22.3 The Process of Breathing

Mechanics of Breathing

Breathing depends on pressure changes inside the thoracic cavity. Muscles alter the cavity's volume, which changes pressure, which moves air in or out. Two physical laws govern this process, and the nervous system coordinates it all automatically.

Mechanisms of Inhalation and Exhalation

Inhalation (inspiration) is an active process. The diaphragm contracts and flattens downward while the external intercostal muscles contract to lift the rib cage outward. Both actions increase thoracic cavity volume, which drops the pressure inside the lungs (intrapulmonary pressure) below atmospheric pressure. Air flows in down this pressure gradient.

Exhalation (expiration) during quiet breathing is largely passive. The diaphragm relaxes and domes upward, the external intercostals relax, and the rib cage drops back down. Thoracic volume decreases, intrapulmonary pressure rises above atmospheric pressure, and air flows out.

During forced exhalation (heavy exercise, blowing out candles), the internal intercostals and abdominal muscles actively contract to push air out faster.

Pressure-Volume-Resistance Relationships

Boyle's Law is the foundation of breathing mechanics:

$P_1V_1 = P_2V_2$

Pressure and volume are inversely related at constant temperature. When the thoracic cavity expands, intrapulmonary pressure drops; when it shrinks, pressure rises. That pressure difference between the lungs and the atmosphere is what drives airflow.

Airflow resistance depends heavily on airway diameter. Poiseuille's Law describes this relationship:

$Flow = \frac{\Delta P \pi r^4}{8 \eta L}$

The key takeaway: airflow is proportional to the fourth power of the airway radius ($r^4$). A small decrease in airway diameter causes a dramatic increase in resistance. This is why bronchoconstriction during an asthma attack makes breathing so difficult. The trachea and bronchi offer relatively low resistance due to their wide diameter, while the smaller bronchioles are the primary site of variable resistance.

Steps of Pulmonary Ventilation

1. Inspiration: The diaphragm and external intercostals contract, expanding the thoracic cavity. Intrapulmonary pressure drops below atmospheric pressure (roughly 1 mmHg below at rest). Air flows into the lungs through the airways.
2. Gas exchange: Oxygen diffuses from the alveoli into pulmonary capillary blood, and carbon dioxide diffuses from the blood into the alveoli. This occurs passively down partial pressure gradients.
3. Expiration: The diaphragm and external intercostals relax. Elastic recoil of the lungs and chest wall decreases thoracic volume. Intrapulmonary pressure rises above atmospheric pressure, and air flows out.

Respiratory Volumes and Capacities

These values are measured using spirometry. Typical adult values:

Capacities are combinations of two or more volumes:

• Inspiratory Capacity (IC) = TV + IRV (how much you can inhale from the end of a normal exhale)
• Functional Residual Capacity (FRC) = ERV + RV (air remaining after a normal exhale)
• Vital Capacity (VC) = TV + IRV + ERV (maximum air you can move in one breath)
• Total Lung Capacity (TLC) = TV + IRV + ERV + RV (all the air the lungs can hold)

Note that residual volume (and any capacity that includes it) cannot be measured by spirometry alone because you can never fully empty your lungs.

Respiratory Rate and Influencing Factors

Normal adult respiratory rate is 12–20 breaths per minute. Several factors shift this rate:

• Age: Infants and children breathe faster than adults
• Physical activity: Exercise increases rate and depth to meet higher oxygen demand
• Emotional state: Stress and anxiety activate sympathetic responses that speed breathing
• Body temperature: Fever raises metabolic rate, which increases respiratory rate
• Blood gases: Rising $CO_2$ (hypercapnia) or falling $O_2$ (hypoxemia) stimulates faster, deeper breathing
• Blood pH: Acidosis increases ventilation (to blow off $CO_2$); alkalosis decreases it

Lung Mechanics and Protective Mechanisms

The pleura consists of two serous membranes: the visceral pleura (on the lung surface) and the parietal pleura (lining the thoracic wall). A thin layer of serous fluid between them reduces friction during breathing. The intrapleural space normally has negative pressure (about $-4$ mmHg at rest), which keeps the lungs inflated by pulling them against the chest wall. If air enters this space (pneumothorax), the lung collapses.

Surfactant is produced by type II alveolar cells and coats the inner surface of alveoli. It reduces surface tension, which prevents smaller alveoli from collapsing into larger ones and makes it much easier to inflate the lungs. Premature infants often lack sufficient surfactant, leading to respiratory distress syndrome.

Lung compliance refers to how easily the lungs stretch. High compliance means the lungs expand easily; low compliance means more effort is needed. Compliance depends on:

• Elastin and collagen fiber content in lung tissue
• Adequate surfactant production
• Normal intrapleural pressure

Conditions like pulmonary fibrosis decrease compliance (stiff lungs), while emphysema actually increases compliance (lungs expand easily but lose elastic recoil and can't exhale effectively).

Respiratory Control

The Medulla and Pons in Breathing Control

The brainstem sets the automatic rhythm of breathing through several groups of neurons:

• Dorsal Respiratory Group (DRG) in the medulla: primarily drives inspiration by sending signals to the diaphragm via the phrenic nerve
• Ventral Respiratory Group (VRG) in the medulla: mostly inactive during quiet breathing but activates during forced breathing to drive both strong inspiration and active expiration
• Pneumotaxic center in the pons: sends inhibitory signals to the DRG to limit the duration of inspiration, which helps set breathing rate. Stronger signals from this center produce shorter, faster breaths.
• Apneustic center in the pons: promotes prolonged inspiration by stimulating the DRG. The pneumotaxic center normally overrides it.

The DRG is the primary pacemaker for the basic breathing rhythm. It fires in a cyclical pattern, producing the regular inhale-pause-exhale cycle.

Chemical and Physical Factors

Chemical factors are the most powerful regulators of breathing depth and rate. Chemoreceptors detect changes in blood gases and pH:

• Central chemoreceptors in the medulla respond to $CO_2$ indirectly. $CO_2$ crosses the blood-brain barrier, reacts with water to form carbonic acid, and lowers cerebrospinal fluid pH. This pH drop is the strongest chemical stimulus for increasing ventilation.
• Peripheral chemoreceptors in the carotid bodies (at the bifurcation of the common carotid arteries) and aortic bodies (in the aortic arch) detect drops in arterial $O_2$, rises in $CO_2$, and drops in blood pH. They respond faster than central chemoreceptors but are less sensitive to $CO_2$.
• $CO_2$ is the primary chemical driver of breathing under normal conditions. Oxygen levels only become the primary driver when $O_2$ drops significantly (below about 60 mmHg).

Physical factors provide additional feedback:

• Pulmonary stretch receptors trigger the Hering-Breuer reflex: when the lungs inflate excessively, these receptors signal the medulla to inhibit further inspiration and promote exhalation. This protects against overinflation.
• Irritant receptors in airway mucosa detect particles, chemicals, or mucus, triggering coughing, sneezing, or bronchoconstriction.
• J receptors (juxtacapillary receptors) in alveolar walls respond to pulmonary congestion or edema, producing rapid shallow breathing and a sensation of dyspnea.

Nervous vs. Chemical Breathing Control

These two systems work in layers:

Together, nervous control provides the rhythm and chemical control tunes the intensity.

Exercise and Other Physiological States

Exercise dramatically increases ventilation, sometimes from about 6 L/min at rest to over 100 L/min during intense activity. Several mechanisms contribute:

• Rising $CO_2$ production and falling pH stimulate chemoreceptors
• Proprioceptors in active muscles and joints send signals to respiratory centers, contributing to the rapid increase in ventilation at the start of exercise (even before blood gas levels change)
• Cortical motor areas that activate skeletal muscles simultaneously stimulate respiratory centers (anticipatory response)

Other states that alter breathing:

• Sleep: Metabolic rate drops, chemoreceptor sensitivity decreases, and breathing becomes slower and more regular. During REM sleep, breathing can become irregular.
• Pregnancy: Elevated progesterone stimulates the respiratory centers, increasing tidal volume and producing mild hyperventilation. The growing uterus pushes the diaphragm upward, reducing FRC, though tidal volume actually increases.
• High altitude: Lower atmospheric $O_2$ partial pressure causes hypoxemia, stimulating peripheral chemoreceptors to increase ventilation. Over days to weeks, acclimatization occurs through sustained hyperventilation, increased red blood cell production (via erythropoietin), and increased 2,3-BPG to improve oxygen unloading at tissues.

Integration of Respiratory Control Mechanisms

All of these control systems converge on one goal: maintaining blood gas and pH homeostasis. Chemoreceptors continuously sample $CO_2$, $O_2$, and $H^+$ levels and feed that information to the medullary respiratory centers. The medulla and pons adjust the rate and depth of breathing accordingly.

When $CO_2$ rises (or pH falls), ventilation increases to blow off more $CO_2$. When $CO_2$ drops (or pH rises), ventilation decreases to retain $CO_2$. This negative feedback loop keeps arterial $CO_2$ near 40 mmHg and blood pH near 7.4 under most conditions.

The nervous and chemical systems don't work in isolation. Proprioceptive input during exercise, cortical override during speech, and protective reflexes like the Hering-Breuer reflex all interact with chemoreceptor-driven adjustments to produce a breathing pattern matched precisely to the body's current needs.