Acute Mountain Sickness

PHYSIOLOGICA
LY CRITICAL
ALTITUDES:
Up to 10,000 ft (3,000
m)safe zone of rapid
ascentclassically
defines high altitude
At 18,000 ft (5,500 m)
upper limit of
permanent human
inhabitation
Above 20,000 ft (6,000
m) life is endangered
without supplemental
oxygen
From 40,000 ft(12,000
m) Ozone layer starts

 COMMON HYPOXIC EFFECTS WITH

DIFFERENT ALTITUDES:
ALTITUD INSPIRE
E LEVEL D AIR
PO2
In feet
(metre)

In mm of Hg

0 (i.e.sealevel)

160

Upto 10,000
(3,000)

110

10,000
15,000
(3,000
4,500)

98

15,000
20,000
(4,500
6,000)

70

HbSATURATI
ON
in %
~ 97 %
~ 90 %

~ 80 %

< 70 %

EFFECTS
Stages (if any)
NIL
Usually none, +/- some nocturnal
visual reduction
( of
indifference)
Mod. Hypoxic symptoms
Drowsiness, headaches ,Mental
and muscle fatigue
Severe hypoxic symp
aggravated CNS involvement
Seizures and muscle twitching

PHYSIOLOGICAL RESPONSES TO
HIGH ALTITUDE HYPOXIA:
I) Acute responses
Refers to immediate reflex
adjustments of
respiratory and
cardiovascular system to hypoxia
II) Long term responses (acclimatization)
Refers to changes in body tissues in
response to long term exposure to
hypoxia

ACCOMMODATION AT HIGH ALTITUDE:

Respons akut tubuh saat terjadi
hipoksia :

Hyperventilation:
arterial PO2 stimulasi
kemoreseptor perifer
meningkatkan ventilasi.

Tachycardia:
O2 jaringan Respons
frekuensi jantung distribusi
oksigen ke jaringan.

Neurological :
Considered as warning signs
Depression of CNS feels
lazy, sleepy, headache
Release Phenomena like
effect of alcohol, lack of
coordination, slurred speech,
slowed reflexes,
overconfidence
At further height cognitive
impairment, poor judgment,
twitching, convulsion & finally

Acute Mountain Sickness

Bisa terjadi pada ketinggian diatas 1500
m (4920 ft) umumnya pada ketinggian
2500 m.
Symptom-complex occurring in a lowlander, who ascends to very high
altitudes over 1-2 days for first time.
No predeliction based on gender
More likely if :
Rapid ascent
Lack of acclimatization

insidensi
Sudden ascent > 10,000 feet (3000
meters) : 30 %
Sudden ascent > 14,000 feet : 75 %
Report from Colorado ski resort : 12 %
Can occur in those with no prior
problems with altitude exposure
Can recur (no consistent tolerance or
"immunity")

Acute Mountain Sickness:

Cause exactly not known appears to be
assoc. with Cerebral oedema (pO2
arteriolar dilatation limit of cerebral
autoregulatory mechs are crossed
cap.pressure fluid transudation into
brain tissue) or Alkalosis
In the minority, more serious sequelae highaltitude pulmonary oedema and high-altitude
cerebral oedema develop.

Adaptive
mechanisms
As PaO2 declines to 60mmHg
chemosensors in the carotid body
trigger an increase in minute
ventilation:

Hypoxic Ventilatory
vesponse (HVR)
PCO2 drops --> resp alkalosis -->
limits HVR.

Himalayan Peaks over Kathmandu, Nepal

Adaptive
mechanisms
24-48h: bicarbonate diuresis -->
compensatory metabolic acidosis --> minute
ventilation increases.
Catecholmine release --> increase in HR and
PAP. Acclimatization correlates with return of
resting HR to baseline except at extreme
altitude.
Increase in cerebral blood flow: offset by the
vaso-constrictive effect of hypocapnea.
4-5days: hematopeisis
Himalayan Peaks
Nepal
afterover
4-5Kathmandu,
days. (Lundby

Gejala
Gejala terjadi pada 8-24 jam setelah
tiba, dapat berlangsung selama 4-8
hari.
Gejala khas : HEADACHE disertai one or
more symptom:
Anorexia, nausea or vomiting
Fatigue or weakness
Dizziness or lightheadedness
Difficulty sleeping

 Symptoms can be reduced by

Cerebral oedema by large doses of
Glucocorticoids
Alkalosis by Acetazolamide (inhibits
CAH+ & HCO3- excretion through
kidneys)

If remain untreated ,
it may cause Ataxia,
Disorientation,coma &
Finally Death(d/t tentorial
herniation of the
brain-tissue)

AMS - Pathophysiology