can be estimated as
2.5 + (0.21)(Age in Years)

Martha Burk, MD

UpToDate

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
Higher than expected values indicate one of the following 1. V/Q mismatch 2. Right to Left Shunt 3. Diffusion defect FiO2 21% 30% 40% 50% 60% 70% 80% 90% 100%
Martha Burk, MD

A-a 10-15 89 160 232 303 374 445 517 588

Influences on A-a Gradient
Anything that interferes with Ventilation Diffusion Perfusion will increase the A-a gradient.

Martha Burk, MD

Image from Mariemakings.blogspot.com

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 paramediastinal pneumothorax
Martha Burk, MD

Pneumothorax with subcutaneous emphysema

Images from radiopaedia.org

Treatment Options in Stable COPD
GOLD Stage Mild I
FEV1/FVC <70% FEV1 >80% Investigations Screening Spirometry

Moderate II
FEV1/FVC <70% FEV1 50-79% Pre- & PostBronchodilator Spirometry

Mod Severe III
FEV1/FVC <70% FEV1 30-49% Annual PFT, ABG, CXR

Severe IV
FEV1/FVC <70%
OR <50% with Chronic Respiratory Failure

FEV1 <30%

PFTs every 6 months Annual ABG, CXR

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] Fewer moderate and severe exacerbations in patients taking inhaled steroids compared with those taking only long acting bronchodilators No change in number of hospitalizations for severe exacerbations or change in mortality UpToDate Martha Burk, MD

Tiotropium + Long Acting Beta Agonist +/- Methylxanthines Supplemental Oxygen as needed Lung Volume Reduction Surgery

The Role of Long Acting Bronchodilators in the Management of Stable COPD Chest 2004; 125:249-259

Treatment Options Acute Exacerbations
Cough increases in frequency or severity Sputum increases in volume or character Dyspnea increases 50-60% due to infection
Martha Burk, MD

Supplemental oxygen

Goal 90-94% Albuterol and Ipratropium combined have a greater effect than either individually IV administration for those intolerant of oral intake Oral steroids are as effective as IV

Short acting bronchodilators

Steroids
  

Dosed as 1mg/kg IBW (Ideal Body Weight)

60mg orally for 7 days

 

Antibiotics, if appropriate No Benefit

Mucolytics, methylxanthines or chest physiotherapy

Ventilatory Support
Precise , high oxygen concentration High flow rates Noninvasive Reduced mortality in appropriate patient

Martha Burk, MD

NIPPV (Noninvasive Positive Pressure Ventilation)

Important Contraindications
Altered Mental Status  Vomiting or High Aspiration Risk  Cardiac or Respiratory Arrest  Need for intubation or expecting prolonged ventilatory support  Inability to cooperate, protect the airway or handle secretions  Recent esophageal anastomosis

When in doubt, INTUBATE
aic.cuhk.edu.hk UpToDate

NIPPV Candidates Inpatient Setting
IMPORTANT Evaluate patients for signs of improvement within 30 minutes Patients who worsen in this time should be intubated immediately

Hypercapneic respiratory failure
 PCO2

>45  pH <7.3
 

Cardiogenic pulmonary edema Post extubation management

Martha Burk, MD

UpToDate

Nocturnal NIPPV
Improvements seen only with patients with chronic hypercapnea NOT with severe but stable COPD

Nocturnal BiPAP helps patients with chronic hypercapnea by
 Decreasing
 Seen

hypercapnea  Decreasing residual volume
as decreased RV/TLC
 Increasing
 Inspiratory

Capacity  Vital Capacity  FEV1
Martha Burk, MD

UpToDate

Evaluating Need For Long Term Oxygen
Documentation Need Flow rate Duration Activity Delivery vehicle Portable or Ambulatory

PaO2 <55mm Hg or Sats <89% PaO2 <60 or Sats <90%

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

SLEEP
 

PaO2 <55 or Sats <89% PaO2 falls >10mm Hg and/or Sats drop >5%

EXERCISE
 

PaO2 <55 or Sats <89% 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 requirements should include adequate levels to prevent desaturations with usual activity or sleep PaO2 on Room Air 50 45 40 35 FIO2 % 24 28 32 35 Flow Rate (L/min) By Nasal Cannula 1 2 3 4
UpToDate

Martha Burk, MD

Oxygen Conserving Devices
Reservoir Mechanism Store during exhalation 2:1 to 4:1 Obtrusive Adequate Few Low Demand Pulse Early inspiratory delivery 3:1 to 7:1 Adequate Adequate Mechanical failure Significant Transtracheal Store Bypass dead space 2:1 to 3:1 Excellent Good Mucous plug Malposition Significant
UpToDate

Efficacy Cosmetics Comfort Complications Cost

Martha Burk, MD

Summary

History of chronic or progressive
   

Additional therapy
  

Dyspnea Cough Sputum Smoking Diagnosis Severity Bronchodilators Inhaled steroids Annual influenza vaccine Pneumococcal vaccine

Pulmonary rehab Supplemental oxygen therapy Nocturnal BiPap Supplemental oxygen NIPPV versus intubation Antibiotics Bronchodilators Steroids

Evaluate pulmonary function
 

Severe exacerbations
    

Initiate treatment
   

Martha Burk, MD

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