12. Altitude and Diving Flashcards

1
Q

Altitude

Highest habitation

How high does atmospheric pressure half

How does this affect oxygen

What would happen if i was taken to the top of everest

A

The highest permanent habitation
in the world is found in the Andes
mountain range at 4877 m (16 000 ft)
above sea level.

In the northern Andes, the majority of inhabitants live above 2743 m (9000 ft).

The capital cities of 
Bolivia (La Paz), 
Ecuador (Quito) 
and Colombia (Bogotá) 
are all high-altitude cities. 

La Paz is the highest
capital city in the world at 3630 m (11 910 ft).

> Atmospheric pressure

halves every 5500 m (18 000 ft).

> The percentage of oxygen in the

atmosphere at sea level is about 21%

and the barometric pressure is around 101 kPa.

As altitude increases,
the percentage remains the same

but the number of oxygen molecules
per breath is reduced.

At 3600 m (12 000 ft) the barometric pressure

is only about 64 kPa (480 mmHg),

so there are roughly 40% fewer oxygen

molecules per breath
thus the body must adjust to
having less oxygen.

> A t 19 200 m (63 000 ft) barometric pressure

is 6.25 kPa, meaning inspired PiO2 is zero

(as the partial pressure of water is 6.3 kPa and PiO2 = FiO2 × (Patm − PH2O)).

If a human being who resides
at sea level were to be

suddenly taken to the top of Mount Everest
(8848 m/29 028 ft) he or she
would succumb to hypoxia and lose consciousness.

The body requires a period of
acclimatisation during 
which physiological adaptation 
occurs in response
to the relative lack of oxygen.
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2
Q

Describe the acute and chronic physiological responses to high altitude

6 responses

A

The alveolar gas equation is
key to understanding the fundamental
physiological response to high altitude:

                          PACO2 PAO2  =PiO2  –    \_\_\_\_\_\_
                              R

Where:

PAO2 Alveolar partial pressure of oxygen

PiO2 Inspired pressure of oxygen = FiO2 ⋅ (PATM − PH2O)

PACO2 Alveolar partial pressure of carbon dioxide (approximates with PaCO2)

R Respiratory quotient = CO2 production / O2 consumption (N = 0.8)

1 Hyperventilation

2
> Oxyhaemoglobin dissociation curve:

3
> Polycythaemia:

4
> Cardiovascular responses:

5
> Hypoxic pulmonary vasoconstriction:

6
> Angiogenesis and enzyme changes:

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3
Q

> Hyperventilation:

A

On ascent to altitude
there is an increase in minute ventilation
as a result of hypoxic stimulation
of the peripheral chemoreceptors
located in the aortic and carotid bodies.

The hyperventilation results in a

lowered arterial PaCO2,

which increases alveolar pressure of oxygen,

as can be seen from the alveolar gas
equation.

The hypocarbia secondary to
hyperventilation results in CSF
alkalosis.

However, this is transient as
bicarbonate is excreted from the
CSF over 24 – 48 hours and renally excreted.

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4
Q

> Oxyhaemoglobin dissociation curve:

A

At moderate altitudes there is a right shift

in the oxyhaemoglobin dissociation curve

caused by increased levels of 2,3-DPG,

thereby favouring oxygen unloading.

At high altitudes there is an overall

left shift in the oxyhaemoglobin

dissociation curve favouring

oxygen uptake in the pulmonary capillaries.

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5
Q

> Polycythaemia:

A

Increased erythropoietin secretion
results in a slow increase in red cell count
in order to increase oxygen-carrying capacity.

However, this also results in a raised haematocrit, which can lead to thrombosis.

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6
Q

> Cardiovascular responses:

A

Increase in heart rate and stroke volume

from sympathetic stimulation

from the effects of hypoxia

in an attempt to maintain oxygen delivery to the tissues.

Overall rise in myocardial work.

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7
Q

> Hypoxic pulmonary vasoconstriction:

A

Results in an increase in
pulmonary vascular resistance,

which can lead to right heart failure.

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8
Q

6

> Angiogenesis and enzyme changes:

A

Increase in capillary density with time,

thereby reducing oxygen diffusion distance.

This is associated with a change in intracellular

oxidative enzymes favouring cellular

respiration under hypoxic conditions.

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9
Q

How does high altitude affect volatile anaesthesia?

A

See Chapter 77, ‘Vaporisers’,
for an in-depth explanation on this topic.

> Gas and vapour analysers measure
partial pressure and assume sea
level atmospheric pressure (101 kPa).

E .g. an oxygen analyser measuring 21 kPa
will assume atmospheric pressure to be 101 kPa
and provide a percentage of oxygen on the
display of 21% or 0.21;

however, if the analyser is used at an altitude
where atmospheric pressure is only 70 kPa,
the analyser will under-read,
displaying 21% when it should be 33%.

> TEC vaporisers function normally at altitude.

The output of these vaporisers is a
constant partial pressure of volatile
agent not a constant volume percentage.

E .g. Vaporiser dialled to deliver 1% isoflurane:

• Gas from the vaporising chamber is
fully saturated with volatile agent

(i.e. it has achieved its
saturated vapour pressure (SVP)
at that ambient temperature).

• SVP is not affected by
ambient pressure
(i.e. does not change with altitude).

• 1% isoflurane at sea level will
have a partial pressure of 1%.

• 1% isoflurane at altitude – 
the volatile agent from the vaporising
chamber will be diluted 
into a less dense gas stream 
and therefore the concentration of 
isoflurane will be

higher but the partial pressure remains
the same as it would be at sea level.

Clinical effect is dependent on the
partial pressure and therefore
remains the same.

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10
Q

What is acute mountain sickness (AMS)?

How common

Depends on

Symptoms

A

AMS is very common at high altitude.

At over 3000 m (10 000 ft), 75% of people
will have mild symptoms.

The occurrence of AMS is
dependent upon the elevation,
the rate of ascent and
individual susceptibility.

Many people will experience
mild AMS during the
acclimatisation process.

The symptoms usually start 12–24 hours
after arrival at altitude and
begin to decrease in severity
around the third day.

The symptoms of mild AMS include:
> Headache

> Nausea and dizziness

> Loss of appetite

> Fatigue

> Shortness of breath

> Disturbed sleep

> General feeling of malaise

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11
Q

What is high-altitude pulmonary oedema (HAPO)?

A

HAPO results from increased
pulmonary extravascular lung water,
which prevents effective oxygen exchange.

As the condition progresses,

severe hypoxaemia develops,
which leads to cyanosis,
impaired cerebral function
and death.

Symptoms of HAPO include:

> Shortness of breath at rest

> Tightness in the chest and
a persistent cough bringing up white, watery
or frothy fluid

> Marked fatigue and weakness

> A feeling of impending suffocation at night

> Confusion and irrational behaviour

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12
Q

What is high-altitude cerebral oedema (HACO)?

A

HACO is a potentially
life-threatening complication
of high altitude resulting from swelling of
brain tissue secondary to fluid leakage.

Symptoms of HACO include:

> Headache

> Weakness

> Disorientation

> Loss of coordination

> Decreasing levels of consciousness

> Loss of memory

> Hallucinations and psychotic behaviour

> Coma

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13
Q

Describe the treatment of AMS.

A
The only cure for mountain sickness 
is either 
acclimatisation 
or 
descent.

Symptoms of mild AMS can be treated with
analgesics for headache
(e.g. ibuprofen),

acetazolamide and
dexamethasone.

> Acetazolamide: 
carbonic anhydrase inhibitor, 
which reduces bicarbonate formation 
and increases 
hydrogen ion concentration in the body, 
leading to development of a 
metabolic acidosis, 
which causes a respiratory 
compensation response resulting 
in an increase in minute
ventilation and 
thus further lowering of PaCO2.

> Dexamethasone:
corticosteroid with
predominantly glucocorticoid
actions.

It has anti-inflammatory properties
and is useful in reducing cerebral oedema.

Many pilgrims at the annual festival at Gosainkunda
Lake in Nepal suffer from HACO following a rapid rate of ascent, and respond remarkably well to dexamethasone.

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14
Q

Other treatments for altitude

sickness include the following

A

> Nifedipine:
calcium channel blocker,
most commonly used as an antihypertensive.

It also has the effect of rapidly reducing pulmonary artery pressure by

inhibiting hypoxic pulmonary vasoconstriction,

thereby improving oxygen transfer.

It can therefore be used to treat HAPO,
though unfortunately its effectiveness
is not anywhere as good as that of
dexamethasone in HACO.

> Furosemide: loop diuretic,
may be used to treat pulmonary oedema
acutely.

However, furosemide may also lead to
collapse from low-volume
shock if the victim is already dehydrated.

> 100% oxygen also reduces the effects of altitude sickness.

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15
Q

Diving

How much does atm pressure increase

what are the problems seen

A

During diving the opposite problems to
altitude are seen.

Barometric pressure increases by 1 atm for
every 10 m descent

(e.g. at a depth of 30 m barometric pressure will be 4 atm).

The following specific issues relate to respiratory physiology during diving:

> Effects of compression and decompression

> Inert gas narcosis

> Decompression sickness

> Oxygen toxicity

> High-pressure nervous syndrome

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16
Q

What mechanics are involved during compression and

decompression?

A

During diving, as depth increases
so too does barometric pressure.

This increase in pressure is not a problem
as long as it is balanced,

i.e. there is no pressure gradient.

Compression of gas-filled cavities
such as the lungs,
middle ear and
sinuses

will occur on descent.

On rapid ascent the pressure difference 
between these cavities 
and 
barometric pressure 
may not have time to equilibrate, 
potentially resulting in complications 
such as
pneumothoraces 
or 
perforated tympanic membranes.
17
Q

What are the problems for scuba divers using an air mixture at depth?

A

Air contains 79% nitrogen.

At high barometric pressures
nitrogen has narcotic properties.

This means that air can only
be safely used up to a depth of 30–50 m.

At depths exceeding 50 m
helium/oxygen gas mixtures are used.

Helium does not exhibit the
narcotic properties of nitrogen.

18
Q

What limits the depth under water that a human can breathe via a snorkel?

A

A snorkel has an apparatus dead space,
which means that if it is beyond a
certain length, rebreathing of expired gas will occur, resulting in hypercarbia
from impaired CO2 elimination.

As the diver descends deeper under water,
barometric pressure increases,
which increases pressure within the circulation.

However, because the diver’s lungs
are exposed to atmospheric pressure
via the snorkel, a situation develops

whereby pulmonary vascular pressure is
greater than alveolar pressure,
causing pulmonary oedema.

It becomes difficult to breathe via a
snorkel at depths exceeding 1 m as a
result of the compression effects on the chest.

19
Q

Describe the physiology of decompression sickness.

A

> At depths exceeding 20 m
nitrogen is absorbed into body tissues,
especially fat.

However, nitrogen has a low solubility and,
therefore, equilibration between
environment and body takes hours.

If rapid ascent occurs, nitrogen comes
out of solution forming bubbles.

These bubbles can cause severe
microvascular complications by
obstructing blood flow;

in the brain this can lead to
visual disturbances
or
convulsions;

joint pain can be severe.

> Treatment of decompression sickness is recompression,

which forces nitrogen back into solution.

> Using a non-air gas mixture
such as helium/oxygen reduces the risk of
decompression sickness.

Helium is 50% less soluble than nitrogen
so less dissolves into tissues,
reducing subsequent risk.

> As a rough rule of thumb it is safe for a 
diver to rapidly halve their
ambient pressure, e.g. a rapid 
ascent from 10 m depth 
(2 atm) to the surface (1 atm).
> Commercial saturation divers 
who work at great depths 
live in high pressure
chambers so that their bodies 
remain saturated in nitrogen,
thus avoiding decompression sickness. 

At the end of their period of diving they
decompress, a process that will
take a considerable amount of time!

20
Q

What would happen if a diver performing a breath hold dive hyperventilated prior to the dive?

A
Competitive apnoea is an 
extreme sport in which competitors 
attempt to attain great depths, 
times or distances on a single breath 
without direct assistance of self-contained underwater breathing apparatus (scuba).

The adaptations made by the human body
while under water and at high pressure include:

> Bradycardia

> Vasoconstriction:
redistribution of blood flow to myocardium, lungs
and brain

> Splenic contraction
The record breath hold dive is 140 m.
Hyperventilating prior to such a dive
is not a sensible manoeuvre! 
Hyperventilation results in hypocarbia. 

The normal stimulus to terminate descent and commence ascent would be the
development of hypoxia and hypercarbia.

If the diver hyperventilated prior
to such a dive, the only stimulus to
ascend would be hypoxia.

On ascent as barometric pressure falls 
so too would alveolar inspired oxygen 
(via alveolar gas equation), 
resulting in severe hypoxaemia 
and possible hypoxic seizures
on ascent or even loss of consciousness.
21
Q

Can oxygen toxicity develop during diving?

A

Yes.

> At oxygen partial pressure of greater than
2 atm oxygen toxicity is a risk;

this equates to air diving at
depths greater than 40 m (=5 atm / PO2 > 2 atm).

CNS excitation can lead to nausea, tinnitus, twitching and convulsions.

> The exact aetiology of the
CNS toxicity from hyperoxia
is not fully understood.

The implication for divers is the
use of a hypoxic gas mixture to overcome
this problem.

For increasingly deep dives the
oxygen concentration in the
tank will be less than 21% and
at extreme depths as low as 1%!

22
Q

What is the physiological basis for hyperbaric oxygen therapy?

A

Increasing the arterial
partial pressure of oxygen
via increasing barometric
pressure has a number of effects:

> Increases amount of dissolved oxygen

> Improves oxygen diffusion (Fick’s law of diffusion)

> Promotes angiogenesis

> Improves function of polymorphs

> Inhibits growth of anaerobes (useful in gas gangrene)

> Displaces carbon monoxide
from haemoglobin

At a barometric pressure of 3 atm there is sufficient dissolved oxygen alone to meet body oxygen requirements.

This may be of use in a Jehovah’s
Witness patient with an acute perioperative anaemia refusing blood transfusion.

23
Q

What are some of the clinical
indications for hyperbaric oxygen
therapy

A

1
> Gas lesions:
air or gas emboli
and decompression sickness

2
> Infections: 
refractory osteomyelitis, 
necrotising soft tissue infections and
clostridial infections

3
> Global hypoxia:
carbon monoxide poisoning and severe anaemia

4
> Regional hypoxia: 
compromised grafts or free flaps, 
osteoradionecrosis
and crush injuries.
24
Q

What are the contraindications

to hyperbaric oxygen therapy?

A

1
> Untreated pneumothorax

2
> Gas trapping in the lungs, e.g. lung bullae/bronchospasm

3
> Unusual drugs, e.g. doxorubicin