ASTHMA

Asthma is usually a reversible process Involves periodic episodes

Pathologic Changes
Hypersensitivity response Bronchoconstriction May become chronic with irreversible changes

Presentation
Bronchospasm Increased mucus secretion Dyspnea Wheezing Cough

pollution, pollen, exercise, mold

Asthma
Allergic asthma is triggered when an allergen cross-links IgE receptors on mast cells, which are then activated to release histamine and other inflammatory mediators (early-phase response). A late-phase response may occur due to further inflammation
. Lewis ed 8 Fig. 29-2

Asthma
Factors causing obstruction (especially expiratory obstruction) in asthma. A, Cross section of a bronchiole occluded by muscle spasm, swollen mucosa, and mucus in the lumen. B, Longitudinal section of a Bronchiole Lewis 8th ed Fig 29-3

Fig. 29-1. Pathophysiology of asthma. IL, Interleukin.

Nursing Management: Asthma

Asthma

Lewis 8th ed, Fig. 29-4. Drug therapy: stepwise approach for managing asthma.

example of medication via a nebulizer

Example of an Aero Chamber spacer used with a metered-dose inhaler

Example of a dry powder inhaler (DPI).

Peak Flowmeasure peak expiratory flow volume

Med Surg Nsg 5th ed 1997, Black page 1053

Chronic Obstructive Pulmonary Diseases (COPD) Chronic Airflow Limitation (CAL) Emphysema Chronic Bronchitis

Emphysema
Loss of lung elasticity Hyperinflation of the lung Formation of Bullae Small airway collapse and air trapping VQ mismatching

Effects of Tobacco Smoke on the Respiratory Stystem

Table 29-17. Effects of Tobacco Smoke on the Respiratory System.

Emphysema: Damage of Aveoli

Hereditary Emphysema or Alpha 1-Antrypsin Deficiency (A1AD) is an inherited disorder that results in low or non-existent levels of AAT in the blood.

AAT Deficiency
Alpha-1 antitrypsin (AAT) deficiency Alpha1 is an inherited condition in which there are low levels or no levels of AAT in the blood. *Also known as AAT Deficiency, AATD, A1-PI deficiency, alpha-1 proteinase deficiency, A1AD, or hereditary or genetic emphysema. Alpha-1 antitrypsin (AAT), also known as alpha1-proteinase inhibitor (A1-PI), is an enzyme produced by the liver and released into the bloodstream. One of the primary roles of AAT is to protect the lungs from neutrophil elastase (NE), an enzyme released by white blood cells. Neutrophil elastase can attack healthy lung tissue if not controlled by AAT. http://www.alpha1health.com/paf/respiratory_system.html

Chronic Obstructive Pulmonary Disease

Classifying Emphysema
Panlobular

Centrolobular

Chronic Obstructive Pulmonary Disease and Therapy by Stages

Client with Emphysema

Clinical Manifestations
Progressive dyspnea on exertion Prolonged expiratory phase & tachypnea Increased work of breathing Anorexia, weight loss Barrel Chest Flattened diaphragm

Clinical Manifestations (cont)

Formation of blebs and bullae Hyperresonance Polycythemia (pink puffer) Chronic hypoxia Pneumothorax Chronic respiratory acidosis (end stage)

Normal muscles which assist in respiration

Accessory Muscles

A/P diameter with COPD

Clubbing of Fingers

Cor Pulmonale secondary to COPD

Consequences of patient with emphysema

ABGs
Initially normal ABG followed by decreased PaO2 and O2 saturation Increased PaCO2 with an increase in HCO3 to compensate

Compensated Respiratory Acidosis and Hypoxemia

Chest cavity/ autopsy: reveals numerous large bullae apparent on the surface of the lungs in a patient dying with emphysema

Collaborative Management of COPD

Medical management
Maximize oxygenation, ventilation and perfusion Manage environment, prevent infections, smoking cessation, drug therapy, O2 therapy, etc Also see notes

Surgical management
Bullectomy Lung volume reduction surgery

Video-Assisted Lung Volume Reduction Surgery (may also be called thorascopic or endoscopic LVRS)

Preoperative CXR of client with COPD