Anatomy and Physiology of the Respiratory Tract

The respiratory tract consists of organs involved in breathing, the transport of respiratory gases, and the exchange of gases between air and blood.

It can be divided into two main portions: the conducting portion and the respiratory portion.

Nasal Cavity and Bronchioles:

• Nasal Cavity: The initial part of the conducting portion, responsible for filtering, warming, and humidifying inhaled air.
• Bronchioles: Smaller airway branches that carry gases during inspiration and expiration.

Larynx:

• Structure: Consists of nine pieces of cartilage joined by membranes and ligaments.
• Epiglottis: Covers the glottis during swallowing to prevent the entrance of food.
• Thyroid Cartilage: Protects the front of the larynx.

Trachea:

• Structure: A flexible tube with four layers.
• Mucosa: Pseudostratified ciliated epithelium that helps sweep debris away from the lungs.
• Submucosa (areolar connective tissue): Surrounds the mucosa and is composed of areolar connective tissue.
• Hyaline Cartilage: Forms 16 to 20 C-shaped rings that that wrap around the submucosa. The rigid rings prevent tracheal collapse during inspiration.
• Adventitia: The outermost layer composed of areolar connective tissue.

Mainstem Bronchi and Bronchioles:

• Tracheal bifurcation at the carina into right and left mainstem bronchi.
• Primary bronchi divide into secondary (lobar) bronchi, tertiary (segmental) bronchi, and numerous order bronchioles (1 mm or less in diameter).
• Terminal Bronchioles: Smallest bronchioles with a diameter of 0.5 mm or less and microscopic respiratory bronchioles.

Alveoli and Alveolar Ducts:

• Alveoli: Tiny air sacs in the lungs where gas exchange occurs. There are approximately 300 million alveoli per lung, each one 200 to 300mm in diameter.
• Alveolar Ducts: Final branches of the bronchial tree leading to alveoli.
• Alveolar Sac: Cluster of adjoining alveoli. - Alveolar Pores: Connect adjacent alveoli.

Respiratory Units:

• Acinus: A respiratory bronchiole, its corresponding alveolar duct, and alveoli together constitute a respiratory unit.
• Respiratory Membrane
• Structure: Composed of alveolar and capillary walls.
• Gas Exchange: Oxygen diffuses across the alveolar wall into the capillaries.

Epithelial Cells and Capillaries:

• The alveoli are lined by two types of epithelial cells.
• Type I Cells (95% of the alveolar surface): Predominant cell type lining the alveolar wall, responsible for oxygen diffusion.
• Type II Cells (5% of the alveolar surface area): Secrete pulmonary surfactant.
• Basement Membranes: Thin outer layer of the alveolar wall, surrounded by capillaries.

Lobes and Fissures:

• Right Lung: Divided into three lobes separated by the horizontal and oblique fissures.
• Left Lung: Divided into two lobes separated by a single horizontal fissure.

Root (Hilum) of the Lung:

• Entry and Exit: Bronchi, pulmonary vessels, bronchial vessels, and lymphatics enter and leave the lung through the root.

Blood Supply:

• Pulmonary Arteries and Veins: Supply deoxygenated blood and remove oxygenated blood from the alveoli, respectively.
• Bronchial Arteries and Veins: Supply oxygenated blood and remove deoxygenated blood from the lung tissue.

The Pleura:

• Visceral Pleura: Inner layer surrounding each lung.
• Parietal Pleura: Outer layer lining the inner wall of the thoracic cavity.
• Pleural Cavity: Narrow space between the two pleural membranes

Boundary of the Lower Respiratory Tract:

• Cricoid Cartilage: Marks the line of demarcation between the upper and lower respiratory tract.

Infections and Terminology:

• Upper Respiratory Infections: Involve anatomic areas above the cricoid cartilage.
• Lower Respiratory Infections: Involve anatomic areas below the cricoid cartilage.

• The goals of respiration are to provide oxygen to the tissues and to remove carbon dioxide. To achieve these goals, respiration occurs through four major functions:
• Pulmonary ventilation which involves the inflow and outflow of air between the atmosphere and the alveoli.
• Diffusion of oxygen and carbon dioxide between the alveoli and the blood – gas exchange.
• Transport of oxygen and carbon dioxide in the blood and body fluids to and from the body's tissue cells.
• Regulation of ventilation and other facets of respiration.

• Involves sequential expansion and emptying of the lungs in two ways.
• Mechanical processes involved consist of
1. Downward and upward movement of the diaphragm (to lengthen or shorten the chest cavity) or
2. The elevation and depression of the ribs (to increase or decrease the antero-posterior diameter of the chest cavity).
• Compliance - describe the distensibility of tissues and organs of the respiratory pump such as the lungs and chest wall. The higher the compliance, the larger the delivered volume per unit changes in pressure.
• Alveolar surface tension affects the compliance of the lungs. If the surface tension is not kept low, there is the inevitable tendency for the alveoli to collapse at smaller volumes during expiration.
• Resistance – describes the inherent capacity of the air conducting system (e.g. airways) and tissues to oppose airflow towards the lungs.
• Airway resistance depends on the radii of the airways (total cross-sectional area), the length of airways, the flow rate, and the density and viscosity of gas.
• In general, resistance is governed principally by Poiseuille’s law stated as:R = 8 lη ÷ πr4
• (where R - resistance, η - viscosity, l - length, and r – radius).
• Thus, airway resistance is inversely proportional to its radius raised to the 4th power. If the airway lumen is decreased by half, there is a corresponding 16-fold increase in the resistance.
• Newborns and infants with their inherently smaller airways are especially prone to marked increase in airway resistance from inflamed tissues and secretions. This age-related difference airway dimension accounts for why croup and bronchiolitis are almost entirely confined to infants and pre-school children.
• Also, in patients with increased airway resistance (as is the case in bronchiolitis and pneumonia), a fast respiratory rate does not allow enough pressure equilibration to occur between the proximal airway and the alveoli, with a resulting tendency to develop hypoxia.

• Gaseous exchange in the respiratory system occurs only in the terminal segments of the airway.
• The gas occupying the part of the respiratory system that is not available for gas exchange with pulmonary capillary blood constitutes the dead space.
• This space comprises the anatomic dead space (respiratory system volume exclusive of alveoli), and the physiologic (total) dead space (volume of gas not equilibrating with blood).
• In healthy individuals, the two dead spaces are identical. However, in disease states such as atelectasis and pneumonia, there may be no exchange between the gas in some of the alveoli and the blood, either as a result of compensatory under-perfusion or over-ventilation of some of the alveoli.
• Gas exchange occurs by the process of diffusion and equilibration of alveolar gas with pulmonary capillary blood.

Diffusion depends on

• The expansive surface area of the lungs which promotes extensive diffusion, and
• The amount of available time for equilibration.
• The minute diffusion distance of the thin alveolar and capillary walls (the alveolar-capillary barrier is less than 0.5 mm in thickness) enhances the rate of diffusion.
• In health, the equilibration of alveolar gas and pulmonary capillary blood is complete for both oxygen and carbon dioxide.
• In diseases in which alveolo-capillary barrier is abnormally increased (alveolo-interstitial diseases), and/or when the time available for equilibration is decreased (increased blood flow velocity) diffusion is incomplete.

• O₂ diffuses through the respiratory membrane from the alveoli to the blood from where it is transported to the tissues for utilization.
• O₂ is transported in blood in two forms, the majority is bound to hemoglobin (oxyhemoglobin) and the rest is dissolved in plasma.
• The relationship is exemplified by the O₂-Hb dissociation curve
• 1gram of Hb combines with 1.34ml of O₂ while 100mls of arterial blood dissolves 0.3ml of O₂
• CO₂ is transported back to the lungs as HCO₃ (60%), carbaminoHb (30%) & in plasma (10%).
• The saturation of haemoglobin with oxygen is expressed as a percent saturation in which each gram of normal haemoglobin can hold 1.34 milliliters of oxygen.
• The dissolved fraction is dependent upon the partial pressure of oxygen.
• Under normal conditions each 100ml of blood contains about 20 ml of oxygen bound to haemoglobin and about 0.3 ml dissolved in plasma
• The dissolved fraction is available to tissues first, and then the fraction bound to haemoglobin.
• As tissues metabolize oxygen or if oxygen transport is inadequate, the dissolved oxygen and the haemoglobin-bound oxygen will eventually become depleted.
• The pulse oximeter calculates the percent of oxyhemoglobin from the total hemoglobin present.

The delivery of oxygen to a particular tissue depends on:

• The amount of O₂ entering the lungs,
• The adequacy of pulmonary gas exchange,
• The blood flow to the tissue, and
• The capacity of the blood to carry O₂.

• The control and maintenance of normal breathing are largely within the respiratory control centers (bulbopontine region of the brainstem).
• Neurons within this area of the brain respond to multiple afferent inputs to modulate their own inherent rhythmicity and provide efferent output to the respiratory control muscles.
• Multiple afferent inputs induce modulation of the central respiratory center efferent outputs to the respiratory and airway muscles and lungs.
• Among these inputs are signals from central and peripheral chemoreceptors, pulmonary stretch receptors, cortical and reticuloactivating system neurons.
• The carotid bodies detect changes in PO2, PCO2, pH,
• The medullary chemoreceptor monitors PCO2 and pH alone.
• The ventilatory drive is stimulated by PO2 and PCO2 levels, although the body demonstrates far greater sensitivity to PCO2 levels.
• In response to the decrease in pH, the central chemoreceptors stimulate the respiratory center to increase the rate of inspiration. Conversely, an increase in PCO2, and a decrease in pH or PO2, causes the peripheral chemoreceptor to stimulate the respiratory center.

• The partial pressures of oxygen (PO2) and carbon dioxide (PCO2) are tightly regulated by the central nervous system.
• Any alteration in their values can be taken as an indication that either the regulatory system (the central control of breathing) or its effector organs (the respiratory muscles and lungs) have become impaired or overwhelmed.
• After being integrated with other afferent (sensory) information from the lungs and chest wall, chemoreceptor activation triggers an increase in the neural output to the respiratory muscles with the resultant physical signs that characterize respiratory distress
• Respiratory distress - a conglomerate of clinical features reflecting respiratory ill health.
• Features - tachypnoea, use of accessory muscles of respiration like the intercostals muscle, lower chest wall indrawing, grunting, hypoxaemia and cyanosis.
• The patient with respiratory distress develops a subjective perception of difficulty in breathing or ‘air hunger’ (dyspnoea) and, consequently an increase in respiratory muscle effort.
• The physical signs of respiratory distress can be explained by:
• A decrease in pleural pressure during inspiration,
• Recruitment of the accessory muscles that do not participate in normal (quiet) breathing at rest,
• The activation of the dilator muscles of the upper airway as reflected by a visible nasal flaring.
• Grunting, which is due to decreased lower airway compliance.
• Grunting - physiological mechanism that generates high pressure in the alveoli.
• The increase in intrapulmonary pressure at the initial phase of grunting is associated with the epiglottis covering the glottis during expiration. When the epiglottis subsequently opens abruptly, gas rushes past the vocal cords producing the expiratory grunting sound.
• Produced by expiration against a partially closed glottis and is an attempt to maintain positive airway pressure during expiration for as long as possible.
• Grunting -a self-administered form of peak end expiratory pressure. By maintaining a high intrapulmonary pressure, more oxygen is expected to diffuse into the blood in the lungs.
• Beneficial in diseases that produce widespread loss of the functional residual capacity, such as in extensive pneumonic consolidation or one associated with pleural effusion
• It is characteristically seen in infants, and is a sign of severe respiratory difficulty.
• Disappearance of grunting may suggest fatigue.
• End-organ hypoxia of the central nervous system causes lethargy and confusion, sometimes alternating with agitation. The arterial hypoxaemia causes haemoglobin desaturation, which if severe could manifest as central cyanosis.