Med Phys Pharm 552 L11 Respiratory Phys I 2025 PDF

Lecture #11: Respiratory Physiology I: Mechanics Julia M. Hum, Ph.D. Monday/Wednesday/Friday: 2:00-2:50pm Office Hours: Monday/Wednesday/Friday 11:00am-12:00pm [email protected]  L11: Learning Objectives 1. List the prima...

Lecture #11: Respiratory Physiology I: Mechanics Julia M. Hum, Ph.D. Monday/Wednesday/Friday: 2:00-2:50pm Office Hours: Monday/Wednesday/Friday 11:00am-12:00pm [email protected]  L11: Learning Objectives 1. List the primary functions of the lung and know the non-respiratory functions of the lung 2. Compare/contrast the conducting and respiratory zones 3. Understand the importance and roles of pneumocytes 4. Illustrate the alveolar surface and alveolar-capillary interface 5. Describe the lung’s blood supply 6. Understand how surface tension is generated in the lung and the role surfactant plays 7. Recognize the key players in the mechanics of breathing 8. Define the forces behind dynamic lung mechanics, compliance, and transpulmonary pressure; predict transpulmonary pressure. 9. Draw the pressure-volume curves during inflation and exhalation under normal breathing and disease states Unless otherwise noted, figures in today’s lecture are from: Lippincott Illustrated Reviews: Physiology 1e Wilson (Ch. 22)  Primary Functions of the Lung Pulmonary gas exchange ventilation (frequency x depth of breathing) perfusion (cardiac output of right ventricle) close matching (volume air = volume blood, “ideal”) Maintenance of partial pressures of gases in tissues (Diffusion) carry oxygenated blood to tissues carry deoxygenated blood (CO2) to lungs for elimination LO1  Non-Respiratory Functions of the Lung Phonation Pulmonary Defense Protect against pollutants and infection Blood Filter Remove clots/emboli Acid-Base Balance Carbonic anhydrase reaction CO2 + H2O H2CO3 H+ + HCO3- Substrate conversion Angiotensin I - Angiotensin II (ACE) LO1 Pulmonary Ventilation  Conducting Zone & Respiratory Zone Lower respiratory tract LO2  Alveolar Sacs: Pneumocytes Type I pneumocytes Thin, flat Bulk of alveolar surface area (~90%) Type II pneumocytes “Granular” Present in equal part, more compact Contain lamellar inclusion bodies Pulmonary surfactant Rapidly divide, aid in alveolar wall damage repair LO 2,3  Alveolar-Capillary Interface Pulmonary capillaries and alveoli form a blood-gas interface Alveolar capillary membrane is extremely thin (~ 0.2 - 0.5 mm) Diffusion distances for gases are very small LO4  The Lung’s Blood Supply Two different sources: 1. Pulmonary circulations 2. Bronchial circulations LO5  1. Pulmonary Circulation Receives entire output of the heart Pulmonary veins – carry O2-rich blood to the left side of the heart for delivery to systemic circulation Pulmonary arteries – Brings O2-poor venous blood from the RV to the blood-gas interface significantly less smooth muscle than systemic Readily distend Pulmonary circulation has low vascular resistance 2-3 mm Hg/L/min (5x less than systemic) LO5  2. Bronchial Circulation Vascular beds that supply the conducting airways with O2 and nutrients Bronchial arteries arise from the aorta Feed capillaries that drain either via anastomoses with pulmonary capillaries into veins of the pulmonary circulation Connections allow for small amounts of deoxygenated blood to bypass the blood-gas interface and reenter systemic circulation without being oxygenated – example of a physiological shunt LO5  Pulmonary Surface Tension Each alveolus moistened with a thin film of alveolar lining fluid Generates surface tension – serious consequences for lung performance LO6 Guyton and Hall Medical Physiology 13th ed  Pulmonary Surfactant Synthesized and released by Type II pneumocytes Mix of lipids and proteins Function to counter the effects of surface tension Composition: Dipalmitoyl phosphatidylchloine (DPPC) Stored in lamellar bodies and exocytosed onto the alveolar surface Form monolayer, head group immersed in the superficial aqueous layer Polar head groups allow them to interact with water molecules – weakening surface tension LO6 Clinical Connection: Infant Respiratory Distress Syndrome Miall, Lawrence & Wallis, Sam. (2011). The management of respiratory distress in the moderatel y preterm newborn infant. Archives of disease in childhood. Education and practice edition. ht tp:/ /www2.hawaii.edu /~yzu o/imgs/RD S.jpg 96. 128-35. 10.1136/adc.2010.189712.  Pulmonary Surfactant: Importance 1. Stabilizing alveolar size 2. Increasing compliance 3. Keeping lungs dry LO6  Pulmonary Surfactant: Importance 1. Stabilizing alveolar size LaPlace Law: “when two bubbles of unequal size are connected, the smaller bubble collapses and the larger one inflates” LO6  Pulmonary Surfactant: Importance 1. Stabilizing alveolar size Surfactant molecules compacted at low lung volumes (deflation) resists compression  surface tension Surfactant molecules spread apart at high lung volumes (inflation) limit expansion  surface tension LO6  Pulmonary Surfactant: Importance 2. Increasing compliance Amount of pressure needed to inflate lungs to a given volume Compliance Diagram Surface tension decreases lung compliance and therefore increases the effort required for inflation Surfactant reduces surface tension’s adverse effect on compliance making it easier for lungs to inflate By decreasing muscular effort to inflate lungs  compliance  work of breathing LO6,8 Clinical Connection: Infant Respiratory Distress Syndrome Example of compliance - ht tp:/ /www2.hawaii.edu /~yzu o/imgs/RD S.jpg  Pulmonary Surfactant: Importance 3. Keeping lungs dry Surfactant reduces the pressure gradient and helps keep lungs fluid free A collapsing fluid bubble within an alveolus exerts negative pressure on the alveolar lining Pressure creates driving force for fluid movement from interstitium onto the alveolar surface Fluid within alveolar sac would interfere with gas exchange and negatively impact lung performance LO6  Mechanics of Breathing Pump structure- Lung tissue not attached to muscles or tendons “Hermetically” sealed to the lining of the thoracic cavity Relies on pleura and pleural fluid LO7  Mechanisms of Breathing: Pump cycling Inspiration Operated by skeletal muscles Diaphragm – phrenic nerve Muscle contracts – intrathoracic volume increases Cross-sectional area of lungs increases during inspiration Contraction of external intercostal muscles LO7  Dynamic Lung Mechanics At rest lung’s volume is subject to two forces: 1. Inward Favors smaller lung volumes Elasticity Surface tension 2. Outward Elastic elements associated with the lungs favor outward movement of the chest wall Muscles and connective tissue Net Effect = create negative pressure within intrapleural space (PpI) LO8  Transpulmonary Pressure Transpulmonary pressure equals: PA - Ppl 758 - 754 = 4 mmHg Pressure around the lungs determine degree of inflation/deflation Lung expand/inflate when pressure around lung is less than atmospheric LO8  Transpulmonary Pressure & Pneumothorax Rupture or puncture of chest wall causes air to flow into pleural space (collapse lung – pneumothorax) Lung retracts to size far below residual volume LO8  Pressure-Volume Curves Studying a collapsed lung allows for understanding the effort required to inflate during normal breathing Inflation – can occur 1 or 2 ways, both modify transpulmonary pressure (PL) PL = PA – PpI LO9  Transpulmonary Pressure ▪ Pressure across the alveolar wall: TPP Alveolus (PL) = PA – PPl ▪ If TPP is positive → alveoli are open. Chest wall ▪ If TPP is 0 → no force across the TPP alveolar wall to 0 0 prevent collapse. ▪ To keep the alveoli Intrapleural space -4 Intrapleural space 0 from collapsing, the Ppl must be negative. TPP = 0 – (-4) = +4 TPP = 0 – 0 = 0 = Bad LO8 Modified from Ryan Sullivan, DO, MS  Inhalation & Exhalation Air flow Diaphragm Diaphragm 0 contracts -- relaxes ++ +4 ---- --- Intrapleural space -4 Intrapleural space ---- --- Resting State Inhalation Exhalation Just enough TPP to keep the alveoli Intrapleural pressure becomes more negative → Intrapleural pressure becomes less negative → open, but not enough to expand. makes alveolar pressure negative → air flows in makes alveolar pressure positive → air flows out (You’re creating more suction force to draw air in) (You’re creating less suction force to push air out) Air will flow into the alveoli until it equilibrates with Air will flow out of the alveoli until it equilibrates Patm → becomes 0. with Patm → becomes 0 and you are back at the resting state. LO8 Modified from Ryan Sullivan, DO, MS  Pressure-Volume Curves: Inflation LO9  Pulmonary Compliance The lungs are compliant Compliance depends on: Lung volume (distensible), elastic structures Lung size Elastic/fibrous tissue in lungs Alveolar surface tension Compliance- ease with which an object can be deformed Pulmonary compliance is  by: Measure of distensibility high lung volume Inversely related to stiffness (i.e. fibrotic disease elastance) alveolar edema ( surfactant) vascular congestion Pulmonary compliance is  by: destruction of elastic tissue (emphysema) LO8  Clinical Connection…Compliance and Pulmonary Disease http://www.tabletsmanual.com/img/wiki/copd.jpg Emphysema -  TLC, FRC and compliance lung easily distended LO9  Clinical Connection…Compliance and Pulmonary Disease Fibrosis -  TLC, FRC and compliance stiffens the lung LO9