2.2 Cardiopulmonary Anatomy, Mechanics of Breathing, and Gas Exchange

Cardiopulmonary Anatomy, Breathing and Gas Exchange

Ventilation moves gas to the alveoli. Diffusion transfers gas across the alveolar-capillary barrier. Perfusion supplies the blood that receives oxygen and releases carbon dioxide. Distinguish these processes when interpreting a change in oxygenation or planning treatment.

1. The Airway Tree

The nose and pharynx warm, humidify and filter inspired air. The larynx helps protect the airway during swallowing. Below the vocal folds, the trachea divides into the main bronchi, which branch into lobar and segmental bronchi and then into bronchioles. The trachea has cartilage rings and the bronchi have cartilage plates. Bronchioles lack cartilage. Their caliber is influenced by smooth muscle, airway pressure and support from the surrounding lung. Mucus and coordinated ciliary motion help move trapped material towards the pharynx. Epithelial structure changes along the tree.

The conducting zone ends at the terminal bronchioles. It delivers gas to the exchange units and contributes to anatomical dead space. The respiratory zone starts where alveoli appear in respiratory bronchiole walls and continues through alveolar ducts and sacs. Real branches vary in length, caliber and number along a path.

Weibel's regular branching model

These figures describe regularized Model A rather than exact measurements or generation labels for an individual. Starting with generation 0 means there are 24 numbered levels through generation 23. The combined luminal area is the sum of cross sections through the branches at that level. The small reduction across the first few model levels precedes a large distal increase.

For an illustrative comparison, if the same total flow of 250 cm³/s passes through two sections of the model, mean bulk speed is flow ÷ combined area. At 2.5 cm², it is about 100 cm/s. At 180 cm², it is about 1.4 cm/s. This calculation assumes the stated total flow through the compared levels. During breathing, flow divides among branches and gas enters and leaves alveoli along the acinus. Molecular diffusion becomes increasingly important for gas mixing distally, and convection can still contribute. The site where the two contributions are comparable depends on conditions such as flow and geometry.

Alveolar structure and surfactant

The alveolar exchange surface is the area of the alveolar walls, not a cut across an airway. In Model A, 11,800 cm² of distal luminal cross section equals 1.18 m². In a separate morphometric study, electron microscopy gave an average alveolar surface estimate of approximately 143 m², greater than earlier light microscopy estimates. Estimates depend on the lungs sampled, inflation and the measurement method. A stereologic study found a mean of about 480 million alveoli in its sample, with substantial variation.

Thin type I pneumocytes cover most of the alveolar surface. Type II cells produce surfactant and contribute to epithelial repair. Surfactant lipids and proteins lower surface tension at the air–liquid interface. For a simplified spherical air space with one interface, the pressure difference is 2 × surface tension ÷ radius. At fixed surface tension, a smaller radius raises this pressure difference. In the lung, surfactant changes surface tension as the interface changes, and alveoli share walls and tissue support. The spherical model illustrates surface forces and cannot predict whether an individual alveolus will collapse.

2. Bronchopulmonary Segments and Positioning

A bronchopulmonary segment is supplied by a segmental bronchus and a pulmonary arterial branch. Pulmonary veins commonly run along boundaries between segments. The names below help describe imaging or target an assessment. Bronchial branching variants occur, including left-sided common trunks.

Clinical positioning. A posterior basal target is anatomically different from the superior segment of the same lobe. A traditional positioning approach may use prone head-down drainage for a posterior basal target. Positioning is an adjunct to clearance and is selected after considering symptoms, imaging, ability to clear secretions, and medical stability. Some patients with bronchiectasis can use modified drainage without head-down tilt. If reflux increases in that position, use an appropriate sitting technique. See Airway Clearance Techniques and Chest Physiotherapy for the position comparison and technique selection.

Worked safety decision. A patient with posterior basal mucus retention also has active intracranial hypertension and an ordered head-elevated position. Avoid head-down drainage and maintain the prescribed position while consulting the neurocritical care and respiratory teams. A flat prone position, a positive expiratory pressure device, manual techniques or suction should not be presumed safe based on the drainage target. Select the approach with the team, considering airway protection, stability, monitoring and applicable device restrictions.

3. Pressure and the Respiratory Muscles

During quiet spontaneous inspiration the diaphragm, supplied by the phrenic nerves from C3–C5, contracts and descends. Rib cage muscles, including parasternal intercostals and scalenes, also contribute. Thoracic expansion lowers pleural pressure and expands the lungs. When alveolar pressure falls below atmospheric pressure, gas flows inward. At the end of inspiration with an open airway and no flow, alveolar pressure again equals atmospheric pressure even though pleural pressure remains below it. Zero cm H₂O here is gauge pressure referenced to atmosphere. Boyle's inverse pressure–volume relationship applies to a fixed amount of gas at constant temperature. Air entering an open lung changes the amount of gas.

The pump-handle description emphasizes forward and upward displacement of the anterior rib cage and increased anteroposterior diameter. The bucket-handle description emphasizes lateral rib elevation and increased transverse diameter. Lower floating ribs can also move outward in a caliper-like fashion. Real rib motion combines components and varies across levels. The sternocleidomastoid can help elevate the upper chest when ventilatory demand rises. With arms fixed, some shoulder girdle muscles can assist rib cage expansion.

Quiet expiration in a healthy resting adult is largely passive as inspiratory muscles relax and net elastic recoil lowers lung volume. Forced expiration recruits the abdominals and expiratory portions of the rib cage muscles. The parasternal portion of the internal intercostals has an inspiratory action. Distinguish it from internal interosseous portions that can assist expiration. An observable increase in respiratory effort must be interpreted with symptoms and vital signs.

4. Pulmonary Volumes and Capacities

The numbers form a single example and are not reference values for a patient. In a passive respiratory system, FRC is the balance point between inward lung recoil and outward chest wall recoil. In obstruction, gas trapping can increase end-expiratory volume. At an illustrative VT of 0.5 L, anatomical dead space of 0.15 L and frequency of 12 breaths per minute, total ventilation is 6.0 L/min and calculated alveolar ventilation is (0.5 − 0.15) × 12 = 4.2 L/min, assuming negligible additional alveolar dead space.

Ordinary spirometry measures gas moved through the mouth. It cannot measure FRC, RV or TLC by itself. The ERS/ATS technical standard describes methods such as body plethysmography, multiple-breath washout and inert gas dilution for measuring FRC. With linked volumes, calculate RV = FRC − ERV and TLC = FRC + IC. Methods can differ in marked obstruction because slowly communicating gas may not be fully captured by dilution or washout. A low forced vital capacity can suggest restriction. TLC below the lower limit of normal establishes the restrictive ventilatory pattern.

5. Alveolar-Capillary Transfer

The Fick diffusion model gives gas transfer rate proportional to area × a gas-specific transfer coefficient × partial-pressure difference ÷ barrier thickness. With the same area, coefficient and gradient, doubling thickness halves the predicted transfer rate. In the lungs, oxygen and carbon dioxide normally travel in opposite directions according to their gradients.

Emphysema can reduce exchange area and fibrosis can lengthen the diffusion path. Carbon dioxide is more soluble and has a substantially greater effective diffusibility in tissue than oxygen. The usual approximate comparison is about 20-fold at the same pressure gradient and under comparable conditions. This comparison alone does not predict when a patient will retain carbon dioxide. Ventilation, perfusion and disease stage also affect arterial gases.

DLCO measures uptake of an inhaled test gas, carbon monoxide, under standardized conditions. It reflects transfer across the membrane and uptake by hemoglobin. Hemoglobin concentration, available alveolar volume and pulmonary capillary blood volume affect the result. Interpret the measurement with the rest of the pulmonary function and clinical findings.

6. Ventilation, Perfusion and West Zones

Alveolar ventilation divided by pulmonary blood flow is the V/Q ratio. For example, 4.0 L/min of alveolar ventilation and 5.0 L/min of blood flow give a whole-lung ratio of 0.8. Both ventilation and perfusion commonly increase toward the base in an upright person. Perfusion increases more steeply in the classic regional measurements, so the apex has a higher ratio than the base. Where there is still perfusion, a relatively high ratio tends toward higher alveolar oxygen and lower alveolar carbon dioxide.

These pressure relationships are not fixed anatomical bands. True zone 1 may be absent in a healthy resting person. Reduced pulmonary arterial pressure or increased alveolar pressure can create it. A normally perfused apex can have a high but finite V/Q ratio without being zone 1.

Shunt is perfusion of an unventilated unit, with a local V/Q of zero. Complete collapse can produce this pattern if perfusion persists. Supplemental oxygen can increase oxygen in ventilated units but cannot directly oxygenate blood crossing a truly unventilated unit. Alveolar dead space is ventilation of an unperfused unit, such as a unit downstream of a complete vascular obstruction. Local alveolar hypoxia can constrict small pulmonary vessels and redistribute flow toward better-ventilated units. Widespread sustained hypoxia can raise pulmonary vascular resistance and increase right ventricular load.