Respiratory Unit

The respiratory unit or the respiratory lobule is the basic structural unit where gaseous exchange takes place. It comprises a respiratory bronchiole along with its associated alveolar ducts, atria and alveoli.

It is pertinent to note that alveoli are not the only sites of gas exchange but the exchange of gases occurs throughout the membranes of the respiratory unit. All the membranes of the respiratory unit that take part in gaseous exchange are known as the respiratory or pulmonary membrane (Fig. 7.4).

7.6.1 Respiratory Membrane

From inside to outside, the sequence of different layers of respiratory membrane (thickness of 0.2-0.6 μm) is (1) layer of fluid containing surfactant lining the alveolus; (2) a thin layer of alveolar epithelium; (3) basement membrane; (4) an interstitial space between the alveolar epithelium and capil­lary membrane; (5) the basement membrane of capillary, which at some places may form a continuous membrane by fusing with the alveolar epithelial basement membrane; and (6) the membrane endothelium of the capillaries.

Table 7.2 Partial pressures of respiratory gases as they enter and leave the lungs (at sea level)

Fig.

7.6.2 Diffusing Capacity of the Membrane

The respiratory membrane’s diffusing capacity is a measure of the pulmonary membrane’s capacity to permit gaseous exchange between the alveoli and the pulmonary blood. This is defined as the volume of a gas (either O₂ or CO₂) that can diffuse through the membrane at a pressure differ­ence of 1 mmHg in 1 min.

The factors that determine the diffusion capacity are (1) the distance of diffusion determined by membrane thick­ness; (2) the surface area available for diffusion; (3) the diffusion coefficient of the gas, which depends upon the solubility of a gas and its molecular weight; and (4) the partial pressure difference of the gas between the two sides of the membrane.

7.6.2.1 Diffusing Capacity (DI) for Oxygen

It is also called the “transfer factor”, and it is the measure of rate of gas transfer from alveolar space to alveolar capillary blood. The diffusing capacity depends upon the number of functioning alveolar-capillary units, i.e. the surface area available for gas exchange and the volume of blood or haemoglobin available in the pulmonary capillaries. In a human being, the diffusing capacity for oxygen during rest is approximately 21 mL/min/mmHg, increasing up to three times during heavy exercise, and for carbon dioxide, it is 400-450 mL/min/mmHg and 1200-1300 mL/min/mmHg during rest and heavy exercise, respectively.

7.6.3 Ventilation-Perfusion Ratio

The ventilation-perfusion ratio expressed as (VA/Q) is a quantitative measurement or ratio of all the air entering the alveoli to the total blood flowing to both the lungs per minute.

When the alveolar ventilation and perfusion are normal, an optimum exchange of respiratory gases occurs via the pulmonary membrane. If (V_A/Q) is subnormal, there is ineffi­cient oxygenation of the deoxygenated blood in the alveolar capillaries due to poor ventilation. Under such conditions, some fraction of blood fails to become oxygenated, which is termed as shunted blood. The physiologic shunt measures the total quantity of shunted blood formed in 1 min. A higher value of physiologic shunt is indicative of the quantum of blood that fails to be oxygenated.

Normoventilation refers to normal ventilation, whereby the P_aCO₂ is maintained at 40 mmHg. Hyperventilation occurs when the alveolar ventilation increases, which lowers the P_aCO₂ below 40 mmHg. In hypoventilation, the alveolar ventilation decreases, elevating the P_aCO₂ above 40 mmHg. Hypoventilation is associated with respiratory acidosis, which disturbs the body’s acid-base equilibrium and blood pH. Hyperventilation leads to respiratory alkalosis, wherein excess deep breathing exhales out more CO₂ leading to a rise in pH due to a fall in H⁺ ions as given in the equation. The reverse happens during hypoventilation, where excess carbon dioxide is retained by the body, elevating the H⁺ ion concen­tration, and reduces blood pH causing respiratory acidosis:

The reversible reaction influences the rise and fall in H⁺ ions with the increase and decrease of carbon dioxide.

7.6.4 Common Anomalies of the Respiratory System

Atelectasis: A congenital or an acquired defect whereby the alveoli fail to open with air entry at birth or the alveoli have collapsed after inflating. Congenital atelectasis is seen in newborns when the lungs fail to inflate after inhaling a few breaths resulting from airway obstructions with clogged amniotic fluid and meconium. In premature newborns with inadequate quality and quantity of pulmo­nary surfactant, it is termed infant respiratory distress syndrome. This defect is also observed in piglets and foals, where newborns show a characteristic sign of gasping commonly termed “barkers”. Acquired atelectasis most commonly occurs owing to obstructions caused by abscesses and tumours in the pleural cavity, the other reasons being pneumothorax, hydrothorax and bloat.

Acute respiratory distress syndrome (ARDS): It occurs in adult humans and animals characterised by several patho­logical manifestations such as intravascular accumulation of neutrophils, pulmonary hypertension, diffuse damage of the alveoli and acute lung injury accompanied by oedema with the formation of hyaline membranes. Several factors contribute to the pathogenesis of ARDS, resulting in diffuse alveolar damage from systemic diseases or from lung injury that generates a cytokine storm triggered by TNF-α, IL-1, IL-6 and IL-8, causing the release of cyto­toxic enzymes and free radicals from neutrophils, which damages the lungs.

Pneumonia: Pneumonia occurs in all species and is characterised by acute inflammation of the lungs from

several causes. The capillaries get filled with blood, and serous fluid occupies the alveoli. Eventually, the RBC, leukocytes and fibrin mix with this fluid. In the final stage, the debris is liquefied and removed along with repair and regeneration of the alveolar epithelium.

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