Summary

This document seems to be notes or an outline of the respiratory system. It explains the internal and external layers of the pleura which includes the visceral pleura and the parietal pleura. The notes also show how the pressure variation (such as intra-pulmonary, intra-pleural, atmospheric, transpulmonary, and transthoracic pressures) affects lung volume and function.

Full Transcript

Respiratory system Tuesday, October 22, 2024 9:42 PM Internal and external...

Respiratory system Tuesday, October 22, 2024 9:42 PM Internal and external Visceral pleura : inner layer , covers lungs Pleural cavity : pleural fluid Parietal pleura : outer layer , covers mediastinum , chest wall and diaphragm Pleural fluid : helps lungs to easily contract during inhalation and exhalation --> excess fluid is removed by lymphatic drainage 760 mm Hg (0 mm Hg) Intra-pulmonary : the pressure inside the alveoli of the lungs At rest : Intra-pleural : the pressure in the pleural space Atmospheric pressure : the pressure exerted by the air in the surrounding environment Intra-pulmonary = 760 mm/hg = 0 mm/Hg ↠ alternate betwwen negative (inspiration ) and positive ( expiration ) Transpulmonary pressure : The difference between intrapulmonary and intrapleural pressure Intra-pleural = 756 mm/Hg = -4 mm/Hg ( keeps lung inflated ) ↠ always negative Transthoracic pressure : The difference between intrapleural and atmospheric pressure Atmospheric = 760 mm/Hg = 0 mm/Hg Transpulmonary = intra-pulmonary - intra-pleural → Defines lung volume = 0 - ( -4 ) → Prevents lung from collapsing = 4 mm/Hg → Pneumothorax : transpulmonary is negative Transthoracic = intra-pleural - atmospheric = -4 - 0 = -4 mm/Hg Intra-pulmonary Smaller alveoli require higher pressure to stay open: For a smaller radius (r), the pressure (P) needed to counteract surface tension (T) increases. This means smaller alveoli are more prone to collapse compared to larger !" Excess pressure : P= ones without additional stabilization mechanisms. # The body counteracts this potential collapse by producing surfactant, a substance secreted by type II alveolar cells. Surfactant reduces surface Boyle's law : P1V1 = P2V2 tension (T) When volume increases , pressure decreases LaPLace law PS : Gases move from area of high pressure to area of lower pressure Gases exert a pressure proportional to Surfactant reduces surface tension proportionally more in smaller alveoli. their abundance More gas = higher pressure During quite inspiration : During forced inspiration : Intra-pulmonary = -1 mm/Hg Intra-pulmonary = -2 mm/Hg Intra-pleural = -6 mm/Hg ( or -8 ) Intra-pleural = -7 mm/Hg Atmospheric = 0 mm/Hg Atmospheric = 0 mm/Hg Transpulmonary = intra-pulmonary - intra-pleural Transpulmonary = intra-pulmonary - intra-pleural = -1 - ( -6 ) = -2 - ( -7 ) = 5 mm/Hg = 5 mm/Hg Transthoracic = intra-pleural - atmospheric Transthoracic = intra-pleural - atmospheric = -6 - 0 = -7 - 0 = -6 mm/Hg = -7 mm/Hg During quite expiration : During forced expiration : Intra-pulmonary = +1 mm/Hg Intra-pulmonary = +2 mm/Hg Intra-pleural = -3 mm/Hg ( or -5 ) Intra-pleural = -2 mm/Hg Atmospheric = 0 mm/Hg Atmospheric = 0 mm/Hg Transpulmonary = intra-pulmonary - intra-pleural Transpulmonary = intra-pulmonary - intra-pleural = 1 - ( -3 ) = 1 - ( -3 ) = 4 mm/Hg = 4 mm/Hg Transthoracic = intra-pleural - atmospheric Transthoracic = intra-pleural - atmospheric = -3 - 0 = -2 - 0 = -3 mm/Hg = -2 mm/Hg From C4-C5 , Phrenic nerve innervate diaphragm From T1-T11 , intercostal nerves innervate the internal and external intercostal muscles. DRG Medullary centers : VRG DRG : dorsal respiratory group VRG : ventral respiratory group C3-C5 T1-T11 ( Compliance represents inverse of stiffness ) Factors that affect lung compliance : Δ𝑉 ↑ Compliance Elastic recoil of the lungs ( tendency to inflate ) 𝐶𝑜𝑚𝑝𝑙𝑖𝑎𝑛𝑐𝑒 = ↓ Pressure Δ𝑃 Elasticity of the chest wall ( tendency to expand outward) Surface tension → Maintain the negative pressure Δ𝑃 ↑ Elasticity Elasticity refers to the tendency of a → Prevent lungs from fully collapsing 𝐸𝑙𝑎𝑠𝑡𝑖𝑐𝑖𝑡𝑦 = ↓ Volume structure to return to its initial size after Δ𝑉 → Created by H2O and air being distended → Keep lungs attached to chest wall → Pneumocytes type 2 ( Which are only 5-10% of the alveolar surface area ) produce surfactant which reduce surface tension ↠ Atelectasis : Insufficient surfactant production = lung collapsing Surface tension is the force exerted by water molecules on the surface of the lung tissue as those water molecules pull together ( Water (H2O) is a highly polar molecule, so it forms strong covalent bonds with other water molecules) The force of these covalent bonds effectively creates an inward force on the surface of the lung , with the effect of lowering the surface area of that surface as the tissue is pulled together. As the air inside the lungs is moist, there is considerable surface tension within the tissue of the lungs. Because the alveoli of the lungs are highly elastic, they do not resist surface tension on their own, which allows the force of that surface tension to deflate the alveoli as air is forced out during exhalation by the contraction of the pleural cavity. The force of surface tension in the lungs is so great that without something to reduce the surface tension, the airways would collapse after exhalation, making re-inflation during inhalation much more difficult and less effective Fortunately, the type II epithelial cells of the alveoli continually secrete a molecule called surfactant that reduces the force of surface tension from water molecules on the lung tissue Pulmonary ventilation VA : volume of air reaching the alveoli per minute when dead space in unknown 𝑉𝐸 𝐶𝑂2 ×0.863 VE CO2 : volume of CO2 exhaled per minute 𝑉𝐴 = 𝑃𝐴 𝐶𝑂2 PA CO2 : alveolar CO2 Airway resistance L : length of the tube Airway resistance is the resistance of the respiratory 8𝐿𝜂 𝜂 ∶ viscocity tract to airflow during inhalation and exhalation. 𝑅= r: radius of the tube 𝜋𝑟 # Diameter increases = Surface area increases = lower resistance of air flow Diameter decreases = Surface area decreases = high resistance of air flow +2 Inspiration Expiration - Diaphragm pulls down - Diaphragm pulls out - Pressure ↓ - Pressure ↑ - Volume ↑ - Volume ↓ - Action potential ↑↑ - Action potential ↓↓ Muscles involved Muscles involved Quiet inspiration : Quiet expiration ( passive process ) Diaphragm External intercostal muscle No muscles involved Depends on elasticity of lungs Forced inspiration : High resistance Sternochleidomastoid Scelene Forced expiration ( breathe out more air ) Anterior serattus Pectoralis minor Abdominal muscles Internal intercostal muscle ( internal and external oblique ) Diseases Interstitial pulmonary fibrosis : Pneumothorax : Parenchyma becomes thicker The pleural space is open to atmospheric pressure and the intrapleural pressure ↓ Compliancy can increase to the point where it is the same as or greater than the intrathoracic ↑ Elasticity pressure (transpulmonary pressure between the ambiguous nucleus and the retrotrapezoid nucleus Believed to be the pacemaker that generates the basic rhythm for breathing. The DRG sends signals to the diaphragm for regular, quiet inspiration. When deeper or forced breaths are needed, the VRG activates additional muscles: Inspiration: External intercostals and accessory muscles. Expiration: Internal intercostals and abdominal muscles for forceful exhalation. Feedback loops and neural input to both the DRG and VRG allow for adjustments in breathing rate and depth, responding to the body's oxygen and carbon dioxide needs The respiratory control center These are the muscles that respond to signals from the respiratory control center to adjust breathing. In the lungs Forced inspiration Forced expiration The respiratory control center in the brain (specifically in the medulla and pons) receives signals from the sensors and integrates this information. It compares current conditions to the body's respiratory needs and sends out appropriate signals to maintain homeostasis. PS : The pulmonary stretch receptors are stimulated by the distention of the lungs during inspiration. Lung distension triggers the pulmonary stretch receptors to send impulses through the vagus nerve to the medulla, inhibiting the activity of DRG thus the inspiration in order to prevent lung overinflation. The Hering-Breuer reflex : Inhibits inspiration when lung volume is high, preventing overinflation. Pulmonary receptors

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