7.1 Respiratory Physiology and Mechanics

Lung Volumes and Capacities

Lung volumes and capacities describe how much air the lungs can hold and move during different phases of breathing. These measurements form the foundation of spirometry and are directly used to diagnose restrictive and obstructive lung diseases.

Tidal Volume and Vital Capacity

Tidal volume ($V_T$) is the volume of air you breathe in and out during a normal, relaxed breath. At rest, this is roughly 500 mL per breath. No extra effort is involved.

Vital capacity (VC) is the maximum volume of air you can exhale after the deepest possible inhalation. It captures the full usable range of your lungs.

• Typical VC is about 4600 mL in men and 3200 mL in women
• Calculated as: $VC = IRV + V_T + ERV$ (inspiratory reserve volume + tidal volume + expiratory reserve volume)
• Clinically, VC is one of the primary indices of pulmonary function measured by spirometry. A significantly reduced VC can point toward restrictive lung disease.

Residual Volume and Dead Space

Residual volume (RV) is the air that stays in your lungs even after you exhale as hard as you can, roughly 1200 mL. This isn't wasted space. It prevents alveolar collapse and keeps alveolar $\text{PO}_2$ stable between breaths, so gas exchange doesn't stop every time you exhale.

Dead space refers to portions of the airway where no gas exchange occurs:

• Anatomical dead space is the volume of the conducting airways (nose, trachea, bronchi, down to the terminal bronchioles), about 150 mL. Air sitting here never reaches the alveoli.
• Physiological dead space includes anatomical dead space plus any alveolar dead space. Alveolar dead space consists of alveoli that receive air but have little or no blood flow (ventilated but not perfused), so gas exchange there is ineffective.

In healthy lungs, physiological and anatomical dead space are nearly equal. In disease states like pulmonary embolism, alveolar dead space can increase significantly.

Ventilation and Gas Exchange

Moving air into the lungs is only half the job. The real purpose is getting oxygen into the blood and carbon dioxide out. This section covers the two processes that make that happen: ventilation (bulk airflow) and diffusion (gas movement across the alveolar membrane).

Ventilation and Diffusion

Ventilation is the mechanical process of moving air in and out of the lungs through inspiration and expiration. It's driven by pressure changes created by the diaphragm and intercostal muscles.

Diffusion is the mechanism that actually transfers gases between the alveoli and pulmonary capillaries. Oxygen diffuses from the alveoli (high $\text{PO}_2$) into the blood (low $\text{PO}_2$), and carbon dioxide diffuses in the opposite direction. The rate of diffusion depends on:

• The partial pressure gradient of each gas across the alveolar-capillary membrane
• The thickness and surface area of the membrane (Fick's law of diffusion)

Conditions that thicken the membrane (like pulmonary fibrosis) or reduce surface area (like emphysema) impair diffusion and compromise gas exchange.

Perfusion and Alveolar Ventilation

Perfusion is the flow of blood through the pulmonary capillaries that surround the alveoli. Efficient gas exchange requires a good match between ventilation (air reaching the alveoli) and perfusion (blood flowing past them). This is called the ventilation-perfusion (V/Q) ratio.

Alveolar ventilation ($\dot{V}_A$) is the volume of fresh air that actually reaches the gas-exchanging alveoli per minute. It's the ventilation measurement that matters most physiologically because dead space air doesn't participate in gas exchange.

$\dot{V}_A = (V_T - V_D) \times f$

Where $V_T$ is tidal volume, $V_D$ is dead space volume, and $f$ is respiratory rate.

For example, at rest: $(500 \text{ mL} - 150 \text{ mL}) \times 12 \text{ breaths/min} = 4200 \text{ mL/min}$

Alveolar ventilation directly determines alveolar $\text{PO}_2$ and $\text{PCO}_2$, which in turn drive the partial pressure gradients for diffusion.

Respiratory Mechanics

The mechanics of breathing involve two key physical properties: how easily the lungs expand (compliance) and how easily air flows through the airways (resistance). These properties determine the work of breathing and are central to distinguishing between restrictive and obstructive lung diseases.

Lung Compliance and Airway Resistance

Lung compliance measures how much the lung volume changes for a given change in pressure:

$C = \frac{\Delta V}{\Delta P}$

High compliance means the lungs stretch easily. Low compliance (stiff lungs) means more pressure is needed to inflate them. Conditions like pulmonary fibrosis reduce compliance, making the lungs harder to expand. This is the hallmark of restrictive lung disease.

Airway resistance opposes airflow through the bronchial tree. The key relationship comes from Poiseuille's law:

$R \propto \frac{1}{r^4}$

Because resistance depends on the fourth power of the airway radius, even a small decrease in radius causes a large increase in resistance. Bronchoconstriction (as in asthma) or mucus buildup (as in chronic bronchitis) dramatically increases resistance and the work of breathing. This is the hallmark of obstructive lung disease.

Respiratory Rate and Minute Ventilation

Respiratory rate is simply the number of breaths per minute. Normal resting rate in adults is 12 to 20 breaths/min.

Minute ventilation ($\dot{V}_E$) is the total volume of air moved in and out of the lungs per minute:

$\dot{V}_E = V_T \times f$

At rest with a tidal volume of 500 mL and a rate of 12 breaths/min, minute ventilation is 6000 mL/min (6 L/min).

The body can increase minute ventilation to meet higher metabolic demands (during exercise, for instance) by increasing tidal volume, respiratory rate, or both. Increasing tidal volume is generally more efficient because it raises alveolar ventilation without proportionally increasing the fraction of each breath wasted on dead space.