Respiratory System.docx

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Department
Kinesiology & Health Science
Course
KINE 3012
Professor
Michael Connor
Semester
Winter

Description
Introduction st - 1 cell we start as has no function – multiplies o Multiple omnipotent cells – all the same, no specialization, ‘stem cells’can become anything – multiply  Highly specialized organ systems – i.e. epithelial, connective-tissue, nerve, and muscle cells 14 • End up with 10 cells - Levels – each step makes up the next, work together to keep homeostasis o Chemical o Cellular o Tissue o Organ o Body system o Organism - Differentiation: how one cell becomes many diverse cells o Signals within the embryo trigger the specialization of cells o Cells with common functions fuse to form organs o Highly complex tightly regulated process – the smallest deviation can throw off the balance  i.e. cystic fibrosis – 1 amino acid difference = disease - Homeostasis – our body wants to get back to its set norms when they are altered o Regulation of homeostasis occurs at many levels  Intracellular – within cells  Intercellular – between cells  Local – specific area, i.e. organ, hand  System  Organism – whole body integration, organs and systems communicating o Maintain homeostasis by balancing:  What we put in our bodies with what is removed from them  What our body produces with what it consumes o Failure to balance inputs and out puts (maintain homeostasis) results in disease  i.e. diabetes = the inability to balance insulin - Feedback systems – used to coordinate the responses of different organs/systems o Consists of:  Sensory system  Relay station – via brain and chemical messengers  Response system o Are organ specific o Are environment and stimulus specific o Used to maintain homeostasis o Negative feedback: response counteracts the initial stimulus  Ex: when you’re too hot, you sweat to cool off  Occurs at whole body, organ, tissue and cell levels  The most common form of feedback o Positive feedback: response adds to the initial stimulus  Ex: when you cut yourself, what is produced in response to exposure to the external environment increases the speed of clot formation  Ex: oxytocin is present during child birth, increases ability to give birth - Feedforward regulation – primes the system for challenges to come o Anticipatory situations o Ex: smell food, stomach churns/you salivate as if you’re actually eating o Ex: athlete’s HR increases same as when exercising… before the game starts o Potentially a learned response (inconclusive) - Homeostatic control summary: o Stability is achieved by balancing inputs and outputs o Sensory mechanism detects deviations from set points o Set points are maintained over a small range  Body responds to the smallest changes o Set points can be reset (up or down) o Hierarchy of control – some things are more important than others  i.e. more important to warm the core than the extremities Respiratory System - Passageway for O i2to the body and CO out2of the body - Helps regulate body pH (with the kidneys) o pH = the presence of H , 7.4 is normal - Phonation (speech) – air flows over our vocal chords - Maintains air quality – filters, warms, moistens - Uptake and removal of second messengers (i.e. hormones) - Dissolves small clots - Anatomy: o Lungs divided into L and R lobes o Nasal and mouth passages meet at the pharynx, divides into  Esophagus, to stomach, runs behind trachea  Larynx, vocal chords • Becomes the trachea – cartilaginous horseshoe rings in from (protective) – begins the conducting zone - Conducting zone – no gas exchange here, air moves quickly to the lungs o Consists of trachea, bronchi, bronchioles, terminal bronchioles o Airways lined on the outside with smooth muscle – can alter tube radius  Can alter air flow rates • So can changing the rate and depth of breathing o Airways lined on the inside with cilia, secrete mucus  Traps particles, pushes them upwards • Defect = cystic fibrosis  Respiratory bronchioles also lined this way - Respiratory zone – gas exchange occurs here o Consists of respiratory bronchioles, alveolar ducts, alveolar sacs o Airways branch – good for gas exchange:  Slows air  Increases surface area - Gas exchange occurs at alveoli o Alveoli are perfect for gas exchange  Are lined with epithelial cells and surrounded by blood vessels • Epithelial cells and capillary walls are only 1 cell thick  Distance between alveolus and capillary is only 0.5 μm  Balloon shape of alveoli gives greater surface area for diffusion to occur o Two types of alveolar epithelial cells  Type 1: flat for gas exchange  Type 2: reduces surface tension in alveoli • By secreting surfactant, a detergent-like substance • Makes alveoli easier to inflate o Reduce the strength of bonds between H O2molecules (are attracted to each other & want to collapse the alveoli) - Respiratory system is located in the thorax (chest cavity) – contains the lungs o Protective boundaries:  Top – muscles and connective tissue  Bottom – diaphragm  Walls – spine, ribs, intercostal muscles, connective tissue o Airtight – air can only get in through the larynx - Each lung is surrounded by a sac – pleura o Visceral pleura – attached to the outer surface of the lung o Parietal pleura – attached to the thoracic wall and the diaphragm o Pleura are very close to each other, separated by intrapleural fluid  Allows membranes to move over each other smoothly  Hydrostatic pressure of fluid = ip(intrapleural pressure) - Ventilation – air moves in and out of lungs o By bulk flow (F) – everything in, no selection or filtration o Movement of substances needs a pressure gradient  F = ∆P/R • ∆P = P alv → ipessure difference • R – resistance → airway diameter - Boyle’s Law determines pressures: P V = 1 V1 2 2 o P and V are inversely proportional - ∆P = air movement into/out of the lungs, no ∆P = no air movement o P atmdoesn’t really change o ∆P is what changes  ∆P is transpulmonary pressure (P ) tp • Ptp P -alv ip o PipP talvrevent collapse of lung  Pipushes in on alveolar walls  P pushes against P alv ip - Elastic recoil prevents the alveoli from always expanding o Elasticity from lung tissues work against P to tpose the lung o Dependent on the size of the lung  i.e. bigger lung = bigger elastic recoil o Passive, only changes because lung volume changes  When P > tpastic recoil – lung expands  Expanding lung increases elastic recoil  When recoil = P thtplung stop expanding  When P inipeases, P decrtpses  P tpelastic recoil causing lungs to get smaller  As lung gets small, recoil decreases  When recoil = P thtplung stops getting smaller - Before inspiration there is no net movement of air o P atm= Palv o P tpelastic recoil - Inspiration: pressure differences cause air to move in to the lungs o Diaphragm and intercostal muscles contract o Thoracic cavity expands, ↑V *we control this o P ip * we control this o P tpb/c there is a bigger difference between P and alv ip o Lungs expand b/c P > etpstic recoil o Palv– lower than P atm o Air flows into alveoli b/c P > P atm alv - Expiration: pressure differences cause air movement out of lungs (passive process) o Diaphragm and intercostal muscles stop contracting o Thoracic cavity recoils, ↓V o Pip o Ptp o Lungs recoil b/c P tpelastic recoil o P ↑ alv o Air flows out of alveoli b/c Patm< P alv - Negative P iiportant o Counteracts lung recoil pressure by making P > 0tp o Keeps the alveoli open - When anatomical structure is compromised P can bipome equal to P alv o Thorax is no longer airtight i.e. puncture wound in chest wall, hole in lung  Air goes into intrapleural space (P ipP )alv • Ptp 0 → recoil > P → tpng collapse o i.e. pneumothorax: P =ip = alv atm  No ∆P = lung collapse, nothing to counteract recoil pressure  Cure: drain fluid, seal hole – creates negative Pip lung can inflate - Compliance = ∆V/∆P tp o How easily the lung can expand and contract - Stiffness = opposite of compliance - Lung diseases affect compliance, making it more difficult to breathe o Increased compliance – small changes in P cause large changes in V  ↑ compliance, ↓ stiffness  Lungs are easy to inflate, but there is a loss of elasticity • Decreased recoil makes it difficult to breathe out o Decreased compliance – large P changes are required to cause changes in V  ↑ stiffness, ↓ compliance  Lungs recoil easily but require great pressure differences to open the lungs • High recoil makes it difficult to breathe in - Lung compliance determined by o Stretchability of connective lung tissue  The thicker the tissue, the less compliant (harder to inflate) o Surface tension at air-water interface  Water lining of alveoli want to collapse the sac • Resist expansion in inspiration  Makes breathing more difficult  Surfactant counteracts this – decreases work of breathing - Surfactant is important because it counteracts the Law of Laplace: P = 2Tension/radius o If there wasn’t any surfactant, P would be greater in smaller alveoli and would move along its gradient into larger alveoli  Eventually the smaller alveoli would collapse  Less alveoli is bad for gas exchange  Large alveoli are inefficient – gas exchange only occurs with the air near the membrane but there is a lot of air in the middle of the alveoli that won’t have an opportunity to participate in gas exchange o Surfactant is more concentrated in smaller alveoli so its effects are greater  There is more surface tension in smaller alveoli  This equalizes the pressures throughout the lung  Smaller alveoli don’t collapse b/c air doesn’t flow from small to big Airway resistance (R) - F = ∆P/R - Inversely proportional to bulk flow – increasing one decreases the other - R is usually low in airways – air moves in and out easily - Dependent on: o Tube length (fixed) – ↑length, ↑R o Interaction between gas molecules – lighter gases move more easily (i.e. He) o **Airway radius (regulated) – most important – changes with every breath  Area = πr2 - Influenced by: o Physical factors  Transpulmonary pressure: ↓R, ↑F  Mucous accumulation: ↑R  Elastic connective tissue (connects airways to alveoli): ↓R when lungs expand – tissues pull and airways also expand o Neuroendocrine (produced by nervous system)  Parasympathetic (acetylcholine): ↑R by constricting airways (↓r)  Epinephrine: ↓R, causes smooth muscle to dilate airways (↑r)  Vasoactive peptide: ↓R, dilates trachea when blood vessels dilate o Paracrine (produced in airways)  Histamine: ↑R, dilates blood vessels, constricts airways • Airways fill with blood and mucous • i.e. allergic reactions, bee stings  Eicosanoids: have effects ** All have effects in conductive zone (barriers to alveoli) except mucous - Any change in R, affects airflow Airway diseases: - Obstructive diseases – air passages are obstructed o Asthma:  Smooth muscles surrounding airways contract (protective)  Airways become inflamed in response to irritants  Hyperresponsive to triggers: • Exercise (most grow out of this), smoke, pollutants  Treat with: • Anti-inflammatories (orange) – glucocorticoids, leukotriene inhibitors – steroids taken on a regular basis to make airways less responsive to triggers o Not good for immediate effects (i.e. attack) o Long-term steroid treatment is harmful to the body • Bronchodilators (blue) o Relax airways – mimic epinephrine, inhibit acetylcholine o Immediate affects (for attack), also taken on a regular basis o Chronic Obstructive Pulmonary Disease (COPD):  Emphysema – destruction/collapse of small airways • Connective tissue where alveoli are located is lost, not available for gas exchange • Lung easily inflate, can’t deflate (↑ compliance)  Chronic bronchitis – excessive mucous production in smaller airways • ↓ airway r, line alveoli making diffusion more difficult ** Same agents cause COPDS – if you have one, you probably have both - Each diseases results in ↑ R and ↓ F o Gas exchange is compromised o Oxygenation of blood is impaired o Breathing is more work – greater ∆P is required - Restrictive diseases – lungs lose their normal elasticity o R is normal, lung capacity is reduced o Caused by diseases of:  Pleura – ability of pleural space to controipP (and thus lung inflation) is compromised, i.e. pneumothorax  Pulmonary fibrosis – thickening of alveolar walls • Elastic tissue turns into connective tissue, lung unable to stretch/inflate as well  Neuromuscular disorders – affect nerve or muscle function, loss of control over diaphragm and intercostals – unable to control pressures as well • i.e. polio, amyotrophic lateral sclerosis (ALS), myasthenia gravis, muscular dystrophy - Memorize lung volumes – see Lab. 1 - Minute ventilation = tidal V (mL/breath) x respiratory rate (breaths/min) o Amount of air moved per minute o V E V xtf = 500 mL/breath x 12 breaths/min = 6 L/min - Not all air that is inhaled is available for gas exchange - Alveolar ventilation (VA) – amount of air moved into/out of the alveoli/min OR amount of air available for gas exchange/min o 500 mL of air moves in and out between the atm. and the respiratory system  350 mL of fresh air reaches the alveoli  150 mL of air is trapped in the mouth/trachea/bronchioles and doesn’t make it to the alveoli – “dead space” o 500 mL of air move in and out of the alveoli with each breath  150 mL is old air from the dead space (left from preceding inspiration)  350 mL is fresh air from the atmosphere o Only 350 mL are actually exchanged between the atmosphere and the alveoli o V E (V –tV ) D f = (500 – 150) mL/breath x 12 breaths/min = 4.2 L/min  1.8 L/m is lost to dead space, never makes it to the lungs - V A V E o If you take more breaths, more air is moved o But if the breaths are shallow, less air can be exchanged (↑f, ↓t) o Therefore: ↑ V Eoesn’t necessarily ↑ V A  This is why dead space can have a big effect on V A if only 150 mL is inhaled in a breath, that air is trapped in the airways • No air is available for gas exchange no matter how many breaths are taken - Diffusion – interaction between alveoli (air) and blood vessels (liquid) o Movement from areas of high concentration to low concentration o Until equilibrium is reached o Biggest barrier to diffusion is distance - Gas exchange o Takes place between:  Blood and alveoli – uptake O , 2ump CO 2  Blood and tissue – uptake CO , d2mp O 2 o Is dependent on pressure differences; pressure is dependent on:  Temperature  ** Concentration – # of molecules/volume • Concentration is proportional to pressure - Dalton’s Law of Partial Pressures – in a mixture of gases, the P of each gas is independent of the others o P = total pressure (P ) x gas fraction (F ) p atm gas  Patm(760 mmHg) consists of: • 79% N →2F = 0N29 • 21% O →2F = 0O21 • 0.3% CO → 2 CO2= 0.003 - Normally P iO2higher and P CO2 is lower in the alveoli than in the blood o This difference allows to two gases to move along their pressure gradients - PO2s lower at altitude – remember P = Pp atmx Fgas o F is constant O2 o Patmis reduced – 250 mmHg o Bad – high P aO2 low P CO2is required at the lung to drive O 2nto the blood and CO out of the blood to be exhaled 2  If these pressures aren’t maintained, O c2n’t be transported to the tissues b/c the pressure is higher there than in the lung • Pressures flow from high to low – pressure differences in alveoli and blood drive gas movement o P can be increased by increasing F – why people bring O tanks to Everest O2 O2 2  Inhaling 100% O in2reases the driving pressure of O 2 - In expired air PO2s lower and P CO2 is higher than in inspired air o FO2 0.17 – we take up 4% of O and 2eplace it with CO o FCO2 = 0.037 - Henry’s Law: the volume of [gas dissolved in a liquid] is proportional to the P of phe gas o C gas P gasx k  C – concentration of gas in a liquid (mL/dl) gas  k – solubility coefficient of the gas in the liquid • Lower k, higher P required to dissolve that gas into a liquid o i.e. N2doesn’t dissolve into our blood because it’s k is so low, Patmisn’t high enough to dissolve it • k > k – CO dissolves more easily into our blood than O CO2 O2 2 2 Oxygen and Carbon Dioxide Exchange caused by Partial Pressure Gradients - In the atmosphere: o PO2s high, 160 mmHg o PCO2 is low, 0.23 mmHg - #1 In the alveoli: o P O is relatively high, 100 mmHg A 2 o PACO i2 relatively low, 40 mmHg - #2 In the veins coming back from the tissues: o PVO 2s relatively low, 40 mmHg o PvCO i2 relatively high, 46 mmHg - There is a partial pressure gradient between the alveoli and the veins – causes passive diffusion of O 2nto the blood and CO in2o the alveoli o Until blood and alveolar pressures become equal  #3 Happens in the arteries leaving the lungs – deliver to the tissues • PaO 2s relatively high, 100 mmHg • P CO is relatively low, 40 mmHg a 2 - #4 In the tissues: o O 2s consumed, low, < 40 mmHg o CO 2s produced, high, > 46 mmHg - There is a partial pressure gradient between the arteries and the tissues – causes passive diffusion of O 2nto the tissues and CO i2to the blood o Until blood and tissue pressures become equal  Blood is now venous (#2) – returns to lungs to pick up O an2 dump CO 2 - In disease states: o Hyperventilation  Over ventilation  Ventilation > metabolic rate (CO p2oduction)  Breathe out more CO th2n can be breathed back in • In alveoli – PCO2↓, PO2 • More like atmospheric air • Throws off body pH o Increasing O c2uses a decrease in CO whic2 has a direct effect on H levels (↓)  Enzymes won’t work • Breathe into a paper bag, bring up CO levels 2  Different than hyperpnea, which occurs during exercise • Ventilation and metabolic rate are proportional o Hypoventilation  Under ventilation  Ventilation < metabolic rate (CO 2roduction)  In alveoli – PO2, P CO2↑ Factors that affect A O2and P AO 2 P A 2 PACO 2 Altitude - ↓ Patmauses ↓ P O2
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