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Chapter 13

KINE 3012- THE RESPIRATORY SYSTEM (chap#13) thorough textbook notes

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Kinesiology & Health Science
KINE 3012
Michael Connor

Physiology II- Chapter#13 Notes Thurs, Jan 17/13 CHAPTER#13- THE RESPIRATORY SYSTEM INTRODUCTION: -function of respiration obtain 02 for cells + eliminate CO2 produced by cells THE RESPIRATORY AIRWAYS (fig. 13-1, pg. 472): -respiratory system respiratory airways to lungs, the lungs, structures of thorax (chest), to produce movement of air in/out of lungs (gas exchange organ) -respiratory airways tubes that carry air b/w atmosphere + air sacs -air sacsonly site gases are exchanged b/w air (alveoli) and blood (capillary) -track of airway nasal passage (nose)/mouth-> pharynx (throat) leads to both respiratory and digestive-> trachea (windpipe for air) or oesophagus (for food) -larynx (voice box) at entrance of trachea, front lump of larynx “Adam’s apple”, vocal cords found at opening of larynx -vocal cords 2 bands of elastic tissue across opening of larynx, as air moves by they vibrate to produce diff. sounds, also close off trachea during swallowing -track of trachea larynx (voice box at opening)-> 2 branches: left + right bronchi (enter left + right lungs)-> bronchioles (smaller branches within lungs)->alveoli -alveoli clustered at ends of bronchioles, tiny air sacs that exchange gases b/w air and blood -airflow in/out of lungs happens when entire track of trachea from larynx to alveoli remain open - trachea and 2 large bronchi are rigid, nonmuscular tubes of cartilage rings to prevent tubes from closing -smaller bronchioles have no cartilage but have smooth muscle sensitive to hormones/local chemicals thus vary in degree of contraction and regulate amount of air passing b/w atmosphere and alveoli PARTICIPATION OF RESPIRATORY SYSTEM: -respiration2 separate/related processes: internal and external respiration Internal/cellular respiration: -metabolic reactions in cells that produce bio. chemical energy from fuel molec. (glucose, fat), using oxidizing agents (O2) (eg. glycolysis/Kreb’s cycle) -aerobic respiration oxygen as final electron acceptor, by product is CO2 -chemical energy stored as ATP is used for locomotion (walking/moving) -respiratory quotient (RQ) ratio of CO2 produced to O2 consumed RQ= CO2 produced 02 consumed External respiration: -sequence of events exchanging O2/CO2 b/w external envir. (atmosphere) and body cells (alveoli) -4 steps of external respiration: 1. breathing/ventilation air moves in/out of lungs, exchanging air b/w atmosphere (external envir.) and alveoli (lung’s air sacs) -breathing/ventilation rate adjusted to control O2 uptake/CO2 removal 2. O2/CO2 exchanged b/w air in alveoli and blood in pulmonary (lung) capillaries through diffusion 3. blood in capillaries transport O2 and CO2 b/w lungs and tissue cells 4. O2/CO2 exchanged b/w tissues and blood by diffusion of systemic (tissue) capillaries *Respiratory system: step 1/2 and circulatory system: step 3/4 Nonrespiratory functions of the respiratory system: -route for water loss/heat elimination -inspired air is humidified/warmed/moistened before expiring to prevent drying out of alveolar lining -helps maintain normal acid-base -defends against foreign inhaled matter/removes, modifies, activates matter passing through pulmonary circulation -mouth enables speech, singing, vocals/nose for smell ALVEOLI: -Fick’s law of diffusion shorter the distance/greater the surface area, greater the rate of diffusion -alveoli thin-walled, inflatable, one-cell thick, grape-like sacs at bronchiole terminals -Type I alveolar cells flattened single layer of cells that make the alveolar walls -interstitial space space b/w alveoli (air) and capillaries (blood) 0.5um, ideal for gas exchange -Type II alveolar cells cells on alveolar epithelium, secrete pulmonary surfactant -surfactant a phospholipoprotein that facilitates lung expansion -pores of Kohn exist in walls b/w adjacent alveoli, permitting airflow b/w adjacent alveoli cells -collateral ventilation airflow b/w adjacent alveoli cells. important for fresh air to enter an alveolus whose terminal ends are blocked by disease THE LUNGS: -two lungs, each supplied by one bronchi each -lung tissue consists of highly branched airways, alveoli, pulmonary blood vessels, elastic connective tissue -smooth muscles in lungs only in walls of arterioles/bronchioles, no muscle in alveolar walls -changes in lung/alveolar volume are made by changes in size of thoracic (chest) cavity, where lungs occupy most of the volume of the thoracic cavity -communication b/w thorax and atmosphere is through respiratory airways into alveoli PLEURAL SACS: -pleural sac double-walled, closed sac that separates each lung from thoracic wall/surrounding structures, air cannot leave/enter -pleural cavity interior of pleural sac -surfaces of pleura secrete a thin intrapleural fluid -intrapleural fluid lubricate pleural surfaces as they slide past each other during respiration -pleurisy inflammation of the pleural sac, causes painful breathing b/c of inflation/deflation of lungs causing “frictional rub” RESPIRATORY MECHANICS: -air moves from higher pressure to lower pressure (down pressure gradient) INTERRELATIONSHIPS AMONG PRESSURES: -air flows in/out of lungs by cyclic respiratory muscle activity during breathing according to pressure gradients b/w alveoli and atmosphere -3 diff. pressure considerations for ventilation: 1. atmospheric (barometric) pressure weight of air in atmosphere on objects on Earth’s surface (760mmHg) 2. intra-alveolar pressure/intrapulmonary pressure pressure within alveoli, air flows in/out to equilibrate with atmospheric pressure 3. intrapleural pressure/intrathoracic pressure pressure within the pleural sac, usually less than alveolar pressure and does not equilibrate b/c there is no direct communication b/w pleural cavity and atmospheric or intra-alveolar pressure STRETCHING OF THE LUNGS: -thoracic cavity larger than unstretched lungs -2 forces, intrapleural fluid’s cohesiveness and the transmural pressure gradient hold the thoracic wall and lungs in close proximity, stretching lungs to fill the larger thoracic cavity Intrapleural fluid’s cohesiveness: -water molec. in intrapleural fluid resist being pulled apart b/c polar molec. attract thus holds pleural surfaces together creating “stickiness” -intrapleural fluid’s stickiness ensures that changes in thoracic dimension cause changes in lung dimension -when thorax expands, lungs being stuck to thoracic wall by intrapleural stickiness also expands Transmural pressure gradient (figure 13-8, pg.477): -intrapleural pressure pushes/stretches lungs b/c it is smaller than atmospheric/intra- alveolar pressure, BUT 760mmHg pressure pushes inward on lungs thus chest wall is “squeezed in” -transmural pressure gradient across lung wall= intra-alveolar pressure -intrapleural pressure -transmural pressure gradient across thoracic wall=atmospheric pressure -intrapleural pressure Reason that the intrapleural pressure is subatmospheric: -thoracic wall and lungs try to repel each other, although they are held close to one another by the interpleural fluid’s cohesiveness and transmural pressure gradient -stretched lungs pull inward away from thoracic walls and thoracic walls move outward away from lungs -the slight expansion of the pleural cavity by these forces cause the pressure to fall to 756mmHg from 760mmHg since the fluid inside the pleural cavity cannot expand to fill additional volume thus creating a vacuum Pneumothorax (fig13-9, pg.478): -air does not enter the pleural cavity b/c there is no direct communication b/w pleural cavity and alveolus or atmosphere -BUT if there is a puncture in chest wall, air will flow into pleural cavity down pressure gradient, thus the pressure in alveolus, pleural cavity, and atmosphere will equilibrate and eliminate the transmural pressure gradient -no transmural pressure gradient= no restricted positioning of thoracic wall and lungs thus can lead to lung collapse -pneumothorax (air in chest) abnormal flow of air into pleural cavity FLOW OF AIR INTO AND OUT OF LUNGS (fig. 13-13, pg.480): -inspiration air flows into alveolus when atmospheric pressure is greater -expiration air flows out of alveolus when alveolar pressure is greater -intra-alveolar pressure can be changed by altering volume of lungs (Boyle’s Law) -Boyle’s lawat constant temperature, pressure exerted by gas varies inversely with volume of gas (pressure increase, volume decrease, v.v) -respiratory muscles during breathing do not directly change lung volume but change thoracic cavity volume, which causes change in lung volume by the intrapleural fluid’s cohesiveness+ transmural pressure gradient Onset of inspiration: Contraction of inspiratory muscles -inspiratoy muscles muscles that contract at the onset of inspiration to enlarge thoracic cavity, include diaphragm, external intercostal muscles -diaphragm sheet of skeletal muscle that forms floor of thoracic cavity, innervated by phrenic nerve, requires a lot of O2, moves downward when contracted enlarging thoracic cavity volume -internal/external intercostal muscleslie b/w ribs, fibers run up/down ribs and when contracted they elevate ribs and enlarge thoracic cavity -as thoracic cavity enlarges, lungs are also forced to expand and alveolar pressure drops since the alveolus still holds same amount of air molec. in larger volume, thus air will flow in down the pressure gradient until equilibrium Role of accessory inspiratory muscles: -deeper inspiration/more air breathed in, accomplished by contracting diaphragm/ external intercostal muscles more forcefully using accessory inspiratory muscles accessory inspiratory muscles found in neck, raises sternum, elevates ribs, further enlarge thoracic cavity/lungs, dropping intra-alveolar pressure, so larger inward flow of air Onset of expiration: relaxation of inspiratory muscles -at end of inspiration, inspiratory muscles relax and diaphragm returns to normal, lack of forces causing expansion of chest wall/lungs, lungs recoil/become smaller in volume -during expiration intra-alveolar pressure is higher, thus air moves into atmosphere until equilibrium - at end of inspiration/expiration intra-alveolar pressure=atmospheric pressure -intrapleural pressure< intra-alveolar pressure, thus keeping constant transmural pressure gradient and lung is always stretched even during expiration Forced expiration: Contraction of expiratory muscles -expiration passive process, by elastic recoil of lungs when inspiratory muscles relax and no muscle exertion/energy expenditure BUT does become active when expiring lungs completely/deeply/forcefully/during exercise, to further reduce volume of thoracic cavity/lungs with expiratory muscles -inspiration ALWAYS active process b/c only by contracting inspiratory muscles using energy -expiratory muscles muscles of abdominal wall and internal intercostal muscles, where abdominal wall contracts pushing diaphragm into thoracic cavity making it smaller/internal intercostal muscles contract to pull ribs down/in making thoracic cavity smaller -smaller thoracic cavity=smaller lung volume, so the air in lungs are conformed to a smaller volume thus intra-alveolar pressure rises -during forceful expiration, intra-pleural pressure rises to 766mmHg and intra-alveolar pressure rises to 770mmHg above atmospheric pressure, transmural pressure gradient keeps lung from collapsing AIRWAY RESISTANCE AND AIRFLOW RATES (table 13-1, pg. 483): -airflow affected not only by pressure gradients but also by resistance to airflow F (airflow rate)= delta P (atmospheric-intra-alveolar pressure) R (resistance of airways, determined by airway radius) -radius of conducting airways determine the resistance to airflow, but pressure is the significant determinant of airflow when airway radius is large enough to ignore -bronchodilation larger airway radius=smaller resistance -bronchoconstriction smaller airway radius=larger resistance AIRWAY RESISTANCE AND CHRONIC PULMONARY DISEASE: -chronic pulmonary diseases increases airway resistance from narrowing of lumen of lower airways, must work harder to breathe -a larger airway resistance requires a higher pressure gradient to maintain airflow -asthma thickening of airway walls, plugging of airways with mucus, exaggerated bronchoconstriction from smoking, dust, most common chronic disease -chronic obstructive pulmonary disease (COPD) slowly damages airways from smoking, coal dust, may lead to chronic bronchitis/emphysema -chronic bronchitis inflammatory condition of lower respiratory airways where airway lining thickens, mucous builds caused by smoking, polluted air, allergens -emphysema collapse of smaller airways, breakdown of alveolar walls, cause by destructive trypsin enzymes from alveolar macrophages that emerge to protect against cigarette smoke/other irritants, a-trypsin then inhibits trypsin but also lung tissues, which leads to breakage of alveolar walls, collapse of small airways -difficulty expiring increase in airway resistance from pulmonary disease makes expiration harder than inspiration since small airways may collapse during expiration LUNG ELASTICITY (fig.13-15, pg.485): -during respiratory cycle, lungs expand during inspiration/ recoil during expiration -2 interrelated concepts for pulmonary elasticity: compliance and elastic recoil -compliance effort/force required to stretch lungs (eg. work to blow balloon)  measure of how much change in lung volume results from change in transmural pressure volume, the force that stretches lungs -highly compliant lung stretches farther than a lower compliant lung for a given pressure difference -lower compliant lung needs larger transmural pressure gradient to stretch lung during normal inspiration, by greater expansion of thorax by inspiratory muscles -elastic recoil how readily lungs rebound after a stretch to preinspiratory volume -pulmonary elastic behaviour of lungs dependent on 2 factors: -pulmonary elastic connective tissue -alveolar surface tension Pulmonary elastic connective tissue -pulmonary connective tissue made by meshwork of bouncy elastin fibres Alveolar surface tension -alveolar surface tension thin liquid film ling each alveolus -an air-water interface causes a strong attraction b/w water molecules creating surface tension and elastic recoil and reduces alveolus size -greater surface tension= less compliant lungs ALVEOLAR STABILITY (table 13-2, pg.488): -if alveoli were lined with water alone, lung would collapse b/c of high attraction of water molecules and very low compliant lungs would require exhausting muscular efforts -2 factors that prevent alveolar collapse/alveolar/lung stability: -pulmonary surfactant -alveolar independence Pulmonary surfactant (fig. 13-16, pg.487): -pulmonary surfactant complex mixture of lipids/proteins secreted by type II alveolar cells, spreads b/w water molecules in fluid lining alveolus/lowers surface tension, thus increases pulmonary compliance reducing work of inflating lungs, reduces lungs tendency to recoil -law of LaPlace P= 2T P= inward-directed collapsing pressure r T= surface tension r= radius of alveolus -smaller alveolus= smaller radius= greater tendency to collapse BUT surfactant molecules are closer together in smaller radius thus preventing collapse Alveolar independence (fig. 13-17, pg. 488): -alveolar stability increases by interdependence of neighbouring/surrounding/ interconnected alveoli connected by connective tissue -when an alveolus collapses, surrounding alveoli stretch b/c they are pulled in direction of collapsing alveolus, BUT surrounding alveolus recoil from being stretched and exert expanding forces on collapsing alveolus to keep it open Newborn respiratory distress syndrome: -when premature babies don’t have enough production of pulmonary surfactant to prevent collapse of lungs, or will require strenuous inspiratory efforts -treated by surfactant replacement/drugs THE WORK OF BREATHING: -during normal breathing, respiratory muscles work for lung expansion against recoil forces/airway resistance during inspiration (active) but do not to expire (passive) - approx.. 3% body energy used for normal breathing with normal highly compliant/low airway resistant lung -4 forces that increase work/energy of lung: 1. decreased pulmonary compliance (pulmonary fibrosis) 2. increased airway resistance (COPD) 3. decreased elastic recoil (emphysema) 4. need for increased ventilation (exercise) HALF-FULL (fig.13-18, pg. 489): -healthy young adult male can hold maximum average 5.7L air, female 4.2L -normal/quite breathing is NOT maximal, but around 2.2L-2.7L -spirometer device that measures volume of air breathed in/out -know pg. 490 + fig.13-21, pg.491 EXAM!! Respiratory dysfunction: -2 general categories of respiratory dysfuntion: 1. obstructive lung disease 2. restrictive lung disease -other conditions affecting respiratory function: 1. diseases impairing diffusion of O2/CO2 across pulmonary membrane 2. reduced ventilation by neuromuscular disorders/respiratory muscles 3. failure of enough pulmonary blood flow 4. ventilation abnormalities/ poor matching of blood/air -diagnosis include spirometry, x-rays, blood-gas determination ALVEOLAR VENTILATION AND PULMONARY VENTILATION: -pulmonary/minute ventilation volume of air breathed in/out in 1 minute -respiratory rate averages 12 breathes/min -pulmonary ventilation= tidal volume x respiratory rate (mL/min) (mL/breathe) (breathe/min) Anatomic dead space (fig.13-22, pg. 492): -anatomic dead space portion of inspired air that stays in conducting airways and does not enter site of gas exchange in alveolus (approx. 150mL) -if 500mL is breathed in/out, only 350mL is actually exchanged b/w atmosphere/alveoli Alveolar ventilation: -NOT pulmonary/minute ventilation BUT amount of actual air in/out of alveolus -alveolar ventilation volume of air exchanged b/w atmosphere/alveoli per min. -alveolar ventilation= (tidal volume-dead space volume) x respiratory volume Effect of breathing patterns on alveolar ventilation (table 13-3, pg.493): -an increase in tidal volume increases alveolar ventilation BUT increase in respiratory rate is not fully toward increasing alveolar ventilation -increase in respiratory rate= increase in frequency with which air is wasted in dead space Alveolar dead space: -alveolar dead spaceany ventilated alveoli that do not participate in gas exchange with blood b/c they are poorly perfused -not all alveoli are equally ventilated with air/ perfused with blood LOCAL CONTROLS (fig.13-23, pg.494): -resistance of individual airways supplying specific alveoli can be adjusted independently by changes in airway’s local environment Effect of CO2 on bronchiolar smooth muscle: -if alveolus receives too little airflow (ventilation) than blood flow (perfusion), the CO2 levels will increase in alveolus/surrounding tissue b/c of CO2 from blood drops than is exhaled into atmosphere -increase in CO2 promotes relaxation of bronchiolar smooth muscle->dilation of the airway->decrease in airway resistance->increased airflow so airflow matches blood supply -decrease in CO2 promotes alveolus receiving too much air compared to blood, causing increased contractile activity of airway smooth muscle, constricting airway supply Effect of 02 on pulmonary arteriolar smooth muscle (table 13-4, pg.495): -cardiac output to diff. alveolar capillary networks can be controlled by adjusting resistance to blood flow through pulmonary arterioles -if blood flow greater than airflow to given alveolus, the O2 level in alveolus/surrounding tissues fall below normal causing vasoconstriction of pulmonary arteriole -vasoconstriction reduces blood flow to match lower airflow -increase in alveolar O2 from large airflow, small blood flow causes vasodilation -vasodilation increases blood flow to match larger airflow -systemic arterioles work opposite to pulmonary arterioles -2 mechanisms for matching blood flow/airflow work concurrently for efficient exchange of O2/CO2 GAS EXCHANGE: -purpose of breathing pickup of O2 by blood/remove CO2 unloaded from blood -blood transport system for O2/CO2 b/w lungs/tissues -tissue cells pick up 02 from blood and eliminate CO2 into blood to transport PARTIAL PRESSURE GRADIENTS (fig.13-24, pg.495): -gas exchange b/w pulmonary capillaries/tissue capillaries involve passive diffusion of O2/CO2 down partial pressure gradient, NO active transport for O2/CO2 Partial pressures: -partial pressure individual pressure exerted by a specific gas in a mixture of gases, proportional to the percentage of gas in the total air mixture Partial pressure gradients: -difference in partial pressure b/w capillary blood/surrounding structures -exists b/w alveolar air/pulmonary capillary blood causing gradient for diffusion of air OXYGEN ENTERS, CO2 LEAVES (fig. 13-25, pg.497): -magnitude of alveolar Po and Pco2, creates partial pressure gradient that moves the gases b/w alveoli/pulmonary capillary blood Alveolar Po2 and Pco2: -alveolar air does NOT equal atmospheric air b/c of 2 reasons: 1. different environments, as soon as atmospheric air enters respiratory system, contents of the body such as H2O/temperature changes the air 2. alveolar Po2 is lower than atmospheric Po2, b/c of dead space remaining in lungs/only small portion of alveolar air is exchanged with each breathe -O2 moves by passive diffusion down partial pressure gradient from alveoli into blood -CO2 continually produced by tissues as metabolic waste, and is continually added to blood through systemic capillaries -in pulmonary capillaries, CO2 diffuses down partial pressure gradient from blood into alveoli, and removed through expiration -alveolar O2 (100mmHg) and CO2 (40mmHg) stay relatively constant throughout respiratory cycle Po2 and Pco2 gradients across the pulmonary capillaries: -blood passing through lungs picks up O2 and drops off CO2 by partial pressure gradient b/w blood/alveoli -ventilation constantly supplies O2/removes CO2, thus maintains partial pressure gradient b/w blood/alveoli -blood entering pulmonary capillaries is systemic blood returned from tissues low in O2 (40mmHg) and high in CO2 (46mmHg), pumped from pulmonary arteries -alveolar air with Po2 (100mmHg) diffuses into this returning blood til’ no gradient, opposite for CO2, blood Pco2 (46mmHg) diffuses into alveolar air of Pco2 (40mmHg) til’ no gradient -again this blood flows back to tissue cells through the heart as systemic arterial blood -there is always a reserve of Po2 and Pco2 in blood and air at all times, O2 for tissue demand and CO2 (generates carbonic acid) for acid-base balance -amount of O2 consumed by tissue cells= amount of O2 diffused from alveoli/amount of CO2 picked up from tissue cells= amount of CO2 given to alveoli OTHER FACTORS (table 13-5, pg.498): -diffusion b/w alveoli/blood not only dependent on partial pressure gradients but also surface area/thickness of membrane/diffusion coefficient of the particular gas Effect of surface area on gas exchange: -surface area available for exchange increases during exercise b/c pulmonary blood pressure is raised and opens previously closed pulmonary capillaries -alveolar membrane are also stretched farther by increases tidal volume (deep breathing), increasing alveolar surface area/decreasing alveolar thickness -capillary transit time amount of time in which blood is in capillaries (at rest 0.75 sec/during exercise 0.4 sec) Effect of thickness on gas exchange: -gas exchange speeds when thickness separating air/blood decreases b/c gas takes longer to diffuse through larger thickness -thickness can increase in: 1. pulmonary oedema excess accumulation of interstitial fluid b/w alveoli/pulmonary capillaries 2. pulmonary fibrosis replacement of lung tissue with thick fibrosis tissue 3. pneumonia inflammatory fluid accumulation within/around alveoli Effect of diffusion coefficient on gas exchange: -diffusion coefficient(D) constant value related to solubility of a particular gas in lung tissues and to its molecular weight (D= sol sqrt. mw) -diffusion coefficient of CO2 is 20X higher than that of O2, but the partial pressure gradient of O2 at 60mmHg is higher so they balance out GAS EXCHANGE ACROSS THE SYSTEMIC CAPILLARIES: -just as in alveolar capillaries, O2/CO2 move b/w systemic capillary blood/tissue cells by passive diffusion down partial pressure gradient -arterial blood that reaches systemic capillaries is the same blood that left the lungs through pulmonary veins -only 2 places in circulatory system that facilitates gas exchange is in pulmonary capillaries/systemic capillaries, which both have equilibrated Po2 (100mmHg)/Pco2 (40mmHg) Po2 and Pco2, gradients across the systemic capillaries: -cells constantly pick up O2/produce CO2 through oxidative metabolism -O2 moves by diffusion down partial pressure gradient from entering systemic capillary blood (Po2 100mmHg) to adjacent cells (Pco2 40mmHg) til’ equilibrium -CO2 moves by diffusion down partial pressure gradient out of cells (Pco2 46mmHg) into systemic capillary blood (40mmHg) -this
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