no 44 course for the diploma in aviation medicine

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)?

Venti

latio

n (li

tres

per

min

ute)

Arterial PO2

60

50

40

30

20

10

04 8 12 160

Ventilatory response to O2

acute exposure to 10,000 feet

60 120

(kPa)

(mmHg)

Values if ventilation had not changed

Mean values for 30 subjects exposed acutely to altitude

0 5000 10,000 15,000 20,000 25,000 feet

20

0

40

0

0 3,000 6,000 m

5.3

Altitude

80

60

40

0

20

100

120

0

16

8

Alveolar PO2

mmHg kPa

Alveolar PCO2

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.

0 20 40 60 80 100 120 1400

10

20

30

40

50

60

70

80

90

100

0 5 10 15 20 kPa

MI patient

COPD

% sat

PO2

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.

mmHg100

kPa13

60 8

100%

20 2.7

50%

stopbreathing

30 seconds

arterial PO2

O2 saturation

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.

Q. At roughly what altitude will he pass out if he fails to notice and take action?

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.

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?

b)In a severely hypoxic patient?

No

Yes

mmHgPO2 0 50 100 150

0 2 4 6 8 10 12 14 16 18 20 kPa

Oxygen saturation (%)

100

75

50

25

0

PCO2 = 5.3 kPa (40 mmHg)pH = 7.4Temperature = 37oC

Small error in saturation

All measurements have some potential errorIf we are measuring oxygen saturation in a normal person at sea level:

Large possible range of PO2

So if the pulse oximeter read 96% there is a wide range of possible arterial PO2s

mmHgPO2 0 50 100 150

0 2 4 6 8 10 12 14 16 18 20 kPa


100

75

50

25

0


Little effect on saturation

If we are measuring arterial PO2 in a normal person at sea level:

Small error in PO2

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?

mmHgPO2 0 50 100 150

0 2 4 6 8 10 12 14 16 18 20 kPa


100

75

50

25

0


Yes, on the steep part of the dissociation cure=ve PO2 predicts saturation quite well and saturation predicts PO2 quite well.

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: NO2 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: O2 sat: O2 cont:

2. Polycythaemia Rubra Vera


3. Severe hypoxia with normal blood. E.g. marked hypoventilation in a patient with a head injury or at very high altitude.


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.


L slightly Lslightly L

N N H

L L L

L L L or N or H

6. Anaemia with a normal respiratory system.


7. Anaemia with the patient breathing oxygen enriched air.


8. Carbon monoxide poisoning.


N NL

H NL

N (usually) LL

Q. How would (a) arterial PO2 and (b) oxygen saturation by pulse oximetry be affected in a patient with carbon monoxide poisoning?

(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.

1

c.f. low oxygenated Hb, high deoxygenated Hb where it correctly records low oxygen saturation

(a) PaO2 is unaffected by CO poisoning. (FIO2 normal; PaO2 only affected when ill enough for ventilation to be depressed.)

http://www.forensicindia.com/forensic_pictures/copoisoning.jpg




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.

0

50

100

150

0 50 100 150 200 250 300

Perfusion Pressure (arterial – venous pressure)

Cer

ebra

l blo

od fl

ow (m

l/min

/100

g tis

sue)

immediate

after a few minutes

Autoregulation: maintenance of a fairly constant blood flow in the face of changes in perfusion pressure F = DP/R

Q. Where are the arterial baroreceptors?

Q. What are the main reflex cardiovascular effect of stimulating the arterial baroreceptors by increasing arterial BP?

Carotid sinusAortic archand coronary arterial

firing carotid sinus and aortic arch baroreceptors

BP Brainstem (NTS)

glossopharyngeal and vagus nerves

parasympathetic

sympathetic

sympathetic

heart blood vessels

heart ratecontractility

vasodilatationvenodilatation

Arterial baroreceptor reflex

BPNTS = Nucleus of the tractus solitarius

Q. What is/are the important differences between the carotid sinus and the aortic arch baroreceptor reflexes?

Aortic baroreceptors: less sensitive to pulse pressure.

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

95 mmHg

75 mmHg

The aortic baroreceptor reflex may have a relatively stronger effect on heart rate than on vascular resistance and the carotid baroreflex the other way round

Q. What mechanism(s) help to both:

1. to reduce foot swelling with prolonged standing and2. to minimize the all in cardiac output with prolonged standing?

Mechanisms limiting increase in capillary pressure in the foot:

may lower foot venous pressure to 20-30 mmHg.

a. skeletal muscle pumping - aids venous return to the heart valves

From Levick JR, An introduction to cardiovascular physiology. 4th editionArnold

Foot venous pressures standing and with walking

Veno

us p

ress

ure

in fo

ot (c

m H

2O)

120

80

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.

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

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.

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.

Q. Apart from the oxygen delivered to a tissue, what else affects the oxygen consumption of a tissue?

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?

Q. What is usually considered to the highest altitude at which most people will show only minor physical and psychometric deficit when breathing air?

Q.* What will their alveolar PO2 be at this altitude?

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?

Q. What is the maximum altitude at which the alveolar PO2 in Q* can be achieved by breathing 100% Oxygen at ambient pressure?

Approx 103 mmHg, 13.3 kPa

Approx 55 mmHg, 7.5 kPa

Approx 10,000 feet

Approx 40,000 feet

Approx 33,700 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?

25,000 feetbreathing O2 enriched air

O2

PAO2 = 103 mmHg

40 103 103

LA

LV

95

RVRA

25,000 feet

breathing air

O2

PAO2 falls progressively to 30 mmHg

40

LA

LVRVRA

PAO2 falls at a rate which depends on alveolar ventilation. Note as PO2 falls to 30 mmHg O2 moves from blood to alveolus.

Loss of oxygen supply:

800040000

65

PAO2

Altitudeatmospherecabin

rapid change to 40000

40000

15

108

tracheal PO2

20

A rapid decompression can cause a much faster fall in alveolar and arterial PO2

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?

* 2 seconds after time 0** 8 seconds after time 0If area under critical line > 140 mmHg.sec consciousness will almost certainly be lost

***

A

At A ‘cabin’ (or hypobaric chamber) altitude from 8000 to 40,000 feet in 1.6 seconds

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 hypoxiaAltitude

Length of time of the exposureExercise

ColdIllnessFatigue

Drugs/AlcoholSmoking (carbon monoxide)

mechanisms: low PaCO2 cerebral vasoconstriction cerebral hypoxia

Hypocapnia = low PaCO2 due to hyperventilation (caused by: anxiety, pain, low PaO2, acidosis, excessive mechanical ventilation)

symptoms: dizzinessvisual disturbances

pins and needles esp. handsstiff muscles, tetany and feet

low PaCO2 alkalosis plasma [Ca2+] nerve and muscle excitability

Hyperventilation

Alveolar ventilation is increased relative to CO2 production. PACO2 (and PaCO2) CO2 production

alveolar ventilationNormal PaCO2 = 40 mmHg, 5.3 kPa

PaCO2 < 25 mmHg: significant fall in psychomotor performancelightheadedness/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

Neurological effectsBelow 10,000 feet: little effect on well-learned tasks(PAO2 ≈ 55mmHg slightly impaired performance novel tasksO2 sat ≈ 87%) reduced night vision

10,000 - 15,000 feet: with increasing altitude / hypoxia difficulties(PAO2 ≈ 55 - 45mmHg in more complex tasks (as tested by choice-O2 sat 87 - 80%) reaction time), first then simpler tasks (tested

by pursuit-meter tasks) e.g.:

12,000 feet 10% fall in ability to air speed, heading etc

15,000 feet 20-30%increasing problems with memory,

drowsiness,judgementalso reduced muscle coordination

15,000 - 20,000 feet: headaches, dizziness, somnolence, euphoria, (PAO2 55 - 45mmHg fatigue, air hungerO2 sat 80 - 65%)

20,000 - 23,000 feet: confusion and dizziness occurs within a few(PAO2 29 - 22mmHg minutes of exposure and total incapacitationO2 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)

Alveolar ventilation (VA) is the volume taking part in gas exchange each minute.

.

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.

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

VT

Tidal Volume (VT) (at rest) 500 ml

V.C

Vital capacity (V.C.) 5,500 ml

I.R.V.

Inspiratory Reserve Volume (I.R.V.) 3,300 ml

T.L.C.

Total Lung Capacity (T.L.C.) 7,300 ml

F.R.C.

Functional Residual Capacity (F.R.C.) 3,500 ml

R.V. 0?

Residual Volume (R.V.) 1,800 ml

E.R.V.

Expiratory Reserve Volume (E.R.V.) 1,700 ml

Note: all volumes depend on height, age & sex

Lung volumes

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)

1 kPa = 7.5 mmHg

atmospheric air 159 0 variable(21 0)

CO2O2

trachea (during insp.) 150 0 47(20 0 6.3)

alveolar gas 100 40 47 (13.3 5.3 6.3)

mixed expired air* 120 26 variable(16 3.5)

*mixture of alveolar and dead space gas

PO2 PCO2 PH2O mmHg (kPa)

At sea level:

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

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.

buccal mucosa and lips

conjunctiva(ear lobes)central cyanosis:-

arterial hypoxaemia - buccal mucosa and lips are best sites.

Central cyanosisThis babies PaO2 was 7.5 kPa (56 mmHg)

Peripheral cyanosis

0

50

100

150

200

0

5

10

15

20

25

PO2

mmHgkPa

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

The Oxygen Cascade

See also Fig 3.5, Ernsting’s Aviation Medicine. Note typo in legend alveolar CO2

PACO2 and PaCO2 CO2 production alveolar ventilation

CO2 production = alveolar CO2 fraction x alveolar ventilation

eg. 250 ml.min-1 = 5 x 5000 ml.min-1

100

alveolar PCO2 and arterial PCO2 alveolar CO2 fraction(PACO2 ) (PaCO2) (FACO2)

PACO2 and PaCO2 CO2 production alveolar ventilation

alveolar ventilation

arterial PCO2VCO2 = CO2 production

.

Breathing air (CO2-free), alveolar and therefore arterial PCO2 is determined by the balance between CO2 production and alveolar ventilation:

Hypercapnia = high PaCO2 due to hypoventilation (possible causes of hypoventilation are head injury, anaesthetics, drugs, chronic lung disease)

+vevery high PaCO2 (> 10 kPa or 75 mmHg) confusionconvulsionscomadepressed ventilationdeath

The effects of a high PCO2 are: flushed skinfull pulse, extrasystolesBP often raisedmuscle twitching, “hand flap”

Venti

latio

n (l

itres

per

min

ute)

Alveolar PCO2 (kPa)

60

50

40

30

20

10

04 5 6 7 8 11

Effect of changes of PO2 on the ventilatory response to raising PCO2

PO2 = 13 kPaPO2 = 5 kPa

hypoxia increases the ventilatory response to CO2

PONSM

EDU

LLA

OBL

ON

GATA

Central chemoreceptors

IX

X

XI

XII

VVIIVIII

VI Location of Chemosensitive areas – there are several areas esp:

Ventrolateral surface of medulla, near the exit of IX and X. Note: Chemoreceptors are separate from the respiratory neurones.

Glial cells

Capillary

CSF

Blood

Chemoreceptor

O2

CO2

H+ , HCO3-

HCO3-

H+

Blood brain barrier

Neurone

CSF

Bifurcationto internal & externalcarotid

carotid sinus nerve

glossopharyngealnerve

carotid body

common carotid artery

scattered around aortic arch, afferents in vagus: in man probably play little role in respiratory responses

Peripheral Chemoreceptors: in carotid and aortic bodiesCarotid bodies Aortic bodies

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 flowIncreased 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.

Time in pulmonary capillary (s)at rest takes ≅ 0.75s, less in exercise

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).

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.

A.

B.

Revision

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.

no 44 course for the diploma in aviation medicine

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