The Respiratory system Flashcards

Question

quiet insipiration

Answer 1

1. diaphragm contracts to inc height of thoracic cavity (by pulling down) 2. external intercostal muscles contract to lift ribcage up and out small changes in all 4 direction= overall inc in volume of 0.5L = drop in P of 1 mmHh air rushes in, inspiration ends when intrapulm P = atmo P at same time, intrapleural P drops to about -6mmHgq

Answer 2

passive, depends more on elastic recoil of lungs than on muscle contraction inspiratory muscles relax, rib cage descends, lungs recoil thoracic and intrapulmonary volumes dec = sp intrapulmonary pressure inc, +1mmHg, so breathe out = gas out to relieve P and go back to atmo P

Answer 3

accessory muscles (neck and chest) raise ribs more by straightening spine

Answer 4

contract abdominal wall muscle,s inc intra-abdominal P depress rib cage using internal intercostal muscle

Answer 5

airway resistance Alveolar surface tension lung compliance

Answer 6

gas flow = P gradient/resistance resistance det by diameter of conduction tubes insig in healthy indv - airway diam at beginning are large -as d dec = number of branches inc - gas flow stops at terminal bronchioles, so resistance is no longer an issue since greatest resistance is at the levels of medium bronchi neural influences - parasympathetic NS = inhaled irritants, histamine, consitrcts bronchioles also during astham attack sympathetic ns = dilates bronchioles disease = mucus, infectious material, tumours, = source of airway resistance

Answer 7

surface tension in gen, at any gas/liquid boundary, the molecs of liquid are more attracted to e/o than the gas, so a) liquid molecs are drawn more closely together, reducing contact w gas molec b) resist inc SA water has extremely high surface tension, if only water in alveoli, would cause collapse, bc strong attraction would cause the alveoli to shrink into itself surfactant = detergent like lipoprotein, prod by type II cells, interferes w cohesiveness of water molecs, prevents alveolar collapse during expiration

Answer 8

premature babies don't prod enough surfactant so alveolus must be re inflated w every breath, too much work

Answer 9

refers to ease w which lungs can be inflated the more a lung expands for a given inc in transpulmonary P, the greater its compliance depends on a)distensibility of lung tissue (flexibility/elasticity) b) alveolar surface tension high surface tension = low surfactant = more resistant = harder to inflate + vice versa compliance is dec by any factor that a) reduced the natural resiliance of lungs (fibrosis) (becomes more fibrous, less elastic) b) inc surface tension of alveolir fluid, dec surfactant, makes more polar c) impair flexibility of thoracic cage, normal w aging, rib cage can't move as easy

Answer 10

tidal volume = amount of air inhaled or exhaled per breath during normal, quiet breathing = 500 mL inspiratory reserve volume= amount of extra air that you can inhale after a normal breath = 3100 mL expiratory reserve volume =amount of extra air that you can exhale after a normal breath = 1200 ml residual volume = no matter what, can't be pushed out, protects against collapsing = 1200 mL

Answer 11

inspiratory capacity = air that can be inspired after tidal expiration ex. breathe out like normal , pull in as much as you can functional residual capacity = volume of air in lungs after tidal expiration, can't be measured bc includes residual volume vital capacity = total amount of exchangeable air, push as much as you can, pull in as much as you can total lung capacity = sum of all lung volume can't be measured bc involves residual volume.

Answer 12

= air that fills passageways but doesn't participate in gas exchange ex. if tidal volume is 500 mL, and dead space is always going to be 150 mL so alveolar ventilation will be 350 mL if some alveoli are dysfunctional then total dead space V = 150 mL + alveolar dead space so V = normal V + additional dead space if volume of air exchange inc per breath, relative V of dead space dec, absolute V won't change, but more V of air would make up the alveolar ventilation portion of the equation

Answer 13

better index of effective lung ventilation takes into account the volume of air in dead space areas and measures flow of fresh gases in/out of alveoli per unit time AVR (mL/min) = frequency (breaths/min) x (total V - dead space) (ml/breath) if healthy, 12 x (500-150) = 4200 ml/min better to inc volume of each inspiration than to inc respiration rate bc dead space volume stays the same, so if you inc rate, you're taking less volume in but still subtracting 150, so TV is less if dec rate, you're getting more in at a time

Answer 14

1. spasm of diaphragm = irritation of phrenic nerve air hits vocal folds of closing glottis 2. very deep inspiration that ventilates all alveoli not triggered by O2 or CO2 levels in blood 3. blast of air from lungs through briefly opened glottis to dislodge foreign particles, or mucus from resp tract 4. like a cough, but through nasal cavity to clear upper resp passageways.

Answer 15

Total P exerted by a mixture of gases = sum of P exerted by each gas in the mixture partial P is directly prop to its % in mixture high altitudes = all partial P dec in direct proportion total P is less, so ratio is same but partial P is lower, absolute amount is less below sea level = atmo P dec by 1 atmo for ever 33 ft, partial P inc accordingly in atmo N = 79% O= 21% in alveoli the air is gonna pick up moisture on its way down and exchange/comnine w gas all in there, that has all unloaded Oxygen + picked up Co2 so partial P of ____ = ____ N= dec O = dec CO2 = inc water = inc

Answer 16

diff from atmo, (more H20 and Co2, less O2) bc 1. O2 from air to blood and Co2 from blood to air in lungs **O2 has already unloaded and CO2 picked up 2.conducting zone pathway has humidified and moisturized air 3. alveolar gas mixed w new atmo gas w every breath inc depth of breathing inc alveolar O2 P and decreases CO2 P breathing more in from atmo = more oxygen, less in CO2,

Answer 17

PP gradients and gas solubulites structural characteristic of respiration mb ventulation/perfusion coupling

Answer 18

very short time to give O2 and pick up Co2 is PP grad is steep = moves more easily, shallow = still moves but not as quick for oxygen, steep, 104 vs 40 mmHg, in lungs vs caps eqm Is met in 0.25seconds, 1/3 of the time RBC is in the pulmonary capillary, so if blood is circulating more rapidly, under excerise, there is still plenty of time for that gas to exchange or for o2 retrieval to occur. for CO2, gradient is flatter, 40 vs 45 mmHg in lungs vs caps eqm at 40 mHg and gradually expelled during resp gas solubilizes = how easy is it for that gas to move from air to fluid, for O2 from air to blood, for CO2 from blood to air. even if gradients are diff, same amounts of CO2 and O2 are exchanged, because CO2 is 20x more soluble in plasma and in alveolar fluid than O2

Answer 19

thickness = if healthy no problem, 0.5 too 1 micrometer if has pneumonia = fluid buildup inc thickness and dec gas exchange = harder to diffuse through a significant amount of fluid. we want a thin barreier so resp gases can exchange easily Surface area = health = huge amount 40x the SA of skin, why is so easy to get O2 and unload Co2, a lot to work w reduced by emphysema, tumours (block entry), mucus, infmatory material emphysema = alveoli are damages, blown up, less SA to work w

Answer 20

coupling bn amount of gas reaching alveoli and blood flow in pulmonary capillaries (local auto regulation) arteriole diameter changes based on O2 P in alveoli, when ventilation is poor, PO2is low, so arterioles constrict for blood to be redirected to where PO2 is high bronchiole dameter changes based on PCO2 high alveolar PCO2 causes bronchioles to dilate so CO2 can be eliminated more rapidly where PCO2 is low, constrict lungs can comensate for any problem, will redirect to alveoli that are well ventilated, if blocked off, won't send blood to them, matching how much blood is sent based on how well there is gas exchange going on

Answer 21

same sort of PP but in opp direction 40 vs 104 in tissues vs arterials = PO2 45 vs 40 in tissues vs arterials = PCO2 exchange occurs and venous blood draining tissues has PO2 of 40mmhg and PCO2 of 45 mmHg, like that entering the lungs

Answer 22

2 ways 1. bound to Hb within RBC = majority Hb = 4 polypeptide chain, each w heme group, w Fe 2. dissolved in plasma, little bc poorly soluble in water

Answer 23

oxyhemoglobin = HbO2, reduced hemoglobin = HHb HHb + O2 <=> HbO2 + H+ when O2 comes off the iron in hemoglobin, there is a H+ assoc w the heme grp that takes its place until another O2 comes and kicks it off

Answer 24

O2 is loosely bound, if too tight, won't be able to get to tissues, we want it to be able to come off to O2 poor tissues affinity of Hb for O2 depends on level of saturation fully sat = all 4 hemes have O2 partially sat = 1, 2 or 3 hemes have O2 **if Hb has no O2, hardest thing is to get 1st one to get in, when 1st binds, it changes shape to make it easier for rest to bind vice versa, easier for first 3 to come off, harder for 4th

Answer 25

PO2, temp blood pH PCO2 BPG in blood = produced by RBC when they metabolize glucose

Answer 26

steep at first, plateaus further down Hb in blood leaving lungs is 98% saturated, just topped off their supply O2 poor tissues = 75% sat high altitudes= Hb is almost completely sat at 70 mmHg, but at high altitudes, PO2 in air is lower, so alveolar PO2 drops. but since Hb is still 90% sat, it is still tolerable for it to be drastically changes, PO2 must drop further. Cardiopulmonary Disease → buildup of fluid in lungs, no good gas exchange, PO2 will be lower, since at 70mmHg is pretty full, a mild drop won't be too bad but a significant drop will cause a problem in O2 delivery. venous reseve = only 25% of O2 is unloaded during first pass through tissues excerise becomes a signal that body is using O2 faster(bc PO2 is dropping) so we unload more O2, gradient becomes steeper, easier for exchange

Answer 27

so with high PO2, large changes in PO2 causes small change inHb sat, ex. from 100 to 80 mmHg of PO2, drop is only 3% of saturation (high altitudes) at low PO2, large changes in PO2 cause large changes in Hb sat. ex. resting tissue = 75% saturation = 40 mmHg of PO2 active tissues = 40% sat, at 20 mmHg when excising drop is 3% vs. 35% within the same drop of mmHg

Answer 28

increasing O2 unloading from blood = inc in temp, inc PCO2, H+ (dec in pH) decreases affinity for Hb for O2 goes R Decreasing factors = increases Hb affinity for O2, holds on more tightly, shifts left. BPG = produced by RBC, binds reversibly to Hb to dec affinity for O2, changes shape a little, makes it easier for O2 to come off and go to tissue. made more rapidly if tissue is warmer and more metabolically active.

Answer 29

CO2 is highest at level of tissues = Co2 buildup in tissues encourage more O2 to come In CO2 released to blood inc H+ content of blood inc CO2 = inc formation of bicarb and H+ **Bohr effect = weakening bond of Hb and O2, by adding H+, makes it so that O2 is released more quickly to tissues heat is a by poriduct of metabolic activity, higher temp in RBC= dec affinity for O2, + inc BPG = more O2 unloading

Answer 30

1. dissolved in plasma = 7-10% 2. bound to Hb as carbaminohemolobin binds to aa of Hb, so no competition w O2 for binding. loading and unloading of CO2 on Hb is depending on a. PCO2: low in lungs so dissociate from Hb high CO2 in tissues so ends to Hb b. Hb saturation. HHb binds more CO2 in tissues, than HbO2 in lungs = Haldane effect = HHb unloaded O2 so diff shape that can accommodate the CO2 than a fully sat O2) 3. bicarbonate ion in plasma (70%) conversion to an unstable H2CO3 then HCO2 and H+ in RBC = carbonic anhydrase Cl shift = bicarb diffuses to plasma, so influx of Cl0 to balance negative charge.

Answer 31

1. dissolved in plasma= moves out of plasma 2. bound to Hb= released and moves out 3. Back into RBC, back to CO2 and H2O and moves out

Answer 32

CO2 + H20 = H2CO3 = HCO3- + H+ H+ buffered by Hb or proteins in RBC or plasma, when Hb doesn't have O2, it picks up a H+ in its place HCO3- = diffuses into plasma, alkaline reserve part of H2CO3 - HCO3 buffer system a) shallow, slow breathing = CO2 accumulates in blood, H2CO3 accumulates, inc H+, blood pH drops b) rapid deep breathing = hyperventilating = blowing off CO2 faster than making it, CO2 flushed out of blood, H2CO3 drop, H+ drop, pH rises we can adjust blood pH and blood acid/base balance by respiratory ventilationr

Answer 33

2 areas. ventral respiratory group dorsal respiratory group VRG pacesetting resp centre = inspiratory centre = in charge phrenic and intercostal nerve stim contraction of diaphragm = thorax expands = so you breathe in, when relax those muscles (VRG expiratory neurons fire), you breathe out eupnea = normal rate of breathing, 12-15 breaths/min OD on sleeping pills, morphine, alcohol = complete suppression of VRG = not telling you to breathe, id not conscious = resp is shut down = won't breathe

Answer 34

PCO2 is the actual boss that regulate breathing rate, breathe more rapidly to get rid of CO2 if too high (as well as H+) chemoreceptors 1. central = bilaterally in medulla (assoc w brain areas) 2. peripheral = vessels of neck (aortic arch and carotid arteries_ less important is O2

Answer 35

most closely controlled peripheral receptors only weakly influenced by CO2, regulation is mainly influenced by medullary chemoreceptors (to brain) were trying to keep arterial PCO2 at an okay level, if CO2 build in CSF of brain, turns into HCO3 + H+, so inc in H+, but CSF doesnt have plasma proteins so can't buffer that accumulation, so pH of CSF drops, signals central receptors inc rate and depth of breathing to get rid of CO2 ***inc H+ is the trigger for receptors, even if initiated by inc in CO2

Answer 36

hypercapnia = inc PCO2 hyperventilation = inc rate/depth of breathing = ends when PCO2 goes back to normal

Answer 37

critical importance of CO2 during respiration if you take breaths before eyou jump, you artificially dec CO2 levels, but O2 stays the same, body only initiated breathing by accumulation of CO2, but since you artificially dec it, delays the urge to breathe Oxygen levels are dropping but brain doesn't signal to breath in time dec level of O2 = black out zone, we meet this point before our body sees an accumulation of CO2, before out body says to breathe.

Answer 38

O2 sensors in aortic and carotid arteries small changes trigger inc sensitivity of PCO2 receptors large drops = imp stimulus for inc ventilation emphysema = chronically high PCO2 levels, chemoreceptors become used ot it and become unresponsive, so PO2 takes over= hypoxic drive

Answer 39

used to be thought of as the inspiratory centre, now VRG has that role not completely understood, role = integrates info coming from chemoreceptors and peripheral stretch

Answer 40

pH can alter breathing even if P of CO2 and O2 are normal H+ diffuses into CSF, inc resp mediated by peripheral receptors

Answer 41

hyperventilates involunatrily = hypocapnia = cerebral vessels constrict = could feel dizzy and faint solution = breath in and out of paper bag, breathing same CO2 that breathing out

Answer 42

inflation reflex lungs inflate strongly = stretch receptors in pleurae and conducting zones sends inhibitor impulses to medulla resp centres to stop inspiration and allow expiration lungs recoil, receptors quiet, loop starts again goal = protect the lungs from being damaged (from overstretching) , only kick in under extreme conditions

Answer 43

involuntary in strong emotion/pain gasp = surprised holding breath when angry gasping for breath in cold water

Answer 44

conscisos control over rate/depth of breathing holding breath or deciding to take. deep breathe bypass medulla centre = if CO2 in blood is too high, resp centre take over

Answer 45

breathing deeply during and after as excising, going through more O2, and more CO2 production hypervent = breathing more rapidly and deeply than need to, dec CO2 levels intensely hyperpnea = in a marathon, making CO2 maintained at right level, matching rate and depth of breathing to what you need to unload 1. increase ventilation as you begin to exercise due to - anticipation and learned resposne -muscles moving around more, contracting more, body temp inc as muscles generate heat - activation of SNS, 2. gradual inc to steady state, matching things well 3. when stop, esp abruptly , breathing dec to baseline levels 4. gradual decline = repaying oxygen debt.

The Respiratory system Flashcards

Lecture 7, part B + L8 + L9