Static Lung Mechanics-MHS F23-1.pptx

Static and dynamic Lung Mechanics Paul McDonough, PhD Resources • Costanzo, L. Physiology, chapter 5, 195-250 • Cloutier, M. Respiratory Physiology, chapter 3, 29-43 Learning objectives 1. Describe how a pressure gradient is created. 2. Define airway resistance and its measurement. 3. Discuss th...

Static and dynamic Lung Mechanics Paul McDonough, PhD Resources • Costanzo, L. Physiology, chapter 5, 195-250 • Cloutier, M. Respiratory Physiology, chapter 3, 29-43 Learning objectives 1. Describe how a pressure gradient is created. 2. Define airway resistance and its measurement. 3. Discuss three factors that contribute to or regulate airway resistance in health and disease. 4. Describe the concepts of flow limitation, the equal pressure point, and dynamic airway compression. 5. Define work of breathing and the factors that contribute to work of breathing. Muscles of breathing • Muscles of inspiration • Diaphragm • • • Accessory muscle of inspiration • • • Main muscle of ventilation Only skeletal muscle necessary for life External intercostals Scalenes and SCM Muscles of expiration • • Passive at rest Accessory muscles of expiration • • Abdominal muscles Internal intercostals Mechanics of breathing Pressures in the pulmonary system • Typically we express these relative to barometric pressure • • So, for the following: Alveolar pressure (PA) at rest is essentially barometric pressure • • So it is either 760 (absolute) or 0 (relative) mmHg Pleural pressure is always less than barometric pressure, so at rest: • 755 mmHg (absolute) or -5 cmH2O (relative) • • 1 cmH2O = 0.75 mmHg Usually, relative values are expressed Compliance of the chest wall • Relationship between the lungs and the chest wall • Obviously the intrapleural space is exaggerated here, but… • Negative pleural pressure (PPl) keeps the lung adhered to the chest wall • • • This PPl becomes more negative during inspiration to higher lung volumes • • Caused by the tendency of the rib cage to expand outward and the lung to collapse inward Essentially a vacuum pressure Needs to fight greater elastic recoil of the lung as it is stretched PPl becomes positive during expiration (and can be very positive during forced expiration) Pneumothorax • Hopefully not caused by a giant x-acto knife • Puncture wounds • • • Stabbing Broken rib Air enters the intrapleural space and PPl becomes equal to atmospheric • Lung not vacuum sealed to the chest wall • Elastic recoil now causes the lung to collapse • Chest wall expands outward Pressure-volume curves for the lungs, chest wall and combined • How we understand the interaction between the lung and the chest wall better • Here we are looking at the compliance curves for the lung, the chest wall and the combined curves • • • • Lung curve is the compliance curve during expiration Chest curve is the compliance curve for the rib cage It is looking at changes in volume for changes in pressure (which is compliance) Compliance = ∆V/∆P Combined compliance curve: expiration • Let’s start at FRC (functional residual capacity) • Resting or equilibrium point for the system • • Here • PRS = zero • For lung= translung pressure (PL) • For chest wall = Transmural pressure (PW) • Collapsing force of the lung is exactly matched by the expansion force of the chest wall If we move to a volume less that FRC (so down on the graph) • • • Reduced lung volume Reduced amount of collapsing force of the lung Increased expanding force of the chest wall • Muscular effort is the only thing keeping the chest wall from expanding • This makes the system “want” to expand Combined compliance curve: Inspiration • Now, lets look at volumes above FRC (up on the graph from FRC) • Inspiration increases volume of lungs • • • Increases the elastic recoil Chest wall recoil is much less So system wants to collapse back to FRC • Elastic recoil is unopposed by chest wall recoil here Diseases of lung compliance • Chest wall compliance really doesn’t change much with disease • The main thing that changes with disease is lung compliance • COPD (emphysema) • • • Increases lung compliance Importantly, this reduces elastic recoil pressure This allows the chest wall to expand out as there is less “opposing force” from elastic recoil • This pulls the combined lung+chest wall curve up and to the left • That is, to a higher FRC • So emphysematous people breathe from a higher lung volume Diseases of lung compliance • Conversely, in fibrosis (e.g. Cystic fibrosis) we see a decrease in lung compliance (enhanced elastic recoil) • • This is shown in the compliance curve for the lung As the chest wall is not impacted, the enhanced elastic recoil pulls the combined curve down and to the right • • Leads to a reduced FRC Hallmark of restrictive disease Surface tension • An attractive force between water molecules at air-liquid interfaces • • • Ex. Bugs walking on water High surface tension is bad in the lung where we also have an airliquid interface (capillary-alveolar membranes) Thus, we need to keep surface tension low in the lung • • • Due to the Law of Laplace P=2T/r Surfactant, produced by type 2 alveolar cells reduces surface tension and helps to keep the alveoli a uniform size Compliance • Compliance is a measure of the distensibility of a compound • Here it means a change in volume for a change in pressure • • • So, we generate changes in pressure with respiratory muscles and this causes changes in volume Compliance is a measure of how easily (high compliance) or how hard (low compliance) it is to inflate the lungs Note that the compliance curve during expiration is different for that during inspiration • This is called hysteresis • As the average slope of the compliance less for expiration, it’s compliance is less • Due to differences in surface tension Compliance • Surface tension is the attraction of water molecules for one another at the air-fluid interface • So, why are the slopes different? • Inspiration • Very high surface tension at low lung volumes • • Expiration • • Begin at high lung volume Surfactant not necessary here as elastic recoil causes the lung to deflate • Surfactant actually inhibits the process at high lung volumes • • This decreases as lung volume increases • Mostly due to surfactant which reduces surface tension Low compliance at the beginning of expiration Saline filled lung • • Eliminates the air-fluid interface Significantly reduces surface tension • Compliance is high and both curves are the same Compliance curve • Difference between lungs inflated with air and saline • Compliance is greater in saline inflated lungs • WHY? • Note also that the inflation and deflation curves are different in air breathing • More work to inflate to deflate • Suggests something in lung resists lung expansion Surfactant • In the saline filled lungs, the air-liquid interface is eliminated • Thus, something must be in the air-liquid interface that is interfering with lung inflation • • Surface tension This is the attraction of adjacent water molecules for one another • This is why small insects can walk on water Surfactant reduces surface tension • It does this by essentially replacing water molecules at the air-liquid interface • The surfactant molecules have hydrophobic tails which want to get out of the water and thus pull the surfactant molecule to the surface • This is very important for allowing the lung to function with a minimum of work • It reduces the “attraction” of water molecules for each other Effect of lung volume on surface tension • As the alveoli inflate • • The radius of the alveoli increases, increasing the distance between surfactant molecules Thus, surface tension rises as the alveoli expands • At end-expiration • The opposite ensues • • Surfactant molecules are closer Easier to expand alveoli Components of surfactant • Mostly lipids, particularly phospholipids • The principal phospholipids • Phosphatidylcholine • Dipalmitoyl phosphatidylcholine • Phospholipids • Key component of cell membranes • Amphiphilic • Both hydrophilic and lipophilic • Good for areas where we have a lipid-water interface Alveolar interdependence • This helps to stabilize the alveoli • All alveoli are surrounded by other alveoli • Except at the pleural surfaces • Thus, the collapse of one alveoli is prevented by the others • In addition, alveoli have small holes in them called • These allow collateral ventilation as well as equalizing pressure which helps to prevent collapse Airflow resistance • The volumetric flow rate Is given by the Fick equation • • • Q = ∆ P/R L/min Resistance is given by Poiseuille’s law • • R = (8ⴄl)/πr4 ∆P/∆V • Opposite of compliance . V = Q or flow Dynamic properties of the lung • When air is flowing • • • V with a dot is airflow (L/s) As always flow = Pressure/resistance A = alveolar; B = barometric So, airflow increases when the pressure gradient goes up OR airway resistance falls • • • Not only must exert force to maintain chest wall and lung volume Also, must overcome inertia and resistance of the tissues Equation 1 • • • • “Flow” This (falling resistance) is normally the case whenever we have increased airflow needs (e.g. exercise) WHY? Equation 2 • • Resistance (R) is dominated by vessel radius Normally when airflow demands increase, bronchodilation occurs Gas viscosit y Vessel length radius Airway resistance • Rearranging • Airway resistance is defined as a change in pressure for a given flow rate • So, RAW falls due to bronchodilation, which allows a higher flow rate at a given ∆P This allows us to achieve increased airflow rates without a rise in RAW • Factors that contribute to airway resistance • Resistance = Pressure/flow • In healthy individuals • • RAW is 1cmH2O/L/s Lung volume • Increasing lung volume, decreases airway resistance • • • Decreasing lung volume, increases airway resistance Airway mucus, inflammation and bronchoconstriction • • Pulls open the airways All increase airway resistance Conductance = Flow/pressure • • Explains different shapes Airflow is higher at higher lung volumes where resistance is low Neurohumoral regulation of airway resistance • Autonomic nervous system • Vagal stimulation • • Sympathetic nerve stimulation • • Decreased resistance by increased diameter Airborne irritants • • Increases resistance by reducing diameter Smoke, dust, cold air • Airway constriction (causes bronchoconstriction) • Cough reflex Allergens • • Histamine, thromboxane A2, prostaglandins F2 and various leukotrienes Increase airway resistance and cause bronchoconstriction Airway resistance across the lung • RAW = RLAW + RMAW + RSAW • • • AW = airway L, M, S = large, medium and small Poiseuille’s law • • • Written to solve for Resistance R = ∆P/V R = 8nl/πr4 • Note that the biggest effect of resistance will be changes in radius • However, resistance is LOWEST in the small airways • WHY? Cross sectional area Total crosssectional area • While the cross-sectional area of each individual tube goes down as we progress deeper in the lung • The TOTAL cross-sectional area (the summed CSA of all segments) increases • Quite a bit, several orders of magnitude Breathing cycle • Note how changes in pressure cause changes in volume • Increase lung volume-inspiration • • • Diaphragm contracts Alveolar pressure falls Intrapleural pressure becomes more negative • • To fight the greater elastic recoil at higher lung volumes Decrease lung volume-expiration • • • Diaphragm relaxes Alveolar pressure becomes positive Intrapleural pressure falls back to “resting” • Less elastic recoil at low lung volumes Pressures during the breathing cycle A. Rest • • • PA = zero (same as atmospheric) PPl = -5 cmH2O PL = 5 cmH2O • Remember • This positive pressure opposes elastic recoil and keeps the lung open B. Inspiration • • • PA = -1 cmH2O PPl = -6.5 cmH2O PL = 5.5 cmH2O • Helps keep the lung open at higher volumes and higher elastic recoil pressures Pressures during the breathing cycle C. Rest at higher lung volume • PA = zero (same as atmospheric) • • PPl = -8 cmH2O • • Greater elastic recoil PL = 8 cmH2O • D. Even though lung volume has increased This is what opposes the greater elastic recoil Expiration • • • PA = 1 cmH2O PPl = -6.5 cmH2O PL = 7.5 cmH2O • Helps keep the lung open at higher volumes and higher elastic recoil pressures Dynamic airway compression • Forced expiration in patient without lung disease • • PA = 35 cmH2O Pairway = 25 cmH2O • • PPl = 20 cmH2O • • • • This is due to alveolar pressure “bleeding off” Now moving with the chest wall which is collapsing and is positive due to the fact that the individual is “bearing down” PL = 15 cmH2O Closing pressure • Pairway – PPl = 5 cmH2O • This means the airway has a positive pressure keeping it open Forced expiration in patient with emphysema • PA = 25 cmH2O • • • • • Reduced elastic recoil reduces this Pairway = 15 cmH2O PPl = 20 cmH2O PL = 5 cmH2O Closing pressure • Pairway – PPl = -5 cmH2O • Airway closes • Only in unsupported airways