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Block 2 > Ventilation & Perfusion > Flashcards

Ventilation & Perfusion Flashcards

1
Q

What are the functions of the respiratory system?

A

Primary purpose = gas exchange between air + blood - O2 in, CO2 out

But also:

  • Reservoir for blood + O2 (70% of blood remains in circulation if blood stopped moving)
  • Metabolism of some circulating compounds (e.g. ACE in lungs)
  • Filter blood (e.g. stop microthrombi getting to brain)
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2
Q

What makes up the respiratory tract?

A

LRT = series of branching tubes that lead to blood-gas barrier at alveolar membrane (provide large SA for gas exchange)

1st 16 divisions trachea -> terminal bronchioles are conducting airways: no gas exchange (anatomical dead space) - bulk flow

17-21st division respiratory bronchioles -> alveolar sacs are respiratory airways: gas exchange - diffusion

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3
Q

What is the purpose of conducting airways?

A

To provide a convoluted tube for air to get down to gas exchange areas (dependent on pressure differences)

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4
Q

What is the tissue conversion as you move from the bronchi to the bronchioles? Why does the type of tissue change?

A

Bronchi made of cartilage whereas bronchioles made up of SM so they can vary their radius allowing a big increase in resistance + flow

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5
Q

What is the structure at the alveoli of the respiratory system?

A

Dense capillary network around each alveoli

Blood vessels are distensible + regulated by hypoxic vasoconstriction for e.g.

Thin blood-gas barrier further aids gas exchange

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6
Q

What is hypoxic vasoconstriction?

A

Vessels around alveoli will constrict if the alveoli has inadequate/low O2 levels + blood directed to alveoli with high O2 levels to maximise gas exchange

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7
Q

Why are alveoli blood vessels distensible?

A

If flow is increased, the tubes radius will increase, decreasing resistance + accommodating increased flow through vessels w/o having to increase pressure a lot

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8
Q

What does the composition of the alveolar air depend upon?

A

Relative rates of ventilation + perfusion

Concentration gradient must be established for diffusion to occur - gases move from high to low concentration area

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9
Q

What will happen to the pO2 + pCO2 if ventilation and perfusion are changed?

A

Increased ventilation: pO2 increase + pCO2 decrease in alveoli

Increased perfusion: pO2 decrease + pCO2 increase

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10
Q

What makes up the diffusion barrier in the alveoli?

A 
Epithelial cell of alveolus
Tissue fluid + connective tissue
Endothelial cell of capillary
Plasma
RBC membrane + cytoplasm
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11
Q

What is the calculation for diffusion rate?

A

A x D x ∆P / T

A = area
D = diffusion (sol/√MW)
∆P = pp difference (gradient)
T = thickness
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12
Q

Why is gas exchange in the alveoli perfusion limited in healthy individuals?

A

O2 fully saturated Hb by the time it is 25% along capillary length (reserve for increased demand)

So gas exchange is limited by extent of blood perfusion of alveoli so O2/CO2 transfer is perfusion limited

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13
Q

What happens to gas exchange in disease states?

A

Perfusion limited -> diffusion limited with full equilibration not occurring by the end of the capillaries i.e. exchange is now limited by diffusion instead

Now need 100% of capillary length to fully saturate Hb with O2 or in severe cases, Hb will not become fully saturated at all (no reserve in increased demand)

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14
Q

How is the composition of alveolar gas kept relatively constant?

A

Exchange between alveolar gas + mixed venous blood would reduce alveolar pO2 + elevate pCO2

However, this is prevented by movement of O2 from atmospheric air into it + CO2 out of alveolus into atmospheric air by ventilation

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15
Q

Define ventilation.

A

Movement of gas in + out of lungs

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16
Q

What muscles + nerves are involved in ventilation?

A

Diaphragm (innervated by phrenic nerve C3, 4 + 5)

Intercostal muscles (innervated by intercostal nerves)

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17
Q

What occurs in the process of ventilation?

A

Inspiration bought about by expansion of chest wall + contraction/depression of diaphragm -> increases volume + reduces pressure in respiratory airways -> gas then flows down pressure gradient into lungs -> relaxation of muscles leads to reversal of process

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18
Q

What are the 4 lung volumes picked up by spirometry?

A
  1. Tidal volume (TV): volume of air moved in + out of lungs at rest
  2. Inspiratory reserve volume (IRV): extra volume that can be breathed in over rest
  3. Expiratory reserve volume (ERV): extra volume that can be breathed out over rest
  4. Residual volume (RV): volume left in lungs following maximal expiration
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19
Q

What are the 4 main lung capacity’s? How do you find them out?

A
  1. Total lung capacity: total volume of air present in lungs at end of max inspiration (IRV + TV + ERV + RV)
  2. Inspiratory capacity: biggest breath that can be taken in from resting expiratory level/lung volume at end of quiet expiration(IRV + TV)
  3. Vital capacity: volume from max inspiration to max expiration (IRV + TV + ERC)
  4. Functional residual capacity: volume of air in lungs at resting expiratory level (ERC + RV)
20
Q

How are lung capacities measured?

A

From fixed points in breathing cycle determined by properties of individual lungs, chest wall + muscles

Relatively reproducible so should stay similar if measured in same patient at different visits

21
Q

What is the difference between lung volumes and capacities?

A

Lung volumes change with breathing pattern whereas capacities do not

22
Q

What is Total/Minute Ventilation (MV)? How is it calculated?

A

Amount of air moved into + out of the lungs per minute

MV = Vt x RR

Vt = tidal volume i.e. volume moved per breath
RR = resp rate
23
Q

What is the typical Total/Minute Ventilation (MV)? How much can it go up in exercise?

A

6-8 L/min at rest (because Vt = 0.5 L + RR = 12-16 typically)

Can exceed 80 L/min in exercise

24
Q

What is the Alveolar Ventilation Rate (AVR)? How can you calculate it?

A

Amount of air that actually reaches the alveoli per minute

Need to allow for ‘wasted’ ventilation of dead space to calculate it

25
Q

What is dead space?

A

Last bit of air entering the lungs stays in the airways + this same bit of air is the first breathed out of the lungs - does not reach alveoli so is ‘wasted’ + does not take part in gas exchange

Dead space volume (Vds) is completely filled with air at each breath

26
Q

What are the 2 main types of dead space?

A
  1. Serial: volume of conducting airways i.e. anatomical dead space
  2. Distributive: some parts of lungs are not airways but do not support gas exchange e.g. damaged alveoli or alveoli with poor perfusion
27
Q

What it total physiological dead space? What is the volume typically?

A

Serial dead space + distributive dead space = ~0.15L

28
Q

How is Alveolar Ventilation Rate (AVR) calculated? What does this indicate?

A

(Vt - Vds) x RR

For a given minute of ventilation, rapid shallow breathing amplifies effect of dead-space whereas slower deeper breathing is a more efficient way of ventilating the alveoli

29
Q

What effect will increasing Alveolar Ventilation Rate (AVR) have on CO2?

A

CO2 will be removed lowering alveolar pCO2 + increasing the partial pressure gradient = increased CO2 diffusion from blood + removal from body

30
Q

What is the ideal relationship between ventilation (V) and perfusion (P)? What happens in reality?

A

Ideally each area should be optimally/equally ventilated + perfused to allow optimal diffusion of gases i.e. V/Q ratio of 1

However, amounts of V + Q vary in different areas of lung in reality

31
Q

What is it called when variations in V and Q do not parallel each other?

A

V/Q mismatch

32
Q

What is the outcome of a physiological V/Q mismatch?

A

Physiological mismatch does not cause gas exchange problems under normal circumstances

33
Q

What is the outcome of a V/Q mismatch in respiratory disease?

A

Respiratory disease may make mismatch worst + is main reason for defective gas exchange in disease

34
Q

What will happen to the V/Q ratio if there is no ventilation?

A

Decreased V/Q because the gas composition of blood coming into + leaving the alveoli has not changed i.e. no gas has been picked up or dropped off so Q will keep increasing to try + compensate

35
Q

What will happen to the V/Q ratio if there is no perfusion?

A

Increased V/Q because the gases in the alveoli do not reach the blood at all so V will just keep increasing to compensate

36
Q

Why is there different V/Q ratios in different parts of the lung?

A

V + Q increase slowly from top -> bottom of lung

But increase at different rates as Q increases more rapidly

37
Q

How does gravity affect the perfusion (Q) of the lungs?

A

Q greater at base due to gravity causing higher blood flow to more dependent areas of the lung

Lung Q varies with vertical distance from heart e.g. absent at top, sporadic in the middle + constant at the bottom

38
Q

How does gravity affect the ventilation (V) of the lungs?

A

Basal lung relatively compressed in resting state so more potential for expansion than in apex of lung which is already partially open i.e. has less expansion potential

So more air moved in + out i.e. V increased at base than at the apex of the lungs

39
Q

How does gravity affect the V/Q ratio? Why?

A

Apex alveolar pO2 is relatively high due to lower blood flow i.e. low perfusion (high V/Q ratio)

Base over-perfused (low V/Q ratio) so will have lower O2 + higher CO2 gas tensions in alveoli + arterial blood

= V/Q ratio decreases moving down the lung

40
Q

What is oxygen uptake dependent on?

A

Perfusion (Q)

41
Q

What happens to the lung apex blood vessels during exercise?

A

Normally collapsed but open during exercise to accommodate increased CO -> increased perfusion increases O2 uptake at the lung apex

42
Q

What does the mismatch of whole lung ventilation (V) and perfusion (Q) result in often in disease states?

A

Arterial hypoxaemia

43
Q

What happens to the V/Q ratio in pneumonia?

A

Reduced V of alveoli so blood perfusing these areas is less oxygenated = decreasing V/Q ratio

44
Q

What happens to the V/Q ratio if a patient has a pulmonary embolus?

A

Reduced Q to area of lung it affects = increasing V/Q ratio

45
Q

Why is it not possible for the effects of high and low V/Q areas (i.e. significant V/Q mismatch) to cancel each other out? I.e. why does this still result in arterial hypoxaemia?

A

Low V/Q areas: significant O2 decrement in mixed capillary blood i.e. Hb is not fully saturated + it drops resulting in a low O2 content

High V/Q areas: add little O2 content to blood which already has fully saturated Hb at lower ratios i.e. Hb already saturated + cannot increase further

= SaO2 is 98% from high V/Q + 58% from low V/Q = blood returning from lungs has an SaO2 = 78%

Block 2 (45 decks)

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