Between the trachea and the alveolar sacs, the airways divide 23 times The first 16 generations of passages

s form the conducting zone of the airways that transports gas from and to the exterior. The remaining seven generations form the transitional and respiratory zones where gas exchange occurs; they are made up of respiratory bronchioles, alveolar ducts, and alveoli. These multiple divisions greatly increase the total cross-sectional area of the airways, from 2.5 cm2 in the trachea to 11,800 cm2 in the alveoli Consequently, the velocity of air flow in the small airways declines to very low values

 The trachea and bronchi have

cartilage in their walls little smooth muscle a ciliated epithelium that contains mucous and serous glands.

Cilia are present as far as the respiratory bronchioles Glands and cartlidge are absent from the epithelium of the bronchioles and terminal bronchioles, their walls contain more smooth muscle, of which the largest amount relative to the thickness of the wall is present in the terminal bronchioles

 Muscarinic receptors are abundant, an cholinergic discharge causes bronchoconstriction. 2-adrenergic receptors mediat bronchodilation They increase bronchial secretion 1 adrenergic receptors inhibit secretion a noncholinergic, nonadrenergic innervation of the bronchioles that produces bronchodilation mostly VIP

 BRONCHIAL TONE The bronchi dilate during inspiration and constrict during expiration. Dilation is produced by sympathetic discharge and constriction by parasympathetic discharge Stimulation of sensory receptors in the airways by irritants and chemicals such as sulfur dioxide produces reflex bronchoconstriction that is mediated via cholinergic pathways Cool air also causes bronchoconstriction, and so does exercise, possibly because the increased respiration associated with it cools the airways There is a circadian rhythm in bronchial tone, with maximal constriction at about 6:00 AM and maximal dilation at about 6:00 PM.

Airflow Measurements of Obstructive & Restrictive Disease

NORMAL OD RD

FVC

5L

3L

3L

FEV1

4L

1.3

2.8

FEV1/FVC

80%

42%

90%

Volume-time curve in obstructive lung disease: FEV1 low, FET higher

Volume-time curve in restrictive lung disease: FEV1 too low, FET normal

OD

RD

CAUSES

Bronchial asthma, chronic bronchitis, emphysema airways

Lung fibfrosis, pulmonary congestion and edema, chest wall abnormalities Lung abnormalities or chestwall inspiration

ANATOMY

BREATYHING DIFFICULTY

expiration

PATHOPHYSIOLOGY

Airway obstruction

Lung elasticity

PULMONARY FUNCTION

airflow

Lung volumes

EMPHYSEMA

This loss of elasticity prevents full expansion of the lung, or airway restriction, during breathing. The most common cause of emphysema is heavy cigarette smoking. The smoke causes an increase in the number of pulmonary alveolar macrophages macrophages release a chemical substance that attracts leukocytes to the lungs. The leukocytes in turn release proteases including elastase, which attacks the elastic tissue in the lungs. At the same time, 1-antitrypsin, a plasma protein that normally inactivates elastase and other proteases, is itself inhibited. The 1-antitrypsin is inactivated by oxygen radicals, and these are released by the leukocytes. The final result is a proteaseantiprotease imbalance with increased destruction of lung tissue. Similar protease antiprotease imbalance can occur through congenital deficiency 1-antitrypsin.