Premed · Premed · Anatomy Physiology 2
Lecture 11: Pulmonary Ventilation and Gas Exchange
Anatomy and Physiology II
Learning Objectives
By the end of this lecture, students will be able to:
- Describe the mechanics of inspiration and expiration
- Explain the role of pressure gradients, lung compliance, and surfactant in ventilation
- Define lung volumes and capacities and interpret spirometry data
- Explain Dalton's law and Henry's law as they apply to gas exchange
- Describe the process of external respiration (pulmonary gas exchange)
- Describe the process of internal respiration (systemic gas exchange)
Lecture Content
I. Mechanics of Pulmonary Ventilation
Ventilation, or breathing, is the physical movement of air into and out of the lungs. It is driven by pressure gradients between the atmosphere and the alveoli, and its mechanics are governed by Boyle's law, which states that at constant temperature, the pressure and volume of a gas are inversely related (P1V1 = P2V2).
Key Pressures
Three pressures are critical to understanding ventilation. Atmospheric pressure (Patm) is 760 mmHg at sea level. Intra-alveolar pressure (intrapulmonary pressure) is the air pressure inside the alveoli, which fluctuates during breathing but equalizes with atmospheric pressure between breaths. Intrapleural pressure (Pip) is the pressure in the pleural cavity, which is always subatmospheric (negative) during normal breathing, approximately 756 mmHg or -4 mmHg relative to atmospheric pressure. This negative pressure is maintained by the opposing elastic recoil forces of the lungs pulling inward and the chest wall pulling outward, supplemented by lymphatic drainage of pleural fluid. The transpulmonary pressure, defined as alveolar pressure minus intrapleural pressure, keeps the lungs inflated against their tendency to collapse.
Inspiration (Inhalation)
Quiet inspiration is an active process requiring muscle contraction. The diaphragm, the most important inspiratory muscle innervated by the phrenic nerve (C3-C5), contracts and flattens, accounting for approximately 75% of air movement during quiet breathing. Simultaneously, the external intercostal muscles contract, elevating the ribs through bucket-handle and pump-handle movements. These actions increase the volume of the thoracic cavity, causing intrapleural pressure to become more negative, the lungs to expand, and intra-alveolar pressure to drop below atmospheric pressure. Air then flows in along this pressure gradient. During forced inspiration, additional muscles such as the scalenes, sternocleidomastoid, and pectoralis minor are recruited to further elevate the ribs and sternum.
Expiration (Exhalation)
Quiet expiration is a passive process requiring no muscle contraction. The diaphragm and external intercostals simply relax, and the elastic recoil of the lungs and chest wall reduces thoracic volume. Intra-alveolar pressure rises above atmospheric pressure, and air flows out. Forced expiration is an active process that recruits the internal intercostal muscles to depress the ribs and the abdominal muscles (rectus abdominis, obliques, transversus abdominis) to compress the abdominal contents and push the diaphragm upward.
Factors Affecting Ventilation
Lung compliance measures the ease with which the lungs expand, defined as the change in volume per change in pressure. High compliance means the lungs expand easily. Compliance is decreased by fibrosis (stiff lungs), decreased surfactant, and reduced chest wall mobility. It is increased in emphysema due to destruction of elastic fibers, though this comes at the cost of impaired recoil.
Airway resistance is the opposition to airflow caused by friction and is determined mainly by airway diameter. Bronchoconstriction, mucus accumulation, and inflammation all increase resistance. Asthma is characterized by reversible bronchoconstriction that increases airway resistance and causes difficulty breathing.
Pulmonary surfactant reduces the surface tension of the fluid lining the alveoli. Without surfactant, small alveoli would collapse according to LaPlace's law and inflate larger ones at their expense. Surfactant equalizes pressures across alveoli of different sizes, preventing this collapse. It is produced by type II pneumocytes, and its deficiency causes respiratory distress syndrome in premature infants.
<image>A diagram of the mechanics of breathing. Panel A: Quiet inspiration — anterior view of the thorax showing the diaphragm contracting and descending, external intercostals contracting to elevate the ribs, the thoracic cavity expanding (arrows pointing outward), intrapleural pressure becoming more negative, lungs expanding, and intra-alveolar pressure dropping below atmospheric pressure (a manometer or pressure gauge showing -1 mmHg relative to Patm) with an arrow showing air flowing into the lungs. Panel B: Quiet expiration — the diaphragm relaxing and ascending, external intercostals relaxing, thoracic volume decreasing, elastic recoil compressing the lungs, intra-alveolar pressure rising above atmospheric (manometer showing +1 mmHg relative to Patm), and air flowing out. Panel C: A graph showing changes in intrapleural pressure, intra-alveolar pressure, and lung volume over two complete breathing cycles, with inspiration and expiration phases labeled.</image>
II. Lung Volumes and Capacities
Lung Volumes (measured by spirometry)
Tidal volume (TV) is the volume of air moved in a normal, quiet breath, approximately 500 mL. Inspiratory reserve volume (IRV) is the additional air that can be forcibly inhaled after a normal inspiration, about 3,100 mL. Expiratory reserve volume (ERV) is the additional air that can be forcibly exhaled after a normal expiration, approximately 1,200 mL. Residual volume (RV) is the air remaining in the lungs after a maximal forced expiration, about 1,200 mL. The residual volume cannot be measured by spirometry and serves to keep the alveoli open.
Lung Capacities (sums of two or more volumes)
Inspiratory capacity (IC) equals TV plus IRV, approximately 3,600 mL. Functional residual capacity (FRC) equals ERV plus RV, about 2,400 mL. Vital capacity (VC) equals TV plus IRV plus ERV, approximately 4,800 mL, representing the maximum volume of air that can be exhaled after a maximum inhalation. Total lung capacity (TLC) equals TV plus IRV plus ERV plus RV, approximately 6,000 mL.
Pulmonary Function Tests
Forced vital capacity (FVC) is the total volume of air exhaled as forcefully and quickly as possible. FEV1 is the volume exhaled in the first second of this maneuver. Normally, the FEV1/FVC ratio is 70 to 80% or higher. In obstructive diseases such as asthma and COPD, FEV1 is reduced more than FVC, producing a decreased ratio. In restrictive diseases such as pulmonary fibrosis, both FEV1 and FVC decrease proportionally, producing a normal or increased ratio.
Minute Ventilation and Alveolar Ventilation
Minute ventilation is calculated as tidal volume multiplied by respiratory rate, yielding approximately 6,000 mL/min at rest (500 mL times 12 breaths per minute). However, not all of this air reaches the gas exchange surfaces. The anatomical dead space, the volume of the conducting airways where no gas exchange occurs, is approximately 150 mL. Alveolar ventilation, the volume of fresh air actually reaching the alveoli per minute, is calculated as (TV minus dead space) multiplied by respiratory rate, yielding about 4,200 mL/min. This measurement is physiologically more important than minute ventilation because it reflects the air available for gas exchange. This is why shallow, rapid breathing is less efficient than slow, deep breathing: a greater proportion of each shallow breath is wasted ventilating the dead space.
III. Gas Exchange — Physical Principles
Dalton's Law of Partial Pressures
Dalton's law states that the total pressure of a gas mixture equals the sum of the partial pressures of each individual gas. The partial pressure of any gas equals the total pressure multiplied by the fractional concentration of that gas. In the atmosphere at 760 mmHg, the partial pressure of oxygen (PO2) is approximately 159 mmHg, while the partial pressure of carbon dioxide (PCO2) is only about 0.3 mmHg. In the alveoli, where the air has been humidified and mixed with residual gases, the values shift: alveolar PO2 (PAO2) drops to approximately 104 mmHg (because oxygen has been removed and carbon dioxide added), and alveolar PCO2 (PACO2) rises to about 40 mmHg.
Henry's Law
Henry's law states that the amount of gas that dissolves in a liquid is proportional to its partial pressure and its solubility coefficient. Carbon dioxide is approximately 20 times more soluble in blood than oxygen. This explains why significant amounts of CO2 dissolve even though its partial pressure is lower than that of oxygen.
IV. External Respiration (Pulmonary Gas Exchange)
External respiration is the exchange of gases between alveolar air and pulmonary capillary blood. It occurs across the respiratory membrane by simple diffusion and is driven by partial pressure gradients.
For oxygen, the alveolar PO2 is approximately 104 mmHg while the PO2 of deoxygenated blood entering the pulmonary capillaries is about 40 mmHg. This 64 mmHg gradient drives oxygen from the alveoli into the blood. By the time blood leaves the pulmonary capillaries, its PO2 has equilibrated to approximately 104 mmHg. For carbon dioxide, the alveolar PCO2 is about 40 mmHg while the PCO2 of incoming blood is approximately 45 mmHg. Although this 5 mmHg gradient is much smaller than for oxygen, it is sufficient because CO2 is far more soluble and diffuses much faster.
Factors Affecting Gas Exchange Efficiency
Several factors influence how efficiently gas exchange occurs. Surface area is reduced in emphysema, where destruction of alveolar walls impairs exchange. Membrane thickness is increased in pulmonary edema and fibrosis, slowing diffusion. Partial pressure gradients are reduced at high altitude, where lower atmospheric pressure decreases alveolar PO2 and limits oxygen uptake. Ventilation-perfusion (V/Q) matching is essential for efficient exchange: local autoregulatory mechanisms ensure that ventilation and blood flow are matched. When alveolar PO2 is low, pulmonary arterioles constrict to redirect blood to better-ventilated areas. When alveolar PCO2 is low, bronchioles constrict to redirect air to better-perfused areas. Notably, this pulmonary vasoconstriction in response to hypoxia is opposite to the vasodilation that occurs in systemic circulation.
V. Internal Respiration (Systemic Gas Exchange)
Internal respiration is the exchange of gases between systemic capillary blood and tissue cells, again driven by partial pressure gradients. For oxygen, arterial blood PO2 is approximately 100 mmHg while tissue PO2 is about 40 mmHg, so oxygen diffuses from the blood into the tissues. Blood leaving the systemic capillaries has a PO2 of approximately 40 mmHg. For carbon dioxide, tissue PCO2 is about 45 mmHg while arterial blood PCO2 is approximately 40 mmHg, so carbon dioxide diffuses from the tissues into the blood. Blood leaving the systemic capillaries has a PCO2 of approximately 45 mmHg.
<image>A diagram of gas exchange at the lungs and tissues. Panel A (External Respiration): An alveolus next to a pulmonary capillary, with partial pressure values labeled — PAO2 = 104 mmHg in the alveolus, PO2 = 40 mmHg in incoming deoxygenated blood, PO2 = 104 mmHg in outgoing oxygenated blood; PACO2 = 40 mmHg in the alveolus, PCO2 = 45 mmHg in incoming blood, PCO2 = 40 mmHg in outgoing blood. Arrows show O2 diffusing into blood and CO2 diffusing into the alveolus. Panel B (Internal Respiration): A systemic capillary next to tissue cells, with PO2 = 100 mmHg in arterial blood, PO2 = 40 mmHg in tissue, PCO2 = 40 mmHg in arterial blood, PCO2 = 45 mmHg in tissue. Arrows show O2 diffusing into tissue and CO2 diffusing into blood. Panel C: A summary circuit diagram showing the full pathway: pulmonary capillaries (gas exchange with alveoli) → pulmonary veins → left heart → systemic arteries → systemic capillaries (gas exchange with tissues) → systemic veins → right heart → pulmonary arteries → back to pulmonary capillaries, with PO2 and PCO2 values at each stage.</image>
