Lecture 2 & 3

• Breathing is the bodily function that leads to ventilation of the lungs, also known as (external) respiration.
• Ventilation is the process of moving gases in (inspiration) and out (expiration) of the lungs.
• Mechanics of breathing describes the structural and physiological bases of ventilation.
• The importance of a pressure gradient is a key learning objective in the mechanics of breathing.
• Mechanism and muscles of inspiration and expiration are also key learning objectives in the mechanics of breathing.
• Lung volumes and capacities are important learning objectives in the mechanics of breathing.
• In obstructive conditions, the work of breathing is minimised with large volume slow breaths.
• The work of breathing is relevant to functional residual capacity, compliance, closing capacity, and surfactant.
• Normal values for lung volumes and capacities are crucial for understanding changes in obstructive and restrictive diseases.
• In restrictive conditions, the work of breathing is minimised with rapid small volume breaths.
• The physics of ventilation involves understanding the role of the ventilatory muscles and their interaction with lung volumes and capacities.
• At maximal hyperventilation, the work of breathing increases to 30% of energy expenditure.
• In health at rest, the work of breathing accounts for 2-5% of energy expenditure.
• Elastic recoil of lungs and chest wall are key learning objectives in the mechanics of breathing.
• Compliance and surfactant are key learning objectives in the mechanics of breathing.
• Resistance to flow is a key learning objective in the mechanics of breathing.
• Diseases affecting ventilation include obstructive conditions such as asthma, chronic obstructive pulmonary disease, and lung cancer, and restrictive conditions like pulmonary fibrosis.
• Gas will flow through patent airways according to the pressure gradient between atmosphere (barometric pressure) and alveoli: Atmosphere is a constant pressure, while Alveoli is a variable pressure.
• Generation of ΔP is dependent on a cycle of pressure changes in the chest.
• Alveolar pressure changes occur secondarily to thoracic volume changes.
• Inspiratory muscles include the diaphragm and external intercostals, which stabilise the rib cage during quiet breathing, and increase effort, causing the diaphragm and external intercostals to lift and expand the rib cage.
• Expiratory muscles include the elastic recoil of tissues during quiet breathing, and internal intercostals and abdominal wall muscles during increasing effort.
• The pleura are important in transmitting thoracic cage expansion into lung volume expansion.
• The volume of air moving in and out of the lungs during ventilation can be measured using a spirometer.
• Tidal volume is the volume of air moved in or out of the lungs during normal breathing, with typical values at rest and during exercise.
• Forced expiratory measurements are used clinically, with a Vitalograph spirometer used to measure the forced vital capacity (FVC) and the forced expiratory volume in 1 second (FEV1), and a peak flow meter used to measure the peak expiratory flow rate (PEFR).
• Surfactant is produced by type II alveolar cells and is 90% phospholipid and 10% protein.
• Surfactant prevents atelectasis and aids alveolar recruitment.
• Hysteresis in breathing occurs at small lung volumes due to reduced compliance of elastic structures and airway calibre.
• The FEV1/FVC ratio is used to distinguish between obstructive and restrictive conditions, with a ratio < 0.7 indicating obstructive and a ratio > 0.7 indicating restrictive.
• Breath sounds are generated in the large airways during high flow rate, turbulent flow and are attenuated by the distal airways during less turbulent flow.
• Inspiratory reserve volume is the volume of air that can be taken in after a normal expiration.
• Peak Expiratory Flow Rate (PEFR) is a convenient way of measuring airways obstruction.
• Measurements of FEV1 and PEFR are made before and after inhalation of a bronchodilator (e.g. the β-adrenoceptor agonist salbutamol) in asthma, where the airways constriction is reversible, so that the FEV1 and PEFR would be restored to normal after salbutamol.
• Surfactant acts as a detergent to reduce alveolar surface tension and increases pulmonary compliance.
• Surfactant becomes more dispersed as alveolar volume increases and equalises pressure between alveoli of different size.
• Infant respiratory distress syndrome is deficient in surfactant.
• During tidal breathing, the relationship between intrathoracic pressure and lung volume is: -5 cm H2O to -9 cm H2O.
• In COPD, the airways constriction is irreversible or nearly irreversible, with less than 15% or 200 mL/s improvement in FEV1 and PEFR after salbutamol.
• Surfactant minimises alveolar fluid.