CHRONIC OBSTRUCTIVE PULMONARY DISEASE

WENDY MCKENZIE, MMM, CD, RN, BSN,MSN, ADEC

Functional Components of the Respiratory System (Review)

Neurochemical Control of Ventilation
(resp center, central and peripheral chemoreceptors)

Mechanics of Breathing
(major and accessory muscles, lung elasticity, aw resistance, Alveolar surface tension, work of breathing

Gas Transport

(distribution of ventilation and perfusion, O2 transport, CO2

transport

Control of the Pulmonary Circulation

(distribution of pulmonary blood flow)

Neurochemical control of ventilation (Review)

Breathing is involuntary normally to maintain homeostasis Voluntary breathing is necessary for talking, singing, laughing and holding ones breath Respiratory center located in the brain stem controls several groups of bilateral neurons that transmit respiratory nerve impulses Five groups of neurons:

Mechanics of Breathing (Review)

3 components 1. Major and accessory muscles of inspiration and expiration 2. Elastic properties of lungs and chest wall 3. Resistance of airflow through conducting airways

Major and accessory muscles

Major diaphragm, external intercostal muscles Accessory muscles sternocleidomastoid and scalene muscles Work of breathing (effort) increases with:

Elastic properties of the lung and chest wall

Elastic properties permit expansion during inspiration and return to resting volume during expiration Elastin fibres in alveolar walls and surrounding small AW, around pulmonary capillaries, and by surface tension Elastic recoil Compliance

Airway Resistance

Similar to blood flow Determined by length, radius and crosssectional area of AW, viscosity and velocity of gas (Poiseuilles law) Normal AW resistance is low Causes of increased resistance:

Swelling (edema) Obstruction (mucous) Spasm (bronchospasm)

Surface Tension

Occurs at any liquid/gas interface Tendency for liquid molecules when exposed to air tend to adhere to one another Example:

In the body increased surface tension makes expansion difficultsurfactant in alveoli enables us to overcome this

Chronic Obstructive Pulmonary Disease

Definition

COPD denotes a group of respiratory disorders characterized by chronic and recurrent obstruction of airflow in the pulmonary airways.

Causes

Mechanism Underlying Airflow Limitation in COPD

INFLAMMATION

Small airway disease

Parenchymal destruction

AIRFLOW LIMITATION

Vocabulary

FEV forced expiratory volume FVC forced vital capacity FEV1 forced expiratory volume 1 second FEV1/FVC ratio expressed as a %
80-120%

normal 60-79% mild obstruction 40-59% moderate obstruction Less than 40% obstruction

Stages of COPD

Stage 0: At Risk Normal spirometry Chronic symptoms (cough/sputum)

Minimum of 3mths/year for 2 consecutive yrs. 2 tbsps sputum/day or more

Stage 1: Mild COPD FEV1/FVC < 70% FEV1 > 80% predicted (post bronchodilator) With or without chronic symptoms

Stage II: Moderate COPD FEV1 60-80% predicted With or without chronic symptoms (dyspnea)

Stage III: Severe COPD FEV1 < 60% predicted Respiratory failure

p02 of < 60 mm Hg with or without a pCO2 > 50 mm Hg while breathing air at sea level

Or Clinical signs of right heart failure

cor pulmonale

Stages of COPD

Stage IV
FEV1/FVC

< 70% FEV1<30% predicted, <50% predicted plus chronic respiratory failure

Pathophysiology of COPD

Process starts with an irritant like cigarette smoke Stresses the tracheobronchial cellular environment

Cellular adaptation and initiation of AIR

Cellular Adaptation
Hypertrophy and hyperplasia submucosal glands in the large bronchi Hyperplasia of the goblet cells (purpose) Metaplasia
i.

i.

ii. iii.

Ciliated epithelial cells stratified squamous epithelial cells

AIR

Release of the chemical mediators

Eventually CIR - fibrosis

Complications of COPD
1. 2. 3. 4. 5. 6. 7.

Mucus Hypersecretion Ciliary Dysfunction Airflow Limitations Pulmonary Hyperinflation Gas Exchange Abnormalities Pulmonary Hypertension Cor pulmonale

1.

Mucus Hypersecretion

Leukotrienes
Stimulate mucus secretion

Hyperplasia of the goblet cells

Increased mucus production Tenacious sputum

Mucus Plug

Ciliary Dysfunction
( mucociliary escalator function)

Replacement of ciliated epithelium to stratified squamous epithelium Smoking destroys cilium

2. Ciliary Dysfunction
( mucociliary escalator function)

Thick mucus interferes mucociliary escalator stasis of mucus in lungs

Mucus accumulates Mucus stagnates Viral/bacterial infections are common

3. Airflow Limitations

Irreversible

Hypertrophy/hyperplasia submucosal glands CIR fibrosis and narrowing of the small airways

Reversible

AIR mucosal edema and mucus production Presence of secretions Bronchial smooth muscle contraction

4. Pulmonary Hyperinflation

Parenchymal destruction (emphysema)

Alveolar destruction loss of elastic recoil of lung Loss of radial traction intra-alveolar pressure driving exhalation Traps gas in the alveoli permanent over inflation and distal airways collapse FEV1 and FVC will when airway resistance

4. Pulmonary Hyperinflation

Parenchymal destruction (emphysema)

Alveolar destruction loss of elastic recoil of lung Loss of radial traction intra-alveolar pressure driving exhalation Traps gas in the alveoli permanent overinflation and distal airways collapse FEV1 and FVC will when airway resistance

5. Gas Exchange Abnormalities

V/Q mismatch Chronic hypercapnia Polycythemia Clubbing of the fingers

Parenchyma destruction Peripheral airway obstruction Pulmonary vascular abnormalities

Leads to hypoxemia and hypercapnia

Ventilation/perfusion mismatch

Ventilation/Perfusion Ratio (V/Q)

Normal V(A)/Q= 4/5 or .8 Low V/Q, V(A)/Q, no change in Q, therefore decreased ventilation High V/Q, V(A)/Q, no change in V(A) therefore decreased perfusion

Chronic Hypercapnia

Inadequate ventilation - receptiveness of the medullary chemoreceptors to pC02 Peripheral chemoreceptors to stimulate ventilation Hypoxic drive

Polycythemia

Chronic hypoxia

Stimulates the release of erythropoietin Bone marrow produces more RBC Increase oxygen carrying capacity

Pulmonary Hypertension and Cor Pulmonale (Rt HF)

Destruction of the pulmonary-capillary bed Alveolar hypoxia compensatory vasoconstriction initially beneficial Vasoconstriction Pulmonary hypertension

Destruction of the pulm-cap bed Chronic hypoxemia Pulm. vasoconstriction ( afterload) RV hypoxia
( workload)

Oxygen supply

RV force of contraction RV O2 demand RV pressure RV hypertrophy RV preload

Rt. sided heart failure

Extrinsic asthma
Type

I - Hypersensitivity Response

Asthma 3 Main Pathologic Features

Smooth muscle spasm/bronchoconstriction

1.

Hypertrophy of smooth muscle Airway Hyperresponsiveness

2.

Mucosal Edema

3.

Mucus hypersecretion

Pathogenesis/Pathophysiology
1. 2.

3.

4.

Antigen (allergen) enters the body Formation of sensitized antibodies (IgE) IgE antibodies bind to the surface of tissue mast cells and basophils Ag-Ab reaction basophils/mast cells degranulate release of chemical mediators

Clinical Features of Asthma

5.

Leukotrienes bind to receptors on smooth muscle bronchoconstriction

Prolonged expiration, wheezing, dyspnea

Chemical mediators

Edema mucosa, mucus secretion, mucociliary escalator Narrowed airways, high pitched wheeze, resp distress

Comparison of Asthma and COPD

Asthma
Sensitizing agent

COPD
Noxious agent

Asthmatic airway inflammation CD4 T lymphocytes Mast cells/Basophils

COPD airway inflammation

Macrophages and neutrophils

Reversible

Airflow Limitation Irreversible

The End.for now.