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Respiratory Physiology > Review of normal respiratory physiology > Flashcards

Review of normal respiratory physiology Flashcards

1
Q

What are the roles of the respiratory system?

A
  • exchange O2 and CO2 between systemic venous blood in the pulmonary arteries and alveolar air
  • contribute to the maintenance of acid-base balance
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2
Q

What affects the rate of O2 and CO3 exchange?

A

Consumption of O2 and production of CO2

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3
Q

What is normal resting PaO2?

(a = arterial)

A

90-98mmHg

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4
Q

What is normal resting PaCO2?

(a = arterial)

A

38-42mmHg

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5
Q

What is normal resting arterial pH?

A

7.38-7.42

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6
Q

What is normal resting mixed venous PO2?

A

~40mmHg

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7
Q

What is normal resting mixed venous CO2?

A

~46mmHg

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8
Q

What is normal resting mixed venous pH?

A

less than arterial pH (

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9
Q

What is normal resting PAO2?

(A = alveolar)

A

~100mmHg

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10
Q

What is normal resting PACO2?

(A = alveolar)

A

~40mmHg

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11
Q

What do the respiratory suffixes a, A, v, and i refer to?

A

a - arterial

A - alveolar

v - mixed venous

i - inspired air

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12
Q

What is the capacity of the respiratory system at rest vs during exercise?

A

Rest: (aerobic metabolism, RQ = 0.8)

  • supplies 250mL/min O2
  • removes 200mL/min CO2

Exercise: (aer & anaer metabolism, RQ = 1.2-1.5)

  • supplies > 4000mL/min O2
  • removes > 4000mL/min CO2

RQ = CO2 elim/O2 consumed

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13
Q

Inadequate respiratory function (in adaptation to exercise) can cause

A

hypoxaemia

hypercapnoea and respiratory acidosis

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14
Q

Ventilation is

A

the movement of air in and out of the lungs

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15
Q

Respiration is

A

gas exchange across the alveolar-capillary membrane

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16
Q

Ventilation ensures that

A

concentrations of O2 and CO2 in alveolar air are optimal for achieving the roles of the respiratory system

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17
Q

In ventilation, PAO2 and PACO2

A

remain relatively constant as O2 is removed and CO2 is added

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18
Q

Ventilation involves the movement of air between the

A

nose and mouth and the alveoli via the

upper airway, trachea, bronchi, and bronchioles

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19
Q

Ventilation is achieved by

A

inspiratory muscles generating a negative intrapleural (intrapulmonary) pressure, an anergy-dependent process

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20
Q

Manual/mechanical ventilation generates

A

positive intrapulmonary pressure

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21
Q

The ‘respiratory pump’ is comprised of

A

rigid chest wall, lung, and pleural space (and respiratory muscles)

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22
Q

Inspiratory muscles are

A

diaphragm

external ICMs

(sternocleidomastoids)

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23
Q

Expiratory muscles are

A

internal ICMs

abdominal muscles

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24
Q

At rest, tidal volume is

A

~500mL

tidal volume: volume of air moved in or out of the lungs during quiet breathing

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25
Q

At rest, minute ventilation is

A

7-8L/min

minute ventilation: volume of gas inhaled or exhaled per minute (volume of each breath x respiratory frequency per minute)

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26
Q

At rest, exhalation is achieved by

A

relaxation of the inspiratory muscles

and elastic recoil of the lungs

until FRC is reached

functional residual capacity: volume in lungs at end-expiratory position

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27
Q

Total lung capacity

A

volume of air in lungs at maximum inhalation

~5700mL or 5.7L

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28
Q

Residual volume

A

volume of air in lungs at maximal exhalation

~1200mL or 1.2L

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29
Q

Vital capacity

A

volume of air exhaled from TLC to RV

~4500mL or 4.5L

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30
Q

Tidal volume

A

volume of any breath

~500mL at rest

~50% of VC (~2250mL) at peak exercise

31
Q

FEV1

A

forced expiratory volume in 1 second

~70-80% of forced vital capacity

**forced vital capacity: **determination of VC from maximally forced expiratory effort

32
Q

Functional residual capacity

A
  • volume remaining after passive exhalation where ‘zero’ pressure occurs - lungs are prevented from recoiling further by the chest wall
  • ~2200mL or 2.2L
  • volume at the balance of intrinsic lung elastic recoil and chest wall expansion
    • i.e. no muscle use
  • residual volume+expiratory reserve volume
33
Q

Normal respiratory rate

A

14-18 breaths/min

34
Q

During exercise, tidal volume

A

can increase to about half VC (~2250mL)

35
Q

During exercise, the respiratory rate is

A

30-40 breaths per min

36
Q

During exercise, minute ventilation is

A

>100L/min

37
Q

Increased tidal volumes, respiratory rates, and minute ventilation during exercise are achieved by

A

use of accessory inspiratory muscles and expiratory muscles in addition to the diaphragm

38
Q

The total work of breathing involves

A
  • **resistive work of breathing: **overcoming the friction of air flowing through the airways
  • elastic work of breathing: work required to expand the lungs and chest wall
    • no work required for up to ~80% expansion of the ribcage
39
Q

Diffusion in the lungs is driven by

A

the difference in partial pressures of gases on either side of the alveolar-capillary (A-C) membrane

40
Q

The rate of diffusion of a gas is determined by

A

Fick’s Law

**diffusion rate of CO2 is 20x that of O2**

COMMON EXAM Q

41
Q

Diffusion of O2 takes

A

~0.25sec

42
Q

How long does the RBC contact the alveolus?

A

0.75s

43
Q

What is the significance of the extra time spent by the RBC at the alveolus?

A
  • in contact ~0.75 sec
  • O2 diffusion takes ~0.25 sec
  • tf ~0.5 sec where no diffusion occurring that provides a reserve that may be useful when O2 demand increases (i.e. exercise)
44
Q

Why is O2 transfer across the A-C membrane perfusion limited, and not diffusion limited?

A
  • O2 transfer is not limited by diffusion
  • O2 transfer is limited by the amount of blood in the capillaries, and the number of available O2 binding sites (i.e. perfusion)
45
Q

Diffusion limitation of O2 transfer occurs when

A
  • at rest if the A-C membrane is grossly abnormal
  • or, in less severe disease during exercise
    • transit time decreases tf RBC spending less time in contact with alveolus
46
Q

Abnormalities in gas exchange are not so much due to abnormalities in diffusion as they are to

A

abnormalities in matching ventilation and perfusion of individual alveolar capillary units

47
Q

Gas exchange is most efficient when

A

ventilation (V) and perfusion (Q) are matched i.e. V/Q = 1 in individual A-C units

48
Q

How many A-C units are there?

A

300 x 10^6

49
Q

What are low V/Q units?

A

ventilation (V) is relatively lower than perfusion (Q)

i.e. alvelous (L) with narrowed airway leading to it but adequate flow

50
Q

What is a shunt?

A

extreme form of low V/Q unit where V/Q = 0

i.e. alveolus (R) with a blocked airway and tf no ventilation, but adequate flow

does not respond to supplemental O2

51
Q

What is the most clinically important cause of reduced PaO2?

A

low V/Q units

decreased PaO2 will respond to supplemental O2

52
Q

What characteristic structures ensure homogenous ventilation and perfusion to most regions of the lungs, and even V/Q matching?

A

fractal design of the bronchial tree and pulmonary arterial circulation

air and blood to each alveolus tf travels the same distance

53
Q

How many divisions are there of the bronchial and pulmonary arterial trees?

A

23

54
Q

Diffusion of CO2 relative to O2 is

A

20x faster

CO2 is more soluble in the A-C membrane

55
Q

Diffusion limitation for CO2 occurs only with

A

severe abnormalities of the A-C membrane

56
Q

Elevated PaCO2 is due to

A

inadequate alveolar ventilation (VA)

i.e. PaCO2 is inversely proportional to VA

57
Q

Stimuli to respiratory muscles from the respiratory centres in the brainstem are sent via

A

phrenic nerves

(motor info to diaphragm, sensory from diaphragm)

58
Q

Central chemoreceptors respond to

A

H+ concentration, a biproduct of the reaction of CO2 + H2O

H+ is sensed in the CSF, not the CO2

59
Q

Peripheral chemoreceptors respond to

A

CO2, H+ ions, and O2

60
Q

Breathing is regulated by

A
  • CO2
  • H+ ions
  • O2
  • emotional and cortical stimuli
  • stretch receptors in the lungs
  • proprioceptors in joints detect position
    • i.e. movement stimulates ventilation
61
Q

On hyperventilation in asthmatics, CO2 is

A

low; pt is not hypoxic or acidotic

tf stimulus to hyperventilate is coming from stretch receptors, anxiety, possible fever, etc.

62
Q

Changes in ____ affect ventilation more than changes in ____

A
  • PCO2, PO2
  • respiratory centre responds more to small changes in CO2 more than small changes in O2
    • small +PCO2 = hyperventilation
    • -PO2 (e.g. 98 to 60mmHg on a flight) = no change to ventilation
63
Q

Hb saturation is calculated by

A

(O2 combined with Hb/O2 capacity)*100

64
Q

How is CO2 transported in blood?

A
  • 10% dissolved in plasma
  • 30% attached to proteins e.g. Hb globin as carbamino compounds
  • 60% bicarbonate dissolved in the blood cell (formed by carbonic anhydrase, H+ generated may attach to Hb)
65
Q

What is the driving pressure for O2 to bind to Hb?

A

concentration of O2 dissolved in plasma (PaO2 or PvO2)

66
Q

What is the significance of the sigmoid relationship between Hb-O2 binding and PaO2?

A
  • PaO2 can be relatively low but still achieves 90% SaO2
  • in tissues, the steep part of the curve facillitates active removal or unbinding of O2 from the Hb
67
Q

How does temperature affect the oxygen-haemoglobin dissociation curve?

A

decrease:

  • left shift
  • +O2 affinity
    • easier to bind to Hb
    • reluctant to unload O2 (i.e. lungs)

increase:

  • right shift
  • -O2 affinity
    • +PaO2 needed/harder to bind to Hb
    • easier to release O2 from Hb (i.e. tissues)
68
Q

How does pH affect the oxygen-haemoglobin dissociation curve?

A

(Bohr effect: +acidity = Hb binds less O2 for a given PO2, and more H+)

decrease/acidosis:

  • right shift; -O2 affinity; i.e. at tissues

increase/alkalosis:

  • left shift; +O2 affinity; i.e. at lungs
69
Q

How does 2,3-BPG affect the oxygen-haemoglobin dissociation curve?

A

decrease:

  • left shift; +O2 affinity; i.e. at lungs

increase:

  • right shift; -O2 affinity; i.e. at tissues
  • 2,3-BPG stabilizes deoxyHb
70
Q

How does CO2 affect the oxygen-haemoglobin dissociation curve?

A

decrease:

  • left shift; +O2 affinity; i.e. lungs

increase:

  • right shift; -O2 affinity; i.e. tissues
  • production of HCO3- produces H+ ions, released into the plasma = respiratory acidosis
  • also influences intracellular pH (Bohr)
71
Q

Tissue oxygen supply depends on

A

PaO2, [Hb], CO,

and local tissue factors: temperature, pH, vascularity, and PO2

72
Q

Central cyanosis reflects

A

decreased oxygenation of arterial blood (PaO2)

compensated for by: +[Hb], +CO

tissues and organs are not hypoxic

73
Q

In chronic hypoventilation

A
  • PaCO2 is elevated
  • pH decreases = respiratory acidosis
  • restored by normal ventilation or compensatory increase in bicarbonate
74
Q

In induced hypoventiliation (i.e. breath holding)

A
  • PaCO2 will increase and pH will decrease
  • chemical stimuli will override conscious effort to hold the breath, triggering hyperventilation

Respiratory Physiology (8 decks)

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