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Indian J. Anaesth. 2002; 46

ROY : PHYSIOLOGICAL (3) : 175-181AND ANAESTHESIA AT HIGH ALTITUDE
ADAPTATION 175
ORIGINAL ARTICLE

PHYSIOLOGICAL ADAPTATION AND ANAESTHESIA

AT HIGH ALTITUDE
Colonel PK Roy1

SUMMARY
Anaesthesia in abnormal environments is a challenging task for all anaesthesiologists. In order to have safe anaesthesia, the
pathophysiological changes in both the unacclimatized and acclimatized patients at high altitude, which include pulmonary hyperventilation,
polycythemia, rising pulmonary blood volume, pulmonary hypertension and increase in diffusion capacity, are to be considered in
preanaesthetic evaluation. This article also highlights the physical behavior of anaesthetic and respiratory gases and their importance
for the safe conduct of anaesthesia.
Keywards : High altitude, Pulmonary hypertension, Hypoxia and anaesthesia at HA.

Introduction High altitude generally means an elevation of 3000

Some ten million of global population live at
altitudes above 13000 feet, majority in South America
and one fifth of it in the Himalayas of Central Asia.
Man ascends to high altitude in aviation, in
mountaineering, and during conditions when troops are
moved from plain land to high altitudes. Modern mode of
transportation also allows increasing number of tourists
to travel rapidly from sea level to high altitudes1. It is
now more important to understand the effects of high
altitudes associated with other factors on the human
physiology.
Anaesthesia at high altitude is a challenging task
for all anaesthesiologists. It may be required as a result
of illness, accidents or war like situations among the
acclimatized patients and also in unacclimatized ones who
have been recently inducted to high mountains.
In order to have safe anaesthesia, we must consider
the physiological changes occurring in human body and
their adaptation at high altitudes.
Table - 1 : Level of Altitudes
Altitude in Meters
Base line 3000 Meters above mean sea level.
Mild High Altitude 3000 to 3600 meters above mean sea level
up to 4200 meters acclimatized people.
Moderate High Altitude 4200 to 4800 meters above mean sea level.
Extreme High Altitude 4800 meters above mean sea level.
Correspond to :
1. Colonel PK Roy,
Assoc. Prof. of Anaesthesiology,
AFMC,
PUNE- 411040
meters or more, above the sea level [Table-1]. Although
the biological effect of high altitude appear at lower levels,
but at this level onwards, people ascending to high
mountains generally show biochemical, physical or
anatomical changes2.
A. Pathophysiology of unacclimatized and
acclimatized persons at high altitude
1. Respiratory System Changes
(a) Oxygen gradients: The percentage of oxygen in
atmospheric air at sea level remains constant which
is 20.93% upto an altitude of 33000 feet. However,
air is compressible and this means that the number
of molecules in a given unit of a air is more at sea
level than at high altitude. In other words, the
barometric pressure which depends on molecular
concentration of the air decreases with increase in
altitude. This inturn means that the partial pressure
of oxygen in ambient air at high altitude is reduced.
At sea level, the partial pressure of oxygen is 20.93%
of atmospheric pressure of 760 mmHg i.e. a value
of 159 mm Hg. When air is breathed into bronchial
tree, it becomes saturated with water vapour which
exerts a pressure of 47 mm Hg so that partial pressure
of oxygen in inspired air, in contrast to ambient
air is 20.93% of 713 (760-47) mm Hg that is
149 mmHg (Table-2).
At rest, the rate of oxygen consumption per minute
of an individual is 220-260ml. There are four stages
of transport conduction of Oxygen from the
atmosphere to the cells. (i) In ventilation O2 flows
from atmosphere through the trachea and bronchial
tree to alveoli. (ii) In alveoli Pulmonary Diffusion
occurs wherein the oxygen in alveoli comes in contact
with alveolar capillary walls and then passes to blood.
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176 INDIAN JOURNAL OF ANAESTHESIA, JUNE 2002

TABLE 2 : Barometric pressures and oxygen tensions capillaries. The PO2 of ambient air is 159mm Hg
at various altitudes where as in mitochondria at the site of oxidative
enzymatic reaction, it is about 1-2 mm Hg. At each
Altitude Barometric Oxygen Alveolar Alveolar Alveolar level of transport, PO2 level falls and is referred to
in feet Pressure Partial Oxygen CO 2 Water
mm Hg Pressure in Tension Tension Vapour as Oxygen Cascade (Table-3). If PO2 value falls
mm Hg/% mm Hg mm Hg Tension below 1-2 mm Hg then aerobic metabolism stops
of Oxygen mm Hg
and anaerobic metabolism sets in and this is referred
0 760 159.2/ 20.96 103 40.0 47 to as Pasteur Point. Although the PO2 in ambient air
is diminished at high altitudes, the final PO2 achieved
5000 632 132.5/17.41 81 37.5 47
in mixed venous blood of the subject at high altitude
10000 523 109.5/14.39 61 35.5 47 is not diminished.
15000 429 90.5/11.81 49 32.5 47 (b) Oxygen Cascade and Acclimatization : There are
18000 380 79.5/10.45 38 31.0 47 two ways of compensation for shortfall of PO2 at
high altitude.
20000 349 73.1/9.61 35 30.0 47
(i) Modification/Adjustment of tissue metabolism
29.028 236 40/5.26 16 24 47
so that metabolic demand of tissues are satisfied
Mt Everest inspite of reduced availability of oxygen.
(ii) Adjustment in oxygen transport system so that
(iii) The Oxygen is then carried in the blood from
effect of loss of oxygen pressure in atmosphere
capillaries of lungs to those of tissues. (iv) Finally,
is minimised for the tissues. Most features of
in the tissues, the oxygen diffuses from the capillaries
acclimatization fall into oxygen cascade system
to the intracellular mitochondria, the sites of
wherein, inspite of fall in atmospheric PO2 the
utilization of oxygen.
final PO2 achieved at mixed venous blood is
In healthy man at sea level, the diffusion of oxygen not diminished3.
across the alveolar membrane occurs efficiently
because of the wide difference between partial (c) Hypoxia and its effects : High altitude reduces the
pressure of oxygen in atmosphere and the pulmonary starting point of Oxygen Cascade. There are many
inhabitants at 6000 feet altitude wherein inspired
PO2 is only 118 mm Hg equivalent to breathing
TABLE 3 : Oxygen Cascade 16.6% Oxygen at sea level. This results in alveolar
PO2 of about 75 mm Hg that is undesirable in many
OXYGEN
TENSION Inspired Alveolar Arterial Capillary Mitochondria pathological conditions. Sea level PO2 can be restored
(mmHg) at that altitude by increasing the inspired oxygen
160– SEA LEVEL concentration to 26.5%. The highest permanent
habitants are at 16000 feet where the alveolar PO2
140–
is reduced to 45 mm Hg requiring 48.8% of inspired
120– oxygen concentration to restore sea level conditions.
100– 14000 Ft The subject at high altitude hyperventilates and this
replaces more alveolar air with fresh inspired air
80–
and thus elevate alveolar oxygen tension.
60– Hyperventilation is an important ventilatory response
40– due to hypoxia and thus maintains an adequate
alveolar oxygen tension in the alveolar spaces.
20–
It increases alveolar oxygen tension by 25 - 30%.
0–
The initial hyperventilation response is due to hypoxia
Mean O2 Pr gradients from inspired air to capillary blood in person at sea level which originates in chemoreceptor cells in the Carotid
and 14000ft. The O2 Cascade in person at H.A. is seen to be much less steep
than in sea level person, although PaO2 in air at HA is less than sea level, the
and Aortic Bodies, although respiratory centre is
final PO2 not greatly diminished. stimulated by oxygen lack, directly.
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ROY : PHYSIOLOGICAL ADAPTATION AND ANAESTHESIA AT HIGH ALTITUDE
(d) Increased Diffusion Capacity During Acclimatization:
The normal diffusion capacity for oxygen through
the pulmonary membrane is 21 ml mmHg-1minute-1
and this diffusion capacity increases three folds during
exercise as well as at high altitude. This increase
probably results from greatly increased pulmonary
capillary blood volume, which expands the capillaries
and increases the surface area for diffusion of more
oxygen into the blood. There is also an increase in
lung volume thereby surface area of alveolar
membrane is also increased. In addition there is
increased pulmonary arterial pressure which forces
blood into alveolar capillaries more than normal
especially in the upper part of the lungs which are
poorly perfused in these conditions4.
2. Circulatory System Changes
Hypoxia is the principal stimulus for an increase
in red blood cell production at high altitude due to
defective saturation of arterial blood with oxygen, which
is more dominant than stimulus of oxygen tension for
erythropoiesis to chronic hypoxia. Bone marrow
shows hyperplasia of erythroid cells rather than
megakaryocytes and myeloid cells. The haematocrit rises
from 40% - 45% to 60% - 65% with an average increase
of haemoglobin from 15gm% to about 22 gm%.
In addition blood volume also increases by about
30% resulting in increase of circulatory haemoglobin from
50% to 90%. This increase in blood volume and
haemoglobin is a slow one having no effect till 2 to 3
weeks, reaching half development in a month or so and
only fully developed after many months.
Diminished oxygen tension in any tissues results in
local vasodilatation which occurs in chronic hypoxia and
results in increased cardiac output. In addition to bone
marrow stimulation for more production of haemoglobin,
there is stimulation of erythropoietin which originates
from the kidney and its production is found to be balanced
between oxygen demand and supply.
On return to sea level/lower altitude, there is
decrease in red cell volume but compensatory increase
in plasma volume. This emphasises that subjects who
have lived at high altitude and then return to sea level
may have higher than normal plasma volume for an
unknown period of time. If such persons return to high
altitude within this period, he may well be more
susceptible to High Altitude Pulmonary Oedema (HAPO)
than the new comers to mountain who will have low
plasma volume 5.
177
3. Pulmonary Hypertension at High Altitude
The normal pulmonary arterial pressure at sea level
is 12mm Hg and that of high altitude is 28 mm Hg.
Hypoxia itself causes pulmonary arterial vessel constriction.
The low barometric pressure and decrease in oxygen
tension in alveolar space are responsible for increase tone
of pulmonary arterial tree. The likely mechanism of
pulmonary vasoconstriction due to decrease in oxygen
tension is related to release of histamine from mast cells
from alveolar space and pulmonary arterioli itself. The
hypoxia may itself have constricting effect directly on
smooth muscle cells of bronchial portion of pulmonary
arterial tree.
Hypervolumia and polycythemia appear to be only
minor important factors in the pathogenesis of increased
pulmonary pressure because when a native from high
altitude is taken to sea level both polycythemia and
hypervolemia disappear, but pulmonary hypertension
persists6.
4. High Altitude Pulmonary Oedema (HAPO)
HAPO can develop rapidly within as little as six
hours after arrival at high altitude. Exposure to HA with
severe exertion is well recognised setting for HAPO in
unacclimatized healthy young persons. Acclimatized HA
natives may also develop HAPO upon return to HA after
a brief sojourn at lower altitude. Young adult and children
are also susceptible to HAPO, may be related to high
levels of growth hormone and thyroxine. Old people above
60 yrs of age, patients of chronic bronchitis and
emphysema whose SPO2 is less than 90% at sea level are
also prone to HAPO when ascend high mountains. Likely
basic mechanism of HAPO are:
(i) Hydrostatic/Over perfusion theory : On
exposure to HA, there is increased pulmonary
arterial pressure leading to patchy uneven
pulmonary vasoconstriction allowing some areas
of lung to receive over perfusion in unprotected
zones leading to interstitial oedema. The high
hydrostatic pressure leads to leakage of fluid
(ii) Permeability mechanism and stress failure of
pulmonary capillaries : There is physical injury
to capillary endothelium as a result of increased
pulmonary arterial pressure, vascular resistance
and increased viscosity of blood leading to
increased cardiac output impacting against the
endothelium causing structural disruption and
leakage of protein rich fluid in alveoli. Some
suggests that hypoxia induced permeability of
endothelium through local release of vasoactive
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178
chemotactic mediators may cause increased
permeability of fluid rich protein.
(iii) Coagulation defect : There appears to be
breakdown of plasma fibrinogen level
responsible for sludging of RBCs, formation
of fibrin thrombi in the lungs. Resulting reduced
cross sectional area of pulmonary capillaries
leads to pulmonary hypertension resulting in
high hydrostatic pressure causing leakage of
fluid. There is also decreased platlet count at
HA, which are sequestrated to obstructed
pulmonary vasculature.
(iv) Roll of Oxygen Free Radicals : On exposure to
HA, there is increased content of oxidized
radicals like peroxides, superoxides and
hydroxyl in skeletal muscles, visceral organs
and blood which react with organic molecules
of the tissues causing oxidation of intracellular
lipids and cell membrane of mitochondria
responsible for oxydative enzymatic reaction
of alveolar epithelium.
5. Neurogenic Pulmonary Oedema
A massive central sympathetic discharge shifts
blood from high resistance systemic circulation to low
resistance pulmonary circulation with resultant
pulmonary hypertension leading to pulmonary oedema.
‘J’ receptors which lie in the interstitial tissue and
which are connected to collagen fibers around alveoli,
have got physiological role in the avoidance of
pulmonary oedema.
6. Body Temperature
Low ambient temperature can be encountered at
HA or Polar region, particularly when anaesthesia is to
be carried out at field condition. Hypothermia is defined
as core body temperature less than 350C. Once the body
temperature falls below 350C, the ability of hypothalamus,
the temperature regulation centre is lost due to depression
of production of chemical heat by each cell.
As temperature decreases, there is fall of blood
pressure, although initially there is rise of B.P. due to
release of catacholamine. There is marked irritability of
AV Bundle leading to atrial and ventricular fibrillation. A
comman cause of death is ventricular fibrillation when
the temperature reaches below 28-290C. Minimum Alveolar
Concentration for inhalation anaesthetic agents decreases
5% per degree C fall of body temperature. This is probably
due to decrease CNS activity and increased solubility of
anaesthetic vapours at low temperature.
INDIAN JOURNAL OF ANAESTHESIA, JUNE 2002
7. CNS Changes
Hypoxia at HA causes high pressure and increased
flow in cerebral blood vessels leading to cerebral
vasodilatation. As a result there is decreased cortical
function. These varying degrees of mental functions
usually are altered behaviour, lack of judgement, in-co-
ordination and speech and sleep disturbances. If not
recognized early and brought to lower altitude, in severe
cases, depression, drowsiness followed by unconsciousness
will occur due to cerebral oedema.
B. ANAESTHESIA AT HIGH ALTITUDE– (HA)
1) General Principles
(a) At high altitude due to reduced PO2 in atmosphere,
the risk of perioperative hypoxia is more common
especially for new comers to altitude who are more
susceptible due to non-acclimatization. Acclimatization
leads to physiological adaptation of human body and
persons coming to high altitude should follow the
normal acclimatization schedule (Table No 4).
(b) Surgical teams are unlikely to be located at extreme
HA. Generally hospital with surgical teams are
located at mild HA. However, life and limb saving
surgeries can be done at moderate HA with due
precaution of giving high concentration of inspired
oxygen along with other measures.
(c) Surgical team should not carry out any operations to
new comers who are not fully acclimatized. If any
patients come for operation during acclimatization
period, it is best advisable to carry out the operation
at lower altitude.
(d) Volume Resuscitation : Whenever indicated, it can
be carried out by using intravenous crystalloids,
colloids, blood or plasma. However, all intravenous
fluids and blood should be warmed to body
temperature before transfusion and great care should
be taken not to overload the patients with fluid in
view of risk of developing pulmonary oedema.
(e) Bleeding : It has been reported that there is
unexpected increased oozing of blood from surgical
wounds at HA [8] . This is attributed to high venous
pressure, increased blood volume, venous dilatation
and increased capillary density. Pre-existing anaemia
where haemoglobin level below that considered to
be normal for natives at high altitude has to be
corrected prior to major surgical operation.
(f) Risk of Infection and Pollution : Risk of infection
and pollution may be due to field service conditions
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ROY : PHYSIOLOGICAL ADAPTATION AND ANAESTHESIA AT HIGH ALTITUDE
where proper OT may not be available. There may
not be any facility to warm OT by air conditioning.
OT may be heated by Bukharies (kerosene heating)
or by steam where chances of infection and pollution
exist.
(g) Fire and Explosion Hazards : It is less due to less
partial pressure of oxygen at HA but in absence of
electricity where kerosene light is used (hurricane
and petromax light) chances of fire and explosion
still persist. However, ether should not be used in
presence of bukharies and open flame. Battery
operated light or generator may be used in OT.
(h) Operation Theatre : In HA the patient’s ability to
control body temperature during anaesthesia is
reduced due to low temperature in OT. All patients
in operation theatre in less than 18 0 C become
hypothermic so OT temperature should be maintained
between 21 - 24 0 C, where 70% of the patient
becomes normothermic. The patient should be kept
warm either by air conditioning or in field service
condition by covering with blankets, hot air blower
or by bukharies.
2) Pre-operative Preparation
(a) Psychological Preparation : Patients are more anxious
and apprehensive due to loneliness, isolation and
monotony of the place. Reassurance and explaining
the anaesthetic and surgical procedure will allay
anxiety.
(b) Pre-medication : At HA above 3000 mtrs opiates
depress tachycardia and hyperapnoea that normally
occurs in response to hypoxaemia, the most important
compensatory mechanism for low oxygen tension.
Opiates should be used with caution in low doses
and supplemented with oxygen only in presence of
pain. Benzodiazepines, barbiturates and NSAIDS can
also be used to allay anxiety and reduce pain.
Injection Atropine and Glycopyrrolate can be used
safely for anti-muscarinic effects.
3. Induction Agents
It has been reported that there is slow recovery of
consciousness, post anaesthetic headache with nausea
following thiopentone with nitrous oxide and oxygen or
breathing air5. However, with oxygen supplement during
spontaneous or controlled ventilation, intraoperatively or
when oxygen is supplemented during postoperative period,
these complications do not occur suggesting that
intraoperative or postoperative hypoxaemia is likely a
pathophysiological factor. Thiopentone causes slower onset
179
of narcosis due to prolonged circulation time of natives
of HA. Non barbiturates like etomidate, propofol and
benzodiazepines like diazepam, midazolam can be used
safely as inducing agent.
4. Inhalational Anaesthesia
(a) Oxygen: A high concentration of oxygen should be
given, at least 40% higher than at sea level during
perioperative period for the following reasons :
(i) Anaesthesia deprives compensatory
hyperventilation at HA.
(ii) Irreversible hypoxic brain damage may occur
in case of apnoea or air way obstruction due
to lower PaO2.
(iii) Patients at HA are unlikely to compensate for
metabolic acidosis following hypertension or
haemorrhage as the buffering capacity is
reduced.
(iv) In HA due to low alveolar and arterial oxygen
tension a high concentration of oxygen should
always been given.
(b) Nitrous oxide : The potency of anaesthetic gases is
proportional to their partial pressure and not the
percentage in mixture of oxygen is important. As
barometric pressure is reduced, fixed concentration
of inhaled anaesthetics will have less potency at
HA. So at HA above 3000 mtrs. There is significant
reduction of efficacy of 50% nitrous oxide in
reducing pain threshold9. Nitrous oxide has got
minimum alveolar concentration over 100% at sea
level. Since at HA, atleast 50% oxygen is to be
given in inspired gas as inhalation mixtures, so it is
of little use as an anaesthetic at 1500 mtrs and of no
value above 3000 mtrs due to its reduced
effectiveness.
(c) Diethyl Ether : With equivalent concentration at sea
level, ether induction at HA is slow and maintenance
also requires higher concentration. Open drop ether
technique is outdated, light ether and oxygen
anaesthesia with assisted or controlled ventilation
with muscle relaxant ensures smooth and rapid
recovery. However, there is explosion hazard with
ether which is increased at HA.
(d) Halothane : It is ideal for its rapid induction, high
potency rapid recovery, and non-inflammable and
less tendency to produce respiratory depression and
laryngospasm. Isoflurane is also suitable at HA.
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180
5. Muscle Relaxants
Short acting muscle relaxant succinyl choline can
be used safely for intubation and other short surgical
procedures with assisted ventilation. Long acting muscle
relaxants like pancuronium, vecuronium and atracurium
can be used safely keeping in mind the fact that the
duration of action of muscle relaxants can be prolonged
in hypothermic patients. Assisted and controlled ventilation
should be continued till patients regain consciousness,
adequate respiration and muscle power. Doses can be
reduced and reversal against muscle relaxant should be
complete as the patients at HA are dependent upon
hyperventilation postoperatively for adequate oxygenation.
6. Regional Anaesthesia
(a) There is high incidence of post spinal headache,
bladder and bowel distension following spinal
anaesthesia. The possible causes are attributed to
intracranial pressure changes to native’s CNS due to
HA. But it is now rare with the use of fine 25G
spinal needle and postoperative oxygen supplement5.
(b) Local Anaesthesia : There is clinical impression that
duration of action of local anaesthetics is shortened.
7. Dissociative Analgesia
Supplemental Oxygen may not be available in some
of HA location so it is important to select an anaesthetic
technique that is least likely to suppress ventilation. The
incidence of hypoxia with ketamine analgesia in unpre-
medicated, spontaneously breathing patients without oxygen
supplement at HA was studied10. Out of 23 patients only
two patients developed decreased SPO2 to 75% or less
but resolved quickly by the end of surgery. Ketamine
anaesthesia is a safe anaesthesia practice in a rural/field
hospital setting at HA if monitored carefully by personnel
who are capable of providing supplemental oxygen
(if available) and manual support of the airway if airway
obstruction occurs.
8. Anaesthesia Equipment
Flow meters are calibrated for use at sea level.
They become inaccurate at HA because of low barometric
pressure leading to low gas density and gives less reading,
especially at higher flows. The error is about 20% at
3000 mtrs. A hazard may arise when low flow oxygen is
mixed with high flow of nitrous oxide. An oxygen analyzer
is essential to measure delivered percentage of oxygen
which is lower than the calculated on the basis of flow
meter readings. Flow meters should be calibrated using a
spirometer at the pressure at which the flow meter should
be used.
INDIAN JOURNAL OF ANAESTHESIA, JUNE 2002
9. Vaporizers
The saturated vapour pressure of any inhalational
anaesthetic drugs does not change with change of ambient
pressure but changes with temprature. Hence at any given
setting the delivered percentage of inhalational agents will
increase with altitude, however, its partial pressure
will remain constant. Individual vaporizers like Fluotec
Mark II and Dragger vaporizers exhibit variation but
changes in the splitting ratio is slight. So, in the clinical
effect with any given dial setting, anaesthetic will be
delivered at a constant potency regardless of altitude11.
10. Oxygen Delivery System
Venturi type gas mixing devices can be used to
deliver high concentration of oxygen at HA than at sea
level11. It has been found that Venturi oxygen mask that
is designed to deliver oxygen 35% at sea level actually
delivers 41% oxygen at 10,000 feet.
11. Gas Pressure Gauges
Changes in barometric pressure at HA has got
hardly any influence on reading of standard pressure
gauges as the reduction of ambient pressure is small
compared to cylinder pressure.
12. Emo Apparatus
It is a draw over ether vaporizer and can be used
with OIB (OXFORD INFLATING BELLOWS) for IPPV
for use at isolated localities where heavy equipment and
gas cylinders cannot be provided.
13. Apparatus Boyles Type ‘F’
This is a field type portable model of Boyles
apparatus incorporated with Goldman vaporizer for
inhalation of halothane which can be safely used.
14. Triservice Anaesthetic Apparatus (PENLON)
This is a draw over system, utilises atmospheric
air for oxygen, used successfully in Falkland Islands war
in 1982. It has got miniature oxford vaporizer for use of
halothane and trilene as volatile anaesthetic agents.
Conclusion
At HA, although there is reduction in ambient
pressure and decrease oxygen tension but anaesthesia can
be safely conducted keeping in mind that physiological
changes that occur at high altitude and management at
altitude requires some modification of sea level techniques
not only because of hypoxia but also because of sub
optimal equipment available at high altitude area.
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ROY : PHYSIOLOGICAL ADAPTATION AND ANAESTHESIA AT HIGH ALTITUDE 181

References 6. Hultgren HN, Kelly J, Miller H : Pulmonary Circulation in

1. MOSSO A (1998) : Life of a man on the high Alps, T Fisher
Unwin, London PP, 179.
2. DGAFMS Medical Memorandum No 60. Anaesthesia at High
Altitude (1993).
3. Kafer ER, Sugioka K; Respiratory and Cardiovascular
Responses to Hypoxaemia and the effect of Anaesthesia. Int
Anaesthesiol Clin 1981; 19 : 85.
4. Rota A, Canepa A, Hurtado A, et al. Pulmonary circulation
at Sea Level and at High Altitude. J Appl physiol : 1956; 9
: 328 - 336.
5. Safer P, Tenicela R : High Altitude physiology in relation to
Anaesthesia and Inhalation Therapy. Anesthesiology 1964;
25 : 515.
Acclimatised man at High Altitude. J Appl Physiol 1965; 20
: 1233 to 1238
7. Singh I, Kapila CC, Khanna PK, et al. High Altitude
Pulmonary Oedema. Lancet 1965;1 : 229-234.
8. Dickinson JG, Severe Acute Mountain Sickness. Postgrad
Med J.1979; 55: 454.
9. James MFM, Manson EDM Dennett JE : Nitrous Oxide
Analgesia and altitude. Anaesthesia 1982;37 : 285.
10. Pederson L, Benumof J: Incidents and Magnitude of
hypoxemia with Ketamine in a rural African Hospital.
Anaesthesia 1993;48 : 67.
11. James MFM, White JF : Anaesthesia Consideration at
Moderate Altitude. Anaesth. Analg 1984;63 : 1097.

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