COPD and Asthma

smoking- primary cause of cb and emphysema

Indoor/Outdoor Pollution 

-Occupational

-Perinatal Lung Development 

-Socioeconomic Status

-Recurrent Respiratory Illness  

-Gender

-Airway Hyperreactivity/Asthma 

-Diet

-Genes (α one antitrypsin def)

submucosal gland enlargement and goblet cell hyperplasia lead to overproduction of mucous

Bronchial wall edema

These 2 factors together narrow airwayand increase airway resistance

loss of elastic recoil/ loss of alveolar capillary surface area

          Loss of Elastic Recoil

          Loss of Cap-Alv SA

leads to increase compliance, increase airway resistance, decrease exp flow rates, hyperinflation

VQ mismatch->hypoxia->pulm vasc comstriction->pulm htn

centrilobular- caused by smoking, Proximal portion terminal bronchiole affected, upper lobe prominence

Panlobular-bronchioles and airsacs affected, has lower lobe prominence, alpha 1 antitrypsin def.

Sputum Production

Dyspnea (Exertional typically)

Fifth decade of Life

Recurrent Respiratory Infections

Thin (severe)

-Pursed Lip breathing (severe)

-Central Cyanosis

-Odor

-Distress? Watch them walk, talk etc….observe

-Depression? Anxiety

-Co-morbidities

-PMH

Assess for presence of heart failure, resp illnesses, GERD, MI, Osteoporosis, Diabetes, Lung Cancer

-Assess for previous history of exacerbations, familial history, smoking history etc

Increase A/P diameter (barrel)

-Tachypnea

-Accessory Muscles, Hoover’s Sign

-Increased resonance to percussion

-Expiratory wheezing

-Decreased breath sounds

Distant heart sounds (listen over xiphoid)

-Check neck veins

α1 Anti-Trypsin Deficiency:

  -<45yrs, caucasian, family history….test everyone?>> ATS says yes

  -Serum concentration < 15-20% of norm = highly suggestive

ABG: (not sensitive)

-Hypoxemia?

-Compensated respiratory acidosis

-Check  if O2 Sat <92% on RA

Hematocrit:

-May be elevated above normal with chronic hypoxemia

Non-diagnostic

-Flattened Diaphragms

-Enlarged Retrosternal Air Space

-Hyperlucency

-Bullous disease?

-Long and Narrow Heart

Chest CT (HRCT):

-Not part of diagnostics > want you to know what to look for 

  if you have it

-Location of abnormalities (upper lobes vs lower lobes)

Spirometry is the best way to diagnose COPD and to monitor its progression and health care workers to care for COPD patients should have assess to spirometry

A diagnosis of COPD should be considered in any patient who has cough, sputum production, or dyspnea and/or a history of exposure to risk factors.  The diagnosis is confirmed by spirometry. 

FVC : Forced Vital Capacity

Total volume of air that can be forcibly exhaled in one breath

FEV1 : Forced Expiratory Volume (1st second)

Volume of air expired in first second of forced exhalation

FEV1/FVC Ratio :

Fraction of air exhaled in the first second to total exhalation volume

VC : Vital Capacity

Maximal volume of air that can be inhaled and exhaled in one breath

TLC : Total Lung Capacity 

Vital Capacity + Residual Volume

Stage II:  Moderate  FEV1/FVC < 0.70 50% < FEV1 < 80% predicted

Stage III: Severe        FEV1/FVC < 0.70 30% < FEV1 < 50% predicted

Stage IV: Very Severe    FEV1/FVC < 0.70 FEV1 < 30% predicted or FEV1 < 50% predicted

    plus chronic respiratory failure

B - Body Mass Index

O - Obstruction

D - Dyspnea

E – Exercise

Higher the score = Higher Mortality Risk

BODE score 0-10

Control stable COPD

Observe, assess and monitor disease

Prevent exacerbations

Decrease risk factors

Anticholinergics

Beta-agonists

Methylxanthines

Combination bronchodilators may have sustained effect

-LA bronchodilator treatment more effective and convenient

-Inhaled is preferred route except for methylxanthines

-Combo SABA & Anticholinergic =

  Fenoterol Ipratropium & Albuterol Ipratropium

Blocks acetylcholine receptors M3 - bronchodilation

- LA Tiotropium bronchodilating effects longer than SABA, up to 24hrs

-Improves symptoms & FEV 1 acutely

-Common side effect dry mouth

-SA-Ipratropium Bromide, LA- Tiotropium

B2 adrenergic agonists – relaxes airway smooth muscles and 

antagonizes bronchoconstriction

-SA-Albuterol, Levobuterol, LA-Salmeterol, Formoterol

-Side Effects: Tachycardia (less tachyphylaxis than we think), Tremors

Non-selective Phosphodiesterase inhibitors? Inc exp flow rate?

-Theophylline, Aminophylline

-High risk for toxicity and drug, food interactions, levels

Not inhaled- theophylline and aminophylline

-In addition to B2-Agonist more effective than alone

-Reduces exacerbations & improve symptoms

-Not been shown to alter natural history of disease

-Long term safety still not known

-Shown to decrease BMD long term, fracture risk?

-Can cause oral candidiasis

-Beclomethasone, Budesonide, Fluticasone, Triamcinolone

-Combo LABA/ICS = Formoterol/Budesonide, 

Salmeterol/Fluticasone

Stage 1- SA bronchodilator as needed

Stage 2: add LA bronchodilator and pulm rehab

Stage 3: add inhaled glucocorticoid if COPD exacerbations

Stage 4: add O2 if resp failur and consider surgical options

Goal to preserve vital organ function

-Only non-pharmacologic treatment that reduces mortality

-Must have room air PaO2 ≤ 55 mmHg or O2Sat ≤ 88%

-If Pulm Htn, Peripheral edema, Polycthemia and PaO2 55-60 or 

O2Sat ≤ 88%.

-Titrate flow to keep Sat 90% or above

-Mortality benefit for > 15hrs/day of oxygen therapy

-Also for exertional and nocturnal hypoxemia

-Infection of tracheobronchial tree

-Air pollution 

-Up to 1/3 unknown etiology…? Evidence of disease   

  progression

Antibiotic Therapy

-Inhaled Bronchodilators (w/wo anticholinergics)

-Oral Glucocorticoids (Oral Prednisone, Methylpred)

-Supplemental O2

-ABG, CXR, CBC

Mild- oral Beta Lactams, Tetra, Bactrim, Macrolides, Cephalosporins

Moderate- oral or IV Beta Lactams, Cephalosporins, or fluoroquinolone

Severe- Fluroquinolone Or Beta Lactam (with Pseudom coverage)

Noninvasive postive pressure ventilation vs ventilator

-Variable recurrent symptoms

-Airway obstruction (Reversible)

-Inflammation (Cellular component)

-Bronchial Hyperresponsiveness

Cellular component = mast cells, eosinophils, T-lymphocytes, macrophages and neutrophils

Ethnicity

Genetic Predisposition

Airway Hyperresponsive

Atopy- allergies

Gender

I/O Allergens

Occupational

Passive Smoking

Respiratory Infection

Obesity

Viral ?

Allergens 

URI-viral 

Exercise 

Cold Air

Sulfur Dioxide 

Meds 

Stress 

Irritants

Inflammation >>> Chronic Repair >>> Eventual Irreversible Narrowing of the Airway  in severe patients

Bronchoconstriction + Airway Edema + Vascular congestion + Luminal Mucous >>>

-Airflow Limitation

-Decrease FEV1 and FEV1/FVC ratio

-Decrease peak expiratory flow (PEF)

-Increased Airway Resistance