No 44 COURSE FOR THE DIPLOMA
IN
AVIATION MEDICINE
June 20th 2011
Revision
Cardiovascular and Respiratory Physiology
Earth’s Atmosphere
Jane Ward MB ChB PhD
Q. How low does PO2 need to be to give a large ventilatory
response?
Q. As a person ascends to altitude in an unpressurised
aircraft, how are his arterial PO2 and PCO2 affected:
a) if the subject failed to increase his ventilation (e.g. a
carotid body resected subject who cannot sense the
hypoxia)?
b) if ventilation increased in the normal way?
Is there any altitude at which the ventilatory response
normalizes alveolar PO2 (i.e. returns it to the sea level
value)?
Ventilatory response to O2
60
Ventilation (litres per minute)
50
40
30
20
10
60
0
0
4
8
Arterial PO2
12
acute exposure to 10,000 feet
120
(mmHg)
16
(kPa)
mmHg
Alveolar PO2
16
120
kPa
100
80
8
60
40
20
Alveolar PCO2
0
0
40
5.3
20
0
0
0
5000
0
10,000 15,000 20,000 25,000 feet
Altitude
3,000
6,000
m
Values if ventilation had not changed
Mean values for 30 subjects exposed acutely to altitude
Two patients both have reduced arterial oxygen contents
of 100 ml/l (instead of the normal 200 ml/l). In Mr A this
is due to anaemia, in Mr C this is due to carbon monoxide
poisoning.
Q. Explain why Mr C is much sicker than Mr A.
Q. Why does raising inspired oxygen concentration from
24% to 28% significantly improve the myocardial oxygen
delivery in a patient with severe chronic obstructive
pulmonary disease (COPD) but not in to a patient with
angina?
Q. Give an example of a condition or situation that
increases arterial PO2 but is associated with symptoms of
cerebral hypoxia.
% sat
MI patient
100
90
80
70
COPD
60
50
40
30
20
10
0
0
0
20
40
5
60
80
10
100
15
PO2
120
20 kPa
140
mmHg
Arterial PO2 vs arterial oxygen saturation
Q. You are measuring arterial PO2 continuously (with an
indwelling PO2 electrode) and oxygen saturation (with a
pulse oximeter) in a patient.
The patient stops breathing.
Q. Describe the way in which arterial PO2 and O2
saturation will change during the apnoea.
mmHg kPa
100
13
arterial PO2
60
8
20
2.7
100%
O2 saturation
50%
stop
breathing
30 seconds
You are measuring alveolar PO2 continuously (with a fast
response O2 meter sampling end-tidal gas) and oxygen
saturation (with a pulse oximeter) in a pilot climbing from
sea level to 40,000 in aircraft with its pressurisation
accidentally switched off.
Q. Describe the way in which arterial PO2 and O2
saturation will change as he ascends.
Steady fall in PO2 with increasing altitude, with rate of fall slowing
a little as ventilation increases above about 10,000 feet. Little
change in saturation until PO2 < 60 mmHg at around 10,000feet.
Q. At roughly what altitude will he pass out if he fails to
notice and take action?
Variable, depending on speed of ascent, activity, individual. The
early balloonists lost consciousness at around 25,000-30,000 feet.
Q. Could you give a reasonable estimate of arterial PO2
if you had an oxygen dissociation cure and a pulse
oximeter oxygen saturation reading:
a)In a normal person at sea level?
No
b)In a severely hypoxic patient?
Yes
All measurements have some potential error
If we are measuring oxygen saturation in a normal person
at sea level:
Large possible range of PO2
100
Oxygen
saturation
(%)
Small error in saturation
PCO2 = 5.3 kPa (40 mmHg)
pH = 7.4
Temperature = 37oC
75
So if the pulse
oximeter read
96% there is a
wide range of
possible arterial
PO2s
50
25
0
0
0
2
4
6
8
50
10
PO2
12
14
100
16
18
20
kPa
150 mmHg
If we are measuring arterial PO2 in a normal person at sea
level:
Small error in PO2
Little effect on saturation
100
Oxygen
saturation
(%)
PCO2 = 5.3 kPa (40 mmHg)
pH = 7.4
Temperature = 37oC
75
50
25
0
0
0
2
4
6
8
50
10
PO2
12
14
100
16
18
20
kPa
150 mmHg
So if arterial
PO2 was 96
mmHg (12.8 kPa)
we can be fairly
confident that
the oxygen
saturation is
fairly close to
97%
Q. In a hypoxic person (P < 8 kPa) with an oxygen
dissociation curve could you reasonably predict PO2 from
saturation or saturation from PaO2?
Yes, on the steep
part of the
dissociation
cure=ve PO2
predicts
saturation quite
well and
saturation
predicts PO2
quite well.
100
Oxygen
saturation
(%)
PCO2 = 5.3 kPa (40 mmHg)
pH = 7.4
Temperature = 37oC
75
50
25
0
0
0
2
4
6
8
50
10
PO2
12
14
100
16
18
20
kPa
150 mmHg
Different situations and conditions affect the arterial
partial pressure of oxygen (PaO2), arterial O2 saturation
(O2 sat) and arterial O2 content (O2 cont) differently.
Compared to a normal person at sea level:
PaO2 :
N
O2 sat:
N
O2 cont:
N
State how are these things affected by the following
situations or conditions:
E.g. Low (L), Slightly L, high (H), normal (N) ….
1. Mild hypoxia with normal blood. E.g. mild respiratory depression or
skiing in the Alps.
PaO2:
L
O2 sat:
slightly L
O2 cont:
slightly L
2. Polycythaemia Rubra Vera
PaO2:
N
O2 sat:
N
O2 cont:
H
3. Severe hypoxia with normal blood. E.g. marked hypoventilation in a
patient with a head injury or at very high altitude.
PaO2:
L
O2 sat:
L
O2 cont:
L
4. Polycythaemia and hypoxia. E.g chronic respiratory diseases esp.
severe COPD. Or a normal person whose has lived in the Himalayas for
several weeks. The polycythaemia is a response to chronic hypoxia.
PaO2:
L
O2 sat:
L
O2 cont:
L or N or H
6. Anaemia with a normal respiratory system.
PaO2:
N
O2 sat:
N
O2 cont:
L
7. Anaemia with the patient breathing oxygen enriched air.
PaO2:
H
O2 sat:
N
O2 cont:
8. Carbon monoxide poisoning.
PaO2: N (usually)
O2 sat:
L
O2 cont: L
L
Q. How would (a) arterial PO2 and (b) oxygen saturation by pulse
oximetry be affected in a patient with carbon monoxide poisoning?
(a) PaO2 is unaffected by CO poisoning. (FIO2 normal; PaO2 only
affected when ill enough for ventilation to be depressed.)
(b) The pulse oximeter is based on
colour of haemoglobin.
Hand of person who died of CO
poisoning.
The simple pulse oximeter will give a
falsely high O2 saturation.
c.f. low oxygenated Hb, high
deoxygenated Hb where it correctly
records low oxygen saturation
1
Q. List the special features of the cerebral circulation:
•High blood flow for weight.
•Total flow relatively constant (but does fall on standing). Local flow
increases with neuronal activity.
•Good autoregulation
•Very sensitive to changes in PCO2 and PO2.
•Hyperventilation lowers PCO2 and can give such marked cerebral
vasoconstriction that oxygen delivery becomes inadequate despite
raised PaO2.
Cerebral blood flow (ml/min/100g tissue)
Autoregulation: maintenance of a fairly constant blood flow in the face of
changes in perfusion pressure
F = DP/R
150
immediate
after a few minutes
100
50
0
0
50
100
150
200
Perfusion Pressure (arterial – venous pressure)
250
300
Q. Where are the arterial baroreceptors?
Carotid sinus
Aortic arch
and coronary arterial
Q. What are the main reflex cardiovascular effect of stimulating
the arterial baroreceptors by increasing arterial BP?
Arterial baroreceptor reflex
 firing
carotid sinus
BP  and aortic  glossopharyngeal  Brainstem
and vagus nerves
(NTS)
arch
baroreceptors
parasympathetic
sympathetic
sympathetic
heart
blood vessels
heart rate
contractility
vasodilatation
venodilatation
NTS = Nucleus of the tractus solitarius
BP
Q. What is/are the important differences between the carotid
sinus and the aortic arch baroreceptor reflexes?
Aortic baroreceptors:
less sensitive to pulse pressure.
The aortic baroreceptor reflex may have a relatively
stronger effect on heart rate than on vascular
resistance and the carotid baroreflex the other way
75 mmHg
round
95 mmHg
On standing aortic baroreceptors remain at heart level
but carotid sinus is now about 25 cm above the heart.
 On standing, even if heart level pressure unchanged,
carotid sinus pressure falls  carotid baroreceptor firing
falls but aortic baroreceptor firing unchanged
95 mmHg
Q. What mechanism(s) help to both:
1. to reduce foot swelling with prolonged standing and
2. to minimize the all in cardiac output with prolonged standing?
Mechanisms limiting increase in capillary pressure in the foot:
a. skeletal muscle pumping - aids venous return to the heart
valves
may lower foot venous
pressure to 20-30 mmHg.
Venous pressure in foot (cm H2O)
Foot venous pressures standing and with walking
120
80
From Levick JR,
An introduction to
cardiovascular physiology. 4th
edition
Arnold
40
0
Time (s)
Normal response to 20
minutes of head up tilt in a
young adult (no faint).
Note: there is actually small
increase in BP - the
%increase in TPR is greater
than the %fall in CO.
Q. What factors determine the oxygen delivery to a tissue?
Oxygen Delivery
Oxygen delivery to a tissue (ml/min) =
arterial oxygen content (ml/ml) x blood flow to the tissue
(ml/min)
Arterial oxygen content depends on:
• the arterial PO2
• the haemoglobin concentration
• the proportion of oxygen binding sites available for
oxygen binding (reduced by CO and methaemoglobin)
• the affinity of the haemoglobin for oxygen (e.g. [H+],
PCO2, temp, 2,3 DPG concentration)
Blood flow to a tissue depends on blood pressure and
vascular resistance.
There are 5 mechanisms which can lead to arterial hypoxia, low PaO2. Of
these, only hypoventilation inevitably leads to a high arterial PCO2.
Mechanisms 3, 4 and 5 increase
the A-a PO2 gradient.
Air or alveolar gas with
normal PO2
Air or alveolar gas with
reduced PO2
Deoxygenated blood (‘mixed
venous’or right-sided)
Normal, fully oxygenated
blood
Incompletely oxygenated blood
Q. Apart from the oxygen delivered to a tissue, what else
affects the oxygen consumption of a tissue?
Oxygen consumption of a tissue (ml/min) = oxygen delivery
(ml/min)) x oxygen extraction (ml O2/ ml blood)
Oxygen extraction is affected by capillary density, tissue oedema,
the affinity of haemoglobin for oxygen.
If the tissue cells cannot use oxygen (e.g. cyanide or sepsis
poisoning the mitochondria) oxygen extraction is also reduced.
Cells furthest from a capillary are exposed to a lower tissue PO2 than
cells near the capillary. These areas (critical zones or lethal corners)
are vulnerable if capillary PO2 falls.
Q. What is normal alveolar PO2 at sea level?
Approx 103 mmHg, 13.3 kPa
Q. What is usually considered to the highest altitude at which most
people will show only minor physical and psychometric deficit when
breathing air?
Approx 10,000 feet
Q.* What will their alveolar PO2 be at this altitude?
Approx 55 mmHg, 7.5 kPa
Above this altitude the raising FIO2 above the usual 0.21 (21%) can be
used to compensate for the low barometric pressure.
Q. What is the maximum altitude at which a normal sea level alveolar
PO2 can be achieved by breathing 100% Oxygen?
Approx 33,700 feet
Q. What is the maximum altitude at which the alveolar PO2 in Q* can
be achieved by breathing 100% Oxygen at ambient pressure?
Approx 40,000 feet
Campbell & Bagshaw, 2002
In plane A a pilot in an unpressurised aircraft lying at 40,000
feet loses his oxygen supply and starts breathing ambient air.
In Plane B, the pilot is breathing cabin air pressurised to 8,000
feet when there is a sudden decompression caused by a large hole
(door sized) suddenly deveolping in the fuselage.
The pilot of which plane is likely to be adversely affected most
quickly?
Loss of oxygen supply:
25,000 feet
breathing O2 enriched
air
25,000 feet
breathing air
O2
O2
PAO2 falls
progressively to 30
mmHg
PAO2 =
103 mmHg
40
RA
RV
103
95
103
40
RA
LA
LV
RV
LA
LV
PAO2 falls at a rate which depends on alveolar ventilation. Note as PO2 falls to 30 mmHg
O2 moves from blood to alveolus.
PAO2
Altitude
atmosphere
cabin
tracheal PO2
40000
8000
108
65
A rapid decompression can cause a much faster fall in alveolar and
arterial PO2
40000
rapid change to 40000
20
15
Q. How quickly does the pilot need to breath oxygen after a
sudden decompression at 40,000 feet?
Q. What determines how likely he is to lose consciousness?
At A ‘cabin’ (or hypobaric chamber) altitude from 8000 to 40,000 feet in 1.6 seconds
A
*
**
* 2 seconds after time 0
** 8 seconds after time 0
If area under critical line > 140 mmHg.sec consciousness will almost certainly be lost
Typical times of useful consciousness (TUC) in a healthy resting
subject.
The values are much more variable at the lower altitudes.
TUC is very much reduced by even light exercise.
Altitude
Feet
Metres
Progressive Hypoxia:
Rapid
As when inspired oxygen Decompression
changed to air
25,000
7,620
3-6 minutes
2-3 minutes
30,000
9,140
1.5-3 minutes
0.5-1.5 minutes
35,000 10, 670
45-75 seconds
25-35 seconds
40,000 12,190
25 seconds
18 seconds
Q. What are the symptoms and signs of hypoxia?
Q. What factors affect an individual’s susceptibility to hypoxia?
Q. What are the symptoms and signs of hyperventilation?
Symptoms and signs of acute hypobaric hypoxia
•personality change
•lack of insight and judgment
•loss of self-criticism
•euphoria
•loss of memory
•mental incoordination
•muscular incordination
•sensory loss
•cyanosis
•hyperventilation specific symptoms (see later)
•clouding of consciousness
•loss of consciousness
•death
Factors affecting the susceptibility to hypoxia
Altitude
Length of time of the exposure
Exercise
Cold
Illness
Fatigue
Drugs/Alcohol
Smoking (carbon monoxide)
Hypocapnia = low PaCO2 due to hyperventilation (caused by: anxiety, pain,
low PaO2, acidosis, excessive mechanical ventilation)
symptoms: dizziness
visual disturbances
pins and needles esp. hands
stiff muscles, tetany and feet
mechanisms: low PaCO2  cerebral vasoconstriction 
cerebral hypoxia
low PaCO2  alkalosis  plasma [Ca2+] 
nerve and muscle excitability
Hyperventilation
Alveolar ventilation is increased relative to CO2 production.
PACO2 (and PaCO2)
 CO2 production
alveolar ventilation
Normal PaCO2 = 40 mmHg, 5.3 kPa
PaCO2 < 25 mmHg: significant fall in psychomotor performance
lightheadedness/dizziness, anxiety, tingling (lips,
fingers, toes)
<20 mmHg muscle spasms in hands and feet (carpopedal spasm)
and face
<10-15 mmHg - clouding of consciousness, unconsciousness
whole body muscle spasms
Below 10,000 feet:
(PAO2 ≈ 55mmHg
O2 sat ≈ 87%)
Neurological effects
little effect on well-learned tasks
slightly impaired performance novel tasks
reduced night vision
10,000 - 15,000 feet:
(PAO2 ≈ 55 - 45mmHg
O2 sat 87 - 80%)
with increasing altitude / hypoxia difficulties
in more complex tasks (as tested by choicereaction time), first then simpler tasks (tested
by pursuit-meter tasks) e.g.:
12,000 feet
10%
15,000 feet
20-30%
increasing problems with memory, drowsiness,
judgement
also reduced muscle coordination
fall in ability to air speed, heading etc
15,000 - 20,000 feet: headaches, dizziness, somnolence, euphoria,
(PAO2 55 - 45mmHg
fatigue, air hunger
O2 sat 80 - 65%)
20,000 - 23,000 feet: confusion and dizziness occurs within a few
(PAO2 29 - 22mmHg minutes of exposure and total incapacitation
O2 sat 65 - 60 %)
and loss of consciousness occurs rapidly after this.
Loss of consciousness - affected by both arterial PO2 and cerebral blood
flow and therefore arterial PCO2.
Occurs when jugular venous PO2 falls to 17-19 mmHg which occurs when
arterial PO2 is 20-40 mmHg. (can occur as low as 16,000 feet)
Tidal volume (VT), is about 500 ml at rest.
Respiratory frequency (f) is about 15 breaths min-1, at rest

.
The minute ventilation (V)= volume entering the lungs each
minute,  7500 ml.min-1 (= 500 x 15) at rest.
.
Alveolar ventilation (VA) is the volume taking part in gas
exchange each minute.
Dead space volume*  150 ml
alveolar ventilation is about 5250 ml.min-1 (= (500 - 150) x 15) at
rest.
*can be measured by various methods such as Bohr method - see appendix
Lung volumes
I.R.V.
T.L.C.
V.C
VT
E.R.V.
F.R.C.
R.V.
Tidal Volume (VT) (at rest)
Vital capacity (V.C.)
Inspiratory Reserve Volume (I.R.V.)
500 ml
5,500 ml
3,300 ml
Expiratory Reserve Volume (E.R.V.)
1,700 ml
Residual Volume (R.V.)
1,800 ml
Functional Residual Capacity (F.R.C.)
3,500 ml
Total Lung Capacity (T.L.C.)
7,300 ml
0?
Note: all
volumes
depend
on height,
age & sex
At altitude, barometric pressure is
reduced, eg. To 33 kPa (250 mmHg),
on top of Everest (29,035 feet).
Fractional concentration of oxygen in
air is unchanged at altitude (0.209).
PIO2 (= FIO2 x PB) falls progressively
with increasing altitude when
breathing air.
Hillary and Tenzing on Everest
May 1953, high FIO2
compensates for the low PB
Calculating PO2 of moist inspired air (PIO2) & alveolar gas, (PAO2)
PIO2
The PO2 of the moistened inspired air at the end of the trachea =
(PB - 6.3) x 0.209 = kPa or (PB - 47) x 0.209 mmHg
PAO2
In the alveolar region CO2 diffuses into the alveolus to replace the oxygen diffusing into the
pulmonary capillary.
If one molecule of CO2 is produced for each molecule of O2 being used then: PAO2 = PIO2 PACO2
but more usually, more O2 is used than CO2 is produced, and then
PAO2 ≈ PIO2 - PACO2 where
R = CO2 production
R
O2 consumption
(Alveolar air equation)
(R is usually about 0.8)
At sea level:
PO2 PCO2 PH2O mmHg
(kPa)
atmospheric air
159
(21 0)
0
variable
mixed expired air* 120
(16 3.5)
26
variable
trachea (during insp.) 150
0 47
(20 0 6.3)
alveolar gas
100
40
47
(13.3 5.3 6.3)
O2
*mixture of alveolar and dead space gas
1 kPa = 7.5 mmHg
CO2
Calculating PO2 of moist inspired air (PIO2) & alveolar gas, (PAO2)
PIO2
The PO2 of the moistened inspired air at the end of the trachea =
(PB - 6.3) x 0.209 = kPa or (PB - 47) x 0.209 mmHg
PAO2
In the alveolar region CO2 diffuses into the alveolus to replace the oxygen diffusing into the
pulmonary capillary.
If one molecule of CO2 is produced for each molecule of O2 being used then: PAO2 = PIO2 PACO2
but more usually, more O2 is used than CO2 is produced, and then
PAO2 ≈ PIO2 - PACO2 where
R = CO2 production
R
O2 consumption
(Alveolar air equation)
(R is usually about 0.8)
Cyanosis is a blue tinge in a tissue due to a high concentration of deoxygenated Hb.
peripheral cyanosis:reduced blood flow to region(s)
Arterial O2 content may be normal.
eg. local obstruction
or low cardiac output
central cyanosis:arterial hypoxaemia - buccal mucosa
and lips are best sites.
conjunctiva
(ear lobes)
buccal mucosa
and lips
When the arterial blood contains > 15 - 20 g.l-1 of deoxygenated haemoglobin cyanosis
is observable even in well-perfused tissues. Occurs when O2 sat. about 85-90% if [Hb]
normal (150 g.l-1).
It appears more easily (higher O2 saturation) in polycythaemic patients. In severe
anaemia central cyanosis is impossible as it would require an O2 saturation
incompatible with life.
Peripheral cyanosis
Central cyanosis
This babies PaO2 was 7.5 kPa (56
mmHg)
The Oxygen Cascade
mmHg
200
150
PO2
100
kPa
25
20
15
10
50
5
0
0
air (sea level)
trachea (moistened)
alveolar (O2 removed)
pulmonary capillary (equilibrates with alveolar)
arterial (R to L shunt blood added, eg bronchial circ.)
mean tissue capillary
mitochondria
mixed venous blood
See also Fig 3.5,
Ernsting’s Aviation
Medicine. Note
typo in legend
alveolar CO2
CO2 production = alveolar CO2 fraction x alveolar ventilation
eg. 250 ml.min-1 = 5
100
x 5000 ml.min-1
alveolar PCO2 and arterial PCO2  alveolar CO2 fraction
(PACO2 )
(PaCO2)
(FACO2)
PACO2 and PaCO2  CO2 production
alveolar ventilation
Breathing air (CO2-free), alveolar and therefore arterial PCO2 is determined by the balance
between CO2 production and alveolar ventilation:
PACO2 and PaCO2  CO2 production
alveolar ventilation
alveolar ventilation
.
VCO2 =
CO2 production
arterial PCO2
Hypercapnia = high PaCO2 due to hypoventilation (possible causes of hypoventilation are
head injury, anaesthetics, drugs, chronic lung disease)
The effects of a high PCO2 are:
flushed skin
full pulse, extrasystoles
BP often raised
muscle twitching, “hand flap”
very high PaCO2 (> 10 kPa or 75 mmHg)

confusion
convulsions
coma
depressed ventilation
death
+ve
Ventilation (litres per minute)
Effect of changes of PO2 on the ventilatory response to raising PCO2
60
50
40
PO2 = 5 kPa
hypoxia
increases the
ventilatory
response to CO2
PO2 = 13 kPa
30
20
10
0
4
5
6
7
Alveolar PCO2 (kPa)
8
11
Central chemoreceptors
Location of Chemosensitive areas – there are several areas esp:
PONSnear the exit of IX and
VI X.
Ventrolateral surface of medulla,
Note: Chemoreceptors are separate from the respiratory neurones.
MEDULLA OBLONGATA
V
VII
VIII
IX
X
XI
XII
Glial cells
CSF
Capillary
Neurone
CSF
HCO3H+
Blood brain barrier
Chemoreceptor
H+ , HCO3-
CO2
O2
Blood
Peripheral Chemoreceptors: in carotid and aortic bodies
Carotid bodies
carotid
sinus
nerve
carotid
body
Bifurcation
to internal
& external
carotid
common
carotid
artery
glossopharyngeal
nerve
Aortic bodies
scattered around aortic
arch, afferents in vagus:
in man probably play
little role in respiratory
responses
Maximum cabin altitude
CAA and FAA regulations stipulate maximum cabin altitude must not exceed 8000 feet
during normal operations.
At usual cruising altitudes is usually no more than 6-7,000 feet in modern jet airliners
Airbus and Boeing 787
Designed for a maximum cabin altitude to 6,000ft – usually operated at 5000 feet.
Cardiovascular effects of acute hypoxia
Heart rate (HR) and cardiac output (CO) increase at rest and in submaximal exercise.
At 15,000 maximum oxygen uptake (VO2 max) is 70% sea level value.
Mean BP usually unchanged during moderate hypoxia.
Effects on regional blood flows
Caused by a mixture of the direct effects of hypoxia on different blood vessels, modified by the
effects of any change in arterial PCO2 and various reflex effects:
•renal blood flow decreased
•coronary flow increased immediately - at 25,000 little or no ECG signs of hypoxia even at point
consciousness lost.
•pulmonary vessels constrict in response to a low PO2 - increases pulmonary artery pressure.
The effects on cerebral blood flow (cbf) are complicated:
Acute high altitude exposure:
Low PaO2
 increased blood flow

Increased ventilation  reduced PaCO2  reduced blood flow
When arterial PO2 > 45 mmHg cbf determined by PaCO2.
If PaCO2 falls from 40 to 20 mmHg cerebral blood flow halves.
As PaO2 falls below 45 mmHg hypoxia leads to vasodilatation and increased cerebral blood flow.
Net effect of increased altitude:
Up to 15,000 feet variable changes in cerebral blood flow. (increases, decreases or no
change)
Above about 17,000 feet increased cerebral blood flow
Mechanism of loss of consciousness
Usually HR, BP and cerebral blood flow are maintained when loss of consciousness occurs and
the main cause is the reduced arterial oxygen content caused by the low alveolar PO2.
In 20% of subjects however loss of consciousness is triggered by a sudden fall in BP - a
vasovagal faint.
Revision
A. At sea level pulmonary capillary PO2
equilibrates with alveolar PO2 both at rest
(time in pulmonary capillary  0.75s) and in
heavy exercise (time in pulmonary capillary 
0.25s).
A.
B. When alveolar PO2 is low, equilibration
takes longer and in exercise pulmonary
capillary PO2 may not reach alveolar PO2.
Leads to increased A-a PO2 gradient and a fall
in arterial PO2.
Signs and symptoms of hypoxia increased by
exercise.
B.
Time in pulmonary capillary (s)
at rest takes ≅ 0.75s, less in exercise
•
•
•
•
•
Causes of hyperventilation
Hypoxia (when PAO2 < about 55 mmHg)
Anxiety (student pilot, experience pilots during emergencies / new aircraft,
passengers with fear of flying)
Pressure breathing (hypoxia protection at very high altitude or G-protection)
Pain
Environmental stress (high temperature, whole-body vibration at 4-8 Hz,
acceleration, cold water immersion)
Note:
1.
some of the symptoms (e.g.. poor psychomotor performance) are similar to those
cause by hypoxia.
2.
Hypoxia causes hyperventilation. Therefore if symptoms/signs of hyperventilation
occur when altitude above 12,000 feet, need to assume and act as if cause is hypoxia
until proven otherwise.