High Yield Pt5 PDF - Pulmonary Function

    Pulmonary Blood Flow  Equal to cardiac output (remember me :)) therefore flow is the same as the systemic circulation  meaning it has relatively high flow  Pulmonary blood circulation is LOW pressure and LOW resistance  Clinical Correlations:  Pulmonary Embolism  Blood clot that is...

    Pulmonary Blood Flow  Equal to cardiac output (remember me :)) therefore flow is the same as the systemic circulation  meaning it has relatively high flow  Pulmonary blood circulation is LOW pressure and LOW resistance  Clinical Correlations:  Pulmonary Embolism  Blood clot that is blocking the pulmonary artery  Obstructs blood flow to portions of the lungs  Causes a buildup of pressure in the right side of the heart and the venous system  Pulmonary Artery Hypertension  Either low NO/Prostacyclin (vasodilators) or high thromboxane/endothelin (vasoconstrictors) are causing vasoconstriction of pulmonary artery  Increases the pressure in the pulmonary circuit  Leads to congestive heart failure due to buildup of pressure in the right side of the heart  Gravity  Blood flow is greater at the base and less at the apex because gravity pulls blood down to the base of the lungs and the vessels are compliant and can take on large volumes  In addition, the base has less vascular resistance and greater transmural pressure Gravity  Blood flow is greater at the base and less at the apex because gravity pulls blood down to the base of the lungs  In addition, the base has less vascular resistance and greater transmural pressure  Zone 1: Apex of lungs ---> Pressure in alveoli is the greatest (low transmural pressure) and pressure in the pulmonary veins is lowest  Flow is more or less 0 here because pressure is alveoli is so great vessels are collapsed  Zone 2: Middle of lungs ---> pressure in pulmonary artery is greatest and pressure in pulmonary vein is lowest  This is a potentially collapsible state for the vessels where flow is equal to Pa - PA  Zone 3: Base of lungs ----> pressure is greatest in the pulmonary arteries and least in the alveoli  Flow is equal to Pa - Pv meaning that the pressure in the alveoli is too small to ever collapse the vessels and it is therefore non-collapsible There is an anatomical shunt that happens between the bronchial artery and pulmonary vein  It is normal and need for blood flow to the bronchial  Reduces amount of O2 in pulmonary vein on its way back to the heart Volume and Resistance  Extra-alveolar: as you breathe in, the intrapleural pressure decreases and the vessels widen, decreasing the resistance  Transmural pressure = PA - Ppl  Intra-alveolar: as you breathe in the alveoli expand and compress the surrounding capillaries making them smaller, increasing the resistance  Total R = Alveolar R + Extra-alveolar R    37: Lung Volumes and Pressures (Mayrovitz)  Volumes  Simple lung model: the lungs are balloons inside a plexiglass chamber.  As you breathe in the intrathoracic pressure decreases below atmospheric pressure leading to a pressure difference of -5 mmHg  Spirometer:  Measures lung volumes and capacities  Inspiration = upward deflection  Expiration = downward deflection  Total lung capacity (TLC) is the absolute maximum your lungs can hold  Vital capacity (VC) is the maximum amount of air you can breathe out  Residual volume (RV) is the air that is left in your lungs despite maximum exhalation  Inspiratory capacity (IC) is the max amount you can breathe in  Functional residual capacity (FRC) is the point at which equilibrium is achieved in that inward and outward forces are opposite but equal  Tidal Volume: amount you breathe in a normal breath  Inspiratory reserve volume (IRV) amount past normal inhale that you could take in up to max (IC)  Expiratory reserve volume (ERV) amount you could exhale past normal up to the max (VC-RV)  He Dilution Calculations  Helium Dilution  Measures FRC and RV  Spirometer is loaded with helium (usually 10%) while valve is closed. At FRC valve is opened for 5 mins until the lungs equilibrate. Then the concentration of He is measured again.  VL x FL_start + Vsp x Fsp_start = (VL + Vsp) FL_end with FL_end = FL_start  FL_start = 0  VL = 0  Vsp = 3000 mL  Fsp_start = 10%  Fsp_end 5%  (0 x 0) + (.10 x 3000) = 0.05 (FRC + 3000)  FRC = 3000  From here we can calculate RV using the formula RV = FRC ERV  ERV is measured with the spirometry (is the Vp number in this case 3 L) Body Plethysmography Calculations  Patient in air tight chamber breathing into a measuring device. Once FRC is met, the valve shutter closes.  Change in airway and box pressures are measured  P1V1 = P2V2  P in the alveoli x V at start = P in the alveoli x (FRC + change in P of the box) Pressures  At any given time there are multiple pressures:  Pressure in the alveoli  Recoil pressure = pressure trying to collapse the alveoli  Intrapleural pressure = Pressure surrounding the alveoli  Translung pressure = pressure across the lung = Palveoli Pintrapleural = Precoil   Fluid Balance  Intrapleural space = space between the visceral and parietal pleura  Has opposing forces that act on this small space  Since one is an inward force and one is an outward force results in a sub-atmospheric pressure in this space  Filtration pressure = (Pc - Pi) - σ(𝝅c - 𝝅i) ---> this is the Starling Force equation (it happens here too :))  There is just enough fluid in the pleural space for lubrication  Starling forces are normally pushing fluid towards the lymphatic drainage in the pulmonary interstitium however if they get unbalanced like in pleural effusion or alveolar flooding it messes with gas exchange  Edema of the respiratory system (same imbalances in forces as before) Alveolar flooding = fluid in alveoli ---> gas exchange cannot occur Pleural Effusion = fluid in intrapleural space ---> Can be Transudative (mostly water) or exudative (inflammatory) can also be hemothorax (blood) or empyema (pus) Interstitial edema = excess fluid in interstitium    The chest wall force is also present as an outward force expanding the lungs  Intrathoracic Pressure = pressure in the thoracic cavity  Wall recoil and lung recoil = the chest wall inward force and lung inward force  Body surface pressure = inward pressure on the chest wall from the body surface area  Transwall pressure = Pintrapleural - Pbodysurface  Total respiratory pressure = Ptw + Ptl  Palveoli = Precoil + Pintrapleural  Inspiration:  Muscles help expand the chest wall (outward force)  As your chest expands the intrathoracic pressure decreases  The pleural are pulled apart causing the intrapleural pressure to decrease  Pressure in the alveoli decreases  Air is drawn into the lung because the pressure in the alveoli is less than atm ---> high to low movement (Q = Patm - Palv) Pressures Cont.  End Expiration:  No flow condition bc Palveoli = Patm  Volume (RV) is determined by Ptl and lung compliance  End Inspiration:  Also no flow condition  Pintrapleural is now more negative  And Recoil pressure is larger, equal and opposite to intrapleural pressure  As you increase volume, the recoil force will increase!  Dynamic Inspiration:  Once the intrapleural pressure decreases the alveoli expand  The pressure in the alveoli decreases  As air enters, the pressure in the alveoli decreases less and less  Once pressure in the alveoli = Patm then inspiration has ended  Q = Patm - Palv / Rairway  Chest Wall Forces  Lung elastic forces = recoil or forces trying to collapse lung  Chest wall elastic forces = forces trying to expand lung  FRC = point where forces are equal and opposite!!  Inspiration:  Lung force increases  Chest force decreases  Thing of this as a set of springs:  The lungs alone only have their recoil or elastic force so the spring is small and closed only volume is the residual volume  The thorax alone only has the chest wall elastic forces trying to expand the wall to the spring is loose and open  Together the forces are equal and opposite and the spring is taught and halfway between the two  Clinical Correlation: Pneumothorax (air in the intrapleural space) there becomes 2 springs independent of each other  Pressure - Volume Relationship  In this graph the red line is the Chest wall recoil force and the blue line is the lung recoil force  The black line is the elastic forces together and represents the total pressure of the respiratory system  The red point in the middle represents FRC where all the forces are equal and opposite  At around 70% of the lung volume, all forces on the airway are due to the recoil pressure of the lung because the chest cannot expand anymore and is therefore at 0 stress.  Compliance is the slopes of these lines and is dependent on both the lung and the chest wall  1/C = 1/Clung + 1/Cwall  Overall C is less than either individual C  Surface Tension  Inward pressure that is reduced by the presence of surfactant  Dependent on area = as area decreases, surface tension decreases  Surfactant:  Increases compliance, reduces closure, reduces fluid transudation and alveolar capture  Respiratory Distress Syndrome  Low surfactant --> as area decreases, there is no decrease in surface tension ---> greater force collapsing the alveoli on exhalation  Once the alveoli have collapsed it takes a larger pressure/work than normal to open the alveoli for the next breath  Muller Maneuver  Forced inspiration against a closed glottis  Causes a greater negative pressure in the lungs (Palveoli is super negative)  Pressure change is more significant at lower lung volumes  Can lead to hemorrhagic danger due to high transmural pressure on blood vessels  Valsalva Maneuver  Forced expiration against a closed glottis  Causes positive pressure in the lungs (Palveoli becomes very positive) 38: Respiratory Compliance and Resistance (Mayrovitz)  Compliance  Compliance of the lung is low until you reach enough pressure to open the alveoli against surface tension ---> then compliance increases with increasing volume until a certain max threshold is met  C=V/P  Can be reduced by scarring, fibrosis, edema, or decreased surfactant  As volume increases pressure increases  The lung is doing 2 types of work  Elastic (2/3): work done to overcome elasticity (recoil forces --> open alveoli and keep it open)  Inelastic (1/3): work to overcome airway resistance and work to overcome tissue viscosity     Pressure change is more significant at higher lung volumes Can lead to alveolar rupture due to decreased venous return and high alveolar pressure Airway Resistance  Turbulent flow (remember me? I happen when the critical Reynolds number is reached)  There is some turbulence during normal quiet breathing  Resistance is greatest in upper airways  Largest values in the bronchi due to size, and branching  Resistance decreases with increasing volume  As you breathe in your airways expand --> increased diameter --> decrease resistance  Clinical Correlation:  Beta 2 agonist drugs cause bronchodilation ---> less resistance  Muscarinic (M3) drugs causes bronchoconstriction and mucus secretion ---> increases resistance  Collapsible Airways (review from cardio)  If Pinside < Poutside the airway will collapse and Q = Palveoli - Pintrapleural /R Dynamic Compression  Small airways can be compressed and are held open by:  Transmural pressure and traction (attachment)  When you breathe out forcefully the intrapleural pressure increases leading the Pi < Pe ---> collapsible!!  In a collapsible state airflow is determined by recoil pressure alone (Q = Prec / R) which remember decreases with lung volume ---> airway closes. This is normal at low volumes  In an obstructive condition however this happens at higher volumes and is abnormal   39: Mechanical Aspects of Obstructive and Restrictive Diseases (Mayrovitz)  Flow-Volume Loop  This loop shows the complete lung function, similar to P-V loops in cardio. Starting at residual volume, the patient maximally inhales to fill the lungs to their total lung capacity, then they maximally exhale to reach the residual volume again. Peak inspiratory flow rate, and peak expiratory flow rate are measured.  The tidal volume lives inside this large loop, we inspire a tidal volume using minimal energy, and exhale that tidal volume quietly back to our functional residual capacity.  The chest wall provides an outward force promoting inhalation until the lungs are at 70% their TLC, chest wall force opposes the recoil force until this point. Past 70% TLC, the chest wall is pulled inward by recoil pressure and the plural attachment to the lung.  Disease states alter the flow-volume loop  Obstructive vs restrictive lung disease  Obstructive: hard to get air out due to increased airway resistance. Can happen from inflammation, mucus plugging, bronchospasm, bronchial smooth muscle hypertrophy and hyperplasia. Increased resistance will lead to air trapping.  Examples are Chronic Bronchitis, Emphysema, Asthma Restrictive: inability to get air in due to decreased compliance. If there is fibrosis, parenchymal edema/hemorrhage, decreased nerve stimulation, or increased abdominal pressure there will be a decreased ability for the lung to expand.  Examples are PAINT: pleural effusion or fibrosis, alveolar edema/hemorrhage, interstitial lung disease or fibrosis, ALS, obesity, ascites Obstructive diseases: increased airway resistance  Chronic Bronchitis: persistent inflammation of the bronchioles, excess mucus secretion, affecting small airways, cough. Low FEV1/FVC  Emphysema: destruction of alveoli, creating air pockets in the interstitium, unable to generate recoil force due to the lack of alveolar wall, the trapped air increases residual volume of the lungs leading to barrel chest  Asthma: larger airway problem where smooth muscle constricts, and mucus is produced in response to neuromuscular (vigorous exercise) and environmental triggers (allergies). Prolonged constriction can lead to hypertrophy, hyperplasia and edema in the airway wall.  Know the differences between asthma and COPD   Obstructive Disease on the flow-volume loop  Inability to get air out due to high airway resistance decreases PEFR, air trapping will increase RV and emphysema will especially increase TLC. The tidal volume loop lives in the flow-volume loop, so FRC will increase as well.  Obstructive disease will cause slow and deep breathing to maintain alveolar ventilation. There is a larger non-elastic work, so to minimize energy spent, the respiratory rate is decreased. To maintain alveolar ventilation tidal volume increases   Restrictive Disease on flow volume loop  Inability to get air in due to low compliance and high recoil will decrease TLC, decrease RV, and since tidal volume lives in the flow volume loop it will also decrease FRC  Restrictive lung diseases will breathe rapid and shallow to maintain alveolar ventilation. There is a large elastic work, to overcome that the tidal volume is decreased. To maintain alveolar ventilation respiratory rate is increased The terms hypo and hyperventilation refer to arterial PCO2, too much CO2 shows we are hypoventilating, too little CO2 shows we are hyperventilating Uneven Alveolar Ventilation  Alveoli have uneven ventilation due to multiple factors, gravity, resistance, and compliance  The pleural space is continuous and pleural fluid will settle at the base, closer to the diaphragm, developing a fluid column. The fluid column will decrease transmural pressure in the alveoli at the base of the lung.  Decreased transmural pressure decreases recoil forces, and increases compliance in these alveoli  Increased compliance allows for better ventilation  The time constant=resistance x compliance, and varies throughout regions of the lung. High RC shows slow gas exchange times in those alveoli. Increased compliance, or increased resistance will slow the gas exchange  This is the alveolar gas equation where R is respiratory quotient, the ratio of CO2 produced to O2 consumed which is 0.8 at sea level. Fatty diets decrease this, Carb heavy diets increase this quotient 41: Gas Diffusion and Transport (Mayrovitz)  Dead Space  These are areas in the airway not participating in gas exchange.  Anatomical dead space: regions like the trachea that hold air but do not participate in gas exchange  Alveolar dead space: some alveoli do not receive the blood flow needed to perform gas exchange, in this situation these alveoli are dead space too. They are ventilated but not perfused  Physiologic dead space: anatomical + alveolar, this is the total amount of each tidal volume that does not participate in gas exchange  Peripheral gas exchange  Many buffers in the blood to maintain PO2 during low ventilation(high blood PO2 when there is low alveolar PO2), however, blood PCO2 will directly increase with increased alveolar PCO2  PO2 in the capillary drops from 95->40 as it reaches the peripheral tissues. Equilibrium is reached in the first ⅓ of the capillary length.  CO2 leaves the peripheral tissues, and is mainly turned into bicarbonate in RBCs, some CO2 binds Hb creating a carbamino compound, some CO2 directly dissolves in plasma to carbonic acid 40: Gas Pressures and Lung Ventilation (Mayrovitz)    O2 in blood  Hemoglobin can bind 4 O2 molecules  Hematocrit is the percentage of blood volume occupied by RBCs  There are 34g Hb/dl RBC  There are 1.34 mlO2 bound to each gram of Hb at 100% saturation  In arterial blood there is 20mlO2/dl blood -> arterial saturation is about 97%  Venous blood has 15mlO2/dl blood -> venous saturation is about 75% Gas partial pressures  As we inhale, our airway warms and humidifies the air we breathe as a protective mechanism for our bronchioles and alveoli. Adding water vapor to the air mixture reduces the partial pressure of O2 our trachea sees, and that PO2 decreases even more as we reach the alveoli when PCO2 increases.  Air going from environment into the airway, down to alveoli, into arteries, then veins loses PO2 at every step  160->150->102->95->40  Arterial blood has less PO2 than alveolar blood because of natural shunting of deoxygenated blood into the pulmonary vein. Bronchial arteries, pleural arteries, alveoli that get no ventilation are examples of natural shunts.  PCO2 increases once we reach capillary beds that participate in gas exchange(in lungs and peripheral tissues)  0->0->40->40->46 Alveolar Gas exchange  The PCO2 of the alveoli matches the PCO2 of the arteries, normally 40mmHg.  PCO2 in the pulmonary artery is 46mmHg. CO2 diffuses from the capillaries into the alveoli, O2 diffuses from alveoli into capillaries. CO2 and O2 are in a steady state