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Hypoxia & Hyperventilation
INTRODUCTION
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Hypoxia is the absence of an adequate supply of O2 to the tissues, in quantity or in concentration.
4 types of hypoxia:
o Hypoxic hypoxia
o Anaemic hypoxia
o Ischemic hypoxia
o Histotoxic hypoxia
ACUTE HYPOBARIC HYPOXIA
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Hypobaric Hypoxia:
o Detectable impairment @ 8000 ft.
o If sudden exposure @ 50000 ft, LOC in 12-15", death in 4-6'
ÆTIOLOGY
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➚ altitude without O2 supply
Failure of personal breathing equipment
Rapid decompression
Respiratory responses to acute hypobaric hypoxia
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Alveolar gases when breathing air
1  FiO2
]
 PiO2  PA O2  PA CO2  [FiO2 
R
 PACO2 is the main determinant in the variation of PO2 between the alveolar and the inspired gas
 PACO2 remains constant on ascent to altitude
 However, in practice:
o Above 8-10000 ft, ➘O2 ⇒➚ Ventilation ⇒➘PACO2
o There are 2 conflicting factors:
 ➘PAO2 ⇒➚ Ventilation
 ➘PACO2 ⇒ ➘ Ventilation
o @ 18000 ft at rest: ➚ Ventilation 20-50%
o @ 22000 ft at rest: ➚ Ventilation 40-60%
o Exercise increases the production of CO2 and thus increases ventilation
Altitude (ft)
Air mix
O2
0
33500
8000
39000
15000
42000
20000
45000
32500
47000
Altitude (ft)
0
10000
12000
18000
25000
©Jean-Michel Ferrieux-2011
PiO2
148
108
80
63
49
mmHg
PAO2
103
64
44,7
36,5
30
PACO2
39
38,5
30,5
26,5
22
PAO2 (mmHg)
103
60
50
40
30
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Alveolar gases when breathing oxygen
After washing out N2
 PAO2 = [PB - PH2O] - PACO2
 PH2O = 47 mmHg (in the body @ 37°C)
 In aviation, there often remains 3-5 mmHg N2,
one must consider a ➘ PO2 of 3-5 mmHg
 If 100% O2 is delivered, ⇒ PAO2 103 mmHg @
33500 ft (equivalent to sea level)
o Physiologically equivalent altitudes
KCL 2011
so
Alveolar gases during rapid decompression
 ➘ PB ⇒ ➘ PA of the different constituents
o ⇒ ↓↓ in PAO2
o If rapid decompression from 8000 to
40000 ft within 1.6":
 PAO2 falls from 65 to 15 mmHg
 PvO2 > PAO2 ⇒ large diffusion of O2 from pulmonary blood to the expired
air
o ⇒ Concept of critical level of PAO2 30 mmHg and critical area under 30 mmHg
where there is a high risk of
LOC if the area is > 140
mmHg/s
o The higher the final altitude +
the longer the exposure ⇒the
greater the degree of hypoxia
o PAO2 at altitude must not fall
below 30 mmHg (critical level)
o ⇒ to avoid neurological disturbances after rapid decompression, 100% O2 must be
breathed before the rapid
decompression, or at least be delivered within 2 seconds after the onset of the
decompression.
Arterial blood gases
 At rest, the PaO2 leaving the pulmonary capillaries is equal to the PAO2
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Altitude (ft)
@ rest
Air mix
O2
PaO2
SaO2
PaCO2
0
33500
95
97%
39-40
11000
40000
45
85%
15-16000
42-43000
36
76
30
Large individual variations
@ exercise, there is a ➘ of transit time of blood in the pulmonary capillaries ⇒ ➘ PaO2 &
SaO2
Cardiovascular responses
Blood flow
 Blood flow is the cardinal determinant of the tension at which O2 is delivered to the
cells
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General cardiovascular changes
@ rest:
 Immediate ➚ heart rate when breathing air above 6000-8000 ft:
o @ 15000 ft, ➚ of 10-15%
o @ 20000 ft, ➚ of 20-25%
o @ 25000 ft, ➚ of 100%
 There is a proportional ➚ in cardiac output
 The mean arterial blood pressure (BP) remains unchanged, but:
o ➚ BPsyst
o ➘ peripheral resistance
o ➚ pulse pressure
KCL 2011
Regional cardiovascular changes
 Immediate ➚ blood flow through the coronary & cerebral circulations
o ➘ renal flow
o ➘ viscera flow
o ➘ skin flow
o ⇒Redistribution of the cardiac output
 The coronary flow increases in parallel with the cardiac output and is effective ++
o @ 25000 ft breathing air ⇒no ischemic signs on the ECG
 @ PaO2 > 45-50 mmHg, the cerebral flow is determined by:
o PaCO2 with a 1-to-1 effect:
 If PaCO2 ➘ from 40 to 20 mmHg ⇒➘ cerebral flow by ½
o If PaO2 < 45 mmHg ⇒hypoxic vasodilatation (VD)
o If PaO2 = 35-40 mmHg ⇒➚ cerebral flow by 50-100%
o There is a balance on cerebral flow between:
 VD effect of hypoxia
 VC influence of hypocapnia
 From 0 to 15000 ft breathing air ⇒ ➘ cerebral blood flow
 From 16000 to 18000 ft breathing air ⇒ ➚ cerebral blood flow
 Pulmonary circulation:
o With exposure to hypoxia such as there is a 20% ➘ of SaO2 ⇒Reversible VC in the
pulmonary circulation.
Syncope
 In 20% of individuals, the immediate cause of LOC is the failure of cerebral blood flow
subsequent to a major fall in arterial BP associated with deep bradycardia.
 Associated symptoms:
o pallor
o sweating
o nausea ± vomiting
Tissue oxygen tension
 The minimum acceptable PO2 in a tissue
depends on the tension of O2 in the
blood flowing its capillaries.
 The form of the oxygen dissociation
curve explains the rate of fall of PO2 under hypoxia
o Protective effect of the haemoglobin (Hb) combination with O2
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Cyanosis
 Cyanosis is caused by the presence of an increased concentration of reduced Hb (Hb R)
in the capillaries and venules of hypoxic tissues.
 > 5g HbR/100ml blood ⇒ cyanosis
 ⇒cyanosis is an unreliable sign of hypoxia
o ➘ if anaemia
o ➚ if polycythaemia
Neurological effects
Impairment of mental performances
 It's of great practical significance in aviation, but with great variability.
 Variations are due to the variations in the respiratory response to hypoxia
o ➘ PaO2 ⇒ ➘ PaCO2 (by hyperventilation—HV) ⇒ ➘ cerebral flow ⇒ ➘ cerebral PO2
o ⇒ ➘ mental performance
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Psychomotor tasks
Well learned and practised tasks are generally preserved until > 10000 ft
If PAO2 < 38-40 mmHg (16-18000 ft) ⇒the reaction time ➚ (by 50% if PAO2 35 mmHg)
Performance at pursuit-meter tasks are unaffected until > 12-14000 ft
Choice-reaction time is impaired ++ @ 12000 ft
Also consider the effect of muscular coordination impairment (tremor @ 15000 ft)
Cognitive tasks
Previously learned tasks are unaffected until > 10000 ft (55 mmHg)
But there is a decline at lower PAO2
o 10-15% @ 15000 ft
o 40-50% @ 18000 ft
Short term & long term memory is affected at as low altitudes as 8-10000 ft (60 mmHg)
@ 8000 ft ⇒ ➘ performance at novel tasks (twice the time for complex reaction-choice
tasks)
Such changes can be demonstrated at altitudes as low as 5-6000 ft.
Impairment of special senses
 Vision
o Subjective darkening of the visual fields (VF) which is actually noticed after O2
restoration (environment seems then much brighter)
o @ 5000 ft ⇒➘ light sensitivity of the dark-adapted eye (scotopic vision)
o Scotopic vision is significantly impaired @ PAO2 < 50 mmHg (12000 ft)
o Photopic vision (bright light vision) is unaffected until PAO2 < 40 mmHg (18000
ft)
o A moderate to severe hypoxia ⇒ ➘ VF (tunnelling) and appearance of a central
scotoma
 Audition
o ➘ auditory acuity by moderate to severe hypoxia
Lost of consciousness (LOC)
 There is a very close correlation between PvJO2 (jugular) and the level of consciousness
o LOC occurs when PvJO2 < 17-19 mmHg (PAO2 < 30 mmHg)
o LOC may occur @ PAO2 40 mmHg associated with hyperventilation
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Effects during rapid decompression
 Rapid decompression (RD) to > 30000 ft breathing air ⇒ ➘++ PAO2 < 30 mmHg
o ⇒ very profound neurological effects (LOC if the subject remains < 30 mmHg
with a "critical" area > 140 mmHg/s
 Time before decrement in performance is about 12-15" after RD
 If 100% O2 is provided within 8" after the RD @ 40000 ft, the performance is recovered
to control level after 60"
 If PAO2 never falls < 30 mmHg and rises rapidly with O2 ⇒performance is maintained
o ⇒It is essential to maintain or restore rapidly a PAO2 > 30 mmHg
Clinical features
 The speed, the order and the severity of symptoms depend on the rate, the degree and the duration of the exposure to hypoxia
 Great variations between individuals
 Factors influencing the clinical presentation:
o Intensity of hypoxia (rate, maximum reached altitude, duration)
o Physical exertion ⇒ ➘ tolerance to hypoxia
o Ambient temperature: cold T° ⇒ ➘ tolerance to hypoxia
o Drugs, alcohol, antihistamins: ⇒ ➘ tolerance to hypoxia
Clinical picture
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0-10000 ft breathing Air (39000 ft with oxygen)
No symptoms @ rest
Impaired performance at novel tasks
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10-15000 ft Air (39-42500 ft oxygen)
A warm resting subject would have no or few signs
Impairment of performance at skilled tasks
If the exposure is prolonged, ⇒headache
There are symptoms if physical exertion and/or extreme T°
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15-20000 ft Air (42500-45000 ft oxygen)
There are signs @ rest
Loss of critical judgment and willpower
The subject is unaware of the deterioration
Changes ++ in emotional state
 ⇒great importance in aviation
 ≈ OH intoxication
Also consider the disturbances due to ➘ PaCO2 (hyperventilation)
Physical exertion ➚++ the severity and speed of onset of symptoms
> 20000 ft Ait (> 45000 ft oxygen)
Marked ➚ of symptoms and signs
Comprehension and performance fall rapidly
LOC with little or no warning
Myoclonic jerks, then convulsions
Death
Covert (early) cerebral features:
 Visual
o ➘ light intensity
o ➘ VA in poor illumination
o ➚ light threshold
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Hypoxia & Hyperventilation — 3/41
o ➘ visual fields
 Psychomotor
o ➘ learning novel tasks
o ➚ choice-reaction time
o ➘ eye-hand coordination
 Cognitive
o ➘ memory
Overt features:
 Personality changes
 lack of insight
 loss of judgment & self-criticism
 euphoria
 ➘ memory
 mental incoordination
 sensory loss
 cyanosis
 hyperventilation and it's symptoms
 ➘ consciousness
 LOC
 Death
Time of useful consciousness
The TUC is the interval between ➘ PAO2 and the point at which there is a specified degree of
impairment of performance.
The main factor is the accepted degree of impairment.
In practical, the TUC is the period during which the affected subject retains the ability to act
to correct his/her predicament.
At a given altitude, the TUC is shorter when due to rapid decompression than to slow ascent.
o When breathing 100% O2 then air:
Altitude (ft)
25000
30000
36000
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KCL 2011
TUC
270"
145"
71"
Recovery from hypoxia & the oxygen paradox
The administration of O2 to a hypoxic subject usually results in rapid recovery.
A generalized headache may persist if there was prolonged hypoxia.
Some subjects may have a worsening of the symptoms during the first 15-60" of oxygenation.
Occurs++ with hypoxic & hyperventilating (= hypocapnic) subjects.
It is mostly important to maintain the oxygenation.
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HYPERVENTILATION
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Condition in which pulmonary ventilation is greater than that required to eliminate CO2 produced
by the tissues.
There is a close relationship between PCO2 and [H+] in blood and tissues
CO2 + H2O ⇌H2CO3 ⇌H+ + HC O3
Aetiology
 Normal response to hypoxia (PO2 < 55-60 mmHg)

 Result of voluntary overbreathing
 ++ Emotional stress, anxiety (20-40% of student aircrew)
 Experienced aircrew if exposed to the mental stress of a sudden emergency
 Pain & motion sickness
 Environmental stress (T°, whole-body vibration @ 4-8 Hz)
 Pressure breathing.
Physiological features of hyperventilation
 Hypocapnia of hyperventilation ➪has no significant effect on cardiac output or BP
 Hypocapnia induces VC++ in cerebral arterioles and vessels in the skin
o ➚ blood flow in skeletal muscles
o ➘➘ the minimum tissue O2 tension
o ➪The many changes due to hyperventilation (including LOC) are due to a combination
of hypoxia and alkalosis in the cerebral tissues.
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A reduction in PaCO2 < 25 mmHg causes significant decrement in the performance of psychomotor tasks
o Such as tracking and complex coordination tests.
o The ability to perform complex mental tasks is compromised by PaCO2 < 30 mmHg
o Steadiness of the hands is impaired with PaCO2 = 25 mmHg
o Manual tasks are impaired by muscular spasms when PaCO2 < 20 mmHg
o Alteration of consciousness and LOC when PaCO2 < 10-15 mmHg.
The rise in tissue pH induced by hyperventilation increases the sensitivity of PNS:
o Paraesthesiae
o Motor disruption
Clinical features of hyperventilation
 Symptoms are manifest when PaCO2 is reduced to 20-25 mmHg:
o Light headedness
o Dizziness
o Anxiety
o Superficial paraesthesiae in the extremities and around the nose and lips
 When PaCO2 = 15-20 mmHg
o Muscles spasms in the limbs and the face (carpo-pedal spasm)
 When PaCO2 < 15 mmHg
o The whole body becomes stiff (tetany)
 The increased irritability of the nervous tissue ➪➚ tendon reflexes (Chvostek's sign)
 Finally, moderate and severe hyperventilation will produce a general deterioration in mental
and physical performance, followed by impairment of consciousness and eventually LOC.
 If severe hyperventilation with LOC by anxiety,, the supervention of coma will be followed by a
gradual recovery as respiration is inhibited and PaCO2 regains normal levels.
 This is not the case if hyperventilation is induced by hypoxia.
 ➪Hypoxia should always be suspected when signs of hypocapnia occur @ altitudes > 12000 ft.
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Hypoxia & Hyperventilation
Introduction
Acute hypobaric hypoxia
Ætiology
Respiratory responses to acute hypobaric hypoxia
Alveolar gases when breathing air
Alveolar gases when breathing oxygen
Alveolar gases during rapid decompression
Arterial blood gases
Cardiovascular responses
Blood flow
General cardiovascular changes
Regional cardiovascular changes
Syncope
Tissue oxygen tension
Cyanosis
Neurological effects
Impairment of mental performances
Psychomotor tasks
Cognitive tasks
Impairment of special senses
Lost of consciousness (LOC)
Effects during rapid decompression
Clinical features
Clinical picture
0-10000 ft breathing Air (39000 ft with oxygen)
10-15000 ft Air (39-42500 ft oxygen)
15-20000 ft Air (42500-45000 ft oxygen)
> 20000 ft Ait (> 45000 ft oxygen)
Time of useful consciousness
Recovery from hypoxia & the oxygen paradox
Hyperventilation
Aetiology
Physiological features of hyperventilation
Clinical features of hyperventilation
©Jean-Michel Ferrieux-2011
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