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
2
Q
What affects the rate of O2 and CO3 exchange?
A
Consumption of O2 and production of CO2
3
Q
What is normal resting PaO2?
(a = arterial)
A
90-98mmHg
4
Q
What is normal resting PaCO2?
(a = arterial)
A
38-42mmHg
5
Q
What is normal resting arterial pH?
A
7.38-7.42
6
Q
What is normal resting mixed venous PO2?
A
~40mmHg
7
Q
What is normal resting mixed venous CO2?
A
~46mmHg
8
Q
What is normal resting mixed venous pH?
A
less than arterial pH (
9
Q
What is normal resting PAO2?
(A = alveolar)
A
~100mmHg
10
Q
What is normal resting PACO2?
(A = alveolar)
A
~40mmHg
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
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
13
Q
Inadequate respiratory function (in adaptation to exercise) can cause
A
hypoxaemia
hypercapnoea and respiratory acidosis
14
Q
Ventilation is
A
the movement of air in and out of the lungs
15
Q
Respiration is
A
gas exchange across the alveolar-capillary membrane
16
Q
Ventilation ensures that
A
concentrations of O2 and CO2 in alveolar air are optimal for achieving the roles of the respiratory system
17
Q
In ventilation, PAO2 and PACO2
A
remain relatively constant as O2 is removed and CO2 is added
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
19
Q
Ventilation is achieved by
A
inspiratory muscles generating a negative intrapleural (intrapulmonary) pressure, an anergy-dependent process
20
Q
Manual/mechanical ventilation generates
A
positive intrapulmonary pressure
21
Q
The ‘respiratory pump’ is comprised of
A
rigid chest wall, lung, and pleural space (and respiratory muscles)
22
Q
Inspiratory muscles are
A
diaphragm
external ICMs
(sternocleidomastoids)
23
Q
Expiratory muscles are
A
internal ICMs
abdominal muscles
24
Q
At rest, tidal volume is
A
~500mL
tidal volume: volume of air moved in or out of the lungs during quiet breathing
25
At rest, minute ventilation is
7-8L/min
**minute ventilation:** volume of gas inhaled or exhaled per minute (volume of each breath x respiratory frequency per minute)
26
At rest, exhalation is achieved by
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
27
Total lung capacity
volume of air in lungs at maximum inhalation
~5700mL or 5.7L
28
Residual volume
volume of air in lungs at maximal exhalation
~1200mL or 1.2L
29
Vital capacity
volume of air exhaled from TLC to RV
~4500mL or 4.5L
30
Tidal volume
volume of any breath
~500mL at rest
~50% of VC (~2250mL) at peak exercise
31
FEV1
forced expiratory volume in 1 second
~70-80% of forced vital capacity
**forced vital capacity: **determination of VC from maximally forced expiratory effort
32
Functional residual capacity
* 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
Normal respiratory rate
14-18 breaths/min
34
During exercise, tidal volume
can increase to about half VC (~2250mL)
35
During exercise, the respiratory rate is
30-40 breaths per min
36
During exercise, minute ventilation is
\>100L/min
37
Increased tidal volumes, respiratory rates, and minute ventilation during exercise are achieved by
use of accessory inspiratory muscles and expiratory muscles in addition to the diaphragm
38
The total work of breathing involves
* **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
Diffusion in the lungs is driven by
the difference in partial pressures of gases on either side of the alveolar-capillary (A-C) membrane
40
The rate of diffusion of a gas is determined by
**Fick's Law**
\*\*diffusion rate of CO2 is 20x that of O2\*\*
**COMMON EXAM Q**
41
Diffusion of O2 takes
~0.25sec
42
How long does the RBC contact the alveolus?
0.75s
43
What is the significance of the extra time spent by the RBC at the alveolus?
* 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
Why is O2 transfer across the A-C membrane perfusion limited, and not diffusion limited?
* 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
Diffusion limitation of O2 transfer occurs when
* 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
Abnormalities in gas exchange are not so much due to abnormalities in diffusion as they are to
abnormalities in matching ventilation and perfusion of individual alveolar capillary units
47
Gas exchange is most efficient when
ventilation (V) and perfusion (Q) are matched i.e. V/Q = 1 in individual A-C units
48
How many A-C units are there?
300 x 10^6
49
What are low V/Q units?
ventilation (V) is relatively lower than perfusion (Q)
i.e. alvelous (L) with narrowed airway leading to it but adequate flow
50
What is a shunt?
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
What is the most clinically important cause of reduced PaO2?
low V/Q units
## Footnote
**decreased PaO2 will respond to supplemental O2**
52
What characteristic structures ensure homogenous ventilation and perfusion to most regions of the lungs, and even V/Q matching?
fractal design of the bronchial tree and pulmonary arterial circulation
air and blood to each alveolus tf travels the same distance
53
How many divisions are there of the bronchial and pulmonary arterial trees?
23
54
Diffusion of CO2 relative to O2 is
20x faster
CO2 is more soluble in the A-C membrane
55
Diffusion limitation for CO2 occurs only with
severe abnormalities of the A-C membrane
56
Elevated PaCO2 is due to
inadequate alveolar ventilation (VA)
i.e. PaCO2 is inversely proportional to VA
57
Stimuli to respiratory muscles from the respiratory centres in the brainstem are sent via
phrenic nerves
(motor info to diaphragm, sensory from diaphragm)
58
Central chemoreceptors respond to
H+ concentration, a biproduct of the reaction of CO2 + H2O
H+ is sensed in the CSF, not the CO2
59
Peripheral chemoreceptors respond to
CO2, H+ ions, and O2
60
Breathing is regulated by
* CO2
* H+ ions
* O2
* emotional and cortical stimuli
* stretch receptors in the lungs
* proprioceptors in joints detect position
* i.e. movement stimulates ventilation
61
On hyperventilation in asthmatics, CO2 is
low; pt is not hypoxic or acidotic
tf stimulus to hyperventilate is coming from stretch receptors, anxiety, possible fever, etc.
62
Changes in ____ affect ventilation more than changes in \_\_\_\_
* 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
Hb saturation is calculated by
(O2 combined with Hb/O2 capacity)\*100
64
How is CO2 transported in blood?
* 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
What is the driving pressure for O2 to bind to Hb?
concentration of O2 dissolved in plasma (PaO2 or PvO2)
66
What is the significance of the sigmoid relationship between Hb-O2 binding and PaO2?
* 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
How does temperature affect the oxygen-haemoglobin dissociation curve?
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
How does pH affect the oxygen-haemoglobin dissociation curve?
(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
How does 2,3-BPG affect the oxygen-haemoglobin dissociation curve?
decrease:
* left shift; +O2 affinity; i.e. at lungs
increase:
* right shift; -O2 affinity; i.e. at tissues
* **2,3-BPG stabilizes deoxyHb**
70
How does CO2 affect the oxygen-haemoglobin dissociation curve?
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
Tissue oxygen supply depends on
PaO2, [Hb], CO,
and local tissue factors: temperature, pH, vascularity, and PO2
72
Central cyanosis reflects
decreased oxygenation of arterial blood (PaO2)
compensated for by: +[Hb], +CO
*tissues and organs are not hypoxic*
73
In chronic hypoventilation
* PaCO2 is elevated
* pH decreases = respiratory acidosis
* restored by normal ventilation or compensatory increase in bicarbonate
74
In induced hypoventiliation (i.e. breath holding)
* PaCO2 will increase and pH will decrease
* chemical stimuli will override conscious effort to hold the breath, triggering hyperventilation
