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Breakdown of Topics in Respiratory Physiology: Ventilation, Gas Exchange, Control of Respiration Respiratory Physiology 1 Functions of the Respiratory System • • • • Respiration Acid-base balance Enabling vocalization Defense against pathogens and foreign particles • Route for water and heat losses 2 General Concepts of Respiration • Ventilate: bring the oxygen to the blood • Gas exchange: diffusion of gasses from alveoli into blood; then gasses go to/from erythrocytes; to /from Hemoglobin • O2 utilization: Mitochondria need the oxygen to break glucose down into ATP (cellular respiration) 3 Ventilation • Ventilation is the process of bringing air into and out of the lungs. • The alveoli in the lungs are the only organs that do not have smooth muscle in them. They are just elastic tissue. • The lungs cannot inflate on their own. They need to be tethered to muscles in order to get volume changes, which causes pressure changes, which regulate air flow. • There are pressure gradients from the partial pressures of gasses. If the partial pressure of a gas is increased, the concentration of that gas increases, too. • Your lungs also contain millions of macrophages, so they are a good line of defense against pathogens. They also get rid of the dust and other debris that accumulates in the lungs. • They are also a route of heat and water loss. When you exhale, you lose water vapor and heat. 90% of the heat lost from your body is from exhaling. 4 Gas Exchange • In the lungs, oxygen moves into the blood, driven by pressure gradients, which are similar to concentration gradients. • Oxygen will diffuse down its concentration gradient (from the lungs, into the plasma, and into the cells) while CO2 moves down its concentration gradient (from the cells, into the plasma, and into the lungs). • These two gas exchanges are called external respiration. 5 Oxygen Utilization • When oxygen enters the cells, some of it enters the mitochondria, which uses oxygen as an electron acceptor (the mitochondria places hydrogen ions on the oxygen and turns it into water). This excess water leaves the cell and enters the tissues. • The removal of oxygen from the plasma and the addition of water in the tissues creates a driving force (known as the Starling principle) to continuously draw oxygen into the tissues, since the water in the tissues has diluted the number of particles there, and oxygen, as a particle, will be sucked into the tissues. • The gas exchange that occurs at the tissue capillary beds is called internal respiration. • The actual use of oxygen as a final electron acceptor(during a process called oxidative phosphorylation) is called cellular respiration. 6 General Concepts: Airway Anatomy Surface area 70 sq meters- each lung (size of a large lecture hall)! Barrier/ thickness to diffusion 0.2 microns 7 Carbon Monoxide • This is an odorless, colorless gas from incomplete burning of fuels. • Carbon monoxide binds to hemoglobin 200x more strongly than oxygen, so it drives the O2 from the hemoglobin, and attaches in its place and stays there. Carbon monoxide decreases the amount of oxygen that can be transported by hemoglobin • The person dies from suffocation; it makes the lips cherry red. • Cyanide poisoning kills in the same way, but the lips are blue (cyanosis). 8 CO2 Transport • When oxygen is on the hemoglobin molecule, it is called oxyhemoglobin. • Dissociation of oxyhemoglobin is when the oxygen is released and enters the tissues. • This dissociation increases as the pCO2 levels increase. • In other words, when the carbon dioxide levels rise, oxygen will jump off the hemoglobin and into the tissues. Therefore, the most effective stimulus to the respiratory center is an increase in pCO2. • The waste product of cellular respiration is carbon dioxide. • CO2 will then attach onto the hemoglobin and be taken 9 to the lungs to be expelled. CO2 Transport • CO2 is carried to the lungs on the hemoglobin, after the oxygen has left to enter the tissues. • The carbon dioxide reacts with water in the RBC to form carbonic acid, which then breaks apart into a hydrogen ion (which lowers blood pH) and a bicarbonate ion (which raises blood pH). CO2 + H2O H2CO3 H+ + HCO3This reaction is reversible, and would go mainly to the right in the tissues and to the left in the lungs. CO2 is transported in the blood predominately in the form of bicarbonate. The number of H+ ions in the blood depends partly on the amount of CO2 in the blood. The more CO2 in the blood, the more H+ in the blood, which makes the blood acidic. If the blood is too acidic, more bicarbonate ions are reabsorbed by the kidneys to raise the pH. If the blood is too alkaline, bicarbonate ions are excreted by the kidneys. 10 CO2 Transport • CO2 carried by the blood is in these proportions: • 85% is in the form of carbonic acid in the erythrocytes • 10% is attached to hemoglobin • 5% is dissolved in plasma 11 Respiratory System Contribution to pH Balance in the Blood • If a person has excess H+ ions in the blood (acidosis), they will breathe more rapidly to blow off the CO2. • If the person has an airway obstruction (such as asthma), they cannot exhale the excess CO2. • Because the H+ are building up, the carbonic acid will also build up, causing a drop in pH (acidosis) in the blood. • Enzymes in the body cannot work outside of their optimal pH range, so chemical reactions come to a halt. • Hyperventilation results in too little CO2 in the blood, so the person has a high pH (alkalosis), which also denatures enzymes. 12 Control of Respiration • Changes in lung volume, and thus ventilation, are dependent upon the change in thoracic cavity volume. • Alterations in the space inside the thoracic cavity are the result mainly of the contraction of the diaphragm, intercostal muscles. • These muscles are innervated by neurons in the respiratory centers of the brain stem (medulla and pons). 13 Respiratory Centers: Medulla oblongata and Pons • Pons (Pneumotaxic Center) – decreases respiratory rate • Medulla – Dorsal respiratory group • Increases inspiration rate – Ventral Respiratory Group • Inactive during quiet respiration • Active during forced respiration Figure 41-1; Guyton & Hall 14 Chemoreceptors • Carbon Dioxide, Hydrogen Ions – Central chemosensitive area of medulla; senses levels of CO2 and H+ in CSF (both are acids) • Oxygen – Peripheral chemoreceptors; sense oxygen levels in blood • Aortic chemoreceptors (CN X) • Carotid chemoreceptors (CN IX) 15 Respiratory Chemoreceptors • In the cardiovascular lecture, we learned about baroreceptors detecting blood pressure in the aortic arch and carotid sinus. • The respiratory system has chemoreceptors in those areas, too. They function to detect the O2 levels of the blood. • The medulla oblongata also has chemoreceptors that monitor pH. This information is sent to the other parts of the respiratory centers (pons and other areas in the medulla oblongata) to allow them to alter breathing rate to maintain proper blood pH. 16 Control of Respiration • Relaxed breathing only requires the diaphragm to contract for inspiration, and for the diaphragm to relax for expiration. • Forced breathing requires the diaphragm plus muscles that raise and lower the ribs (external intercostals for inspiration, internal intercostals for expiration). • The respiratory centers are most sensitive to the level of CO2 in the blood, rather than the levels of oxygen. 17 Control of Gas at Cellular Level • The flow of blood through capillaries is controlled by sphincters on the arterioles and capillary beds to adjust the amount of blood flowing to particular tissues. • Cells and tissues that are undergoing increased aerobic activity have less oxygen and more CO2, lower pH, and increased temperature. • When CO2 levels in the tissues are too high, the smooth muscle sphincters relax to allow more blood flow to increase gas exchange. 18 Ventilation Inspiration (inhalation) Expiration (exhalation) Normal inhalation, normal exhalation Forced inhalation, forced exhalation Concepts: 1. Pressure gradient created by volume changes (Boyle’s Law) 2. Anatomy of lung and chest wall 19 Inhalation and Exhalation vs. Force • Ventilation requires ATP during inhalation, but normal exhalation does not require ATP. • Some people with respiratory problems need to work at exhalation as well by using skeletal muscle, and this means that they need to use more ATP. Lungs are not muscular structures. They need the skeletal muscles in the thoracic cage to change the thoracic volume, which changes the pressure gradients. • Air flows from high pressure to low pressure. 20 Boyle's Law P1V1=P2V2 • Pressure and volume are inversely related (if other variables are kept constant.) Boyle’s Law assumes normal circumstances, not a person who is in high altitude or who has variation in body temperature. 21 Air Pressure in Lungs • Every time a molecule strikes the wall of a container, it causes pressure. In a larger container with fewer molecules, it takes a while to strike the wall randomly, so there is less pressure. • The number of impacts on a container wall is the pressure. • The lungs must have a volume change to create a pressure change, which is required to have air move into and out of the lungs. 22 Air Pressure in Lungs • The diaphragm is the muscle that mostly contributes to the volume change. When it contracts, it pulls downward, and the volume of the thoracic cavity increases. • The external intercostals elevates the ribcage, giving the lungs more room, so they also increase the lung volume. • Those two muscles cause increased volume. 23 Air Pressure in Lungs • Because the lungs are tethered to the thoracic cavity, when your chest wall expands, your lungs expand with it. The lungs are stuck to the chest wall because the serous fluid in the pleural cavity makes the lungs stick to the chest wall like two pieces of wet glass stuck together. • When the lungs expand, their volume expands. That means there is less pressure in the lungs than there is in the outside air. Since air moves from high to low pressure, air flows into the lungs. • As air flows in, the alveoli expand, so the volume in each air sac expands, so the pressure in the alveoli lowers. Air in the conducting passages (bronchi) is at higher pressure, so it will move from high to low pressure areas. Therefore, air will move into the alveoli. 24 Air Pressure in Lungs • Air has weight; atmospheric pressure is 760 mmHg at sea level (much less weight and pressure at high altitudes). • Since air will flow from higher pressure to lower pressure areas, to get the air to flow into our lungs, we need to have a lower pressure in our lungs. • We can decrease the pressure in our lungs by expanding the volume. As we expand the volume of our thoracic cavity (taking a breath), the pressure in the lungs drops, and air flows into the lungs. • It is a small pressure difference, but it is enough to get 500 ml of air to come into your lungs. • At higher altitudes, even though the amount of oxygen is the same (21%) there is less air pressure. At 8,000 feet in elevation, there is ¼ less pressure. This makes it harder to breathe. • When you exhale, you simply relax the muscles, and if the lungs are not being pulled open any more, the elastic tissue there will recoil, making the lung volume smaller, so the pressure there increases. 25 Lung Compliance • Lung Compliance is how much the lung volume changes when the pressure changes. • Compliance can be considered the opposite of stiffness. • A low lung compliance (increase in stiffness) would mean that the lungs would need a greater than average change in pressure to change the volume of the lungs. Instead of needing only 10 mmHg pressure difference between the outside air and the lungs, would now need a 20 mm difference. • A high lung compliance would indicate that little pressure difference is needed to change the volume of the lungs. • More energy is required to breathe in a person with low lung compliance. Persons with low lung compliance due to disease therefore tend to take shallow breaths and breathe more frequently. 26 Gases move down pressure gradients Flow Rule: P atm = 760 torr How are the pressure gradients changed? Patm – Palv Resistance p alveolar = 758 torr Air moves from high to low pressure According to Boyle’s law we will need to create volume changes! PROBLEM! THE LUNGS ARE NOT MUSCULAR STRUCTURES! 27 Air Pressure in Lungs • We are looking at two types of air pressures: atmospheric pressure, and the pressure of air deep in the lungs, called the alveolar (pulmonary) pressure. • As long as there is a difference in pressure between these two, there will be a pressure gradient, and air will flow. • If they equal each other (such as during a punctured lung, called a pneumothorax), air will not flow. 28 Air Pressure in Lungs • Take a breath in and stop. Enough air has come in now so that the air pressure in the alveoli equals the atmosphere, so you no longer get more air flowing in. • When you relax, the lungs recoil, air comes out, and when the two pressures equal each other, air stops flowing out. • You will get zero pressure differences upon maximum inhalation and exhalation. 29 Oxygen-Hemoglobin • Each hemoglobin protein can bind to four oxygen molecules. • After the first O2 molecule binds to the iron, the Hb molecule changes shape. • As a result, it more readily takes up two more O2 molecules, and uptake of the fourth is even more facilitated. 30 Hemoglobin • When 1-3 molecules of O2 are bound, the Hb is considered partially saturated. When all four O2 molecules are bound, it is fully saturated. • Unloading of one O2 molecule enhances the unloading of the next, and so on. In this way, the affinity (binding strength) of the Hb for oxygen changes with the extent of oxygen saturation. 31 • Under normal resting conditions, arterial blood Hb is 98% saturated. • As the blood travels to the capillaries, it releases some O2 and Hb saturation decreases to 75%. • There is still a substantial amount of O2 available in the venous blood which can be used if needed. • This is called the venous reserve. 32 33 34 35 Oxygen-Hemoglobin Shifts • The rate at which Hb binds to O2 or releases O2 is regulated by pO2, temperature, blood pH, pCO2. • An increase in temperature, pCO2, or acidity will modify the 3D structure of hemoglobin, which lowers Hb’s affinity for O2, which will enhance oxygen unloading from the Hb into the blood. • This results in a right shift of the oxy-Hb dissociation curve. • Conversely, a decrease in any of these factors increases Hb’s affinity for oxygen, which decreases oxygen unloading, resulting is a left shift. 36 Oxygen-Hemoglobin Shifts 37 Bohr Effect • Temperature, pCO2, and acidity all tend to be highest in the capillaries, where oxygen unloading is the goal. As cells metabolize glucose and use oxygen, they release CO2, which increases the pCO2 and H+ levels in capillary blood. These conditions weaken the Hb-O2 bond, a phenomenon called the Bohr effect. This enhances oxygen unloading where it is most needed. • Additionally, heat is a by-product of metabolic activity, and active tissues are warmer. The rise in temperature will also cause Hb to unload more O2 to those tissues. 38 Oxygen-Hbg Dissociation Curve • This graph demonstrates that 75% of Hbg is still saturated when pO2 is only 70 mm (when it first arrives in the tissues). • When pO2 reaches 100mm (in the lungs), Hbg becomes 100% saturated. 39 Left shift Oxygen is kept on the Hb CAUSE: Decreased acidity Decreased CO2 Decreased Temperature “Left out in the cold with baking soda” 40 Right shift Oxygen is unloaded from Hb CAUSE: Increased acidity Increased CO2 Increased temperature 41 Shifts • A left shift will increase oxygen's affinity for hemoglobin. – In a left shift condition (alkalosis or hypothermia) oxygen will have a higher affinity for hemoglobin (it won’t leave!). – This can result in tissue hypoxia even when there is sufficient oxygen in the blood. • A right shift decreases oxygen's affinity for hemoglobin. – In a right shift (acidosis or fever) oxygen has a lower affinity for hemoglobin. Blood will release oxygen more readily. – This means more O2 will be released to the cells, but it also means less oxygen will be carried from the 42 lungs in the first place. Vacuum in Lungs • There is another anatomical structure you need to remember: the plural cavity. Each lung is surrounded by a parietal and visceral serousal membrane. • The serousal cells make a lubricating fluid so the lungs don’t rub against the thoracic cavity, causing heat generation, which can denature proteins. • This fluid has cohesive properties. If you put two pieces of wet glass together, you have to use more force to pull them apart than if they were 43 dry. You have to break the vacuum. Vacuum in Lungs • The surface of the lungs are tightly stuck to the surface of the thoracic wall. • If they are disengaged, they will recoil like deflated balloons. • If the vacuum in the pleural cavity is broken, the lung will collapse. • They need to be reinflated by the administration of oxygen. 44 Mechanics of Ventilation • Normal Inspiration • Is an active process (It’s work! It uses ATP) – Contract Diaphragm and it moves inferiorly to increase thoracic volume -60-75% of volume change – Contract external intercostals Forced Inspiration Accessory muscles needed Sternocleidomastoid Scalenes Serratus anterior Others (erector spinae) Diaphragm When the chest wall moves, so do the lungs! Why are the lungs right up against the chest wall? Pleural Space or Cavity 1. a vacuum (contains no air) 2. pleural fluid (water) has surface tension Result? Lung moves with the chest wall Lungs are not muscular organs, they cannot actively move. They move with the chest wall. 46 What happens if the lung dissociates from the chest wall? • • • Pneumothorax: air in the pleural cavity Hemothorax: blood in the pleural cavity How? – Injury (Gun shot, stabbing) – Spontaneous (tissue erosion, disease lung) – Bleeding wound • • Chest wall recoils outward (barrel chest) Lung recoils inward (atelectasis = alveolar, lung collapse) 47 Mechanics of Ventilation • Normal Expiration- • A Passive process • Simply relax the muscles of inspiration • Rely on the elastic properties of lung (like a balloon deflating on its own) • Forced Expiration • Relax muscles of inhalation AND • Contract internal intercostals • Contract Abdominal muscles • Internal and external obliques • Transverse abdominis • Rectus abdominis 48 Emphysema • COPD (chronic obstructive pulmonary disease) is emphysema plus chronic bronchitis. • Emphysema is generally caused by smoking. • The alveoli have broken, leaving spaces where gas exchange cannot take place. • Compliance decreases, so It is difficult to expel the air in the lungs. • Each inhalation is a forced inspiration also. • When the ribs are continually raised with each breath, they eventually remain in the upright position, causing a barrel chest. 49 Exhalation Problem: COPD • Normal exhalation is passive, requires no ATP. But forced expiration (such as emphysema patient) recruits abdominal muscles. The muscles enlarge with time, creating a barrelshaped chest, typical of emphysema patients and COPD. 50 COPD • In everyone, the midsized bronchioles do not have cartilage rings to hold them open, and during exhalation, the sides of the bronchioles collapse and touch each other. • If there is not enough surfactant, they stick to each other with greater strength (like two wet pieces of glass), and the person has to forcefully exhale with each breath to overcome the cohesiveness of the fluid. • Surfactant is like adding soap to the fluid so the surfaces come apart easier. 51 Exhalation • Giving oxygen in high concentration helps get air into their lungs, but it reduces the drive for them to breathe. CO2 is a powerful driving force for ventilation. When a person has COPD and is on an oxygen tank, they have less CO2, and oxygen becomes the driving force. • If we give them oxygen, the drive for them to breathe becomes diminished. They eventually wind up on a positive pressure ventilator, but the disease progresses, and they die from suffocation. • A continuous positive airway pressure machine is called a CPAP machine. 52 CPAP Machine 53 Both the Lung and Chest Wall are Elastic • Both lung and chest wall have the tendency to recoil • What is recoil? Tendency to snap back to resting position (like a stretched rubber band recoils when you let go of one end) The chest wall recoils outward (springs out) The lung recoils inward (ie. it collapses!) 54 Palv (mmHg) • Increase in lung volume decreases intra-alveolar pressure (we now have a pressure gradient) = air goes in. • Decrease in lung volume raises intra-alveolar pressure above atmosphere = air goes out. expiration inspiration Palv=0 Palv=+1 Palv=0 Palv=0 Breath vol. (L) Palv= -1 0.5 When the pressure at the alveoli are at 0 (no difference between their pressure and atmospheric pressure), no air flows in or out of the lungs. Pressures Patm and Palv create the pressure gradient that drives ventilation Atmospheric Pressures (Patm)- pressure of the outside air (760mmHg=760 torr = 1 atm). Intra-alveolar pressure (Palv) pressure within the alveoli of the lungs. Equal to Patm (0mmHg) at rest, but varies during phases of ventilation. Intra-pleural pressure – (Pip) pressure in the intra-pleural space. • Pressure is negative because of the lack of air in the intrapleural space, lymph drainage, and opposing forces of lung and chest wall. 56 Air Flow • If atmospheric pressure is greater than alveolar pressure, air flows into the lungs. • If atmospheric pressure is less than alveolar pressure, air flows out of the lungs. • Transpulmonary pressure is the difference between the alveolar and intra-pleural pressures. 57 Positive vs. Negative Pressure Breathing P atm = 760 torr • • • • Normally, the pressure gradient is produced by changing palv Positive Air moves from high Pressure to low pressure breathing This is called negative pressure breathing If one changes patm, then this is positive pressure breathing Ex. bag, cpr, mouth to mouth p alveolar = 758 torr Is this positive or negative pressure breathing? Negative Pressure breathing 58 18 Iron Lung • This chamber is an iron lung, invented for polio patients, whose respiratory nerves were paralyzed. When we are normally breathing, we are changing thoracic volume, so we are using negative pressure breathing. But a paralyzed person cannot move their respiratory muscles. • It works like a reversible vacuum. There is less air pressure in the tank, so there is less pressure on the chest, to help get air out. The vacuum then reverses, air is pumped into the machine, which increases pressure on the chest, air flows in. 59 Acute Mountain Sickness (Altitude Sickness) • When you visit someone in a high elevation (5,000 m) you might get acute mountain sickness. • Symptoms: – Severe headache, fatigue, dizziness, palpitation and nausea. • Cause: – Pulmonary edema. • Why do you get pulmonary edema? – High elevations have lower pO2 levels. – This causes hypoxia (lack of oxygen) in the pulmonary capillaries – This causes increased pulmonary arterial and capillary pressures (pulmonary hypertension) – That causes the pulmonary edema 60 Respiratory Cycle 61 Ventilation Volume • When you breathe in, you inhale about 500 ml. You exhale about 500 ml. Therefore, 500 ml is your TIDAL VOLUME. • Not all 500 ml gets down deep to your alveoli. About 150 ml of it stays in the conductive zone (bronchi and trachea). About 350 ml reaches the alveoli. That is considered your alveolar ventilation volume. • That is the amount of air that can undergo gas exchange. If you want to calculate how much air moves in and out per minute, take the tidal volume and multiply it by breathing rate (about 12 breaths per minute for adult, 20 for children). 500 x 12 = total ventilation Tidal volume – 150 x 12 = alveolar ventilation 62 Lung function tests • • • Spirometry – Static lung tests • Volumes and capacities • No element of time involved, ie. How long does it take you to push the air out? Normal expiration takes 2-3 x longer than inspiration • Lung volumes are assessed by spirometry. Subject breathes into a closed system in which air is trapped within a bell floating in H20. The bell moves up when the subject exhales and down when the subject inhales. – Dynamic lung tests • Time element, rate of exhale • How much, how quickly? 63 Spirometry measures lung volumes • Such things as the tidal volume, vital capacity, and expiratory capacity volume can be measured directly with a spirometer. • Most air (80%) is exhaled during the first second of exhalation. You take a maximum inhale, then a maximum exhale (vital capacity). The pen moves down the paper, showing time. • You can calculate how much air you blew out (vital capacity), and the amount of air you blew out in one second (expiratory capacity volume in one second). • Expiratory capacity volume in one second, divided by vital capacity should be 80%. If you are less than 80%, it is suggestive of an obstructive or restrictive pulmonary disorder. To tell which one, look at Vital Capacity. If it is normal, it is obstructive. If it is low, they have restrictive lung disease. 64 EC EC/VC =80% VC EC EC/VC =47% VC Dynamic Lung Tests Someone with COPD takes longer than one second to exhale 80%. 65 COPD Severity 66 Obstructive Lung Diseases • Obstructive lung diseases are characterized by inflamed and easily collapsible airways, obstruction to airflow, and frequent hospitalizations. • Examples – Asthma – Chronic obstructive pulmonary disease (COPD) • Bronchitis • Emphysema 67 Restrictive Lung Diseases • These are extrapulmonary or pleural respiratory diseases that restrict lung expansion, resulting in a decreased lung volume (rapid, shallow breathing), an increased work of breathing, and inadequate ventilation and/or oxygenation. Decreased vital capacity. – – – – Cystic Fibrosis Infant Respiratory Distress Syndrome Weak respiratory muscles Pneumothorax 68 Capacities are two or more volumes added together These are measured with a spirometer This is estimated, based on height and age These are calculated FRC = ERV + RV TLC = RV + ERV + TV + IRV 69 Capacities are two or more volumes added together These are measured with a spirometer This is estimated, based on height and age These are calculated FRC = ERV + RV TLC = RV + ERV + TV + IRV 70 Capacities are two or more volumes added together 71 Quiz yourself (what the test will look like) 1 3 8 9 10 4 5 7 2 6 72 Quiz yourself (color version) 1 3 8 9 10 4 5 7 2 6 73 You don’t need to memorize the normal numbers, just the definitions • • Respiratory Cycle: A single cycle of inhalation and exhalation Respiratory rate (RR): number of breaths per minute (usually about 12-18; children higher 18-20). • • • • Tidal Volume (TV): normal breath in and out. Usually about 500 ml. Inspiratory Reserve Volume (IRV): take in a normal breath, stop, now inhale as much more as you can. In other words, this is the amount of air that can be forcefully inhaled after a normal inhalation. ERV = Expiratory Reserve Volume (Expiratory capacity): take a normal breath in, a normal breath out, then breathe out the most you can. In other words, this is the amount of air that can be forcefully exhaled after a normal exhalation. This is the air needed to perform the Heimlich maneuver. The maneuver decreases the thoracic cavity volume, causing increased pressure in lungs. That causes forced air with high pressure to be expelled from the lungs. Residual volume (RV): The amount of air left in your lungs after you exhale maximally. This air helps to keep the alveoli open and prevent lung collapse. This is estimated based on height and age. 74 Capacities are two or more volumes added together 75 You don’t need to memorize the normal numbers, just the definitions •Vital capacity: The volume of air a patient can exhale maximally after a forced inspiration. Maximum deep breath in, then exhale as much as possible. Vital capacity divided by expiratory reserve volume should be 80%. If it is lower than that, the person has either obstructive or restrictive lung disease. To tell which one, look at VC. If it is normal, it is obstructive. If it is low, they have restrictive lung disease. •Total Lung Capacity (TLC): the sum of all lung volumes •Inspiratory Capacity: amount of air for a deep breath in after normal exhalation •Functional residual capacity (FRC): amount of air left in your lungs after a normal exhale. You have to calculate this: •FRC = ERV + residual volume. – In COPD (obstructive), their FRC increases because they were not able to exhale all the way. • • • – They have a barrel chest The lungs don’t have as much recoil, have decreased tidal volume, cannot exhale enough Total Lung Capacity and Residual volume is increased because the air stays in the lungs. In restrictive lung disease, FRC is decreased because their alveoli cannot open all the way. • Total Lung Capacity and Residual volume are decreased. 76 Capacities are two or more volumes added together 77 You don’t need to memorize the normal numbers, just the definitions • • • Dead Space: Area where air fills the passageways and never contributes to gas exchange. Amounts to about 150 ml. Minute Respiratory Volume (MRV): tidal volume x respiratory rate. This calculation does not take into account the volume of air wasted in the dead space. A more accurate measurement of respiratory efficiency is alveolar ventilation rate. Alveolar Ventilation Rate (AVR) AVR = (TV – Dead Space) x Respiratory Rate Summary of lung calculations FRC = ERV + RV TLC = RV + ERV + TV + IRV MRV = TV x RR AVR = (TV – Dead Space) x RR You DO need to know these formulas. 78 Lung Capacity and Disease— Summary • Obstructive Disease: – Normal VC – Increased TLC, RV, FRC. – VC/ERV is less than 80% • Restrictive Disease: – Decreased VC – Decreased TLC, RV, FRC – VC/ERV less than 80% FRC: ERV +RV. Why is this important? It’s the volume of air in your lungs at the end of a normal exhale. It represents the normal equilibrium position of your chest wall trying to spring out and lung to recoil, but forced together due to pleural cavity restriction. 79 Sample Questions Minute Respiratory Rate is the volume of air that enters the airways (passes the lips) each min. MRV = Tidal volume x rate of breathing = (500 ml/breath) x 12 breaths/min = 6,000 ml/min Alveolar ventilation rate is the volume of air that fills all the lung’s respiratory airways (alveoli) each min. In a normal, healthy lung, this might be: AVR = (tidal volume – dead space volume) x rate of breathing = (500 ml/breath – 150 ml) x 12 breaths/min = (350 ml/breath) x 12 breath/ min = 4, 200 ml/min In a diseased, poorly perfused lung, this value may well be much lower. Then, is panting an example of hyper, normal, or hypoventilation???? 80 Hyper and Hypo Ventilation • The deeper regions of your lungs get more blood flow and the upper regions have more air flow. • If you hyperventilate, the rate and depth of ventilations increases, so more air gets to alveoli. After voluntary hyperventilation, apnea (no breathing) may occur b/c the arterial blood contains less carbon dioxide • Hypoventilation is dealing only with conductive zone. When you pant, you are just shifting air in the conducting zone. You are not increasing air to the alveoli. Panting is hypoventilation. 81 Respiratory vs. Metabolic Acidosis and Alkalosis • • • • • • RESPIRATORY ACIDOSIS AND ALKALOSIS is abnormal blood pH which is caused by abnormal breathing rates. It is not necessarily a disease, since hyperventilating from stress is not a disease. Respiratory alkalosis is caused by hyperventilation. This increases the amount of CO2 that you are exhaling. CO2 is an acid, so if you hyperventilate, you are exhaling a lot of acid, so your blood plasma pH will increase (alkalosis) Respiratory acidosis is caused by hypoventilation. This decreases the amount of CO2 that you are exhaling. If you hypoventilate, you are not exhaling enough acid, so your blood plasma pH will decrease (acidosis). Respiratory acidosis can also be caused by interference with respiratory muscles by disease, drugs, toxins. METABOLIC ACIDOSIS AND ALKALOSIS is abnormal blood pH which is not caused by abnormal breathing rate. Metabolic acidosis can be caused by – Salicylate (aspirin) overdose – Untreated diabetes mellitus (leading to ketoacidosis) Metabolic alkalosis can be caused by – excessive vomiting (loss of acid from stomach) – Eating too many antacids (Tums) 82 Compensations for Respiratory vs. Metabolic Acidosis and Alkalosis • Respiratory alkalosis can be compensated by – excreting an alkaline urine (kidneys excrete more bicarbonate) – Cannot hypoventilate since hyperventilation is the problem in the first place! • Respiratory acidosis can be compensated by – excreting an acidic urine (kidneys excrete more H+) • Cannot hyperentilate since hypoventilation is the problem in the first place! • Metabolic acidosis can be compensated by – excreting an acidic urine – hyperventilation • Metabolic alkalosis can be compensated by – Excreting an alkaline urine – Hypoventilation 83 Acid-Base Conditions • Excessive diarrhea Causes the problem of low HCO3 (bicarbonate) Leads to pH in blood (acidosis) Lungs Compensate by: pCO2 (hyperventilation, which decreases the CO2 content in the blood, thereby removing acid from the blood) 84 Acid-Base Conditions • Ingesting excessive stomach antacids Causes the problem of high HCO3 (bicarbonate) Leads to pH in blood (alkalosis) Lungs Compensate by: pCO2 (hypoventilation, which increases the CO2 content in the blood, thereby adding acid from the blood) 85 Acid-Base Conditions • Aspirin overdose Causes the problem of high acid, low HCO3 (bicarbonate) Leads to pH in blood (acidosis) Lungs Compensate by: pCO2 (hyperventilation, which decreases the CO2 content in the blood, thereby removing acid from the blood) 86 Acid-Base Conditions • Anxiety or hysteria with panting (hypoventilation) The patient hypoventilates Causes the problem of high pCO2 Leads to pH in blood (acidosis) Lungs Compensate by: HCO3 (by hyperventilation, which decreases the CO2 content in the blood, thereby removing acid from the blood) 87 Pulmonary Embolism • Pulmonary Embolism: blockage of the pulmonary artery (or one of its branches) by a blood clot, fat, air or clumped tumor cells. The most common form of pulmonary embolism is a thromboembolism, which occurs when a blood clot, generally in a vein, becomes dislodged from its site of formation, travels to the heart, goes into a pulmonary artery, and becomes lodged in the smaller artery in the lungs, blocking blood flow and oxygen to that region of the lung. • Symptoms may include difficulty breathing, pain during breathing, and possibly death. Treatment is with anticoagulant medication. 88