Pulmonary Physiology PDF Study Guide

PSIO441 – Unit 2 Study Guide Exam 4 will cover material from chapters 13 and 14. You should use PowerPoint slides and any notes you have taken as your primary study material. Reaching out to me, consulting the textbook and/or other online resources should be used when further or alternative explanat...

PSIO441 – Unit 2 Study Guide Exam 4 will cover material from chapters 13 and 14. You should use PowerPoint slides and any notes you have taken as your primary study material. Reaching out to me, consulting the textbook and/or other online resources should be used when further or alternative explanations are required. This study guide has been provided to act as a guide for your studying and to remind you of the main topics covered. Please do not rely solely on the topics listed here. Everything on the exam is on this study guide, but just because it is on the study guide does not mean it will be on the exam. This study guide is a comprehensive review of everything covered in this unit. Remember, the exam is 50 questions (1 pt each) and you will have 50 minutes to complete it. There are 23 questions from respiratory and 27 from renal. All questions will be multiple choice, true/false and after reading all the positive feedback on sequential order questions, there will be 2 sequential order questions: one for respiratory, one for renal. **REMEMBER REVIEW SESSION WILL BE ON SUNDAY NIGHT FROM 5-6PM IN OUR LECTURE HALL HOSTED BY PHYSIOLOGY GRADUATE STUDENTS Chapter 13 – Respiratory Pulmonary Physiology -What is respiration? What processes make it up? Respiration: sum of processes that accomplish ongoing passive movement of O2 from atmosphere to tissues to support cell metabolism and continuous passive movement of metabolically produced CO2 from tissues to the atmosphere. Cellular Respiration: intracellular metabolic processes carried out within the mitochondria which use O2 and produce CO2 while delivering energy from nutrient molecules External Respiration: entire sequence of events in the exchange of O2 and Co2 between external environment and the tissue cells. -What is the relationship between PO2 and Hb saturation? This is a proportional relationship: as PO2 increases, Hb saturation increases -What are the four steps to external respiration? 1.)Ventilation (mechanical process): movement of air into and out of the lungs 2.)Diffusion: of O2 and CO2 between air in alveoli and blood within the pulmonary capillaries 3.)Blood Transports: O2 and CO2 between lungs and tissues 4.)Diffusion: of O2 and CO2 between the tissues and blood across systemic (tissues) capillaries -Understand the difference between the tissue of the lungs vs. the airways of the lungs. Lungs are occupied in the thoracic cavity of the body. Lungs are divided into lobes which divide into segments Lobes consist of highly branched airways (tubes to bring air in), alveoli, pulmonary blood vessels, elastic connective tissue Outer Chest Wall: formed by 12 pairs of ribs and variety of skeletal muscle -Understand the anatomy of the lungs: conducting zone vs. respiratory zone, branching, bronchi vs bronchioles, alveoli Conducting Zone: ends after divisions (diameter shrinks with each branch division) No gas exchange (Dead Space: contain air, but no exchange between O2 and CO2, 150 mL of air) Trachea and Bronchi contain Cartilage (Cartilage Rings on Trachea: Give flexibility) Bronchioles: smooth muscle (no cartilage), regulate resistance (lets more or less air in) Respiratory Zone: Respiratory bronchioles to alveolar sacs (air filled sacs) Involved in gas exchange  High surface area for capillary exchange (more diffusion) -What is the mucociliary escalator? Why is it important? Where is it at? Within the conductive zone, the mucociliary escalator is a host defense mechanism that pushes mucous up and out of the system into the throat (keeps junk out) (In patients with asthma, CF, or COPD, the production and secretion of mucus is markedly upregulated) Iclicker: Are the cilia in your trachea beating up or down? - Up, a dust particle comes in and cilia pushes it back out. -What effect does surface area have on the alveoli? Within the respiratory zone, Alveoli’s main function: gas exchange Surface Area allows for the alveoli to have more options to pull from (air) Type 1 Alveolar Cells: walls of alveoli (single layer, flattened) Type 2 Alveolar Cells: Secrete pulmonary surfactant (chemical that helps keep your alveoli from collapsing) -Understand the anatomical set up of the alveoli and why its important to have capillaries nearby. Type 1 Alveolar Cells: walls of alveoli (single layer, flattened) Type 2 Alveolar Cells: Secrete pulmonary surfactant (chemical that helps keep your alveoli from collapsing) Importance of capillaries: pulmonary capillaries encircle each alveolus. Important for gas exchange of CO2 and O2 -Know the anatomical set up of the lungs, how do our different membranes interact to give us the pleural space and its corresponding relationship with thoracic wall and diaphragm. Inner to outer: 1.) The pleural sac encases the lungs 2.) Visceral Pleura: membrane that touches the lung (or organ) 3.) Parietal Pleura: outer membrane that touches the connected to the chest wall 4.) Chest (thoracic wall) 5.) Diaphragm -Know the three important pressures for ventilation: atmospheric pressure, intra-alveolar pressure and intrapleural pressure. Atmospheric Pressure: 760 mmHg at sea level Intra-Alveolar Pressure (lungs): pressure within the alveoli – 760 mmHg when equilibrated with atmospheric pressure Intrapleural Pressure (IPP) (lungs and chest interacting): pressure within the pleural sac – pressure exerted outside the lungs within the thoracic cavity, usually less than atmospheric pressure at 756 mmHg -Be able to interpret spirometry tracing and its corresponding terms. Lung volumes are direct measurements from the tracing, capacities are calculated. Tidal Volume (TV): amount of air that enters or leaves the lung in a single respiratory cycle 500 mL Functional Residual Capacity (FRC): amount of gas in the lungs at the end of a passive expiration A marker for lung compliance Inspiratory Capacity (IC): maximal volume of gas that can be inspired from FRC  Deep inhalation Inspiratory Reserve Volume (IRV): additional amount of air that can be inhaled after a normal inspiration Amount of air that you can take in additionally after a title volume Expiratory Reserve Volume (ERV): additional volume that can be expired after a passive expiration Additional air you can force out of your lungs Residual Volume (RV): maximal volume that can be expired after a maximal inspiration Air left in lungs (will never be able to completely deflate your lungs) Vital Capacity (VC): volume that can be expired after a maximal inspiration Total Lung Capacity: amount of air in the lung after a maximal inspiration Respiratory System: Static Respiratory Mechanics -Understand all of the forces that are going into static mechanics. What are isolated recoil forces? How do they interact to give us FRC? Lung recoil represents the inward force (lungs always want to collapse) Created by the elastic recoil properties of lung tissue and the alveoli As the lungs expand, recoil increases; as the lungs get smaller, recoil decreases Chest wall recoil is the outward force Chest wall always wants to expand FRC: represents the point where the outward recoil of the chest wall is counterbalanced by the inward recoil of the lung. The forces moving in the opposite direction create the negative IPP Negative IPP: no air is moving -Why is the IPP negative (sub atmospheric)? What causes it to be that way? IPP: pressure in the thin film of fluid between the visceral and parietal pleura. The outward recoil of the chest and inward recoil of the lungs create a negative IPP If the pressure of the intrapleural space (756) is greater than the intra alveolar pressure (760), the lung WILL COLLAPSE. -Understand what a transmural pressure gradient is – specifically the transpulmonary pressure gradient. What does it mean when it's positive? More positive? Negative? *remember the bulk of those numbers were given to help you understand what’s going on, it's more important to understand the relationship (ex. What does it mean when Pa > Patm...air is leaving lungs) PTM = PInside - Poutside PTM = 760 -756 = +4 (At FRC, IPP is subatmospheric, so PTM is positive) The positive outward force counters the lung elastic recoil and prevents alveolar collapse PTM = Negative = lungs are collapsed PTM = Positive = lungs are inflated (when you inspire air, PTM increase) When Pa > Patm : air is leaving the lungs -Understand the relationship between compliance and elasticity. Compliance is important for inspiration where elasticity is important for expiration. Think about blowing up a balloon. Compliance (Breathing In): how much effort is required to stretch or distend the lungs The less compliant or stiff the lungs are, the more work required to produce a given degree of inflation High Compliance = High ability to expand Low Compliance = low ability to expand Elasticity (Breathing Out): Driving force going to make it come back to original shape High elasticity: easier to deflate Low Elasticity: harder to deflate -What are the two components of elastic recoil? Which contributes more? Why is it important to have elastic recoil? What happens if elastic recoil forces are too strong? What role does surfactant play in elastic recoil? Elastic Recoil Comes from: 1.) Tissue Itself: collagen and elastic fibers of the lung 2.) Surface Tension inward forces in fluid lining the alveoli where liquid air interface Greatest component of recoil Pulmonary Surfactant decreases surface tension by separating water molecules. Prevents alveoli collapsing and maintains lung volume 3.) Collapsing forces necessary to exhale, but must be countered at the end of expiration to prevent alveoli from collapsing completely during expiration -Be able to think through what happens when there is a deficiency in surfactant. Is it hard to breathe in or out? What are the two conditions we see with surfactant deficiency? If there is a decrease of activity of pulmonary surfactant: Increase surface tension Increase lung elasticity Increase risk of edema Increase lung resistance Decrease of lung compliance (stiff) Decrease of lung volume (collapse) (Patients struggle to breathe in) 1.) Infant Respiratory Distress Syndrome (IRDS): babies are born prematurely and have not produced sufficient surfactant 2.) Adult Respiratory Distress Syndrome (ARDS): caused by airway gastric aspirations, infect surfactant production -Describe Lungs at Rest At rest or FRC, muscles are relaxed Tendency of the isolated lung is to collapse Tendency of the isolated chest wall is to expand -Inspiration is an active process meaning it requires energy. What are the four forces to overcome for Inspiration? Dynamic Force (Use ATP) To actively inflate lungs, the muscles of the chest wall must exert energy to: 1.) Overcome elastic recoil of the pulmonary System 2.) Overcome friction caused by the moving tissue (lungs and chest) rubbing against tissues Tissue Resistance 3.) Overcome friction caused by the moving air rubbing against the conducting airways Flow Resistance 4.) Overcome the forces of inertia associated with the moving tissues and the flowing air -Know the steps for inspiration and expiration. Be able to think through which muscles contract (and why) and how those muscles cause volume changes to cause pressure changes. Remember we breathe air in and out of lungs because we change pressure gradients and the air simply follows its pressure gradient. Inspiration 1.) The diaphragm via phrenic nerve and external intercostal muscles contract  Phrenic nerve: C3, C4, and C5 of the cervical region of the spine 2.) Diaphragm moves down, ribs are elevated 3.) IPP falls from 756 → 752 because more stretch and recoil from the contracting muscles 4.) Lungs expand 5.) Intrapulmonary pressure then drops from 760 → 759 and air enters the lungs Boyle’s Law: Increased Volume, decreases pressure Resting Expiration Cause: relaxation of the muscles contracted during inspiration causes elastic recoil to kick in Relaxation of the diaphragm and muscles of chest wall and the elastic recoil of the alveoli: 1.) decrease the volume of the chest cavity 2.) intrapulmonary pressure increases leading to pressure increases above atmospheric from 759 → 761: air is driven out -When does the expiration stop: when in equilibrium with atmospheric pressure (FRC), marks the end of expiration -What does it mean when the diaphragm is contracted [flattened] relaxed [dome shaped]? Diaphragm is contracted [flattened]: inspiration Diaphragm is relaxed [dome-shaped]: expiration -How do we do a forced expiration? Who is more likely to do a forced expiration? Forced Expiration Includes muscles of anterior abdominal wall (Increases intra-abdominal pressure), Internal intercostals (depress rib cage) Active during high ventilation, compensation for COPD. Also essential for coughing, sneezing, straining Emphysema (Loss of elasticity): struggle to breathe air out! (uses forced expiration) -What does parasympathetic stimulation cause in the airways? Bronchoconstriction or bronchodilation? Anything else? BronchoConstriction: parasympathetic stimulation causes increased resistance leading to closing of the airways 2-Fold Protection System: 1.) Decreased Airflow 2.) Increase in mucus production -What does sympathetic stimulation cause in the airways? Bronchoconstriction or bronchodilation? Anything else? BronchoDilation: sympathetic stimulation increases radius and decreases resistance to airflow Hormonal Control of Epinephrine -Work of Breathing (Ventilation) Normally requires 3% of total energy expenditure for quiet breathing 3 factors must be overcome for ventilation: 1.) Elastic Recoil of Chest and Lung 2.) Frictional resistance to gas flow in exchange 3.)Tissue frictional resistance -Understand alveolar ventilation and that pressure gradients are what drive gases to move. This is the diagram that walks through the exchange of oxygen between blood and tissue. Alveolar Ventilation: the process of exchanging O2 and CO2 between the alveoli of the lungs and the outside environment. INVOLVES PRESSURE GRADIENTS -Gas Partial Pressure Gas Partial Pressure: gas exchange involves simple diffusion of O2 and CO2 down partial pressure gradients Partial Pressure: pressure exerted on gas x % of gas in mixture PO2atm = 760 mmHg x 0.21 (percent of O2) = 160 mmHg Once in the body, does O2 pressure increase or decrease? - Decrease -How is partial pressure affected when there is a change in atmospheric pressure? What if there are other gases around (think about when we breathe oxygen into our trachea (water vapor) and then into our alveoli (CO2)) PO2atm = 0.21 (760 mmHg) = 160 mmHg Inspired air warmed to 37°C and completely humidified Humidifying the air reduces the parietal pressure of other gasses. The -47 below is a correction factor for water vapor: PinspiredO2: 0.21 (760-47) = 150 mmHg -As the air gets into your alveoli, PO2 is going to drop even more to what number? Why? - PO2 will drop to 100 mmHg and this is because of CO2 -PO2: Alveolar Air PAO2= 100 mmHg -Alveolar PCO2 PCO2 = 40 mmHg ^Determined By: rate of CO2 production (VCO2), rate of CO2 removal from lungs (alveolar ventilation) PACO2: VCO2/VA Can be used evaluate alveolar ventilation -Know the two abnormal breathing patterns – what they do to CO2 levels and does it make you acidotic or alkalotic? Hyperventilation: When PACO2 is lower than normal If alveolar ventilation is doubled, PACO2 is cut in half Alkalotic: blood pH is higher is normal because the lungs aren’t removing CO2 Hypoventilation: When PACO2 is higher than normal If alveolar ventilation is cut in half, PACO2 is doubled Shallow Breathing Acidotic: blood pH is lower than normal because the lungs aren’t removing CO2 -Understand why arterial blood gases reflect lung function and venous blood gases reflect tissue function. -What is hemoglobin? How much oxygen does it carry? Hb Major Role: to store O2 and influences the total amount of O2 carried in the blood Only 1.5% of O2 in plasma, important regulator 1 Hb = 4 heme groups (each bind 1 O2) Blood leaving the lungs (arteries) PaO2: 100 mmHg, Hb Saturation: 98% -Be able to think about the relationship graphed on an oxygen-Hb dissociation curve. Right shift vs. left shift. What causes it to shift? How do I know it shifted? What does an increase/decrease in the P50 represent? What are the different points on the graph (arterial vs. venous blood)? What happens when I exercise? What happens to the affinity of oxygen on Hb when it shifts? PO2 is the main factor determining Hb. Saturation Site 4: PO2 = 100 mmHg, Lungs; 98% Hb Saturation Blood leaving the lungs; highest amount of oxygen present Site 3: PO2 = 40 mmHg, Tissue, O2 dissociates; 75% sat Difference between #4 and #3 represents amount of O2 the tissue extracted from the blood (only using 25% of oxygen of the tissue is extracted out of blood) Site 2: Normal PO2 = 26 mmHg P50 = PO2 required for 50% saturation Minimum desaturation under normal conditions -Decrease in HB Saturation in Venous Blood: More active Tissue GOOD -Decrease in Hb saturation in artery blood: lung dysfunction BAD Right Shift: a reflection of the decreased affinity (ability to hold on to something) of Hb in O2 Represents enhanced oxygen release from Hb to tissues under metabolic demand Are we releasing more or less oxygen with the blue curve? - a right shift means more O2 is released in the blood to be utilized by the tissues Are we releasing more or less oxygen with the green curve? - A left shift curve means that oxygen is staying in blood Normal Oxygen Release:Hb-75% saturated which means 25% was offloaded to tissue Enhanced Oxygen Release: Hb-55% saturated which means 45% was offloaded to tissue -What are the three ways that CO2 is transported in the blood? 1.) Dissolved in plasma: 5%, PaCO2 2.) Carbamino compounds: 5% 3.) Bicarbonate: 90% of CO2 is carried as plasma bicarbonate -What happens to Co2 when it gets into a RBC? What does that H+ ion cause? When CO2 gets into a RBC, it is converted to bicarbonate to be diffused into the blood. The H+ ion causes Hb to release oxygen. -What is the Bohr effect? Haldane effect? Bohr Effect: Binding of H+ to Hb to release oxygen Graphed as a right shift On average, body releases 25% total oxygen content for use by tissues (4 → 3) CO2 into tissue, O2 out of tissue Takes place in your tissues Haldane Effect: ability of deoxygenated blood to carry more CO2 than oxygenated blood Binding of O2 with Hb in the lungs promotes dissociation of CO2 from blood O2 into, CO2 out of Takes place in your lungs -What is the DRG? What does it control? DRG: Inspiratory Center of neural control regulation Controls Diaphragm -What are central chemoreceptors? What do they respond to? Where are they located? When are they stimulated (1st or 2nd)? Are they strong or weak? Do they adapt? Central Chemoreceptors : Located in the brain and respond to CO2, stimulated 2nd Actively increase ventilation Stimulated by changes is CSF pH via CO2 Main Drive (initial trigger) for ventilation is CO2 (H+) on the central chemoreceptors ^system ADAPTS within 12-24 hrs Produce significant increase in ventilation with hypercapnia (elevated CO2) There are no central PO2 receptors - What are peripheral chemoreceptors? What do they respond to? Where are they located? When are they stimulated (1st or 2nd)? Are they strong or weak? Do they adapt? Peripheral Chemoreceptors: O2, CO2, H+, Stimulated 1st in changes in arterial CO2 levels Carotid Bodies: near carotid sinus, afferents to CNS in glossopharyngeal nerve (IX) Aortic Bodies: near aortic arch, afferents to CNS in vagus nerve (X) Monitors CO2 and pH of arterial blood: Less sensitive than central, small contribution to normal drive.  Increases firing as PaO2 falls below 80 mmHg and becomes marked and progressive when PaO2 is less than 60 mmHg -What type of chemoreceptor is stimulated last (when O2 Levels have dropped below 60 mmHg)? -know the four types of hypoxia and just the general definition/cause of each. When O2 levels have dropped below 60 mmHg, stimulation of peripheral chemoreceptor -What’s different at altitude? What happens to our PaO2? How does our body respond? Altitude Stress → Abnormal Air Composition: symptoms occurs when atmospheric pressure falls to around 520mmHg If I drop you on the summit of Mount Everest, what is the 1st thing your body does? - hyperventilate because PaO2 dropped below 60 stimulated peripheral chemoreceptors -What happens during acclimatization? increase hematocrit = increase in RBCs = polycythemia Physiological Adjustments: 1.) Increase Ventilation (blow off CO2): peripheral chemoreceptors due to low arterial O2 2.) Increase Hematocrit: due to EPO, increase oxygen carrying capacity in blood EPO: kidney, PRO that tells you to make more RBCs -What is altered when someone has polycythemia/anemia? Lungs are fine, the number of RBCs is different so the total O2 content changes. No change in the P50, graph is not shifted Anemia: reduction in Hb concentration Polycythemia: higher than normal Hb concentration (more RBC) (Your lungs are fine. You have the right amount of O2 in your plasma and the right amount of O2 bound to Hb. You just have more or less RBCs = more or less Hb overall) -What happens with CO poisoning? Which way is the graph shifted? What happens to the P50? Affinity for oxygen? Carbon monoxide binds with Hb → carboxyhemoglobin (COHb) CO poisoning makes Hb affinity for CO be 200x more than for O2, so small amounts of CO tie up large amounts of Hb Co decreases functional concentration of Hb; form of acute-onset anemia (reduced arterial O2 content) What causes Hb to hold to oxygen and not to release it? - Carbon monoxide (very hard to release O2) Condition worsens because Hb-O2 dissociation curve shifts to the left, P50 is decreased, unloading of O2 is hindered Common Symptoms: Headache, nausea and vomiting, dizziness, lethargy and a feeling of weakness Numbers to know: Patm = 760 mm Hg, O2 Air composition = 21%, PO2 = 80-100 mm Hg, Hb saturation = 95-100% Total oxygen content = 20 mL oxygen/ 100mL of blood (20% volume) PAO2 = 100 mm Hg