Pressure Changes in Breathing
Breathing depends entirely on pressure gradients between the atmosphere and the inside of your lungs. Air always flows from high pressure to low pressure, so the respiratory system creates these gradients by changing the volume of the thoracic cavity.
Inspiration and Expiration
During inspiration (inhalation), respiratory muscles contract and expand the thoracic cavity. This expansion lowers the pressure inside the lungs (intrapulmonary pressure) below atmospheric pressure, and air flows in.
During expiration (exhalation), the thoracic cavity volume decreases, intrapulmonary pressure rises above atmospheric pressure, and air flows out.
The physical principle driving this is Boyle's Law: at a constant temperature, pressure and volume are inversely related.
When volume goes up, pressure goes down (and vice versa). That single relationship explains the entire pressure-driven cycle of breathing.
Muscle Actions During Breathing
Inspiration:
- The diaphragm and external intercostal muscles contract.
- The thoracic cavity expands in all dimensions.
- Lung volume increases, intrapulmonary pressure drops below atmospheric pressure.
- Air flows into the lungs down the pressure gradient.
Quiet Expiration:
- The diaphragm and external intercostals relax.
- The elastic recoil of the lungs and chest wall passively decreases thoracic volume.
- Intrapulmonary pressure rises above atmospheric pressure.
- Air flows out of the lungs.
Quiet expiration is a passive process. No muscles need to contract; the lungs simply spring back like a stretched rubber band.
Respiratory Muscle Function
Diaphragm
The diaphragm is the primary muscle of inspiration. It's a dome-shaped sheet of skeletal muscle at the base of the thoracic cavity, separating it from the abdominal cavity.
When the diaphragm contracts, it flattens downward, increasing the vertical dimension of the thoracic cavity. This single action accounts for roughly 75% of air movement during quiet breathing.
The diaphragm is innervated by the phrenic nerves, which arise from spinal cord segments C3, C4, and C5. A helpful mnemonic: "C3, 4, 5 keeps the diaphragm alive." The respiratory centers in the brainstem control diaphragm contraction involuntarily, though you can also override this with voluntary effort (like holding your breath).
Other Inspiratory Muscles
The external intercostal muscles run between the ribs and assist inspiration by lifting the ribs upward and outward. This increases both the anteroposterior (front-to-back) and transverse (side-to-side) dimensions of the thoracic cavity. They contribute about 25% of air movement during quiet breathing.
During deep or labored breathing, accessory muscles get recruited:
- Sternocleidomastoid elevates the sternum
- Scalene muscles elevate the upper ribs
These accessory muscles are typically only active during exercise or respiratory distress (dyspnea). If you see a patient using accessory muscles at rest, that's a clinical red flag for significant breathing difficulty.
Expiratory Muscles
Quiet expiration is passive, but forced expiration requires active muscle contraction:
- Internal intercostal muscles pull the ribs downward and inward, compressing the thoracic cavity.
- Abdominal muscles (rectus abdominis, transverse abdominis, and obliques) contract to push the abdominal contents upward against the diaphragm, further reducing thoracic volume.
These muscles are essential for activities requiring rapid or forceful airflow: coughing, sneezing, singing, and blowing out candles. During exercise, they also increase the rate and depth of expiration to meet higher metabolic demands.
Lung Volumes and Capacities
Lung volumes and capacities describe how much air the lungs can hold and move. Volumes are single, directly measured values. Capacities are combinations of two or more volumes.
Lung Volumes
| Volume | Definition | Typical Adult Value |
|---|---|---|
| Tidal Volume (TV) | Air moved in and out during a normal, quiet breath | ~500 mL |
| Inspiratory Reserve Volume (IRV) | Additional air you can inhale beyond a normal breath | ~3,000 mL |
| Expiratory Reserve Volume (ERV) | Additional air you can forcefully exhale beyond a normal breath | ~1,100 mL |
| Residual Volume (RV) | Air remaining in the lungs after a maximal expiration | ~1,200 mL |
The residual volume exists because small airways close before all air can be expelled, and the inherent elasticity of lung tissue prevents complete collapse. You can never fully empty your lungs.
Lung Capacities
Each capacity is a sum of specific volumes:
- Total Lung Capacity (TLC) = TV + IRV + ERV + RV ≈ 6,000 mL (adult males)
- Vital Capacity (VC) = TV + IRV + ERV ≈ 4,600 mL
- Inspiratory Capacity (IC) = TV + IRV ≈ 3,500 mL
- Functional Residual Capacity (FRC) = ERV + RV ≈ 2,300 mL
Spirometry can measure all of these except residual volume (and therefore FRC and TLC), since you can't exhale the residual volume into the spirometer. Measuring RV requires indirect techniques like helium dilution or body plethysmography. Spirometry is a key clinical tool for diagnosing and monitoring respiratory disorders like asthma and COPD.
Factors Affecting Lung Function
Two major mechanical properties determine how easily you can move air: lung compliance and airway resistance. Problems with either one increase the work of breathing.
Lung Compliance
Lung compliance is a measure of how easily the lungs expand for a given change in pressure. High compliance means the lungs stretch easily; low compliance means they're stiff and hard to inflate.
Two factors determine compliance:
- Elastic tissue components: Elastin and collagen fibers in the lung parenchyma provide structural support and elastic recoil. Elastic recoil is what drives passive expiration and maintains lung architecture.
- Alveolar surface tension: The thin fluid lining the alveoli creates surface tension that tends to collapse them. This is where surfactant becomes critical.
Surfactant is a mixture of phospholipids and proteins secreted by type II alveolar cells. It reduces alveolar surface tension, which does two things: it increases compliance (making inflation easier) and it prevents alveolar collapse (atelectasis), especially in smaller alveoli.
Surfactant deficiency is the underlying cause of respiratory distress syndrome (RDS) in premature infants. Their type II alveolar cells haven't matured enough to produce adequate surfactant, leading to alveolar collapse and severe breathing difficulty.
Conditions that decrease compliance include:
- Pulmonary fibrosis: Excess scar tissue stiffens the lungs
- Acute respiratory distress syndrome (ARDS): Inflammation and fluid accumulation reduce surfactant function and stiffen lung tissue
Airway Resistance
Airway resistance is the opposition to airflow through the respiratory tract, determined primarily by airway diameter. Even small changes in diameter have large effects on resistance because resistance is inversely proportional to the fourth power of the radius.
Factors that increase airway resistance:
- Bronchoconstriction: Smooth muscle contraction narrows the airways. Triggers include irritants (smoke), allergens (pollen), and cold air.
- Mucus hypersecretion: Excess mucus physically obstructs the airway lumen.
- Inflammation: Swelling of the airway walls reduces the available diameter.
- Structural obstruction: Tumors or foreign bodies block airflow.
Diseases characterized by increased airway resistance include asthma (reversible bronchoconstriction), COPD (chronic airflow limitation from emphysema and/or chronic bronchitis), and cystic fibrosis (thick mucus plugging).
Pharmacological treatments target the underlying cause:
- Bronchodilators relax airway smooth muscle to widen the airways. Examples include beta-2 agonists (albuterol) and anticholinergics (ipratropium).
- Corticosteroids reduce inflammation and mucus secretion over time, addressing the chronic component of diseases like asthma.