Pulmonary Physiology I PDF - PHYSIOLOGY

PULMONARY PHYSIOLOGY I PHYSIOLOGY (2ND Shifting) | (Dr. Razon) | (November 20, 2018) OUTLINE Upper Airway – above vocal cords I. Introduction to Respiration Lower Airwa...

PULMONARY PHYSIOLOGY I PHYSIOLOGY (2ND Shifting) | (Dr. Razon) | (November 20, 2018) OUTLINE Upper Airway – above vocal cords I. Introduction to Respiration Lower Airway – below vocal cords II. Anatomy of the Respiratory System A. Respiratory Airways UPPER AIRWAY B. Lungs  Major function of upper airway is to ―condition‖ inspired air so C. Blood Supply of the Lungs that by the time it reaches the lower airway, it is humidified and III. Zones of the Respiratory System close to body temperature A. Conducting Zone  Nose B. Respiratory Zone First passageways IV. Mechanics of Pulmonary Ventilation Offers the greatest resistance (~50%) of airflow resistance to A. Muscles For Lung Expansion And Contraction the air from the atmosphere which is a form of protective B. Pressures That Move Air In And Out Of Lungs mechanism C. Respiratory Airflow  Increased nasal resistance during viral infections and D. Phases of Breathing during increased airflow (e.g., during exercise) V. Work of Inspiration/Expiration Filters, entraps, and clears particles later than 10 μm in size A. Compliance of the Lungs Lined by respiratory epithelial cells, with interspersed B. Compliance Diagram of the Lungs secretory cells C. Determinants of Lung Compliance  Secretory cells produce important immunoglobulins, VI. Surfactant inflammatory mediators, and interferons, which are the A. Composition of Lung Surfactant first line of host defense. B. Function of Lung Surfactant When nasal respiration is not enough, oral breathing is C. Collapse Pressure of the Lungs initiated D. Alveolar Independence VII. Airway Resistance NICE TO KNOW: A. Factors that Contribute to Airway Resistance Acc. to Doc Razon, one puff of cigarate can immobilize cilla is for 6 B. Neurohormonal Regulation of Airway Resistance hours. VIII. Pulmonary Volume and Capacities IX. Alveolar Ventilation  Pharynx X. Ventilation/Perfusion Ratio common passage of air and food; inferiorly, it branches into the esophagus (food conduction) and the larynx (respiratory I. INTRODUCTION TO RESPIRATION tube)  ―When you cannot breath nothing else matters‖- American Lung Divided into three regions: the nasopharynx, oropharynx, and Association laryngopharynx  Breathing is one of the few organ systems that we are  Nasopharynx connects nose and mouth, which enables consciously aware of and can control voluntarily oral and nasal breathing Air containing O2 is transported from the atmosphere down  Soft palate separates nasopharynx and oropharynx, to the level of the lungs, O2 then perfuses to the lungs, and which ends at the epiglottis is then  Laryngopharynx begins at the epiglottis and ends at the distributed to the different tissues of the body esophagus  Epiglottis A. FUNCTIONS OF THE LUNGS Flap preventing food from entering the airways; closed when  Gas exchange – provides O2 to our body from the atmosphere food is swallowed and eliminates CO2 from our body to the atmosphere Covers vocal cords when swallowing food  Regulate blood hydrogen ion concentration - pH  Communication - Phonation (production of speech)  Larynx  Body Defense respiratory tube where the vocal cords are found.  Regulation concentration of chemical messengers - Ex.  Vocal cords Angiotensin Converting Enzyme which converts Angiotensin I to thin fold of elastic tissue responsible for phonation (vibration Angiotensin II caused by the flow of air to the lungs).  Protection from clots - structure of the lungs is like a network that sieves the clots that may be coming from the circulation; most common site for lodging of embolus in the peripheral LOWER AIRWAY circulation  Trachea cartilaginous (primarily) tube opening from the larynx branches inferiorly into two main stem bronchi II. ANATOMY OF THE RESPIRATORY SYSTEM  Bronchus  INSPIRATION: Nose or Mouth → Trachea → Right and left tube entering the lungs; paired; contains cartilage bronchi → Bronchioles → Alveoli  Bronchioles  EXPIRATION is the REVERSE non-cartilaginous tubes terminating in alveoli; supported by  Important complementary organ [not part of the respiratory smooth muscles system] is the Diaphragm 20-25 generation if branches Terminal bronchioles are the smallest airways without alveoli A. RESPIRATORY AIRWAYS  Divide into respiratory bronchioles, which signal the  Divided into two parts by the Vocal Cords (demarkation start of the respiratory zone line): S 02 // T 08 BALIZA, CAMANGON, CRUZ, GESTOPA, LUNARIO, FERRANCOL, TOLENTINO 1 of 14  BRONCIAL CIRCULATION (SYSTEMIC CIRCULATION)  Part of the left ventricular output (2% of the cardiac output is given to the bronchial circulation)  Carries blood to perfuse and supply nutrients to the cells of the lungs PULMONARY CIRCULATION  Brings partially-deoxygenated blood (less 25% O2) from the systemic circuit into the pulmonary circulation via pulmonary artery to be oxygenated; most of the output of the right ventricle  Pulmonary arteries are the only arteries to carry deoxygenated blood  Low pressure circulation (9 to 24 mmHg) Acc to Doc. Razon, lung should not provide obstruction to the blood circulation from the right heart to the left heart.  Pressures in the Pulmonary Artery Figure 1. Respiratory tract At systole: B. LUNGS  Pressure in pulmonary artery = pressure in right ventricle After pulmonary valve closes at the end of systole:  Primary organ of the respiratory system  Ventricular pressure falls  Right lung is divided into three lobes, while left is divided into  Pulmonary arterial pressure falls more slowly as blood two flow through the lung capillaries  Covered by a serous membrane (two layers of pleura)  Decreased alveolar O2 reduces local alveolar blood flow Visceral pleura and regulates pulmonary blood flow  Adhere to the lungs, intimately covering it  When O2 drops below normal, blood vessels constrict,  No sensory innervation = Not sensitive to pain increasing vascular resistance Parietal pleura  Distributes blood flow where lung aeration is better  Intimately related to the under surface of the thoracic  Note that the opposite occurs in systemic circulation cage; outer  Sensitive to pain - innervated by the intercostals and the phrenic nerves III.ZONES OF THE RESPIRATORY SYSTEM A. CONDUCTING ZONE Pleural Cavity  From trachea to terminal bronchioles  Located in between the parietal and visceral pleurae  Potential space because the two pleurae can adhere to  Functions: one another in normal conditions Provides passageway for airways  Interface between the parietal and visceral pleura allows Provides a low resistance pathway for airflow for smooth gliding as the lung expands, producing a Defense against foreign bodies potential space  Physical obstruction / retardation of unwanted particles –  Pressure within the pleural cavity is negative to facilitate cilia, mucus respiration (-4mmHg acc to Doc Razon)  Immune response – phagocytes  caused by constant suctioning effect of lymphatic Acclimatize the air breathe in – to humidify air and to make it drainage the same temperature as that of the body  According to Doc Razon, it is caused by 2 oppposing Speech forces: the elastic recoil of the lungs and chest wall elastic recoil (chest wall is moving outward against the B. RESPIRATORY ZONE atmospheric pressure)  Beyond the terminal bronchioles; from respiratory bronchioles to the level of the alveoli  Respiratory bronchiole → Alveolar Sacs → Alveoli  Function: Site for gas exchange ALVEOLI  Terminal ends of the respiratory tree.  Ground zero for gas exchange  Hollow sacs, continuous with the openings of the airways  Extensively covered by pulmonary capillaries  Blood is never deoxygenated; only 25% of O2 content of blood is used  There are around 800million alveolar sac acc. To Guyton Figure 2. Pleuras C. BLOOD SUPPLY OF THE LUNGS  The lungs have two blood supplies, one for the uptake of O2 and removal of CO2 (pulmonary circulation), and one for supplying O2 to lung tissue (bronchial circulation) PHYSIOLOGY Pulmonary Physiology I 2 of 14  Transudation of fluid (escape of fluid from pulmonary vessel into interstitium; recall Starling forces) Indicates serious pathology; the lungs are over-engineered to do its function  During exercise, we only utilize 70% of the maximal capability of our lungs CELLS IN THE ALVEOLI Figure 3. Alveoli Pulmonary Capillary Network  Largest vascular bed in the body  At any one point, has an area of 70 m2 and only 150 cc of blood circulating through the pulmonary vascular network  Most of the pulmonary capillaries are dormant; there is not enough blood to pass through them  The large area and low blood volume in the pulmonary circulation means that an increase in vascular pressure can easily be dissipated Figure 5. Two types of pneumocytes Pros: Any pathology that will lead to an increase in the  Type I Pneumocytes pulmonary pressure can be dealt with by opening dormant Covers nearly the entire alveolus capillaries 95-98% of the alveolar wall Cons: Most of the symptoms pertaining to the respiratory Contributes to the respiratory membrane system comes in late; when they show up, it is almost always Vulnerable to toxic substances (e.g., cigarette smoke) at the later stages  Causes damage to pneumocytes  Pulmonary systolic/diastolic pressure = 25/8 mmHg  Type II pneumocytes (septal cells) 2-4% of the alveolar wall Relationship Between Pulmonary Vascular Resistance and Secretes surfactants Pulmonary Arterial Pressure  Reduces surface tension to prevent alveolar collapse Can transform into type I cell to replace damaged IV. MECHANICS OF PULMONARY VENTILATION Four major components of respiration:  Pulmonary ventilation – inflow and outflow of air between the atmosphere and the lung alveoli  Diffusion of oxygen (OPHYSIOLOGY 2) and carbon dioxide (CO 2) between the alveoli and the blood LECTURE # 2.09: Pulmonary Physiology I  Transport of oxygenDATEand OF LECTURE: carbon Nov 3, 2017 dioxide in the blood and INSTRUCTOR: body fluids to and from the body’sDr.tissue Razon cells  Regulation of ventilation and other facets of respiration Figure 4. Graphical Representation of relationship between pulmonary vascular resistance and pulmonary arterial pressure  Inverse relationship between Pulmonary vascular resistance and Arterial/Venous pressure  Evidence-based data that indicates that the vast capillary network can deal with increases in pressure  ↑ Pulmonary Arterial Pressure, ↑ CO, ↓ Pulmonary Vascular Resistance  Reason: There are a lot of dormant pulmonary capillaries not participating on a moment by moment basis. Increased blood Figure 13. Forc supply will lead to recruitment of sleeping pulmonary vessels. Figure 11. Summary Figure diagram 6. General of inspiration mechanism (left) and expiration of pulmonary. (right) ventilation at Appendix, Fig A.Muscles Muscles For Lung responsible Expansion for Quiet Breathing And Contraction MECHANISMS OF PULMONARY VESSELS IN INCREASED (Refer to Figure PULMONARY PRESSURE  Lungs 1. expand and contract in two ways: External intercostals At end ins  Low to moderate increase 2.downward Diaphragm and upward movement of the diaphragm (A), wh ich  lengthen or shorten the chest cavity expand ○ Recruitment of dormant pulmonary vessels to accommodate Lungs can be expanded and contracted in two ways: At end e increased pressure 1. Normal Downward quiet breathing and upward movement of the diaphragm to interpleura Pulmonary vascular resistance elevation and lengthen anddepression shorten the chest of the ribs to increase and cavity pqe ssu q e○ decrease 2. Elevationtheandanteroposterior depression of the ribs diameter ofdecrease to increase and the chest  Moderate to high increase atmospher cavity the anteroposterior diameter of the chest cavity distension of pulmonary capillaries  Normal quiet breathing:  High to very high increase Inspiration: contraction of the diaphragm pulls the lower PHYSIOLOGY Pulmonary Physiology I 3 of 14  surfaces of the lungs downward continual suction of excess fluid into lymphatic Expiration: diaphragm relaxes channels maintains a slight suction between the  Elastic recoil of the lungs, chest wall, and visceral surface of the lung pleura and the parietal abdominal structures compresses the lungs and pleural surface of the thoracic cavity, not the lungs expels the air  NOTE: Guyton used cmH2O. 1 cmH2O = 0.73 mmHg  Heavy breathing: elastic forces are not powerful enough to Changes in Pleural Pressure during Respiration cause the necessary rapid expiration Abdominal muscles – contraction which pushes the  Pleural pressure is the pressure of the fluid in the thin abdominal contents upward against the bottom of the space between the lung pleura and the chest wall pleura diaphragm gives extra force (compresses lungs) is normally a slight suction – slightly negative pressure  Raising the rib cageFigure expands the lungs 11. Summary diagram of inspiration (left) and expiration (right) Figure −513. Forces cmH 2Othat contribute to the transpulmonary pressure (More at Appendix, Figure 3) pleural pressure at the beginning of  normal Natural resting position: ribs slant downward, sternum fall backward Muscles towardresponsible the vertebral for Quiet Breathing column inspiration (Refer to Figure 14) When rib cage1. is External elevated: intercostals  amount of suction required to hold the lungs open At end inspiration, there is a larger interpleural negative pressure 2. Diaphragm  ribs project almost directly forward, sternum (A), to whichtheir q esu l tsresting i n ah i glevel he qt qa nspu lmonaqypq essuqe○ lungs moves forward away from the spine  Normalexpandinspiration: ○ air flows expansion from atmosphereofto lungs chest cage pulls lungs Lungs can be expanded and contracted in two ways: outward At with greater force, end expiration, there isincreased lung volume a less negative by 0.5 liter (more positive)  anteroposterior thicknessand 1. Downward of upward the chest aboutof20% movement the diaphragm to greater during maximum  more interpleural negative pressure (B), which P (−7.5 cmHleads 2O) to a smaller transpulmonary lengthen andinspiration shorten the chest cavity e○ = lungs decrease in size ○ a Muscles of inspiration 2. Elevation– elevate the chest and depression of the cage are and decrease ribs to increase  ↑ lung p q e ssu volume q  pleural pressure iqflows f q om l ungst o atmosphere the anteroposterior  External intercostals – mostdiameter of the chest important; cavity others  Essentially reversed in expiration support  Sternocleidomastoid – lift upward on the sternum  Anterior serrati – lift many ribs  Scalene – lift the first two ribs. Muscles of expiration – depress the chest cage  Abdominal recti - powerful effect of pulling downward on the lower ribs - also compress the abdominal contents upward against the diaphragm with the help of other abdominal muscles  Internal intercostals Muscles for quiet breathing Figure 12. Muscles of contraction and its effects on the size of the  Externalthoracic intercostals cage. AP, Anteroposterior  Diapraghm  Ribs during expiration(Refer to are Appendix, Figure 2downward, angled for Muscles of Inspiration and the and Expiration) external intercostals are elongated forward and downward Transpulmonary Pressure  Inspiration: Contraction of external intercostals pull the upper Figure 8. Changes Figure in lung pressure 14. Pulmonary volume, and alveolar pressure, volume changes pleural during pressure, the Difference between alveolar pressure and intrapleural pressure and transpulmonary pressure during normal breathing. ribs forward in relation(Pto -Pthe) lower ribs, which causes the respiratory cycle ALV IP ribs to be raised upwardPressure that keeps the lungs partially expanded Alveolar Pressure—Air Pressure Inside the Lung Alveoli internal intercostals function pressure exactly in space the (-4opposite Negative inside pleural  When glottis V.isWORK mmHg) is a result of two openOFand INSPIRATION/EXPIRATION no air is flowing into or out of the manner – angleopposing between forces the ribs in (lung elastic the recoil and opposite chest wall elastic recoil) lungs: Work pressures of breathinginneeds all toparts of the respiratory tree up to overcome: direction and cause ○ opposite leverage Lungs are elastic organs,(expiration) and are trying to collapse inwards ○ Chest wall is trying to move outward against the atmospheric alveoli1.= PCompliance work atm (0 reference pressure in the airways, 0 cmH2O) 2. Tissue  To cause inwardresistance flow work into the alveoli during inspiration, pressure 3. Airway resistance work Keeps the lungs partially inflated alveolar P must fall to a value slightly below Patm, below 0 −1 cmH2O is enough to pull 0.5 L of air into the lungs Trans By: Gines, Vasquez, Viray in the 2 sec required for normal quiet inspiration Page 6 of 16  During expiration alveolar P rises to +1 cmH2O which forces the 0.5 L of inspired air out of the lungs during the 2-3 sec of expiration  Before inspiration and after expiration: P = 0 cmH2O Transpulmonary Pressure  Difference between Alveolar and Pleural Pressures  between that in the alveoli and that on the outer surfaces of the lungs (pleural pressure) Figure 7. Contraction and expansion of thoracic cage.  measure of recoil pressure – the elastic forces in the lungs B. Pressures That Move Air In And Out Of Lungs that tend to collapse the lungs at each instant of respiration  Pressure that keeps the lungs partially expanded/inflated  Lung is an elastic structure that collapses like a balloon and expels all its air through the trachea whenever there is no  Negative pressure inside pleural space (-4 mmHg) is a result force to keep it inflated of two opposing forces (lung elastic recoil and chest wall  Lung ―floats‖ in the thoracic cavity elastic recoil) surrounded by a thin layer of pleural fluid that Lungs are elastic organs, and are trying to collapse lubricates movement of the lungs within the cavity inwards no attachments between the lung and the walls of the Chest wall is trying to move outward against the Patm chest cage  Keeps the lungs partially inflated  except where it is suspended at its hilum from the  At end inspiration, larger interpleural negative pressure (A), mediastinum – middle section of the chest cavity which results in a higher transpulmonary pressure → lungs  Lungs are held to the thoracic wall as if glued there, except expand → air flows from atmosphere to lungs that they are well lubricated and can slide freely as the chest  At end expiration, there is a less negative (more positive) expands and contracts interpleural pressure (B), which leads to a smaller PHYSIOLOGY Pulmonary Physiology I 4 of 14  DATE OF LECTURE: Nov 3, 2017 INSTRUCTOR: Dr. Razon transpulmonary PHYSIOLOGY IV. MECHANICS pressureOF→ PULMONARY VENTILATION lungs decrease in size → air Phases of Breathing Diaphragm contracts flows from lungs to atmosphere LECTURE # 2.09: Pulmonary Physiology I Lung volume increases, therefore alveolar pressure DATE OF LECTURE: Nov 3, 2017 A.INSTRUCTOR: Respiratory Airflow C. Respiratory Airflow drops (B) Dr. Razon Movement of gasesfrom from atmosphere into lungs PALV < PATM  Movement of gases atmosphere into lungs ○ Air flows from a region of higher pressure to a region of lower Since air flows from high P to low P, air flows into the Air flowsIV.from a MECHANICS region OF of higher PULMONARY pressure to a region of VENTILATION Phases of Breathing lungs pressure. lower pressure Results from a pressure gradient between the atmosphere and the  At the end of inspiration  Resultslungs from a pressure gradient between the atmosphere A. Respiratory Airflow Pressure equalizes, airflow stops (C) and theBoyle’s lungs Law:of gases from atmosphere into lungs Movement PATM = PALV  Boyle’s Law: ○ Air flows from a region of higher pressure to a region of lower pressure. 𝑃𝑎𝑡𝑚 − 𝑃𝑎𝑙𝑣 Expiration 𝐹 = gradient between the atmosphere and the Results from a pressure lungs 𝑅  A passive process, brought about by elastic recoil of the Where: Boyle’s Law: lungs and relaxation of muscles of inspiration Where: F =FFlow  Thoracic cage is compressed (in forced expiration, this = Flowof gas of gas 𝑃𝑎𝑡𝑚 − 𝑃𝑎𝑙𝑣 Patm Patm= =Atmospheric pressure Atmospheric pressure (~760 mmHg) 𝐹 = (~760 mmHg) involves the muscles of expiration) Palv = Alveolar Pressure Palv = Alveolar Pressure 𝑅  Lung volume decreases  alveolar pressure rises (D) R =RResistance = Where: Resistance  PALV > PATM F = Flow of gas  Air flows out of lungs, equalizing pressure; airflow stops (E)  Boyle’sPatm law states = Atmospheric Boyle’s law that statespressure there (~760 that there an isinverse ismmHg) an relationship inverse between relationship betweenPalv = Alveolar pressure pressure andPressure and volume volume R = Resistance V. WORK OF INSPIRATION AND EXPIRATION  If thereIf there is no is no pressure pressure gradientgradient betweenbetween the atmosphere the atmosphere and the and thealveoli, alveoli,there Boyle’s lawwillstates there be no willflow that be ofno there air.flow is an of relationship inverse air between  Work of breathing needs to overcome: Respiration is basically the manipulation manipulation of the Figure 10. Phases of breathing and its effects on the intra-alveolar  Respiration pressure and is basically volume the of lung the volume to lung volume pressure 1. Compliance work create to create a a pressure If there pressure gradient is no pressure gradientgradient between the atmosphere and the 2. Tissue resistance work alveoli, there will be no flow of air. ○ Decreasing the pressure at the alveolus facilitates air uptake Decreasing the pressure at the alveolus Respiration is basically the manipulation of the lung volume to facilitates air Figure 10. (Refer Phases to Figure of 3. Airway breathing 10) resistance and its effects work on the intra-alveolar uptake Physics create a pressure of Boyle’s Law gradient pressure  These 3 factors resist expansion of chest  work Inspiration (Refer to Figure 10)  More negative interpleural pressure needs to be generated ○ Decreasing the pressure at the alveolus facilitates air uptake Physics of Boyle’s Constant motion Law of gas molecules → Gas molecules frequently bump of against At the start of during inspiration,inspiration as compared to expiration Physics Boyle’sone Lawanother → bumping of molecules creates  Constantpressuremotion of gas molecules  Gas moleculesInspiration○ No movement  At any in thoracic lung cagevolume, the pressure that you need to inhale is Constant motion of gas molecules → Gas molecules frequently frequently bigbump In abump against against container, theanother one frequencyone → with another whichof gas bumping bumping  creates molecules molecules bump of At the○start No airflow, of inspiration, as PATM the greater = PALVpressure (ΔP = 0) (A)that you need to afford exhalation molecules creates pressure ○ During inspiration, No movement in thoracic cage pressure against one another would be less than if they are confined in a ○ No airflow,  All as PATM the = Pexpandswork ALV (ΔP = 0) (A)we need to overcome in breathing is done  In a bigsmaller In a container. big container, container, thethefrequency frequency with withwhich gas whichmolecules molecules During○inspiration, gasbump Thoracic cage during inspiration due to contraction of the muscles for bump against against one another would be less than if they are confined in a inspiration one another would be less than if they are ○ Thoracic cage expands due to contraction of the muscles for smaller container. ○ Diaphragm contracts confined in a smaller container (bigger Vol = smaller P) inspiration “Work” of Breathing (Guyton) ○ Lung contracts ○ Diaphragm volume normal increases, therefore alveolar pressure drops (B) quiet breathing: all respiratory muscle contraction ○ Lung○ volume PALV < Pincreases, ATM therefore alveolar pressure drops (B) ○ALV PATM PALV > PATM These 3 factors resist expansion chest → work Figure 9. Visualization of Boyle’s Law Air flows out of the lungs,resistance equalizing to movement pressure; More negative airflow of air into stops (E) interpleural pressure needsthe to lungs be generated during D. Phases Phases ofOf Breathing Breathing Air flows out of the lungs, equalizing pressure; airflow stops (E) NTILATION inspiration asA.compared to expiration Compliance of the lungs At any lung volume, the pressure that you need to inhale is greater  compliance work: compliance and elasticity the pressure that you need to afford exhalation. Trans By: Gines, Vasquez, Viray  extentAlltothewhich theneed lungsPage 5 ofexpand will 16 for each unit during increase gs work we to overcome in breathing is done Trans By: Gines, Vasquez, Viray e to a region of lower in transpulmonary inspiration pressure (ifPage 5 of 16 time is allowed to enough e atmosphere and the reach equilibrium)  total compliance of A. both Lunglungs in the normal adult human Compliance averages 0.2 L of air per cmH2O transpulmonary pressure The extent to which the lungs will expand for each unit increase in transpulmonary every time transpulmonary pressure P increases 1 cmH2O, the Normal lung compliance: 200 cc/cm ofLwater lung volume will expand 0.2 afterpressure 10-20 sec  Normal○ lung If youcompliance: place 1 cm of 200 watercc/cm of lungs, on top of waterthepressure water droplet If you wouldplace 1 cm200 sink around of ccwater on top → compliant of lungs, the water lungs Figure 15. droplet would sink around 200 cc → compliant lungs shows chan ∆𝑉 pressure 𝑐𝑙 = relationship between 𝑃𝐴𝐿𝑉 − 𝑃𝐼𝑃 Where: e atmosphere and the Figure 10. Phases of breathing and corresponding alveolar pressure. Where: CL =CLung Compliance L = Lung Compliance Figure 10. Phases of breathing and its effects on the intra-alveolar 1. Tissue the lung volume to Inspiration ΔV =ΔVchange = changeinin volume volume pressure collage PALVP= Alveolar pressure ALV = Alveolar pressure  acilitates air uptakeAt the (Refer starttoof inspiration C Figure 10) PIP =PIPIntrapleural pressure = Intrapleural pressure No movement in thoracic cage In molecules frequently Inspiration No airflow, as PATM = PALV (ΔP = 0) (A) Additional info: 2. Surfac of molecules creates At the start of inspiration,  Compliance is when Compliance you stretch is when you stretch an an object objectandandremove remove the the fluid th  During inspiration ○ No movement in thoracic cage ○ No airflow, as PATM = PALV (ΔP = 0) (A) stretching force,force, stretching and and thenthen it stays it staysstretched, whileelasticity stretched, while elasticity is is space. gas molecules bump Thoracic cage expands due to contraction of the hey are confined in a During inspiration, when youwhenstretch an object, you stretch an object,and and itit resists and resists and triestries to gotoback go to S muscles for inspiration ○ Thoracic cage expands due to contraction of the muscles for th inspiration back to its itsoriginal form. original Note Note form. that, strictly that, speaking, the lungs arethe strictly speaking, not a ○ Diaphragm contracts compliant material; they exhibit elastic behavior. W PHYSIOLOGY○ LungPulmonary Physiology volume increases, I therefore alveolar pressure drops (B) However, in physiology, the term that caught on is compliance,5 of 14 m ○ PALV < PATM thus compliance is used even though elasticity is more accurate. ch ○ Since air flows from high P to low P, air flows into the lungs. o At the end of inspiration, Elasticity is a measure of stiffness, while compliance is a  lungs are not a compliant material; they exhibit elastic tension forces in the alveoli represent about two thirds behavior.  fluid-air surface tension elastic forces also increase  However, in physiology, the term that caught on is tremendously when surfactant is absent in alveolar fluid compliance, thus compliance is used even though elasticity  Lungs with lower volume are more compliant than lungs with is more accurate. higher volume  Elasticity is a measure of stiffness, while compliance is a Therefore, smaller alveoli are more compliant than measure of compliance larger alveoli A more elastic lung is harder to stretch Larger alveoli are already partially stretched, so the B. Compliance Diagram of the Lungs elastic recoil is greater, so compliance is lower Smaller alveoli have not yet been stretched as much,  relates lung volume changes to changes in pleural pressure, thus they can stretch further (higher compliance) which, in turn, alters transpulmonary pressure Small and large alveoli coexist and sometimes even More (-) pleural pressure  greater transpulmonary connected pressure  increased lung volume  relation is different for inspiration and expiration Why larger alveoli are less compliant at higher lung  each curve is recorded by changing the pleural pressure in volume? small steps and allowing the lung volume to come to a  Stretching larger alveoli require more work than smaller ones steady level between successive steps Since they are already partially stretched  two curves: inspiratory compliance curve and the Elasticity is resistance to stretch expiratory compliance curve If alveoli is already stretched, there is more force that resist further stretching When small, there is still room for stretch Compliance vs Elastance/elasticity  Elasticity is a measure of stiffness; refusal to be stretched E.g. Spring on bed (remove work, comes back to normal) More elastic lung, harder to stretch  Compliance – removing the force (stretch) won’t return it back to normal E.g. spring on notebook (remove work, stays stretched) Figure 11. Compliance diagram in a healthy person. This diagram shows changes in lung volume during changes in transpulmonary pressure (alveolar pressure minus pleural pressure). C. Determinants of Lung Compliance 1. Lung tissue elasticity Contributes 1/3/ of lung elasticity determined mainly by elastin and collagen fibers interwoven among the lung parenchyma In deflated lungs: fibers are in elastically contracted and kinked state. When lungs expand, the fibers Figure 12. Comparison of the compliance diagrams of saline-filled and become stretched and unkinked  elongating and air-filled lungs when the alveolar pressure is maintained at atmospheric exerting even more elastic force pressure (0 cm H2O) and pleural pressure is changed in order to change ↑ elasticity =  compliance less compliant the transpulmonary pressure. 2. Surface tension effect (surface tension elastic force)  Figure above shows how difficult it is to expand the lungs of the fluid that lines the inside walls of the alveoli and when there is the presence of air-water interface other lung air spaces  Air-water interface is removed through flooding with saline much more complex (No surface tension)  Surface tension: pressure generated by water Needs 2 cm H2O molecules when they are exposed to air  To expand alveolus with air-water interface (thus surface  Water, which lines inner surface of alveoli, is a tension is present), around 5 cm H2O is needed, which is bipolar molecule; the positive charges will be greater than that of the saline-flooded alveoli attracted to the negative charges, and vice versa - The attraction between the water molecules VI. SURFACTANTS causes the alveolar walls to contract as well, making the alveoli smaller Principle of Surface Tension - Makes lungs less compliant  When water forms a surface with air, the water molecules on Contributes to 2/3 of lung elasticity the surface of the water have an especially strong attraction When lungs are filled with air  interface between the for one another alveolar fluid and the air in the alveoli water surface is always attempting to contract – what  When filled with saline solution  no air-fluid holds raindrops together interface  surface tension effect is not present; water is bipolar (has + and -) thus they are always only tissue elastic forces are operative in the lung attracted to each other filled with saline solution  Inner surfaces of the alveoli: the water surface is also  transpleural pressures required to expand air-filled lungs are attempting to contract 3x as great as to expand lungs filled with saline solution force air out of the alveoli through the bronchi the tissue elastic forces tending to cause collapse of in doing so, causes the alveoli to try to collapse the air- filled lung represent only about one third of the net effect is to cause an elastic contractile force of the total lung elasticity, whereas the fluid-air surface entire lungs – surface tension elastic force PHYSIOLOGY Pulmonary Physiology I 6 of 14  INSTRUCTOR: Dr. Razon PHYSIOLOGY (Refer 16) Its Effect on LECTURE to Figureand Surfactant # 2.09: Pulmonary Physiology I Surface LECTURE: Tension Nov 3, 2017 Shows how difficult it is to DATE expandOFthe lungs when there is the  Surfactant is a surface active INSTRUCTOR: Dr. Razon presence of air-water interface agent in water greatly reduces the surface tension PHYSIOLOGYof water Air-water interface is removed through epithelial Type II pneumocytes/alveolar flooding with saline (No LECTURE # 2.09: cells Pulmonary Physiology I surface (Refer tension)to Figure special 16) surfactant-secreting DATEepithelial cellsNov 3, 2017 OF LECTURE: o Needs Shows how difficult 2 cm H2O 10% of the alveolar  constitute it is to expand the lungs surfaceDr.area INSTRUCTOR: when there is the Razon To expand presence alveolus of with air-water air-water interface interface (thus  granular, contains lipid inclusions that are secreted surface tension is inAir-water present), around interface the 5surfactant cm H 2O isinto is removed needed, through which the alveoli is floodingthan greater withthat saline of (No surface (Refer to Figure 16) tension)  stimulated the saline-flooded alveoli when stretched Shows how difficult it is to expand the lungs when there is the o Needs 2 cm H2O stretch  release surfactant  hinga ng malalim presence ofwith air-water interface To expandinto  morphs alveolus type I air-wateris interface butis removed (thus surface lessthrough effective tension is Air-water interface flooding(lose with saline (No present), around VI. 5 cm Hability)needed, Surfactants surfactant-secreting 2 O is – so which is greater take care than that of of your surface tension) the saline-flooded type I o Needs alveoli 2 cm H2O Surface active agent in water ConcentrationTodecreases expand alveoluswhen breathsinterface with air-water are small and tension is (thus surface Reducesconstant surface tension. present), around VI.5Surfactants cm H2O is needed, which is greater than that of Secreted by Type II pneumocytes/alveolar the saline-flooded alveoli epithelial cells. (10% Surface active agentofinLung water Surfactants of alveolar A. Composition surface area) Surfactant Reduces  Concentration surface tension. is decreases a complex when VI. breathsofare mixture Surfactants small and several constant phospholipids, Figure 13. Mechanism of how surfactant reduces surface tension in proteins, and Secreted ions by Type II pneumocytes/alveolar epithelial cells. (10% Figure 17. Mechanism of how alveoli. surfactant reduces surface tension in Surface active agent in water of most importantalveolar surface arearea) the tension. phospholipid dipalmitoyl alveoli C. Collapse Pressure of the Lungs Reduces surface Concentration A. Composition phosphatidylcholine, decreases Secretedof by Lung when breathsapoproteins, IISurfactants surfactant Type are small and pneumocytes/alveolar constant and cells. (10% epithelial Figure 17. Mechanism of how surfactant reduces surface tension in  Surfactants helps overcome collapse pressure brought about calcium ions of alveolar surface area) C. Collapse alveoli Complex mixture of several phospholipids, proteins, and ions (most Con