Chapter 7 and 10 ALL (textbook + lecture notes)

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Department
Kinesiology & Health Science
Course
KINE 3012
Professor
Tanya Da Sylva
Semester
Summer

Description
Chapter 11: Respiratory System INTRODUCTION Primary function: to obtain O2 for use of the body’s cells to eliminate CO2 that cells produce External Respiration It is the entire sequence of events in exchange between external environment and cells of body 4 Steps of External Respiration 1. Air is moved in and out of lungs. Between external environment and alveoli done by breathing/ventilation. Ventilation is regulated according to the needs of the body for O2 and CO2 removal 2. O2 diffuses from air into alveoli into blood (pulmonary capillaries), CO2 goes into alveoli (opposite direction) 3. Blood transports O2 from lungs to tissues, and CO2 from tissues to lungs 4. O2 and CO2 are exchanged between tissues and blocked by diffusion across capillaries Anatomy of Respiratory System 2 components: 1. lungs = a)airways b) alveoli 2. chest wall Lungs  Lungs occupy most of the thoracic cavity  2 lungs, separated by lobes, supplied by each of the bronchi a) airways o are between the atmosphere and where exchange of C02 and O2 occurs o nasal pharynx (nose)  pharynx (throat)  esophagus  trachea o since the pharynx is the passageway for food as well, reflex mechanisms close the trachea during swallowing so food enters the esophagus not airways o the esophagus remains closed except when swallowing (controlled in brainstem) o the larynx is located on top of the trachea, anterior = Adams apple o vocal folds are on top of opening of larynx, laryngeal muscles control length and shape of these muscles o lips, tongue, soft palate modify vibrations into recognizable sounds o during swallowing, vocal cords are brought close together to prevent entry of food o after the larynx, the trachea divides into left and right bronchi  bronchioles (some gas exchange occurs)  alveoli (clustered ends of bronchioles, gas exchange occurs between blood and alveoli) o for flow in and out of alveoli, the airway must remain open. o The airways are kept open in many ways: a) the trachea and bronchi are encircled by cartilaginous rings that help airways resist compression during compression (ex. Coughing) - the trachea is an incomplete cartilaginous ring and connects both ends by smooth muscle b) bronchioles have no cartilage, but have smooth muscle controlled by autonomic system, thus can control the resistance between air flow between atmosphere and alveoli (Poiselles Law) o airways = convection, alveoli = diffusion - small arteries =  resistance to flow - larger arteries =  resistance to flow -  SA =  diffusion (alveoli) - the beginning is convective (air flowing through trachea then bronchi) to diffusion (bronchioles/alveoli) b) alveoli o composed of 2 epithelial cells 1. type I: in alveolar wall 2. type II: secrete pulmonary surfactant- helps lung expansion and stabilizes alveolar dimensions Chest Wall  formed by 12 pairs of ribs which join the thoracic vertebrae  ribs 1-7 join the sternum (anteriorily)  rib cage protects lungs and heart  chest wall contains muscles that generate pressure required for airflow  main inspiratory muscles are: 1. Diaphragm: - large sheet of skeletal muscle, forms floor of thoracic cavity and separates it from thoracic cavity - penetrated by only esophagus and blood vessels in thoracic region - innervated by phrenic nerves come from C3-C5 - at rest, diaphragm is dome shaped, round part goes into thoracic cavity - during inspiration, it goes downward, enlarging the volume of the thoracic cavity by increasing cavities vertical dimensions - the abdominal wall pushes outward during inspiration as the descending diaphragm moves abdominal contents outward and forward - 50-75% of enlargement of thoracic cavity during inspiration is due to contraction of diaphragm - when the diaphragm contracts/moves down, the volume of the lungs increases, therefore pressure decreases, since air moves from high pressure to low pressure, air flows into the lungs 2. External intercostal muscles (inspiratory): - internal intercostals lie between ribs and the external intercostals are lie right on top of the internal intercostals - external intercostals help enlarge the thoracic cavity laterally (side-to- side) and anterior-posteriorily - when the external intercostals contract, they elevate the ribs, moving sternum upward and outwards - intercostal nerves activate these intercostal muscles (T1-T12) - many physiologists think that main reason for activating external intercostals is to stabilize the chest wall from being sucked in during inspiration, this increases the efficiency of the diaphragm because contraction is used to inflate the lungs rather than being wasted on moving the chest wall Internal intercostals (expiratory) -expiratory muscles consist of internal intercostals and abdominal muscles (rectus abdominis, transverse abdominis, and external/internal obliques) - these muscles are inactive in healthy humans but activated during exercise, coughing, sneezing (when ventilatory demands increase) - expiratory can generate more pressure than inspiratory muscles since reflexes like coughing and sneezing are so important - internal intercostals innervated by same thoracic nerves as external intercostals - abdominal innervated by nerves coming off T7-L1 The Pleural Space  Lungs + structures covered by visceral membrane and the inside of wall of thorax is covered by parietal membrane  Pleural space/cavity/sac: small space between visceral and parietal membranes  The pleural fluid lubricates the surfaces of the two membranes as they slide past each other during breathing  Pleurisy: inflammation of the pleural membrane, causes pain during breathing because inflation and deflation of the lungs causes a “friction rub” between pleural and visceral membranes RESPIRATORY MECHANICS  All fluids in the respiratory system go down a pressure gradient F= P/R F= bulk flow P= pressure difference R= resistance  This pressure gradience is used to overcome the stiffness, the resistance to flow of the respiratory system  For inspiration, pressure in alveoli must be less than pressure in mouth  For expiration, pressure must be more in alveoli than the mouth Pressures in the Respiratory System 4 different pressures critical to ventilation: 1. Atmospheric/barometric pressure (P ): Bhe pressure exerted by weight of the air in the atmosphere on objects 2. Alveolar pressure (P A: pressure within the alveoli 3. Pleural pressure (P p1 pressure outside the lungs, but within the thoracic cavity (pressure within the pleural space) 4. Transpulmonary pressure (P , also referred to as lung recoil pressure) tp *recoil is the lungs going back to normal after being stretched by inhalation Mechanical Properties of the Respiratory System  The 2 properties of the respiratory system, the lungs and chest wall, each have its own pressure-volume relationship  As lung volume increases, its recoil pressure increases, so the lung is always exerting positive pressure  The recoil pressure of chest wall is mostly negative (inspiratory ) at minimum volume and increases as volume increases, exerts no recoil at 60% of total volume, and above 60% is positive (expiratory)  The recoil pressure of the respiratory system is the sum of the pressures generated by the chest wall and lungs  At functional residual capacity (FRC), the pressures of the chest wall and lung are equal and opposite, therefore net pressure =0 (pg 455) ** use mmHg when discussing partial pressure of gases when discussing diffusion and cmH2O when discussing bulk flow (convection)** Ptp P -AP p1 If P > recoil, then lung expands, but as lung expands, recoil increases tp When recoil = P ltpg stops expanding We change P tpby changing P p1 If Ptp recoil, then lung gets smaller, but as lung gets smaller recoil decreases When recoil = P lung stops getting smaller tp Read pg 456 Source of the Lung’s Elastic Recoil The lungs want to collapse/recoil for 2 reasons 1. Elastic recoil of the tissues 2. Surface tension of the liquid lining the inside the alveoli: - contributes to 70% of lungs elastic recoil pressure - it was seen that air filled lungs had more recoil pressure than saline filled lungs - air filled lungs have more recoil because of surface tension: unequal distribution of charge because water molecules like to stay near each within the surface rather than water molecules above the surface - surface tension has 2 effects: o First: the liquid layer resists an force that increases the SA (opposes expansion of alveolus), because the surface molecules oppose being pulled apart o Second: the SA of the liquid tends to shrink as much as possible because the water molecules are attracted to each other and want to be as close as possible - therefore, the surface tension of the lining in the alveolus tends to reduce alveolar size and expel alveolar gas, this combined with the elastin fibres produces lungs elastic recoil that provides pressure for expiration Emphysema: loss of elastic fibres and reduction of alveolar surface tension because of breakdown of alveolar walls decrease elastic recoil. This along with increases airway resistance gives patient difficulty breathing. They also have increased FRC, outward recoil of chest wall, giving patient barrel- chested look  pulmonary connective tissues as lots of elastic fibres, they are arranged in a meshwork that amplifies their elastic behavior, the entire piece of fabric (lung) is stretchier and tends to bounce back into shape even more than individual elastin fibres (not arranged in meshwork)* Alveolar Stability 2 factors that oppose the alveoli to collapse: 1. pulmonary surfactant: - a complex mixture of lipids and proteins secreted by type II alveolar cells - this mixture spreads out in water molecules in the fluid lining of the alveoli and lowers the alveolar surface tensions because the cohesive (joining) force between the water molecule and adjacent molecule of surfactant is very low - by lowering alveolar surface tension surfactant as 2 benefits (1) it increases pulmonary compliance, reducing work to inflate the lungs (2) it reduces recoil pressure of smaller alveoli more than larger alveoli, allowing different sizes of alveoli to exist Compliance: refers to how much effort is required to stretch/distend lungs. The less compliant lungs are, the more work is required 2 major determinants of lung compliance 1. stretchability of lung tissues 2. surface tension at air-water interface Law of Laplace: the magnitude of the collapsing pressure is directly proportional to the surface tension and inversely proportional to the radius of the bubble (alveoli) P= 2T/r P= collapsing pressure T= surface tension r= radius of bubble (alveolus) - the smaller the radius, the smaller the alveolus so the smaller the radius, the greater the tendency to collapse at a given surface tension - so if small alveolus were to collapse they would empty into larger ones, but that doesn’t happen because of surfactant - in small alveoli, the surfactant molecules are close together and reduce surface tension, so the lower surface tension of the alveoli offsets the effect of the low radius, thus reducing the collapsing pressure Net effect of surfactant: 1. equalize pressures within alveoli of different sizes 2. minimize the tension of small ones to empty into larger ones = stabilizing alveoli and maintain gas exchange 2. Alveolar Interdependence  interdependence amongst neighboring alveoli  each alveolus is surrounded by other alveoli and interconnected to them by connective tissue  if an alveolus starts to collapse, the surrounding alveoli are stretched as their walls are being pulled in the direction of the collapsing alveolus. Then these surrounding alveoli will recoil after being stretched and exert an expanding force on the collapsing alveolus, therefore keeping it open = alveolar interdependence alveoli begins to collapse  surrounding alveoli stretch in direction of collapsing alveoli  stretched alveoli recoil  collapsing alveoli is expanded (kept open) Pneumothorax  It is the abnormal condition of air entering the pleural space  This can happen if the chest wall is punctured and the air flows down its pressure gradient into the pleural space  So now the pleural and alveolar pressure now equal atmospheric pressure, meaning that there is no pressure gradient between the chest wall and the lung wall  With no opposing negative pleural pressure to keep it open, the lung collapses to its unstretched size and the thoracic wall springs outward to its unstretched size How Alveolar Pressure Changes  For air to flow out of lungs, the alveolar pressure must exceed the atmospheric pressure  For air to flow in lungs, the atmospheric pressure must exceed the alveolar pressure  Ptp P -AP p1 Lung recoil pressure = alveolar pressure – pleural pressure Alveolar pressure = lung recoil pressure + pleural pressure (we have to change the alveolar pressure to inflate/deflate the lungs, atmospheric pressure is an arbitrary 0) THEREFORE to change alveolar pressure, must change lung recoil pressure or pleural pressure or both, but we only change pleural pressure because lung recoil takes longer - change pleural pressure by activating muscles in chest wall - activating inspiratory muscles decreases plural pressure and activating expiratory muscles increases it Onset of Inspiration: Contraction of Inspiratory Muscles  Before inspiration, alveolar pressure = atmospheric pressures so no air is flowing in or out  Pleural pressure  and thoracic cavity enlarges, pressure in alveoli  because of decompression  Because alveolar pressure < atmospheric pressure, air flows into lungs down the pressure gradient, inflating the lungs  Air continues to enter lungs until no gradient exists (alveolar pressure = atmospheric pressure) Onset of Expiration: Relaxation of Inspiratory Muscles  End of inspiration, inspiratory muscles relax and decrease their ability to expand the thorax  Pleural pressure then becomes less negative and less than the recoil pressure of the lung  Activation of expiratory muscles is NOT necessary to expiration to occur, only reduction of activity in the inspiratory muscles is needed  Expiration stops when alveolar pressure = atmospheric pressure Role of Accessory Inspiratory Muscles  Deeper inspiration can be done by contracting diaphragm and external intercostal muscles more forcefully and activating the previous inactive accessory inspiratory muscles  This increases the tidal volume Summary of Inspiration  Inspiration occurs when alveolar pressure is less than atmospheric pressure  This drop in alveolar pressure is because of the activation of inspiratory muscles that lower pleural pressure (alveolar pressure = lung recoil pressure + pleural pressure)  The lungs recoil pressure cannot change as quickly as pleural pressure  As the alveolar pressure drops because the pleural pressure drops, air flows into the lungs (into alveoli)  As long as the inspiratory muscles contract to keep the pleural pressure lower (more negative) than the recoil pressure of the lung, it keeps inflating  Towards the end of inspiration, the activity of inspiratory muscles decreases, so the recoil pressure of the lung catches up to the pleural pressure until the 2 pressures are equal and opposite (just like they were at the beginning of inspiration, BUT the lung volume is greater because the recoil pressure of the lung is now greater)  For expiration, since the inspiratory muscle activity decline, the pleural pressure increases (becomes more positive -8 to -7)  The elastic recoil pressure of the lung is now greater than the pleural pressure, the alveolar pressure is now positive = expiration  Expiration ends when recoil pressure of lung = pleural pressure Active Expiration  Expiration is passive in healthy people, but inspiration is always active because of contraction of inspiratory muscles  Forced/active expiration: used to empty lungs faster and more completely  To breath out more forcefully, alveolar pressure must be increased even more above atmospheric pressure  Most important expiratory muscles are in the abdominal wall, when they contract the pressure is pushed into the pleural space increases pleural pressure making a more forceful expiration Airway Resistance and Airflow  Flow in and out of lungs is because of the pressure gradient between alveoli and the atmosphere  F = P/R - flow is inversely related to R - flow resistance is normally very low  Poiseulles Law determines resistance to blood flow R= 8nl/r 4 Where: n= viscosity of fluid (airway resistance and flow is l= length of tube dependent on all 3 of these) r= radius of tube  The radius of the airways is the primary factor determining resistance to airflow  Air way size adjustments can be made through the autonomic system  Parasympathetic: work when at rest, bronchoconstriction- increases airway resistance by decreasing radius  Bronchoconstriction is caused by the airways getting innervated by postganglionic parasympathetic nerves coming from the vagus nerve, releases acetylcholine = bronchoconstriction Sympathetic: associated with epinephrine, muscle relaxation- bronchodilation- decreases airway resistance  So when there is high demand for O2 (exercise), bronchodilation makes sure there is maximum flow and minimum resistance  Low resistance also helps reduce work of breathing (look table page 463)  Dilation can happen in 2 ways by the adrenergic system: 1. releasing nor epinephrine which activates B2-receptors on bronchial smooth muscle 2. indirectly by the adrenal medulla releasing epinephrine which is carried by circulation to the site (airway smooth muscle) (why people with severe reaction carry needles of epinephrine). Then activation of a-adrenergic receptors suppresses parasympathetic activity causing bronchodilation  In the peptidergic system, vasoactive peptide dilates  Histamine constricts and recruited as response to allergies  Resistance can be affected by the swelling of the mucosa in the nose (stuffy nose), this swelling can be reduced by decongestants Airways Resistance and Chronic Pulmonary Diseases  Chronic pulmonary diseases are when there is increased resistance  When resistance increases, a larger pressure gradient must be established to maintain a normal flow, so people with pulmonary disease work harder to breath Asthma:  In asthma airway obstruction is because of: 1. thickening of airway walls because of inflammation and histamine 2. plugging because of excess mucous 3. airway hyper-responsiveness (constriction of the smaller airways resulting from spasm of the smooth muscle on their walls)  These can be triggered by exposure to allergens, irritants (smoke), infections  Most common chronic childhood disease  Treated with bronchodilators (blue) and anti-inflammatory drugs (orange) Chronic Obstructive Pulmonary Disease (COPD):  COPD is a new term for emphysema and chronic bronchitis  Emphysema: -destruction and collapse of smaller airways -breakdown of alveolar walls - happens because of release of destructive enzymes (trypsin) that are produced with cigarette smoking - the body is protected from trypsin with antitrypsin, but these enzymes can overwhelm antitrypsin -loss of lung tissues leads to breakdown of alveolar walls -could also come from genetic inability to produce antitrypsin - treatment: lung transplant  Chronic Bronchitis: -excessive mucous production in smaller airways - lower airways - happens by exposure to cigarettes, smoke, pollution - airways become narrowed by thickening of airway linings - frequent coughing, but the mucous cannot be removed - mucous causes bacterial infections  Increased airway resistance  Decreased air flow  Compromised gas exchange  Impaired oxygenation of blood  Increased work of breathing  Usually happens by cigarette smoking and slowly damages the airways  Can also result from airborne irritants (pollution, dust, silica, asbestos)  4 thleading cause of death in Canada Difficulty Breathing Out  With any type of pulmonary disease, expiration is harder than inspiration  Smaller airways that don’t have cartilaginous rings to keep them open, are kept open by a negative pleural pressure (air can flow in – transummural gradient)  Inspiration dilates these airways and raises volume of alveoli  Dilation of the airways lowers flow resistance (Poiseuille’s Law)  A person with asthma has more difficulty expiring than inspiring because the airway resistance increases by a lot and is noticeable  Patients undergoing asthma complain more about not being able to inspire than expire  The initial problem is obstructive (cant get air out), it becomes restrictive (cant get air in)  Because the person has trouble breathing out, they do not go back to the end-expiratory lung volume, so the next inspiration starts at a higher volume  This is good because airway resistance is lower at higher lung volumes  But at this higher lung volume the person cannot breathe out completely, overtime this process = dynamic hyperinflation  The higher lung volume makes the system less complaint (stretchibility of lungs) making breathing difficult, because the person cannot achieve a good tidal volume (volume of air leaving and entering during a single breath)  In normal people, the smaller airways stay open at rest and during exercise collapse and further outflow of air is stopped at LOW lung volumes (residual volume)  People with pulmonary disease the smaller airways collapse when at rest preventing further outflow (leaving higher volume inside the lungs) = higher end-expiratory volumes Lung Volumes and Capacities  Spirometer: device that measures volume of air breathed in and out (has air-filled drum floating in a water-filled chamber)  Spirogram: pen attached to the spirometer that records volume Tidal Volume: the volume of air entering or leaving the lungs during a single breath = 500ml Inspiratory reserve volume (IRV): the extra volume that can be maximally inspired over and above the typical resting tidal volume = 3000ml Inspiratory capacity (IC): the maximum volume that can be inspired starting from the end of a normal quiet expiration = 3500ml Expiratory reserve capacity (ERV): the maximum volume that can be actively expired starting from the end of a typical resting tidal volume= 1000ml Residual volume (RV): the volume remaining in the lungs after maximal expiration, cannot be measured directly with a spirometer, because this volume of air does not move in and out of lung = 1200ml Functional residual capacity (FRC): the volume of air in the lungs at the end of a normal passive expiration FRC= ERV+RV= 2200ml Vital capacity (VC): the maximum volume of air that can be moved out during a single breath following a maximal inspiration. The subject first inspires maximally and then expires maximally =4500ml Total lung capacity: the max volume of air the lungs can hold (TLC= VC+RV)= 5700ml Forced expiratory volume in one second (FEV ): the volume of air that 1 can be expired in the first second of a maximal expiratory effort starting form TLC (FEV /FVC) 1 (look at figure 11.20 page 467) PULMONARY AND ALVEOLAR VENTILATION  Amount of air moved in and out of the alveoli  Minute ventilation: volume of gas breathed in and out in 1 minute Pulmonary Ventilation: VE= V T f = 500ml/breath x 12 breaths/min = 6000ml/min = 8640L/day Calculated by multiplying average tidal volume (VT) by the respiratory frequency (f) The E after the V in VE indicated that the measurement was made on expired gas  To increase ventilation, both tidal volume and frequency increase at the start, but tidal volume increases more than frequency, but once the limit to tidal volume is reached, frequency increases  Not all of this ventilation can be used for gas exchange because of anatomical space Anatomic Dead Space  Not all air inspired reaches the alveoli. Some remains in conducting airways = anatomical dead space- air that cannot be a part of gas exchange  The volume of conducting airways = 150 ml, so 500ml of air moves in and out of every breath, only 350 reaches the alveoli and are a part of gas exchange How anatomic dead space affect gas exchange: Inspire 500ml  350 goes to alveoli, 150 in conducting airway  500 ml expired (350 from alveoli and 150 old air from conducting airways)  alveoli also has to expire 500, so 150ml goes into conducting airways  next inspiration 500ml is taken in , the first 150 is the one that was in the conducting airways from before (old air)  the last 150 remain in the airways (pg 469-470 figure 11-22) Alveolar Ventilation  Alveolar ventilation: = (V TV D x f (tidal volume – dead space) x respiratory rate = (500-150ml/breath) x 12 breaths/min = 4200ml/min  To have the most amount of O2 going into the blood, we would want most of the lung to be devoted for gas exchange/alveoli, this would require smaller airways, BUT this would make more resistance (Poiselles law r )  Therefore, the respiratory system is compromise between airway (resistance) and alveolar (gas exchange)  Some inspired air never reaches alveoli (150ml) that’s why we need to breath in more than 150 ml  If we breathed in the same tidal volume as the dead space (150ml(), alveolar ventilation would be 0  That’s why we need to take big breaths to maximize alveolar ventilation, so alveolar air is much larger than dead space air  At rest, ventilation is better with large tidal volume and lower frequency  During exercise, the amount of dead space decreases, and amount of air going to alveoli increases = more efficient breathing  This is because the best way to increase ventilation is to increase tidal volume, you have a limit to tidal volume, so after the max is reached, you improve ventilation by increasing the frequency WORK OF BREATHING  Expiration is passive  The energy comes from energy stored in expanded lung (lung recoil)  Lungs are highly compliant and only 3% of body energy is used for quiet breathing   tidal volume +  frequency =  elastic component of work of breathing +  resistive component of breathing   frequency +  tidal volume =  resistive +  elastic  8-16 breaths/min is when we are using min energy Work of breathing increases in 4 different situations: 1. When pulmonary compliance is decreased: ex. Pulmonary fibrosis, more work req’d to expand lungs 2. When airway resistance is increased: ex. Chronic obstructive pulmonary disease/asthma, more work req’d 3. When elastic recoil is decreased: ex. Emphysema, passive expiration may not be enough to push out the normal amount of air pushed out during exhalation, so expiratory muscles work to empty the lungs even at rest 4. When there is a need for increased ventilation: ex. Exercise = more work req’d to generate larger tidal volumes and faster breathing  Usually the need for O2 is never too much for the body to compromise with blood flow, but in hot temperatures, when the body also needs to give blood to skin to cool down, it could result in fatigue and less exercise duration  The respiratory muscles require most of the energy in these situations when work is increased GAS EXCHANGE  The purpose of alveolar ventilation is to provide O2 to the alveoli where O2 is taken up by blood and CO2 is removed and exhaled  Blood is the transporter of O2 and CO2 b/w tissues and lungs, cells extracting O2 and eliminating CO2  A healthy individual with healthy lungs may still have problems with amount of O2, this can happen at the gas exchange level  Gas exchange involves diffusion of O2 from the alveoli to the blood and of CO2 in the opp direction  Factors determining diffusion are pressure gradient and resistance Diffusion at the Alveolar-capillary Membrane 2 factors that determine diffusions 1. Partial pressure gradient of gas: O2: high end = partial pressure in alveoli Low end = partial pressure in pulmonary artery CO2: high end= partial pressure in pulmonary arterial blood Low end= partial pressure in alveoli 2. Resistance to diffusion: a) surface area of membrane b) thickness of membrane c) diffusibility of gas (constant) Partial Pressure Gradients Partial pressure: in a mixture of gases, each gas has a partial pressure which is the hypothetical pressure of that gas if it alone occupied the total volume of the mixture  Partial pressure depends on 1. Temperature 2. Concentration (#mol/vol.)  In a mixture of gases the pressure of each gas is independent of the others  Partial pressure is directly proportional to the percentage of that gas in the mixture Calculating Partial Pressure Partial pressure = total pressure x gas fraction In lung: total pressure = atmospheric pressure Atmospheric air is: 79.04% N2 20.93% O2  CO2 atmospheric pressure = 760 mmHg PO2 = 760 x 0.2093/760 = 159 IF atmospheric pressure = 250 mmHg (high altitude) PO2= 250 x 0.2093/250 = 52  Can see that there is a lower pressure of O2 at higher altitude because there is lower driving pressure of O2 due to low atmospheric pressure (look on slides) Alveolar Partial Pressure of O2 and CO2  The greater the partial pressure the more the gas is dissolved in liquid  Alveolar air does not have same composition as inspired air because: 1. as soon as it enters it becomes humidified, lowering the partial pressure, pressure of H2O = 47 mmHg, so 760-47= 713mmHg, therefore all of the partial pressures decrease 2. alveolar air is also lower because inspired air (humidified) mixes with “old” air that already was in lungs plus dead space air - after inspiration, the amount of each gas that goes into the alveoli is even lower because less than 15% is fresh air (table 11-6 pg 472) - alveolar gas can be calculated by alveolar gas equation  during inspiration, the O2 in the alveoli does not increase because only a small amount of alveolar air is exchanged in each breath, the small volume of the high O2 air mixes with the large volume of the low O2 air already in the alveoli, so alveolar air has O2 of about 100mmHg constant  Alveolar O2= 100mmHg and after it diffuses and goes into blood, arterial O2 is also about the same amount (100 mmHg)  Reverse situation for CO2, it comes from body tissues and diffuses down its pressure gradient from blood to alveoli, CO2= 40mmHg (page 473 figure 11-24) Other factors  According to Fick’s law of diffusion, the rate of diffusion also depends on SA and thickness of the membrane  In healthy people, these factors are relatively constant Effects of Surface Area and Membrane Thickness on Gas Exchange  During exercise, pulmonary capillaries that were closed before open up to increase SA for gas exchange  This reduces diffusion distance for O2  Alveolar membranes are also stretched out more during exercise = high SA and low thickness  Capillary transit time: the amount of time capillary blood is exposed to alveolar gas (affects the spread of O2 and CO2)  At rest, blood remains in the pulmonary capillaries for .75 seconds, so capillary transit time is .75 seconds, which is more than enough time needed for equilibration of O2 and CO2  During exercise, capillary transit time is reduced, but still enough time for O2 and CO2 to equilibrate because SA increases and partial pressure gradients are maintained/increased (pg 475 table 11-7)  This transit time shows that exercise on high altitude is difficult because the lower the atmospheric pressure reduces the alveolar O2  Thickness increases in: 1. pulmonary edema 2. pulmonary fibrosis 3. pneumonia  in a diseased lung, O2 is impaired more than CO2 transfer because of O2’s lower diffusibility  CO2 diffuses faster Alveolar Dead Space  Not all alveoli participate equally in gas exchange  Some alveoli are perfused but not ventilated = shunts  Some alveoli are not perfused but are ventilated  These both are alveolar dead space because gas exchange does not occur  In healthy people this does not have an effect Regional Control of Ventilation and Perfusion Effect of Oxygen  How fast O2 is removed from the lung region depends on its perfusion (delivery of blood to a tissue)  Sink example: Water= O2 Faucet (increased ventilation) Sink = lung Drain = perfusion So with increased ventilation, more O2 will come into the lung, and how fast the O2 is removed from the lung depends on its perfusion  If O2 is low in lung, the low O2 causes constriction (hypoxia) of the blood vessels supplying that lung region – like partially closing the sinks drain, as a result the region partial pressure of O2 rises  The perfusion to hypoxic lung is diverted to the better ventilated (non- hypoxic) regions  The reverse does not happen, increase in O2 does not dilate blood vessels, it would just reduce previous vasoconstriction, but not dilate  Same effect happens with CO2  If perfusion for CO2 is low the partial pressure of CO2 falls  The low pCO2 (hypocapnia) causes constriction in the lung region, so ventilation in that lung decreases  Because all ventilation goes to lungs, any ventilation of an underperfused lung region is diverted to another, better perfused region  An increase in perfusion causes dilation Gas Exchange Across Systemic Capillaries  Only 2 places where gas exchange can occur are systemic and pulmonary capillaries  Arterial pO2 is 100mmHg and arterial pCO2 is 40mmHg pO2 and pCO2 Gradients Across the Systemic Capillaries  In the cells, pO2 is 40 mmHg, whereas arterial pO2 is 100 mmHg  SO O2 easily goes down its gradient from the blood into tissues, until it equilibrates 40mmHg  Therefore, venous blood leaving systemic capillaries (that go to tissues) have a low pO2 of 40  For CO2 the opposite happens  pCO2 in cells is 46mmHg and arterial pCO2 is 40, so it moves down its gradient for the tissues into the blood until it equilibrates  that’s why blood coming from systemic capillaries has pCO2 of 46 mmHg  as tissue uses
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