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Exercise physiology > Lecture 14: Pulmonary Physiology: structure and function > Flashcards

Lecture 14: Pulmonary Physiology: structure and function Flashcards

1
Q

describe the anatomy of the respiratory system (8 parts –> 2 zones)
- function of the zones ish

A

CONDUCTING ZONE
1. trachea
2. primary bronchus
3. bronchus
4. bronchi
5. bronchioles
- Area of No gas exchange
- transports, warms humidifies and filters inspired air
RESPIRATORY ZONES:
6. Respiratory bronchioles
7. alveolar ducts
8. alveolar sacs
- site(s) of pulmonary gas exchange
- large surface area (if all alveolar sacs laid out, would fit half a tennis court = respiratory system is overbuilt ish)

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2
Q

describe the mechanics of ventilation: inspiration (3 steps)
- active or passive?

A
  1. medullary respiratory control center signals the inspiratory muscles to contract through increased phrenic nerve activity
  2. inspiratory muscles contract (rib cage expands, opens up airways, diaphragm descends) which reduces intrapulmonary pressure (from 760 to 754 mmHg) below atmospheric pressure
  3. such that air is literally sucked into the lungs through the mouth, nose, upper and lower airways
  • ACTIVE!
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3
Q

describe the mechanics of ventilation: expiration (3 steps ish)
- active or passive? rest vs exercise

A

1.during inspiration, lung inflation increases activity of pulmonary stretch receptors (PSRs) in lungs
2. PSRs relay sensory afferent information to the medullary respiratory control center –> which progressive “turns off” the neural signal for inspiration (Hering-Breuer reflex) = STOP
3. at rest, PASSIVE recoil of lungs and chest wall in combination with ascent of diaphragm increase intrapulmonary pressure above atmospheric pressure (764 mmHg), which pushes air out of lungs
VS during exercise: expiration becomes active with recruitment of abdominal and intercostal muscles

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4
Q

what are the muscles for inspiration (5) vs expiration (5)?

A

INSPIRATION:
- sternocleidomastoid
- scalenes
- external intercostals
- internal intervostals
- diaphragm
EXPIRATION
- internal intercostals
- external abdominal oblique
- internal abdominal oblique
- transversus abdominis
- rectus abdominis

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5
Q

What is Hooke’s law?
- how does that relate to normal physiological range of tidal breathing?

A

states that an elastic structure changes dimensions in direct proportion fo the amount of force applied
- over normal physiological range of tidal breathing, the amount of lung inflation/expansion for a given change in intrapulmonary pressure conforms fo Hooke’s law
*if you apply force, volume will increase

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6
Q
  • what is O2 cost of breathing?
  • what causes an increase in O2 cost of breathing?

*what analogy?

A
  • amount of O2 used by respiratory muscles to breathe, relative to total oxygen consumed
  • decrease intrapulmonary pressure causes an additional unit of volume to be generated –> increase lung volume –> increase inspiratory elastic recoil –> increase inspiratory work to overcome those elastic recoil forces –> increase O2 cost of breathing
  • ie inflate balloon: the bigger the balloon, the harder it is to inflate it bc of elastic recoil and increased P in balloon
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7
Q

regarding the balloon analogy and Hooke’s law, describe graph of distending pressure (x) vs volume (y)
- what is work?

A
  • at the beginning, pressure change gives proportional volume change (ie you blow into the balloon and it increases volume as you would expect
  • but as the volume gets bigger (and more elastic recoil), pressure change will only give a really small amount of increasing volume bc of extra elastic recoil force
  • work = (delta P)/(delta V)
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8
Q

what is airway resistance? acronym?

  • formula?
A

opposition to airflow caused by forces of friction within tracheobronchial tree
- raw
*ie we need to overcome raw to continue blowing balloon

Raw = (airway length x gas viscosity)/(airway radius)^4
*airway length and gas viscosity stay constant!
*Raw = Poiseulle’s law (simplified) (?)

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9
Q

at any given rate of airflow into the lungs, the ________ __________ (symbol ish?) that must be developed depends on raw
- therefore, raw is an important determinant of what? (2)

A

the driving pressure (delta P)
- thus, raw is determinant of work of breathing (WOB) (energy needed to breathe, but also deltaP/deltaV) and O2 cost of breathing

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10
Q

what is the formula for airflow?
- what happens during bronchoconstriction vs bronchodilation?
- also give examples of when those 2 happen

A

airflow = (P1-P2)/raw

BRONCHOCONSTRICTION:
- ie asthma attack, allergie reaction
- decrease radius = very big increase in raw –> so have to increase work of breathing in order to maintain given rate of airflow

BRONCHODILATION:
- ie exercise, inhaler (ventolin, flovent)
- increase radius = decrease in raw –> decrease work of breathing to keep same airflow

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11
Q

describe the influence of lung volume (x) on raw (y-axis)
- CONCLUSION?
*EXAM!

A
  • at low lung volume (low total lung capacity), raw is high because radius is small
  • at high lung volume/total lung capacity, raw is low
    CONCLUSION:
  • as lung volume increases, airway resistance (Raw) decreases bc airways distends as the lungs inflate, and bigger airways have lower resistance (Poiseulles’ law)
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12
Q

how to we measure the pressure-volume relationships of pulmonary system?

A
  • using a esophageal balloon catheter to measure pressures
  • balloon inflated in esophagus and stomach
  • can measure flow over time, pressure…
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13
Q

explain the pressure-volume relationship curve!

A

pressure: x-axis
volume: y-axis
1. at first, large delta P –> small delta volume (bc slope is very small) = NON-COMPLIANT
- increase RESISTIVE work of breathing bc low volume = increased raw = increase WOB (Poiseulle’s law (?))
2. in the middle of the curve, small delta pressure = large delta volume (big slow) = COMPLIANT!
- “matched” V and P
- elastic and resistive WOB is minimized when tidal volume expansion occurs within compliant (linear) portion of respiratory system’s sigmoid pressure-volume curve
3. at the extreme end of pressure, large delta P –> small delta volume (bc slope is very small) = NON-COMPLIANT
- increase inspiratory ELASTIC work of breathing (Hooke’s law)
- high volume = high elastic recoil (even if low raw) –> so still non-compliant

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14
Q

what is
- TIDAL VOLUME (VT)
- INSPIRATION RESERVE VOLUME (IRV)
- EXPIRATION RESERVE VOLUME (ERV)
- RESIDUAL VOLUME (RV)

  • INSPIRATORY CAPACITY (IC)
  • FUNCTIONAL RESIDUAL CAPACITY (FRC)
  • VITAL CAPACITY (VC)
  • TOTAL LUNG CAPACITY (TLC)
A
  • VT: volume that moves during a respiratory cycle (air that gets in/out during normal breathing) (kinda like stroke volume)
  • IRV: additional volume above tidal volume (when you use neck muscles)
  • ERV: forcefully exhaled after end of normal expiration (when you use abs and internal intercostal muscles)
  • RV: volume of air in respiratory system after maximal exhalation
  • IC = IRV + VT
  • FRC = ERV + RV
  • VC = IRV + VT + ERV
  • TLC = IRV + VT + ERV + RV
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15
Q

how do we call the volume at the end of inspiration? vs at the end of exhale?
- which one is higher?

  • how do we call the volume of air of forced inhale and forced exhale?
A
  • end-inspiratory lung volume (EILV) –> higher than EELV
  • end-expiratory lung volume (EELV)
  • vital capacity! = IRV + VT + ERV
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16
Q

where is the normal breathing pattern situated on the pressure volume curve? place VT, IRV, TLC, IC, EILV, EELV, FRC, ERV and RV on the curve

A
  • bottom: RV
  • top: TLC
  • oval in the middle: top = EILV, bottom = EELV or FRC –> the entire oval represents vital capacity
  • btw EELV and RV = ERV
  • btw EILV and TLC = IRV
  • btw EELV and TLC = IC
17
Q

what happens to your normal tidal breathing when you start exercising? on the curve?

A

the oval gets a little big bigger cause you breathe deeper. so your vital capacity increases

18
Q

what are 3 physiological challenges/examples of how the respiratory system is limited during exercise?

A
  1. exercise induces increase in VO2 and VCO2 –> causes blood returning to lungs from exercising muscle to get progressively more hypoxic (decrease O2) and hypercapnic/acidic (increase PCO2, decrease pH) –> can disturb acid-base balance and compromise O2 delivery to exercising muscles, leading to fatigue
  2. ventilation reqs during exercise might be 20-30x above resting levels –> in order to minimize work and O2 cost of breathing: a) ventilatory response to exercise must increase in direct proportion fo muscle metabolic requirement (particularly VCO2) and b) need precise control of dynamic operating lung volumes
  3. work produced by locomotor and respiratory muscles increase during exercise –> blood flow and O2 reqs of both groups must be met –> excessive work and O2 cost of breathing has potential to steal blood flow away from exercising muscles, leading to peripheral locomotor muscle fatigue (hypothesis)
19
Q

formula for diffusive O2 flux?
- according to which law?

A

flux = diffusive conductance of lung for O2 (DKlungO2) x (PAO2 - PcapO2)
- PAO2 - PcapO2 –> pressure gradient
OR
according to Fick’s law of diffusion
flux = (A x D x (P1-P2))/T
- A: surface area: lung/blood interface (number of alveolar units)
- D: solubility and size of gas molecule
- P1-P2 = driving pressure: PAO2 - PcapO2 gradient
- T = diffusion distance: thickness of alveolar-capillary membrane (o.5um)

20
Q
  • what is the main driving force of arterial blood oxygenation? WHY?
  • what is that main driver dependent on? which in turn is determined by what?
A

pressure! btw alveolar PO2 and pulmonary capillary PO2!
because surface area (A), diffusion coefficient of gas (D) and diffusion distance (T) are all unchanging

  • pressure gradient for diffusion of O2 from lungs to blood is dependent on alveolar PO2 –> which in turn is determined by alveolar ventilation (V’A)
  • alveolar ventilation = amount of air going to alveoli for gas exchange (doesn’t include residual volume)
21
Q

if alveolar ventilation is inadequate –> what is inadequate to ensure what?? –> consequence during heavy exercise?

A
  • if V’A is inadequate –> PaO2 will be inadequate to ensure that the rate of diffusive O2 flux from alveoli into blood is able to fully saturate RBCs with O2 during the brief time that it is in pulmonary capillaries
  • becomes challenge during heavy exercise since amount of time for pulmonary O2 gas exchange decreases due to reductions in both mixed-venous PO2 and the time RBC spends in pulmonary capillary (bc you have higher ventilation/less time btw inhale and exhale/less exchange of O2/CO2)
22
Q

describe impact of alveolar ventilation on alveolar PO2 and arterial O2 content using the conservation of mass model

A

a) alveolar ventilation (V’A) represents inflow of O2 into alveoli
b) movement of O2 from alveoli into the blood, and the flow of blood out of the lungs represents outflow of O2
c) PaO2 to PcapO2 = delta P = what DRIVES inflow and outflow of this model
- balance btw V’A (inflow) with pulmonary blood flow (outflow) determines PaO2 and the efficiency of pulmonary gas exchange
- THUS, any constraint on V’A limits the ability to maintain a high PaO2, which in turn compromises arterial blood oxygenation and O2 supply/delivery to the exercising muscles –> pulmonary limitation to exercise tolerance!

23
Q

1) what is alveolar ventilation? + formula
2) what is minute ventilation? + formula
3) what is dead space ventilation?

A

1) V’A = volume of air that reaches alveoli and participates in gas exchange per minute (in L/min)
- V’A = minute ventilation (V’E) - dead space ventilation (V’D)

2) minute ventilation (V’E, L/min): volume of air moved into and out of lungs per minute
- V’E = tidal volume x breathing frequency

3) volume of air that does not participate in gas exchange per minute
- V’D = (anatomic dead space + physiologic dead space) x breathing frequency

24
Q

what is anatomic dead space? vs physiologic dead space?

A

ANATOMIC DS:
- volume of air that fills the non-diffusible portions of the respiratory system (ie conducting zones: nose, mouth, trachea, bronchi…) –> about 150-200 mL or 30% of VT

PHYSIOLOGIC DS:
- portion of alveoli that are poorly ventilated and/or poorly perfused with blood
- is negligible in health (0.25-0.5 mL) but increases with pulmonary disease

25
Q

alveolar ventilation depends on what (3)
- what does NOT reflex V’A

A

depends on breathing pattern and volume of anatomic and physiologic dead space
- Minute ventilation does NOT reflect V’A:
-ie rapid and shallow: small VT (0.15) + high breathing frequency (40) = V’E of 6.0 –> but then your V’D is also very high bc of high breathing frequency (0.15 (dead space) x 40) = low V’A (0L/min)
- normal breathing: normal VT (0.5) + normal breathing frequency (12) = V’E (6) –> V’D = 0.15 x 12 –> V’A = 4.2 yay
- deep and slow breathing: VT = 1.0, breathing f = 6 –> V’E = 6.0 –> V’D = 0.15 x 6 –> V’A = 5.1 yay

depending on how much your VT and breathing frequency is

V’D is affected by breathing frequency

26
Q

during exercise, respiratory system is faced with challenge of maintaining alveolar gas exchange by protecting (2) via what? especially what?

A
  • by protecting both alveolar PO2 (PAO2) and PCO2 (PACO2) via precise matching of V’A to muscle metabolism, particularly V’CO2!

GOAL = ventilate to decrease CO2! (and not because we want more O2) –> CO2 is really the driving component

27
Q

what are the formulas for PACO2 and PAO2?

A

PACO2 = (V’CO2/V’A) x (Pb - 47)
PACO2 = alveolar PCO2
*Pb = constant
*V’CO2 = rate of CO2 production

PAO2 = PiO2 - (PaCO2/(V’CO2/V’O2)
*PaCO2 = arterial CO2
*PiO2: inspired PO2
*V’O2 = rate of O2 consumption

28
Q

what happens when you exercise and CO2 production increases?
*alveolar gas equations!

A

PACO2 = (V’CO2/V’A) x (Pb - 47)
PAO2 = PiO2 - (PaCO2/(V’CO2/V’O2)

  1. if V’CO2 increases, PaCO2 also increases (more CO2 in alveolis) –> which also means that arterial CO2 increases
  2. if PaCO2 increases, PAO2 decreases so arterial PO2 (PaO2), arterial O2 saturation(SaO2) and arterial O2 content (CaO2) all decrease = BAD

SO body needs to increase V’A in order to match increase in V’CO2, so that PaCO2 doesn’t increase
- by increasing V’A, PaCO2 will decrease, and PaO2, SaO2 and CaO2 will increase back to normal bc you got rid of all the CO2 by increasing alveolar ventilation

29
Q

whats a technique to hold your breath longer?

A

do a lot of shallow breathing (can’t get more O2 in) but CAN get more CO2 out
- than you hold your breath, and because you started at a lower level of CO2, you’ll be able to hold breath longer bc it will take you longer to reach the limit at which your body will gasp for air/want to ventilate to get rid of all the CO2

Exercise physiology (14 decks)

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