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Flashcards covering respiratory anatomy, mechanics of ventilation, pressure gradients, gas exchange, lung compliance, surfactant biology, spirometry volumes, and pulmonary pathophysiologies based on Chapter 18 of Human Physiology.
What are the four primary functions of the respiratory system?
In respiratory bulk flow, what creates the pressure gradient and what is the primary determinant of resistance to flow?
A muscular pump creates pressure gradients (moving air from regions of higher pressure to lower pressure), and resistance to flow is determined primarily by the diameter of the airways (tubes).
What are the three steps of external respiration that coordinate gas transfer between the atmosphere and cells?
Which anatomical structures comprise the upper respiratory tract versus the lower respiratory tract?
The upper respiratory tract consists of the oral cavity, pharynx, and larynx. The lower respiratory tract consists of the trachea, two primary bronchi and their branches, and the lungs.
How many times does the primary bronchus divide, and approximately how many bronchioles are produced by this branching?
The primary bronchus divides 22 more times, terminating in clusters of alveoli and creating approximately 80 million bronchioles.

How do the 'pump handle' and 'bucket handle' motions expand the thoracic cavity during inspiration?
The 'pump handle' motion lifts the sternum and ribs to increase the anterior-posterior dimension of the rib cage, while the 'bucket handle' motion swings the ribs upward and outward to increase the lateral dimension.
What two essential functions are served by the thin layer of pleural fluid in the pleural sac?
What three conditioning steps occur to inspired air as it travels through the airways?

What are the distinct physiological roles of Type I versus Type II alveolar cells?
Type I alveolar cells are thin epithelial cells specialized for gas exchange, whereas Type II alveolar cells synthesize and secrete surfactant.
What is the function of the ciliated epithelium lining the trachea and bronchi?
It forms a mucociliary escalator where cilia continuously beat to push the mucus layer (which traps inhaled particles and pathogens) toward the pharynx to be swallowed or expectorated.
How does alveolar pressure change relative to atmospheric pressure during inspiration and expiration?
During inspiration, thoracic volume expands causing alveolar pressure to decrease below atmospheric pressure (subatmospheric), drawing air in. During expiration, thoracic volume decreases causing alveolar pressure to increase above atmospheric pressure, pushing air out.

What causes the normal intrapleural pressure to be subatmospheric (−3mmHg), and what happens during a pneumothorax?
The outward elastic pull of the chest wall opposing the inward elastic recoil of the lungs creates a negative intrapleural pressure (−3mmHg). If the pleural sac is breached, air flows in until intrapleural pressure equals atmospheric pressure, breaking the bond and causing the lung to collapse.
How do lung compliance and lung elastance differ?
Compliance is the ability of the lung to stretch (high compliance stretches easily; low compliance requires more force). Elastance is the ability of the lung to resist being stretched and recoil back to its resting volume when the stretching force is released.

According to the Law of LaPlace (P=r2T), why is surfactant essential for alveolar stability?
Without surfactant, smaller alveoli (smaller radius r) would generate higher collapsing pressure than larger alveoli and collapse into them. Surfactant reduces surface tension (T) more in smaller alveoli, equalizing pressure across different-sized alveoli.
What causes Newborn Respiratory Distress Syndrome (NRDS) in premature infants, and what clinical signs appear?
NRDS is caused by inadequate surfactant production by underdeveloped Type II alveolar cells, leading to stiff collapsed alveoli. Clinical signs include grunting respirations, use of accessory breathing muscles, and nasal flaring.
Which neural and chemical factors mediate bronchoconstriction versus bronchodilation in the bronchioles?
Bronchoconstriction is mediated by parasympathetic neurons (via muscarinic receptors), histamine, and leukotrienes. Bronchodilation is mediated by increased carbon dioxide (CO2) and epinephrine binding to β2-adrenergic receptors.
How does hyperpnea differ from hyperventilation?
Hyperpnea is an increase in respiratory rate and/or volume matched to an increased metabolic demand (such as during exercise), whereas hyperventilation is an increase in respiratory rate and/or volume without increased metabolism (e.g., emotional panic or blowing up a balloon).
Define the ventilatory terms tachypnea, dyspnea, and apnea.
What is the normal resting alveolar ventilation rate, and how do alveolar PO2 and PCO2 change during hyperventilation versus hypoventilation?
Normal alveolar ventilation is 4.2L/min. During hyperventilation, alveolar PO2 increases (toward 120mmHg) and PCO2 decreases. During hypoventilation, alveolar PO2 decreases and PCO2 increases.
What is the primary physiological distinction between obstructive and restrictive lung diseases, and what is an example of each?
Obstructive lung diseases feature increased airway resistance to flow (e.g., asthma, emphysema, COPD), whereas restrictive lung diseases feature reduced lung compliance and difficulty expanding the lungs (e.g., pulmonary fibrosis).
What are the four non-overlapping pulmonary volumes measured by spirometry?
What are the formulas and typical resting values for Vital Capacity (VC) and Total Lung Capacity (TLC)?
Vital Capacity: VC=VT+IRV+ERV (approximately 4600mL Total Lung Capacity: TLC=VT+IRV+ERV+RV (approximately 5800mL)