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NPB 113 > RESPIRATORY SYSTEM > Flashcards

RESPIRATORY SYSTEM Flashcards

1
Q

respiratory system functions

A
  • involved with speech (phonation)
  • involved in activating angiotensin from its precursor
  • involved with homeostasis
    1. plasma gases: arterial PO2 & PCO2 (dissolved gasses)
    2. plasma pH
    3. body temperature
  • resp fx tied to metabolism: ↑ activity = ↑ resp
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2
Q

atmospheric pressure of O in dry air

A

159.2 mmHg

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3
Q

atmospheric pressure of N in dry air

A

593.5 mmHg

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4
Q

how does gas diffusion occur?

A

with a ΔP (change in gas pressure)

  • independent of other gases
  • PalvO2 = 100 mmHg
  • ParterialO2 = 60 mmHg
  • ∴ ΔP = 40 mmHg
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5
Q

changes in partial pressures of gases in trachea

A
  1. mixing old air w/ newly inspired air ➞ extra CO2 in old air
  2. air is humidified

in the trachea:

  • N (73.26%) = 557 mmHg
  • O (19.65%) = 150 mmHg
  • CO2 (0.03%) = 0.2 mmHg
  • H2O (6.18%) = 6.6 mmHg
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6
Q

pressure of H2O in trachea

A

6.6 mmHg

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7
Q

pressure of CO2 in the trachea

A

0.2 mmHg

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8
Q

pressure of O in the trachea

A

150 mmHg

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9
Q

where does gas exchange occur?

A

btwn alveoli & interstitium and interstitium & capillaries ONLY

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10
Q

pressure of N in the trachea

A

557 mmHg

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11
Q

ficks law of diffusion

A

rate of diffusion of a substance across a membrane is proportional to the concentration gradient

  • Jx = (Pxa - Pxb) x permeability
  • diffusion of gas ∝ ΔPgas x permeability
  • movement via diffusion is via short distances
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12
Q

conductive regions of the respiratory system

A

air moves in/out of the lungs via these pathways

  • bulk air movement
  • nose & nasal passages
  • pharynx
  • larynx
  • trachea
  • bronchi
  • bronchioles
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13
Q

exchange regions of the respiratory system

A

gas exchange btwn alveoli & blood

  • respiratory bronchioles
  • alveolar ducts
  • alveolar sacs & alveoli
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14
Q

upper respiratory system

A
  • conductive pathways
    1. nose & nasal passages
    2. pharynx
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15
Q

lower respiratory system

A
  • conductive pathways
    1. larynx
    2. trachea
    3. bronchi
    4. bronchioles
  • gas exchange surfaces
    1. respiratory bronchioles
    2. alveolar ducts
    3. alveolar sacs & alveoli
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16
Q

pharynx

A
  • throat
  • shared w/ GI tract
  • helps to warm & humidify air
  • upper respiratory system
  • conductive pathway
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17
Q

larynx

A
  • voice box
  • lower respiratory system
  • conductive pathway
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18
Q

trachea

A
  • has cartilaginous rings that stiffen & prevent collapse
  • lower respiratory system
  • conductive pathway
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19
Q

bronchi

A
  • lower respiratory system
  • conductive pathways
  • branch & give rise to smaller bronchi (in diameter) & ↑ # of bronchi
    • arborization = branching
  • has cartilaginous rings stiffen & prevent collapse
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20
Q

bronchioles

A
  • lower respiratory system
  • conductive pathways
  • lose cartilage but gain smooth muscle rings
  • guides ventilation
  • under ANS control
  • can potentially collapse due to lack of cartilage if P outside of it is greater than P inside ➞ flattens it out
    • P(bronchioles) must be larger than P(outside) or collapse when cough/sneeze
  • stay roughly same diameter
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21
Q

respiratory bronchioles

A
  • 1st gas exchange surfaces
  • lower respiriatory system
  • have alveoli ∴ can do exchange
  • smooth muscle rings
  • no cartilage
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22
Q

alveolar ducts

A
  • gas exchange surfaces
  • lower respiratory tract
  • walls are made of type I alveolar epithelium
  • basically alveoli forming a pathway to still conduct air
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23
Q

alveolar sacs & alveoli

A
  • gas exchange surfaces
  • lower respiratory tract
  • don’t usually collapse
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24
Q

branching

A
  • bronchi branch & give rise to smaller & more bronchi
  • bronchioles will show up ~11th gen
  • respiratory bronchioles @ branch 17-19
  • alveolar ducts @ branch 20
  • by the end: respiratory passages branch ~23-25x
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25
Q

type I alveolar epithelium

A
  • 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
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26
Q

type II alveolar epithelium

A
  • 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
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27
Q

thoracic anatomy

A
  • 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
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28
Q

tidal volume

A

TV = amount of air we breathe in/out during normal breathing

  • resting TV ≈ 500 mL
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29
Q

inspiratory reserve volume

A

IRV = amount of air that is voluntarily inhaled above TV

  • ~2-25L
  • inherent (cannot train for)
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30
Q

expiratory reserve volume

A

ERV = max expired air past TV

  • ~1.1-1.5 L
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31
Q

residual volume

A

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

  • residual air
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32
Q

functional residual capacity

A

FRC = amount of air remaining in lungs after normal passive expiration

  • ERV + RV
  • capacity = adding 2+ volumes together
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33
Q

vital capacity

A

VC = overall breathing range

  • ERV + TV + IRV
  • inherent ➞ associated w/ anatomy
  • ↓ w/ age ➞ posture associated
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34
Q

static properties of the chest wall

A
  • 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
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35
Q

transmural force

A

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
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36
Q

to change ΔP

A
  • 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)
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37
Q

P(lung) =

A

P(alv) − P(IP)

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38
Q

intraplural pressures at FRC

A
  • 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
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39
Q

do we use ⊖ transmural forces during normal passive expiration?

A

no

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40
Q

relationship btwn P(lung) & P(ER+ST) to expand the lung

A

transmural forces must be larger than forces of elastic recoil + surface tension

  • P(lung) > P(ER+ST)
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41
Q

relationship btwn P(lung) & P(ER+ST) during expiration

A

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
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42
Q

inspiratory muscles

A
  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
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43
Q

surface tension

A
  • 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
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44
Q

law of laplace

A

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
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45
Q

expiratory muscles

A

passive expiration: ↓ thoracic volume by relaxing inspiratory muscles

  • diaphragm moves up
  • ribcage moves down & inwards

forced expiration

  • internal intercostals
  • abdominal muscles
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46
Q

hysteresis

A
  • 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
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47
Q

posture & breathing

A
  • 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
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48
Q

dynamic compression of the lungs

A

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
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49
Q

static resistance

A
  • radius = major static resistance
  • bronchioles have lowest resistance because of accumulative aggregation of 100,000+
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50
Q

laminar airflow

A

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
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51
Q

turbulent airflow

A

= dynamic resistance

  • associated w/ fast velocities & branches/edges
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52
Q

transitional airflow

A
  • in between laminar & turbulent
  • characteristics of both
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53
Q

reynold’s number

A

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)
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54
Q

resistance in larger airways

A

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

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55
Q

resistance in smaller airways

A

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

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56
Q

autonomic input to bronchiolar SM

A
  • 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)
57
Q

airway resistances

A
  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
58
Q

lung volume effect on resistance

A

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
59
Q

luminar & interstitial gases effect on resistance

A
  • 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
60
Q

airflow & resistance in 1º bronchi & trachea

A
  • 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
61
Q

airflow & resistance in bronchioles

A

have slowest air velocities & smallest radius ∴ Re is small ∴ air flow is laminar

  • resistance due to reynold’s number is low
62
Q

dead space

A

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
63
Q

to change alveolar perfusion

A

↑ 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

64
Q

resistance to pulmonary bf factors

A

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
65
Q

resistance to pulmonary bf from recruitment & distention

A

↑ 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
66
Q

resistance to pulmonary bf from lung volume

A
  • 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
67
Q

resistance to pulmonary bf from lung volume based on zones

A
  • 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
68
Q

resistance to pulmonary bf from lung interstitial/parenchyma PO2/PCO2 content

A
  • 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
69
Q

ventilation-perfusion ratios

A
  • 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)
70
Q

gas exchange between alveoli & pulmonary capillary

A
  • 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)
71
Q

factors influencing gas exchange

A
  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
72
Q

hemoglobin

A
  • 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
73
Q

O2 transport in blood as dissolved O2

A
  • 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
74
Q

O2 transport in blood bound to hemoglobin

A
  • 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
75
Q

compliance of the lung

A
  • 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
76
Q

compliance of the lung & chest wall

A
  • 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
77
Q

oxy-hemoglobin saturation curve

A
  • 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
78
Q

Hb-O2 at tissues

A

Hb-O2 dissociates → O2 unbinding due to a ↓ in tissue interstitial O2 content

  • metabolically active tissue is using O2
79
Q

factors contributing to O2 unbinding

A
  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
80
Q

bohr effect

A

binding of CO2 to Hb reduces affinity for O2 & shifts Hb-O2 dissociation curve to the R

  • occurs at tissues ➞ beneficial for O2 unloading
81
Q

Hb binding in the lungs

A

↑ 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
82
Q

mechanisms of CO2 transport in the blood

A
  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
83
Q

why is the conversion of H2O + CO2 to carbonic acid rapid in the RBC but slow in the plasma

A

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

84
Q

CO2 transport in plasma

A
  • 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
85
Q

methods of CO2 transport in RBC

A
  • ~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
86
Q

CO2 carried as carbamino compounds

A
  • ~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)
87
Q

CO2 carried by bicarbonate

A
  • ~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
88
Q

total CO2 proportions

A
  • 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%
89
Q

as Hb binds O2

A
  • 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
90
Q

ventilation controllers

A
  1. cerebral cortex: during speech, voluntary activities, during exercise
  2. brain stem
91
Q

ventilation control centers in brain stem

A
  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
92
Q

pre-botzinger complex

A

pacemaker of respiration: generates breathing rhythm → central pattern generator

  • neurons self depolarize to threshold & fire AP
  • controls RR involuntarily
93
Q

dorsal respiratory group (DRG)

A
  • 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
94
Q

ventral respiratory group (VRG)

A
  • 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**
95
Q

pontine regions

A
  • 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
96
Q

rostral & intermediate VRG

A

upper motor neurons that innervate lower motor neurons that innervate muscles involved in forced inspiration

  • mouth & tongue
  • nares (nostrils)
  • pharynx & larynx
  • scalenes & sternocleidomastoids
97
Q

rostral & intermediate VRG

A

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

98
Q

control of respiration

A
  • 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
99
Q

peripheral chemoreceptors

A
  • 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)
100
Q

central chemoreceptors

A
  • 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
101
Q

ventilation is stimulated/increased very strongly by a small

A

increase in arterial PCO2

102
Q

transmural forces at FRC during normal breathing

A

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

103
Q

right shift of a pressure-volume compliance curve

A

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

104
Q

Why might inflation of the lung from 70% to 80% of vital capacity (VC) require a greater inspiratory effort
than inflating the lung from 30-40% VC?

A

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

105
Q

what would allow laminar airflow through conducting pathways?

A
  1. decreased air velocity
  2. decreased airway diameter
  3. increased viscosity
  4. fewer branches
106
Q

In the respiratory system, which region exhibits the lowest total resistance?

A

bronchioles

107
Q

What region of the lung exhibits the greatest transpulmonary pressure at FRC?

A

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
108
Q

what describes ventilation in an upright person?

A

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
109
Q

surfactant is important for

A

reducing the effort needed inflating the lung

110
Q

what tends to cause dilation of the airways

A

sympathetic input

111
Q

which respiratory region is the primary site of airflow regulation by the ANS?

A

bronchioles

112
Q

local control of the airways

A
  • 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
113
Q

dead space volume

A

volume w/in conducting pathways

114
Q

why does bf slow down in pulmonary capillaries

A

to allow optimal gas exchange

115
Q

what contributes to low resistance of pulmonary capillaries

A

capillaries are recruited when arterial BP rises

116
Q

during inspiration, the alveolar pressure in zone 1 of the lung prevents flow through the pulmonary capillaries

A

true

117
Q

If exchange of a gas from the alveolus is primarily determined by the rate of blood flow, we would classify that gas exchange as

A

perfusion limited

118
Q

gas movement/diffusion + equilibration affected by solubility in water or large molecular weight

A

diffusion limited

119
Q

approximate PCO2 of plasma once it has equilibrated with the alveolus?

A

40 mmHg

120
Q

Bohr shift of the oxyhemoglobin dissociation curve

A

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

121
Q

What is the major form that carbon dioxide is carried in plasma?

A

as bicarbonate ions

122
Q

Where is the primary pacemaker of respiration found?

A

in the Pre-Botzinger area

123
Q

Most of the inspiratory premotor neurons that control the diaphragm arise from

A

the DRG

  • diaphragm controlled during normal inspiration
124
Q

Inspiratory premotor neurons controlling forced-expiration muscles are located in

A

the VRG

125
Q

What appears to be the primary role of the apneustic center?

A

it likely initiates inspiration during activities such as exercise

126
Q

peripheral chemoreceptors & respiratory control

A

strongly stimulate respiration when arterial PO2 drops below 50 mmHg

127
Q

which muscles are activated during normal expiration?

A

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

128
Q

what is the approximate PCO2 in dry air?

A

0.23 mmHg

129
Q

How do we inflate the lung when the respiratory muscles contract?

A

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

130
Q

pulmonary stretch receptors

A
  • 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
131
Q

irritant receptors

A
  • peripheral sensory afferents
  • monitor noxious stimuli in lungs/airways
  • itch, pain, temp
  • induce sneeze, cough, or forced expiration
  • induces bronchoconstriction → protective effect
132
Q

metaboreceptors

A
  • 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
133
Q

haldane effect

A

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
134
Q

patients with emphysema

A

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
135
Q

what causes pulmonary vasodilation?

A

high PO2 in lung interstitium/parenchyma

136
Q

bohr vs haldane effects

A

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
137
Q

what causes local pulmonary vasoconstriction?

A

low PO2 in lung interstitium/parenchyma

138
Q

what causes local bronchodilation?

A
  1. ↑ interstitial PCO2
  2. ↓ interstitial PO2

NPB 113 (5 decks)

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