Human Anatomy and Physiology - N. I. Fedyukovich 2003

Internal Organs
Respiratory System
Respiratory Physiology

The vital activity of a living Organism involves the uptake of O₂ and the release of CO₂. Therefore, METABOLISM/2.html">THE CONCEPT OF "respiration" encompasses all processes associated with delivering O₂ from the external environment into The Cell and eliminating CO₂ from the cell into the surrounding environment.

In humans, respiration is subdivided into: 1) internal (cellular or tissue) respiration; 2) gas transport by Blood or other Body Fluids; 3) external (pulmonary) respiration. Essentially, all Links of the body's gas transport system, including regulatory mechanisms, serve to maintain the oxygen concentration in Cells required to sustain The activity of respiratory Enzymes.

The transfer of O₂ from alveolar air into the blood, and of CO₂ from the blood into alveolar air, occurs exclusively via diffusion. The driving force for diffusion is the difference in the partial pressures of O₂ and CO₂ on both sides of the alveolocapillary membrane. Oxygen and carbon dioxide diffuse through a thin phospholipid film (surfactant), the alveolar epithelium, two basement membranes, and the endothelium of the blood capillary. The diffusing capacity of the Lungs for oxygen is substantial. This is due to the large number of alveoli and their extensive gas exchange surface area, as well as the minimal thickness (about 1 µm) of the alveolocapillary membrane. The transit time of blood through the pulmonary capillaries is approximately 1 s, and the gas tension in the arterial blood leaving the lungs completely matches the partial pressure in the alveolar air. If pulmonary ventilation is inadequate and the CO₂ content in the alveoli increases, the concentration of CO₂ in the blood rises immediately, leading to an increased breathing rate.

In the lungs, deoxygenated blood is converted into arterial blood, which is rich in O₂ and low in CO₂. Arterial blood flows to the Tissues, where O₂ is consumed and CO₂ is produced As a result of continuous metabolic processes. In the tissues, the O₂ tension is close to zero, while the CO₂ tension is about 60 mmHg. Due to this pressure gradient, CO₂ diffuses from the tissues into the blood, and O₂ diffuses into the tissues. The blood becomes deoxygenated and returns via Veins to the lungs, where the gas exchange cycle repeats.

Gases have very low solubility in liquids. Thus, only a small fraction of O₂ (about 2 %) is dissolved in plasma, and CO₂ accounts for 3–6%. The bulk of oxygen is transported in the form of a unstable compound with Hemoglobin contained within erythrocytes. The molecule of this respiratory pigment comprises a specific protein, globin, and a prosthetic group, heme, which contains ferrous iron. The binding of oxygen to hemoglobin yields oxyhemoglobin, whereas the release of oxygen produces deoxyhemoglobin. For example, 1 g of hemoglobin is capable of binding 1.36 mL of gaseous O₂ (at atmospheric pressure). Considering that human blood contains approximately 15 % hemoglobin, 100 mL of blood can carry up to 21 mL of O₂. This is known as the oxygen capacity of the blood. Hemoglobin oxygenation depends on the partial pressure of O₂ in the medium with which the blood is in contact. The affinity of hemoglobin for oxygen is measured by the oxygen partial pressure at which hemoglobin is 50 % saturated (P₅₀); under normal conditions in humans, this value is 26.5 mmHg for arterial blood.

Hemoglobin readily binds with carbon monoxide (CO) to form carboxyhemoglobin, which is incapable of transporting O₂. Its chemical affinity for hemoglobin is nearly 300 times greater than that for O₂. Consequently, at a CO concentration in the air of 0.1 %, about 80 % of blood hemoglobin binds to carbon monoxide rather than oxygen. This leads to symptoms of oxygen deprivation in The Human Body (vomiting, headache, loss of consciousness). Mild Carbon monoxide poisoning is a reversible process: CO gradually dissociates from hemoglobin and is eliminated through breathing fresh air.

At a CO concentration of 1 %, death occurs within several seconds.

Carbon dioxide has The ability to participate in various chemical bonds, forming, among other things, unstable carbonic acid. This is a reversible reaction dependent on the partial pressure of CO₂ in the gaseous environment. It is sharply accelerated by the enzyme Carbonic anhydrase, located in erythrocytes, into which CO₂ rapidly diffuses from the plasma. About 4/5 of Carbon dioxide is transported in the form of bicarbonate (HCO₃). The binding of CO₂ is facilitated by a decrease in the acidic properties of hemoglobin. Carbonic acid in tissue capillaries reacts with sodium and potassium ions to form bicarbonates (NaHCO^-₃, KHCO^-₃). Carbon dioxide is transported to the lungs in a physically dissolved state and as an unstable chemical compound in the form of carbohemoglobin, carbonic acid, and sodium and potassium bicarbonates. About 70 % of it resides in the plasma, and 30 % in the erythrocytes.

The coordinated contractions of the Respiratory Muscles are driven by the rhythmic activity of Neurons in the respiratory center located in the Medulla Oblongata. In addition, the regulatory apparatus of respiration includes chemoreceptor and mechanoreceptor systems that ensure the normal functioning of the respiratory center in accordance with the body's gas exchange demands. Respiratory neurons are Nerve Cells whose impulse activity changes in phase with the respiratory cycle. A distinction is made between inspiratory neurons, which are active only during the inhalation phase, and expiratory neurons, which are active during exhalation. The activity of respiratory neurons also depends on impulses originating from the chemoreceptors and mechanoreceptors of the Respiratory system. The primary regulator of the central respiratory mechanism's activity is afferent signaling regarding blood gas composition, which arrives from central (bulbar) and peripheral (arterial) chemoreceptors.

The main stimulus controlling respiration is a high level of CO₂ (hypercapnia) in the blood and Brain extracellular fluid. The stronger the excitation of the bulbar chemosensitive structures and arterial chemoreceptors, the higher the ventilation rate. Hypoxia has a minor effect on respiratory regulation. A combination of hypercapnia and hypoxia stimulates respiration; the intensification of oxidative processes leads not only to an increase in oxygen uptake from the blood, but also to a rise in carbon dioxide and acidic metabolic products within it.

The mechanoreceptors of the respiratory system, firstly, participate in regulating the parameters of the respiratory cycle—controlling the depth of inspiration and its duration; secondly, these receptors mediate protective Reflexes such as coughing. Mechanoreceptors include pulmonary stretch receptors, irritant receptors, juxtapulmonary receptors (J-receptors), upper airway receptors, and proprioceptors of the respiratory muscles. Pulmonary stretch receptors are located primarily in the smooth Muscle layer of the tracheobronchial tree walls and are sensitive to pressure and stretching. Irritant receptors reside in the epithelial and subepithelial layers of the airways. They are sensitive to dust particles, mucus, and chemical agents, and also respond to sudden changes in lung volume (collapse). Juxtapulmonary receptors are localized in the lung interstitium near the alveolar capillaries and give rise to unmyelinated C-fibers running within the Vagus nerve. These receptors are sensitive to a range of BIOLOGICALLY ACTIVE SUBSTANCES (nicotine, histamine, etc.). Upper airway receptors primarily serve as the source of protective reflexes (coughing, sneezing, swallowing). Proprioceptors of the respiratory muscles monitor the activity of these muscles under The Influence of central respiratory neurons.

Thus, neural and humoral structures varying in nature and Location take part in the Regulation of Respiration, creating optimal conditions for gas exchange.

At rest, a human inhales and exhales about 500 mL of air. This volume of air is termed the tidal volume. If, following a quiet inspiration, one makes a forced maximal inspiration, an additional 1,500 mL of air can enter the lungs. This volume is called the inspiratory reserve volume. Following a quiet expiration, maximal contraction of the respiratory muscles can expel another 1,500 mL of air. This volume is termed the expiratory reserve volume. After a maximal expiration, about 1,200 mL of air remains in the lungs, which is the residual volume. The sum of the expiratory reserve volume and the residual volume is about 2,500 mL (Note: Translation reflects original text's numerical context, keeping structural integrity) — the functional residual capacity of the lungs (alveolar air). Vital capacity is the sum of the tidal volume, inspiratory reserve volume, and expiratory reserve volume (500 + 1500 + 1500).

The vital capacity of the lungs and the volume of pulmonary air are measured using a specialized device known as a spirometer (or spirograph).

Respiration changes under increased or decreased atmospheric pressure. For instance, when working underwater at depth (divers, aquanauts), it is necessary to supply a breathing mixture that corresponds to the hydrostatic pressure at that depth, otherwise breathing becomes impossible. For every 10 m increase in depth, pressure rises by 1 atm (0.1 MPa). Thus, at a depth of 100 m, a person requires a breathing mixture at approximately 10 times atmospheric pressure. The density of this mixture increases proportionally, creating additional resistance to breathing. Consequently, at depths exceeding 60–80 m, large amounts of gases, including nitrogen, dissolve in the blood and tissues. A rapid transition from high pressure to normal pressure causes numerous nitrogen gas bubbles to form in the human body, which can occlude capillaries and disrupt Blood Circulation. A gradual pressure reduction in a decompression chamber facilitates the elimination of nitrogen via the lungs.

To prevent the Adverse effects of nitrogen on the human body, nitrogen is wholly or partially replaced by helium, whose density is 7 times lower than that of nitrogen.

Exposure to high altitudes is accompanied by a decrease in the partial pressure of oxygen in the inspired air and alveolar gas. For example, at an altitude of 4,000 m above sea level, atmospheric O₂ and alveolar O₂ pressures drop by more than 1.5 times compared to normal levels. Under these conditions, a person may experience inadequate oxygen supply to the body, particularly the brain, manifested by shortness of breath, Central Nervous system disturbances (headache, nausea, insomnia), etc. An individual's physiological resistance depends entirely on their acclimatization. However, at altitudes of 7,000–8,000 m, where atmospheric and alveolar O₂ pressures drop nearly threefold, breathing is considered unsafe for life without The Use of an oxygen-enriched gas mixture.