Mechanics of Respiration and Expiration PDF

Mechanics of respiration, inspiration and expiration ○ The lungs and chest wall are elastic structures ○ Normally no more than a thin layer of fluid is present between the lungs and the chest wall (intrapleural space) ○ The lungs slide easily on the chest wall, but resist being pulled away from it i...

Mechanics of respiration, inspiration and expiration ○ The lungs and chest wall are elastic structures ○ Normally no more than a thin layer of fluid is present between the lungs and the chest wall (intrapleural space) ○ The lungs slide easily on the chest wall, but resist being pulled away from it in the same way that two moist pieces of glass slide on each other but resist separation ○ The pressure in the “space” between the lungs and chest wall (intrapleural pressure) is sub-atmospheric ○ The lungs are stretched when they expand at birth and at the end of a quiet expiration, their tendency to recoil from the chest wall is just balanced by the tendency of the chest wall to recoil in the opposite direction ○ If the chest wall is opened, the lung collapse; and of the lungs lose their elasticity, the chest expands and becomes barrel shaped Inspiration ○ Inspiration is an active process ○ The contraction of the inspiratory muscles increases intrathoracic volume ○ The intrapleural pressure at the base of the lungs is normally -2.5 mm Hg (relative to atmosphere) at the start of inspiration, decreases to about -6 mmHg ○ The lungs are pulled into a more expanded position ○ The pressure in the airways becomes slightly negative and air flows into the lungs ○ At the end of inspiration, te lung recoil begins to pull the chest back to the expiratory position where the recoil pressures of the lungs and chest wall balance ○ The pressure in the airway becomes slightly positive, and air flows pout of the lungs ○ Expiration during quiet breathing is passive in the sense that no muscles that decrease intrathoracic volume contract ○ However, some contraction of the inspiratory muscles occurs in the early part of expiration ○ This contraction of the inspiratory muscles occurs in the early part of expiration ○ This contraction exerts a braking action on the recoil forces and slows the expiration ○ Strong inspiratory efforts reduce intrapleural pressure to values as low as -30 mmHg, producing correspondingly greater degrees of lung inflation ○ When ventilation is increased the extent of the lung deflation is also increased by active contraction of expiratory muscles that decrease intrathoracic muscles Lung volumes and capacities ○ Important quantification of lung function can be gleaned from the displacement of air volume during inspiration and /or expiration ○ Lung capacities refer to subdivisions that contain 2 or more volumes ○ Diagnostic spirometry is used to asses a patient’s lung function for purposes of comparison with a normal population, or with previous measures from the same patient ○ The amount of air that moves into the lungs with each inspiration (the amount that moves out with each inspiration) during quiet breathing is called tudal volumed (TV) ○ Typical vales for TV are on the order of 500-750 mL ○ The air inspired with a maximal respiratory effort in excess of TV is the inspiratory reserve volume (IRV-2L) ○ The volume expelled by an active expiratory effort after passive expiration is the experiatory reserve volume (EVR-1L) and the air left in the lungs after maximal expiratory effort is residual volume (RV: 1.3L) ○ When all four of these components are taken together, they make up the total lung capacity (TLC- 5L) ○ The TLC can be broken down into alternative capacities that help define functioning lungs ○ The vital capacities (VC-3.5L) refers to the maximum amount of air expired from the fully inflated lungs or maximum inspiratory level (represents TV + IRV +EVR) ○ The inspiratory capacity (IC-2.5L) is the maximum amount of air inspired form the end expiratory level (IRV+ TV). ○ The functional residual capacity (FRC- 2.5L) represents the volume of air remaining in the lungs after expiration of a normal breath (RV+ EVR) Restrictive disease -idiopathic pulmonary fibrosis ○ Idiopathic pulmonary fibrosis (IPF) a type of a pulmonary fibrosis is a rare and irreversible interstitial lung disease that usually affects middle aged and older adults (>50 yo) ○ The most common cause of death related to IPF is respiratory failure ○ Other causes of death include pulmonary hypertension, and PH associated with right heart failure, pulmonary embolism and lung cancer ○ Up to 132,000 people in the US are currently affected by IPF and there are 30,000-40,000 new cases each year ○ Alveolar epithelial injury due to epithelial cell apoptosis and endoplasmic reticulum stress and epithelial to mesenchymal transition (EMT) have been implicated as cellular mechanisms involved in the development of IPF Airway resistance ○ Airway resistance is defined as the change of pressure from the alveoli to the mouth divided by the change in flow rate ○ Because of the structure of the bronchial tree, and thus the pathway for air that contributes to its resistance it is difficult to apply mathematical estimates of the movement through the bronchial tree ○ However, measurements where alveolar and intrapleural pressures can be compared to actual pressures show the contribution of airway resistance ○ Airway resistance is significantly increases as lung volume is reduced ○ Also, bronchi and bronchioles significantly contribute to airway resistance ○ Thus, contraction of the smooth muscle that lines the bronchial airways will increase airway resistance and make breathing more difficult Surfactant ○ Surfactant is important at birth ○ The fetus makes respiratory movements in the utero, but the lungs remain collapsed until birth ○ After birth, the infant makes several strong inspiratory movements and the lung is expanded ○ Surfactant keeps them from collapsing again ○ Surfactant deficiency is an important cause of infant respiratory syndroom (IRDS also known as hyaline membrane disease), the serious pulmonary disease that develops in infants born before their surfactant system is functional. ○ Surface tension in the lungs of these infants is high, and the alveoli are collapsed in many areas (atelectasis) ○ An additional factor in IRDS is retention of fluid in the lungs ○ During fetal life, Cl- is secreted with fluid by the pulmonary epithelial cells ○ At birth, there is a shift of Na+ absorption by these cells via the epithelial Na+ channels (ENaCs), and fluid is absorbed with the Na+. ○ Prolonged immaturity of the ENaCs contributes to the pulmonary abnormalities in IRDS ○ overproduction/dysregulation of surfactant proteins can also lead to respiratory distress and is the cause of pulmonary alveolar proteinosis Dead space and uneven ventilation ○ Because gaseous exchange in the respiratory system occurs only in the terminal portions of the airway, the gas that occupies the rest of the respiratory system is not available for gas exchange with pulmonary capillary blood ○ Normally the volume (in mL) of this anatomic dead space is approximately equal to the body weight in pounds ○ As an example, in a man who weighs 150 lb (68kg), only the first 350 mL of the 500 mL inspired with each breath at rest mixes with the air in the alveoli ○ Conversely, with each expiration, the first 150 mL expired is gas that occupied the dead space and only the last 350 mL is gas from the alveoli ○ Consequently, the alveolar ventilation, that is, the amount of air reaching the alveoli per minute is less than the RMV ○ Note that because of the dead space, rapid shallow breathing produces much less alveolar ventilation than slow deep breathing at the same RMV The diffusing capacity of the lungs for a given gas is directly proportional to the surface area of the alveolocapillary membrane and inversely proportional to its thickness The diffusing capacity for CO (DLCO) is measured as an index of diffusing capacity because its uptake is diffusion limited.