RESPIRATORY SYSTEM Flashcards

Question

type I alveolar epithelium

Answer 1

- make up the walls of the alveolus, alveolar ducts, & some parts of the respiratory bronchioles - thin ➞ facilitate gas exchange - form to create alveoli - alveoli adjacent to each other tether together ➞ expanding alveoli pull on adjacent alveoli via tether fibers

Answer 2

- produces surfactant ➞ allows us not to waste energy to breathe - interspersed w/in type I (fewer) - surfactant gets dispersed along surface - ends up on thin layer of water that’s inside alveolus

Answer 3

- **diaphragm** = skeletal muscle at base of thoracic cavity - inspiration - contracts during inspiratory effort - chest wall - ribs & cartilage - intercostal muscles - **parietal pleura** = membrane that lines chest wall & diaphragm - joins with visceral pleura - **visceral pleura** = membrane lining lungs - **pleural cavity/intrapleural space** = space btwn lungs & chest wall btwn parietal & visceral pleura

Answer 4

TV = amount of air we breathe in/out during normal breathing - resting TV ≈ 500 mL

Answer 5

IRV = amount of air that is voluntarily inhaled above TV - ~2-25L - inherent (cannot train for)

Answer 6

ERV = max expired air past TV - ~1.1-1.5 L

Answer 7

RV = amount of air remaining in the lungs after max expiration - residual air

Answer 8

FRC = amount of air remaining in lungs after normal passive expiration - ERV + RV - **capacity** = adding 2+ volumes together

Answer 9

VC = overall breathing range - ERV + TV + IRV - inherent ➞ associated w/ anatomy - ↓ w/ age ➞ posture associated

Answer 10

- higher pressure towards bottom of chest cavity due to gravity & the way the lungs hang - intrapleural space created by 3 tendencies to recoil: 1. lung parenchyma = lots of elastin ∴ when lung stretches it naturally recoils **inwards** 2. **chest wall** at FRC has a natural tendency to recoil **outwards** due to cartilage structure 3. **diaphragm** recoils **upwards**

Answer 11

pressures acting on a wall - P(TM) = P(inside) − P(outside) → alveolus − intraplueral - ⊕ transmural force causes ↑V ∴ lung expands - ⊖ transmural force causes ↓V ∴ lung collapses

Answer 12

- Patm never changes → Patm = 760 mmHg - ∴ Palv must change - inspiration: Palv < Patm - expiration: Palv > Patm - if Palv = Patm → no flow (e.g. at end of expiration (@FRC) or at top of inspiration) - to change Palv: change lung volume using transmural pressures (acts against elastic recoil + surface tension forces) - elastic recoil pushing in (due to elastin) - surface tension pushing in (due to water cohesiveness) - transmural force pushing out aka P(lung) - ⊕ transmural forces will expand the lung (generated by us) - ⊖ transmural forces will collapse the lung (only during forceful expiration, not normal breathing)

Answer 13

P(alv) − P(IP)

Answer 14

- Palv = 760 mmHg (same as atm) - on avg ≈ 756 mmHg ∴ P(lung) = +4 - at top of lungs: 750 mmHg ∴ P(lung) = +10 - at bottom of lungs: 759 mmHg ∴ P(lung) = +1 - elastic recoil + surface tension inwards opposes transmural force at -4 mmHg - P(lung) > P(ER+ST) = ↑ transmural → expansion

Answer 15

transmural forces must be larger than forces of elastic recoil + surface tension - P(lung) > P(ER+ST)

Answer 16

pressure of elastic recoil + surface tension must be larger than transmural force acting on the lung - P(ER+ST) > P(lung) - at top of inspiration: P(lung) = +6 mmHg balances P(ER+ST) = -6 - as we relax inspiratory muscles, thoracic volume ↓➞ P(IP)↑ from 754 → 756 mmHg - now P(lung) = 760 − 756 mmHg = +4 but P(ER+ST) = -6 - larger elastic recoil + surface tension inward is how lung decreases in size

Answer 17

1. **diaphragm**: goes down → expands in caudal direction 2. **external intercostals**: pull rib cage upwards, allow chest wall to recoil 3. **sternocleidomastoids**: pulls chest upwards **during exercise or forced expiration** 4. **scalenes** in upper shoulders elevate the first rib **during exercise or forced inspiration**

Answer 18

- in alveoli in lung due to H2O cohesiveness - in small alveoli: H-bond strength is very large - large alveoli has same # of H2O mol just spread apart ∴ H-bond strength decreases - **law of laplace**: P(collapsing) = (2 x ST)/radius - collapsing pressure is trying to make alveoli smaller - as the radius increases, the collapsing pressure decreases - ∴ small alveoli are harder to inflate while large alveoli are easier to inflate - resistance factor at **small volumes** - **surfactant** from type II alveolar epithelium helps reduce ST - phospholipids sit btwn H2O mol ↓ ST - ↓ amount of energy required at start of inspiration

Answer 19

P(collapsing) = (2 x ST)/radius - as the radius increases, the collapsing pressure decreases - small alveoli are harder to inflate - large alveoli are easier to inflate

Answer 20

**passive expiration**: ↓ thoracic volume by relaxing inspiratory muscles - diaphragm moves up - ribcage moves down & inwards **forced expiration** - internal intercostals - abdominal muscles

Answer 21

- phenomenon that inspiration & expiration take 2 different pathways - our normal breathing shows less hysteresis b/c we don’t go to <50% total lung capacity - #1: hard to increase volume initially (@ TLC =10%) due to cohesive attraction of H2O mol (surface tension) - #4: hard to increase volume at TLC ~90% due to elastic recoil force

Answer 22

- **elderly person** = bent over ∴ more difficult to breathe - prevents easy expansion of the chest volume - overall stiffness of joints - young persons: posture affects how the lung hangs in the thoracic cavity - more squished at the bottom: P @ 759 - more space at the top: P @ 750 - decreased pressure at top creates larger alveoli - in an upright indiv @ FRC - the top alveoli are very large due to large P(lung) (+10) - alveoli at bottom are small due to small P(lung) (+1) - ∴ elastic recoil for top alveoli is larger (-10) compared to bottom (-1) - ∴ inspiratory effort preferentially inflates bottom 1/3-1/2 of the lung because of larger elastic recoil at top - **differential in ventilation of the lung**: preferentially ventilate bottom of lung first

Answer 23

max forced expiration ➞ increased intrapleural pressure which collapses bronchioles in lower airways - contract abdominal muscles + intercostal muscles + posture change (to ↓ thoracic V ∴ ↓P) - P(bronchiole) = P(inside) − P(outside) = 785 - 786 = -1 - bronchioles have no cartilaginous support - ⊖ transmural force collapses the lung - collapse prevents air from flowing out - common in patients with emphysema

Answer 24

- radius = major static resistance - bronchioles have lowest resistance because of accumulative aggregation of 100,000+

Answer 25

air moves in layers - air in center has fastest velocity - outer edges ↓ velocity (↑ resistance from contact w/ walls) - typical of regions where airflow velocity is low

Answer 26

= dynamic resistance - associated w/ **fast velocities & branches/edges**

Answer 27

- in between laminar & turbulent - characteristics of both

Answer 28

assesses whether the flow will be laminar vs turbulent - Re > 3000 = turbulent flow - Re < 2000 = laminar flow - 2000 > Re > 3000 = transitional flow - Re = (2 x r x V x ρ)/η - fastest velocity in biggest airways = turbulent (trachea & bronchi) - bronchioles have slowest velocity - bigger radius = more turbulent flow - smaller radius = smaller reynold’s number = laminar flow (bronchioles)

Answer 29

large airways have less static resistance due to radius size but larger dynamic resistance due to reynold’s number & turbulent flow

Answer 30

smaller airways have more static resistance due to radius but smaller dynamic resistance due to reynold’s number & laminar flow

Answer 31

- autonomic input **changes radius** & **primarily affects static resistance** - SMC contract → makes bronchioles smaller in diameter (bronchoconstriction) → ↑ R - SMC relax = bronchodilation → ↓ R - bronchioles = primary resistance sites 1. response to **↑ PSNS** input = bronchoconstriction → matching bf to lungs w/ air flow 2. response to **↑ SNS** input = bronchodilation & ventilate portions of lung not previously ventilated (**β-adrenergic response**) 3. ↑ **histamine release** from immune cells causes constriction of bronchioles & alveolar ducts (although alveolar ducts do not have SM)

Answer 32

1. static resistance from radius 2. dynamic resistance from airflow & the renold's number 3. autonomic input to bronchiolar sm 4. lung volume 5. luminar & interstitial gases

Answer 33

as lung V↑ → R in bronchioles ↓ - alveoli ↑ in size & are mechanically tethered to the bronchioles - enlarged alveoli pull on the wall of the bronchiole → ↑ radius - maybe allows bronchioles to overcome collapsing transmural forces

Answer 34

- as interstitial PCO2 ↑ → causes causes SMC to relax ∴ bronchodilation ➞ R↓ → ↑ airflow - more predominant effect than PO2 - as interstitial PO2 falls → bronchodilation (SMC relax) ➞ R↓ → ↑ airflow - matching ventilation to perfusion

Answer 35

- have highest velocities & largest diameter ∴ Re is big ➞ turbulent flow = resistance due to reynold’s number - air pressure falls w/ resistance ∴ not enough pressure to withstand surrounding pressure ➞ can lead to dynamic collapse - cartilage protects 1º bronchi & trachea from dynamic collapse

Answer 36

have slowest air velocities & smallest radius ∴ Re is small ∴ air flow is laminar - resistance due to reynold’s number is low

Answer 37

conductive pathways where no gas exchange occurs - **alveolar ventilation**: V(A) = (TV − DS) x RR = 4.2L/min ➞ only in **exchange surfaces** - in a 500 mL tidal volume, typical dead space = 150 mL & exchange surfaces ≈ 350 mL - during an inspiration: 150 mL of old air mixes w/ 350 mL of fresh air → alveolar air after the inspiration has less O2 than the humidified air in the trachea ➞ changes gas composition

Answer 38

↑ magnitude of the gradient: for CO2: **↑ alveolar ventilation** (VA = (TV − DS) x RR) 1. ↑ RR 2. ↑ TV (strongest) - as VA ↑ → PalvCO2 will ↓ - as VA ↓ → PalvCO2 will ↓ for O2: as we ↑ VA → PalvO2 can rise to at most 110 mmHg because of water vapor in inhaled air at alveolus

Answer 39

resistance is low 1. as perfusion ↑ (due to an ↑ CO) the resistance ↓ → **recruitment & distention of bv↓ resistance** 2. **lung volume** induces changes in resistance to blood vessels (effects on septum capillaries, extra-alveolar blood vessels, and zones of the lung) 3. lung interstitial/parenchyma **PCO2** content

Answer 40

↑ perfusion due to↑ CO: 1. **recruitment of blood vessels**: ↑ in bf to closed/unused blood vessels ➞ **↓R** 2. **distention** of pulmonary bv due to ↑ pulmonary arterial BP → **↓R**

Answer 41

- bv sitting in between alveoli/in septum get **squished** during inspiration → **↑ R** - **extra-alveolar blood vessels** are not in septum ∴ do not get squished during inspiration, but actually expand due to transmural force ➞ **↓R**

Answer 42

- in an upright indiv: blood perfuses zone 3 > zone 2 > zone 1 - selectively perfusing bottom 1/2 - 2/3 - **at apex: ↓ in bf due to gravity + bv are squished down by larger alveoli** - transmural force expanding bv is weaker than squishing force of lung tissue ∴ bv at top get squished - **at base**: blood selectively perfuses lower bv + lung tissue is not as expanded so not much squishing force on bv ∴ **more overall blood flow into the lower vessels**

Answer 43

- local effect - **low O2 content** w/in parenchyma causes local **vasoconstriction** of the pulmonary arterioles → **shunts blood away from region that is poorly ventilated** - **high PO2 content** → **vasodilation** of pulmonary arterioles → ↑ bf to that ventilated region - allows us to match blood flow to ventilation - PCO2 effects are not as influential as PO2 - high CO2 causes local vasoconstriction - low CO2 causes vasodilation

Answer 44

- ideal lung VA (alveolar ventilation) should match bf to that alveolus - VA/QC should be 1 → ratio is actually ≈ 0.8 (in middle) - apex is over-ventilated compared to blood flow (1.2) - base is under-ventilated compared to blood flow (0.6)

Answer 45

- **for O2 & CO2: blood has equivilated by 1/3 of the distance** - during exercise: bf is faster b/c CO has ↑ ∴ CO2/O2 equilibration occurs by 1/2 way (slower) - both CO2 & O2 movement/diffusion + equilibration depends on the bf rate ➞ **perfusion limited** - **diffusion limited** = affected by its solubility in water or large molecular weight (e.g. carbon monoxide)

Answer 46

1. **ΔP(gas)**: ↑ ΔP = ↑ gas exchange 2. **perfusion**: more perfusion = ↑ gas exchange 3. **H2O solubility or mw**: more water soluble & smaller mw = faster gas exchange 4. **SA**: ↑SA facilitates exchange 5. **thickness/diffusion distance**: smaller distance facilitates exchange while larger distance ↓ exchange 6. **bf rate**: slower rate = faster gas exchange

Answer 47

- protein structure that reversibly binds to O2 at Fe center of heme group - 4 O2 + Hb → Hb-O2 (oxyhemoglobin) - adult hemoglobin has 4 subunits (2⍺ & 2β) - fetal Hb has a higher affinity to O2 compared to adult → gas exchange occurs through placenta & fetus is competing with mother for O2 ∴ must have higher affinity

Answer 48

- at rest: we consume 250 mLO2/min - CO at rest = 5000 ml/min - O2 solubility constant = 0.003 mLO2/100ml of blood - 15 ml O2/min = oxygen delivery from dissolved O2 → **not enough to sustain life**

Answer 49

- 2% of O2 is dissolved in plasma - low O2 carrying capacity of plasma of blood drove evolution of RBCs (aka erythrocyte) - “formed element” ➞ non-nucleated - packed w/ hemoglobin (≈ 280 million) - to ↑ amount of Hb in blood: ↑ # of RBC - erythropoietin induces RBC synthesis - 1000 mL O2/min ➞ sustains O2 consumption at rest (250ml O2/min) - **in the lungs → Hb must bind O2 w/ high affinity** - **at the tissues → Hb must dissociate from O2 → affinity to O2 must decrease**

Answer 50

- for a normal person: you only have to do a small change in pressure to get a big change in volume - at higher & higher volumes, we have to generate a lot more pressure to change the volume because of elastic recoil - fibrosis → stiffer lungs → must exert a lot more pressure to get volume to change

Answer 51

- at FRC: chest wall naturally recoils outwards - no need to exert ⊕ transmural forces on chest wall when recoil takes care of it - lungs require ⊕ transmural force to expand - once lungs have inflated a bit, we require ⊕ transmural forces on lung & chest wall to get lungs to inflate any more - w/in normal/resting range: recoil of chest wall helps us expand thoracic volume → allows us to exert a lot less force to change volume - at 50%: chest wall transmural force = -4 while lung transmural force = +4 → balance each other out → force = 0 - > 75% = ⊕ transmural force on both chest wall & lung to expand lung

Answer 52

- **allosteric effect**: as Hb binds to O2 → its affinity ↑ to bind even more O2 - Hb loves to bind to O2 & it gets a greater binding capacity as it fills up

Answer 53

Hb-O2 dissociates → **O2 unbinding** due to a ↓ in tissue interstitial O2 content - metabolically active tissue is using O2

Answer 54

1. tissue is producing CO2 → **↑ PCO2** causes ↓ in affinity of Hb to O2 which causes causes Hb-O2 to unbind O2 (R shift of dissociation curve = ↓ affinity ➞ **Bohr effect**) 2. in tissue: **↓pH** from CO2 → H2CO3 (**↑H+**) + **lactic acid** ➞ R shift in Hb-O2 saturation curve causes Hb-O2 to unbind O2 (**Bohr effect**) 3. **↑ temp** at active tissue ➞ heat causes R shift in Hb-O2 saturation curve which causes Hb-O2 unbinding of O2 4. tissue & interstitial **2-DPG** (diphosphoglycerate) produced during metabolic activity ➞ R shift in Hb-O2 saturation curve which causes Hb-O2 unbinding of O2

Answer 55

binding of CO2 to Hb reduces affinity for O2 & shifts Hb-O2 dissociation curve to the R - occurs at tissues ➞ beneficial for O2 unloading

Answer 56

↑ affinity of Hb to O2 (lower saturation at lungs) → left shift of curve - interstitial CO2 is **low** - pH is more neutral (7.4) - temp is cooler

Answer 57

1. dissolved → in the plasma & in ICF in RBC 2. carried by HCO3- 3. bound as carbamino compounds - CO2 is differentially carried by RBC & plasma - 89% carried by RBC - 11% carried by plasma

Answer 58

RBC has carbonic anhydrase to catalyze the rxn while plasma does not

Answer 59

- 11% of total CO2 - **6%** (of 11%) is **physically dissolved** → depends on solubility constant (ability to dissolve in H2O of plasma) - **5%** (of 11%) **rxts w/ H2O** ⇌ H2CO3 → spontaneously **dissociates to H+ & HCO3-** → **very slow rxn** because **no carbonic anhydrase** in plasma

Answer 60

- ~89% of total CO2 - in the cytoplasm of RBC ~**4%** (of 89%) is **physically dissolved** - ~21% (of 89%) of CO2 rxts w/ Hb → forms carbamino compound - Hb-O2 unbinds O2 at tissues → forms deoxygenated Hb - oxygenated Hb has low affinity for CO2 - **deoxygenated Hb has high affinity for CO2 → L shift of the curve = haldane effect** - CO2 binds to AA in globin portion of Hb - ~64% (of 89%) is carried as HCO3- - CO2 + H2O ⇌ H2CO3 → H+ + HCO3- in RBC catalyzed by **carbonic anhydrase ∴ rapid rxn** - **anion transporter** in PM moves HCO3- into plasma & Cl- into RBC (chloride shift) - HCO3- not technically carried by RBC but created by RBC - as CO2↑ the rxn is driven to R ∴ more CO2 can be carried - H+ is buffered out - ↑HCO3- → carries CO2

Answer 61

- ~21% of CO2 carried by RBCs rxts w/ Hb → forms carbamino compound - Hb-O2 unbinds O2 at tissues → forms deoxygenated Hb - **deoxygenated Hb has high affinity for CO2 → L shift of the curve = haldane effect** - CO2 binds to AA in globin portion of Hb - at lungs: Hb starts to bind to O2 → decreases Hb binding to CO2 (right shift of CO2 curve)

Answer 62

- ~64% (of 89% carried by RBC) is carried as HCO3- - in RBC catalyzed by **carbonic anhydrase ∴ rapid rxn** - **anion transporter** in PM **moves HCO3- into plasma** & **Cl- into RBC** (chloride shift) ∴ HCO3- not technically carried by RBC but created by RBC - as CO2↑ the rxn is driven to R ∴ more CO2 can be carried - H+ is buffered out

Answer 63

- **dissolved**: 6% (plasma) + 4% (RBC cytoplasm) = **10%** - **carbamino compounds**: 1% (plasma proteins) + 21% (RBC w/ Hb) = **21-22%** - **bicarbonate**: 4% (formed in plasma directly) + 64% (formed in RBC & moved to plasma) = **68-69%**

Answer 64

- decreases Hb binding to CO2 (right shift of dissociation curve) - carbamino compound (Hb) releases CO2 into RBC cytoplasm → dissolved CO2 diffuses out of cell into plasma - Hb gives up H+, which then rxts w/ bicarbonate (reverse anion transport) → generates CO2 in RBC & releases it into plasma - oxygenation of Hb shifts rxn towards formation of CO2

Answer 65

1. **cerebral cortex**: during speech, voluntary activities, during exercise 2. **brain stem**

Answer 66

1. **pre-botzinger complex** btwn medulla oblongata & pontine region = pacemaker of respiration: generates breathing rhythm → central pattern generator 2. **dorsal respiratory group (DRG)** in medulla oblongata controls normal/passive inspiration 3. **ventral respiratory group (VRG)** in medulla oblongata activated during strenuous activity with elevated metabolism 4. **pneumotaxic center** in pontine region maybe maybe shuts off DRG, limits inspiratory effort 5. **apneustic center** in pontine region maybe provides initial inspiratory drive/signal

Answer 67

pacemaker of respiration: generates breathing rhythm → central pattern generator - neurons self depolarize to threshold & fire AP - controls RR involuntarily

Answer 68

- in posterior medulla oblongata - controls involuntary normal inspiration - receives input from NTS - contains upper motor neurons that project to lower motor neurons in spinal cord that innervate inspiratory muscles - contract during inspiratory efforts - during inspiration: DRG neurons fire AP → synapse to & excite lower motor neurons - **ramping** behavior: at start of inspiration: AP freq is slow → as we progress through inspiration: AP freq speeds up - during expiration (@ rest): DRG neurons shut off → stop activating lower motor neurons → diaphragm & external intercostals relax

Answer 69

- in anterior medulla oblongata - during more strenuous activities (e.g. exercise) → elevated metabolism - **rostral & intermediate VRG**: upper motor neurons that innervate lower motor neurons that innervate muscles involved in **forced inspiration** - musculature of mouth, tongue, nares (nostrils), pharynx & larynx, & scalenes & sternocleidomastoids in thorax - **caudal VRG**: upper motor neurons that innervate lower motor neurons that activate abdominal musculature, internal intercostal muscles →** forced expiration**

Answer 70

- above medulla oblongata in brain stem - communicate w/ DRG, VRG, & pre-botzinger complex → input & output - unclear how they work - **pneumotaxic center →** maybe **shuts off DRG, limits inspiratory effort** - activity ↑ w/ an ↑ in ventilation - apneustic center: - communicates w/ DRG & VRG - hypothesis: provides initial inspiratory drive/signal

Answer 71

upper motor neurons that innervate lower motor neurons that innervate muscles involved in **forced inspiration** - mouth & tongue - nares (nostrils) - pharynx & larynx - scalenes & sternocleidomastoids

Answer 72

upper motor neurons in the VRG in medulla that innervate lower motor neurons that activate **abdominal & internal intercostal muscles** → **forced expiration**

Answer 73

- blood gas content: PCO2 & PO2 on arterial side involve chemoreceptors - blood pH (normal ≈ 7.4) involves chemoreceptors - regulated by: 1. peripheral chemoreceptors 2. central chemoreceptors 3. peripheral sensory afferents

Answer 74

- in aortic bodies & carotid bodies - stimulated by: 1. **↓ arterial PO2** → fall below 60 mmHg activates ventilation 2. arterial **acidity (↓pH/↑[H+])** usually due to ↑ activity/CO2 → ventilation ↑ - rapid response - pH homeostasis response - partial compensation of pH disturbance 3. **CO2 in arterial blood** → rise in arterial PCO2 due to ↑ metabolism &/or a ↓ in ventilation stimulates ventilation (**weak response**)

Answer 75

- found in the brain stem in the medulla - primary sensor, strong response - detects [H+] which is proportional to blood PCO2 - ↑ brain ECF [H+] stimulates ventilation

Answer 76

increase in arterial PCO2

Answer 77

lung transmural force (+4) is equal in magnitude to the chest wall transmural force (-4)

Answer 78

exhibits a smaller than normal change in lung volume for any change in lung transmural pressure

Answer 79

The elastic recoil at 70% VC is stronger than that at 30% VC

Answer 80

1. decreased air velocity 2. decreased airway diameter 3. increased viscosity 4. fewer branches

Answer 81

bronchioles

Answer 82

the top of the lung - bottom of lungs are more squished (due to gravity) → more squished = larger PIP (759) → PTM = 760 − 759 = +1 - more space at top of lungs = decreased pressure (750) ➞ PTM = 760 − 750 = **+10**

Answer 83

the alveoli at the bottom of the lungs are easiest to inflate - alveoli at bottom of lung are more squished & at top have more space → decreased pressure at top creates larger alveoli - larger alveoli have stronger elastic recoil - ∴ inspiratory effort preferentially inflates bottom 1/3-1/2 of the lung because of larger elastic recoil at top

Answer 84

reducing the effort needed inflating the lung

Answer 85

sympathetic input

Answer 86

bronchioles

Answer 87

- bronchodilation may occur in a given lung region when that region's CO2 levels increase - bronchoconstriction may occur to match low perfusion in a given lung's region

Answer 88

volume w/in conducting pathways

Answer 89

to allow optimal gas exchange

Answer 90

capillaries are recruited when arterial BP rises

Answer 91

perfusion limited

Answer 92

diffusion limited

Answer 93

is a right shift with a drop in tissue pH or an ↑ PCO2

Answer 94

as bicarbonate ions

Answer 95

in the Pre-Botzinger area

Answer 96

the DRG - diaphragm controlled during normal inspiration

Answer 97

it likely initiates inspiration during activities such as exercise

Answer 98

strongly stimulate respiration when arterial PO2 drops below 50 mmHg

Answer 99

none, inspiratory muscles (diaphragm & external intercostals) are relaxed

Answer 100

The chest expansion increases the magnitude of PTP. That pressure expands the lung

Answer 101

- peripheral sensory afferents - in lung parenchyma - monitor volume of lungs - inspire: lung volume ↑ → AP freq ↑ → brainstem NTS → **inhibits ventilation** - expire: ↓ lung volume ➞ AP freq ↓ → brainstem NTS → **activates ventilation** - can influence respiration independently of gas content

Answer 102

- peripheral sensory afferents - monitor noxious stimuli in lungs/airways - itch, pain, temp - induce sneeze, cough, or forced expiration - induces bronchoconstriction → protective effect

Answer 103

- peripheral sensory afferents - chemoreceptors found in tissues - monitor ECF chemicals (CO2, pH) - ↑ tissue metabolism releases CO2 that metaboreceptors detect → activates ventilation - contributes to fine-tuning respiration

Answer 104

deoxygenated Hb has high affinity for CO2 → L shift of the curve - binding of O2 to Hb lowers affinity for CO2 - less O2 bound = higher affinity for CO2

Answer 105

experience dynamic collapse of bronchioles → lose strong connective tissue that keeps the wall stiff - wall is so weak that it doesn’t take much P to collapse

Answer 106

high PO2 in lung interstitium/parenchyma

Answer 107

**bohr effect**: binding of CO2 to Hb reduces affinity for O2 (**↑ PCO2** causes ↓ in affinity of Hb to O2 ➞ O2 unloading at tissues ➞ R shift of Hb-O2 dissociation curve **haldane effect**: deoxygenated Hb has high affinity for CO2 → L shift of the CO2 saturation curve - binding of O2 to Hb lowers affinity for CO2 - less O2 bound = higher affinity for CO2

Answer 108

low PO2 in lung interstitium/parenchyma

Answer 109

1. ↑ interstitial PCO2 2. ↓ interstitial PO2