Alternation of Respiratory function (Airway Resistance (Bronchioles and…
Alternation of Respiratory function
determined by the relationship between driving pressure and flow
the radius of the airway tube decreases
others：stress, pulmonary conditioning, and age
The trachea and bronchi contain cartilage and small amounts of muscle. The cartilage assists in maintaining airway passage stability, thus preventing airway collapse.
Bronchioles and terminal bronchioles do not contain cartilage, but have increased amounts of smooth muscle that are innervated by the autonomic nervous system.
Stimulation of the β2-adrenergic receptors leads to bronchodilation
Stimulation of cholinergic fibers leads to bronchoconstriction
bronchial artery system
oxygenated blood to the pleura and lung tissues
pulmonary artery system
for O2 and CO2 exchange
Oxygen-depleted (unoxygenated) blood leaves the right ventricle by way of the pulmonary artery trunk
terminal bronchioles and the acinus
Mechanics of Breathing
respiratory muscle contract
respiratory muscle contract, the chest wall expands, and air flow into the lung.
：the respiratory muscle relax, the lung recoil, and air flows passively out of the lung.
Upper air way
Neurologic Control of Ventilation
neural control centers：
Obstructive Pulmonary disorders：Asthma
airway obstruction that is reversible
increased airway reactivity to a variety of stimuli
defined by paroxysms of diffuse wheezing, dyspnea, and cough(resulting from spasmodic contractions of the bronchi).
regard to smoking cessation and avoidance of passive smoke, aerosols, and odors.
decreasing inflammation and bronchoconstriction, including β2 agonists, corticosteroids, leukotriene modifiers, and mast cell inhibitors.
triggered both by allergens and by stimuli, such as exercise and exposure to cold air.
immunohistopathologic features of asthma airway epithelium, collagen deposition beneath the basement membrane, edema, mast cell activation, and inflammatory cell infiltration by neutrophils, eosinophils, and lymphocytes.
Obstructive Pulmonary disorders：
chronic inflammation and swelling of the bronchial mucosa
increased fibrosis of the mucous membrane
hyperplasia of bronchial mucous glands and goblet cells
se of inhaled short-acting β2 agonists and inhaled anticholinergic bronchodilators, cough suppressants, and antimicrobial agents for infections.
Inhaled or oral corticosteroids. Low-dose oxygen therapy.
hypertrophy of bronchial glands and goblet cells
increased bronchial wall thickness
decreased number of cilia and decreased action of available cilia
shortness of breath on exertion
excess body fluids (edema, hypervolemia)
chills, malaise, muscle aches, fatigue, loss of libido, and insomnia
right-sided heart failure
destructive changes of the alveolar walls and abnormal enlargement of the distal air sacs.
include smoking, air pollution, certain occupations
leading to alveolar destruction are associated with the release of proteolytic enzymes from inflammatory cells such as neutrophils and macrophages.
leads to inflammation in the lung tissue, release of proteolytic enzymes that directly damage alveolar tissue.
inactivates α1-antitrypsin, which normally acts to protect the lung parenchyma.
loss of alveolar walls, there is also a marked reduction in the pulmonary capillary bed, which is essential for exchange of oxygen and carbon dioxide between the alveolar air and capillary blood.
loss of elastic tissue in the lung, decrease in the size of the smaller bronchioles.
loss of radial traction, which normally holds the airway open, and to increasing pressure around the outside of the airway lumen, which in turn increases airway resistance and decreases airflow.
overinflation (barrel chest) is from an increase in lung volume.