Chapter 5 Respiratory Physiology
|Smooth muscle||Present (many layers)||Present (1-3 layers)|
|Epithelium||Pseudostratified columnar||Simple cuboidal|
|Diameter||Independent of lung volume||Depends on lung volume|
|Location||Intraparenchymal and extraparenchymal||Embedded directly within connective tissue of lung|
Clinical note: Primary ciliary dyskinesia is an autosomal recessive disorder that renders cilia in airways unable to beat normally (absent dynein arm). The result is a chronic cough and recurrent infections. When accompanied by the combination of situs inversus, chronic sinusitis, and bronchiectasis, it is known as Kartagener syndrome. Cigarette smoke causes a secondary ciliary dyskinesia. Cystic fibrosis and ventilation-associated pneumonia are other examples of conditions associated with dysfunction of the mucociliary tract.
|Parameter||Conducting Airways||Respiratory Airways|
|Histology||Ciliated columnar tissue||Nonciliated cuboidal tissue|
|Goblet cells (mucociliary tract)||No goblet cells|
|Lacks smooth muscle|
|Presence of cartilage||Yes||No|
|Resistance||Large diameter||Small diameter|
|Arranged in series||Arranged in parallel|
|High resistance||Low resistance|
(From Kumar V, Abbas A, Fausto N: Robbins and Cotran Pathologic Basis of Disease, 7th ed. Philadelphia, Saunders, 2005, Fig. 15-1.)
Pathology note: The alveolar epithelium is primarily populated by type 1 epithelial cells, which play an important role in gas exchange. Type 2 epithelial cells are much less numerous but are important in producing surfactant (stored in lamellar bodies). When the pulmonary membrane has been damaged, type 2 epithelial cells are able to differentiate into type 1 epithelial cells and effect repair of the pulmonary membrane.
5-2 A, Muscles of inspiration. Note how contraction of the diaphragm increases the vertical diameter of the thorax, whereas contraction of the external intercostal muscles results in anteroposterior and lateral expansion of the thorax. B, Movement of thoracic wall during breathing. C, Muscles of expiration.
(From Boron W, Boulpaep E: Medical Physiology, 2nd ed. Philadelphia, Saunders, 2009, Fig. 27-3.)
Clinical note: During normal inhalation at rest, abdominal pressure increases secondary to diaphragmatic contraction. This is evident by watching a supine person’s abdomen rise during quiet breathing (as long as the person is not trying to “suck in their gut”). In patients with respiratory distress, the abdomen may actually be “sucked in” while the accessory muscles of inspiration are contracting. This is known as paradoxical breathing and is an indicator of impending respiratory failure.
5-3 Pressure and volume changes during the respiratory cycle. Note that alveolar pressure equals zero at the end of a tidal inspiration (when there is no airflow). In contrast, at the end of a tidal inspiration, the pleural pressure has decreased to its lowest value (approximately −7.5 cm H2O). The difference between pleural and alveolar pressures is referred to as the transpulmonary pressure.
5-4 Flow-volume curve recorded during inspiration and expiration in a normal subject. Note the linear decline during most of expiration. PEF, Peak expiratory flow; RV, residual volume; TLC, total lung capacity; VC, vital capacity.
(From Goljan EF, Sloka K: Rapid Review Laboratory Testing in Clinical Medicine. Philadelphia, Mosby, 2008, Fig. 3-3.)
Clinical note: If the lung were a simple pump, its maximum attainable transport of gas in and out would be limited by exhalation. During expiration, the last two thirds of the expired vital capacity is largely independent of effort. The best way to appreciate this is to do it yourself. No matter how hard you try, you cannot increase flow during the latter part of the expiratory cycle. The reduction in small airway diameter with resultant increase in airway resistance is the major determinant of this phenomenon. In contrast, large airways are mostly spared from collapse by the presence of cartilage. One can imagine the difficulty asthmatic individuals face during exhalation with the addition of bronchoconstriction.
Pathophysiology note: Airway diameter can be reduced (and airway resistance thereby increased) by a number of mechanisms. For example, airway diameters are reduced by smooth muscle contraction and excess secretions in obstructive airway diseases such as asthma and chronic bronchitis. Work caused by airway resistance increases markedly as a result.
Note that this description is a simplification, because Poiseuille’s equation is based on the premise that airflow is laminar. Although this is true for the smaller airways, in which the total cross-sectional area is large and the airflow velocity is slow, airflow in the upper airways is typically turbulent, as evidenced by the bronchial sounds heard during auscultation.
Pharmacology note: Many classes of drugs affect large-airway diameter by affecting bronchial smooth muscle tone. For example, β2-adrenergic agonists such as albuterol directly stimulate bronchodilation. Most other classes work by preventing bronchoconstriction or by inhibiting inflammation (which reduces airway diameter); these include steroids, mast cell stabilizers, anticholinergics, leukotriene-receptor antagonists, and lipoxygenase inhibitors.
5-6 Compliance curve of the lungs: lung volume plotted against changes in transpulmonary pressure (the difference between pleural and alveolar pressure). During inspiration, maximal compliance occurs in the midportion of the inspiratory curve. The difference between the inspiration curve and the expiration curve is referred to as hysteresis. Hysteresis is an intrinsic property of all elastic substances.
(From West JB: Respiratory Physiology: The Essentials, 8th ed. Philadelphia, Lippincott Williams & Wilkins, 2008, Fig. 7-11.)
Pathology note: In emphysema, destruction of lung parenchyma results in increased compliance and a reduced elastic recoil of the lungs because of destruction of elastic tissue by neutrophil-derived elastases. At a given FRC, the tendency is therefore for the lungs to expand because of the unchanged outward pressure exerted by the chest wall. The lung–chest wall system adopts a new higher FRC to balance these opposing forces. This is part of the reason patients with emphysema breathe at a higher FRC. Breathing at a higher FRC also keep more airways open, which decreases airway resistance and minimizes dynamic airway compression during expiration.
Clinical note: In restrictive lung diseases such as silicosis and asbestosis, inspiration becomes increasingly difficult as the resistance to lung expansion increases in response to increased lung elastance, resulting in reduced lung volumes and total lung capacity. In obstructive lung diseases such as emphysema, there is reduced lung elastance secondary to destruction of lung parenchyma and loss of proteins that contribute to the elastic recoil of the lungs (e.g., collagen, elastin). Expiration may therefore become an active process (rather than a passive one), even while at rest, because the easily collapsible airways “trap” air in the lungs. “Pursed-lip breathing,” an attempt to expire adequate amounts of air, is often seen; it creates an added pressure within the airways that keeps them open and allows for more effective expiration.
5-8 Compliance of air-inflated lungs versus saline-inflated lungs. Note that the saline-inflated lungs are more compliant than air-filled lungs owing to the reduction in surface tension, which reduces the collapsing pressure of alveoli.
Clinical note: The collapse of many alveoli in the same region of lung parenchyma leads to atelectasis. Atelectatic lung may result from external compression, as may occur with pleural effusion or tumor; a prolonged period of “shallow breaths,” as may occur with pain (e.g., rib fracture) or diaphragmatic paralysis; or obstruction of bronchi (e.g., tumor, pus, or mucus).
Clinical note: The collapsing pressure of alveoli in infants born before approximately 34 weeks of gestation may be pathologically elevated for two reasons: (1) the alveoli are small, which contributes to an elevated collapsing pressure (recall Laplace’s law); and (2) surface tension may be abnormally increased because surfactant is not normally produced until the third trimester of pregnancy. There is therefore a high risk for respiratory failure and neonatal respiratory distress syndrome (hyaline membrane disease) in these infants. Mothers in premature labor are frequently given corticosteroids to stimulate the fetus to produce surfactant. After birth, exogenous surfactant or artificial respiration may also be required.
(From Damjanov I: Pathophysiology. Philadelphia, Saunders, 2008, Fig. 5-6.)