Manu Chopra

MD, DNB, MNAMS

Pulmonologist
 High altitude: 1500-3500m above sea level
Very high altitude: 3500-5500m
Extreme altitude: above 5500m Andes
Tibetan plateau &
Himalayan valleys
(6962m) (8848m)

Hackett PH, Roach RC. High

altitude medicine. Widerness
medicine 2007

Ethiopian highlands (4620m)

26 July 2017 6
ALTITUDE TYPE FROM SEA-
LEVEL (In feet)
HIGH 8,000 12,000

VERY HIGH 12,000 18,000

EXTREMELY Above 18,000

Manali 2050m Mussoorie 2006m

Srinagar 1585m

Nainital 2084m Shimla 2205m

 Kanqchenjunga- 8,586 M
Mt K2 8611m

Mt Everest
8848m

Nanga Parbat 8126m Dhaulagiri 1 8167m

 Ladakhi

Thiksey monastery Leh

3650m Kibber Village
4270m

Tabo Monastery Spiti 3280m

Kedarnath
3553m

Korzok Village Ladakh

4600m
 BAROMETRIC PRESSURE
HEAVY SNOW
WINDY CLIMATE
FREEZING TEMPERATURES
DANGERS
RADIATION

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Barometric pressure versus altitude
 Barometric
Inspired PO2 (mm
Altitude (m) Altitude (feet) Pressure (mm
Hg)
Hg)
0 0 760.0 159.1
1,000 3,280 674.4 141.2
2,000 6,560 596.3 124.9
3,000 9,840 525.8 110.1
4,000 13,120 462.8 96.9
5,000 16,400 405.0 84.8
6,000 19,680 354.0 79.1
8,000 26,240 267.8 56.1
8,848 29,028 253.0 43.1
26 July 2017 25
26 July 2017 27
 A combination of air
temperature and
wind speed that
affects the freezing
rate of exposed
skin.
 Wind Chill/Frostbite Chart

As this chart indicates, if the actual temperature is -200 F and the wind is blowing 15
mph, the cold effect on your bared skin is -450 F. At this temperature, frostbite can
begin in as little as 10 minutes.
 16 C to -60 C

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26 July 2017 31
 5% increase in UV
rays/ 300m gain +
snow reflection

26 July 2017 32
 Air Lungs Blood Tissue
Delivery of atmospheric O2 to the tissues normally involve 3
stages---with a drop in PO2 at each stage.
When the starting PO2 is lower than normal, body
undergoes acclimatization so as to
(i) pressure drop during transfer
(ii) oxygen carrying capacity of blood
(iii) ability of tissues to utilize O2
 VENTILATORY ACCLIMATIZATION

Starts within 10- 15 min of exposure 1500m

Mechanism

Ascent to altitude

Hypoxia
Decreased PCO2
Carotid body stimulation

Respiratory centres stimulation

Increased ventilation

CO2 + H2O H2CO3 HCO3- + H+ Improved hypoxia

 1. Ventilation & perfusion matching
Increased Ventilation = Increased cardiac output
Increased Pulmonary Perfusion
Alveolar hypoxia triggers Hypoxic Pulmonary
vasoconstriction
-redistribution of blood flow to areas less
perfused at sea level
- improved gas exchange
LUNG DIFFUSION

Major rate limiting step

High altitude O2 diffusion, because of
a lower driving pressure for O2 from the air to the
blood ( low Po2)
and inadequate time for equilibration ( decreased
transit Time)

Long term adaptation diffusing capacity increases

Cardiac output increases

Tachycardia:
Increased catecholamine release & sensitivity
Also d/t peripheral chemo. Response CO
oxygen delivery to the tissues
Stroke Vol decreases
 Increase in Hb conc in 1-2 days
initially hemoconcentration ( diuresis)
later increased RBC production due to
increased erythropoietin
Hypoxia is the primary stimulus for
erythropoietin secretion
Se erythropoietin levels increase in 24-48 hrs
decline within 3 weeks
 Plasma to cytoplasm 10mmHg
Cytoplasm to mitochondria 1-2mmHg
Diminished ms fibre
Increased myoglobin conc
Increased levels of enzymes involved in
oxidative phosphorylation
 Cerebral Blood flow
Cerebral bld flow increases initially
due to hypoxia
Hypocapnia cerebral
vasoconstriction bld flow decreases
13% greater than sea level
Improved O2 delivery
 Motor, sensory & cognitive abilities impair
New tasks are learned with difficulty at
3048m
Short term memory impaired
Arterial So2 85% - impair concentration and
fine motor coordination
Arterial So2 75% - poor judgement and
irritability
 Diuresis & natriuresis
Peripheral venous constriction
increased central volume
decreased ADH and aldosterone
diuresis
decreased plasma volume and hyperosmolality.
 Cheyne-Stokes Respirations
Above 10,000 ft (3,000 m) most people experience a periodic
breathing during sleep. The pattern begins with a few shallow
breaths increases to deep sighing respirations falls off
rapidly.

During period of breathing-arrest, person often becomes

restless & may wake with a sudden feeling of suffocation.

Can disturb sleeping patterns exhausting the climber.

O2 & acetazolamide help
 At high altitude air is thin. To make up for it, the
blood gets thick, respiration & circulation
improves, provided adequate time is given &
body functions properly still some limitations
remain as implied!!!
Acclimatisation

Process by which people gradually adjust to high altitude

Determines survival and performance at high altitude
Series of physiological changes
O2 delivery
hypoxic tolerance +++
Acclimatization depends on
severity of the high-altitude hypoxic stress
rate of onset of the hypoxia
individuals physiological response to hypoxia
26 July 2017 50
 FIRST STAGE ACCLIMAZATION(Above 2700 m and up to
3600 m): The acclimatization period will be for 6 days as
under:
(i) First and second day: Rest except for short walks in the
unit lines only, not involving any climbs.

(ii) Third and fourth day: walk at slow pace for 1.5 -3Km
avoid steep climbs.

(iii) Fifth and sixth day: walk upto 5 Km and climb upto 300
m at a slow pace.

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 SECOND STAGE ACCLIMATIZATION(Above 3600 m and
up to 4500 m): This is carried out for 4 days as under:
(i ) First & Second day: Slow walk for a distance for 1.5 -3 Km avoid
steep climbs.

(ii) Third day: slow walk and climb upto 300 m.

(iii) Fourth day: Climb 300 m without equipment.

THIRD STAGE ACCLIMATIZATION:(Above 4500 m): This

also lasts for 4 days and is on the same lines as second stage
acclimatization.

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maladaptation
ACUTE CHRONIC

Acute Mountain Sickness Chronic Mountain Sickness

High Altitude Pulmonary Pulmonary Arterial
Oedema Hypertension of HA
High Altitude Cerebral
Oedema
 High altitude retinopathy
UV keratitis
Thrombotic episodes
Hypothermia
Local cold injury
(A) Chilblains
(B) Trench foot
(C) Frost bite

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 Relationships of the Different
Forms of Altitude Illness

Altitude illness may be an interrelated spectrum :

AMS HAPE

HACE
Acute Mountain Sickness :
Etiology
22-50% travellers
Typically occurs at altitude > 8000 feet
Rarely occurs at altitude 6000 to 8000 feet
No predeliction based on gender
More likely if :
Rapid ascent
Lack of acclimatization
Exertion soon after arrival
Alcohol intake
Sedatives (sleeping pills)
Narcotics
Acute Mountain Sickness :
Pathophysiology

Much individual variation in susceptibility

Likely mild cerebral oedema develops
Tight fit hypothesis
 Symptoms: Signs: no characteristic finding
Headache Mild tachycardia
+ Peripheral oedema
Fatigue Crackles
Nausea & Vomiting
Impaired night vision
Anorexia
Dizziness
Sleep Disturbance
 Acute Mountain Sickness :
Differential Diagnosis

Dehydration
Hypothermia
Exhaustion
Alcohol hangover
Respiratory/ CNS infection
Psychiatric disorders
Carbon monoxide poisoning
 Mild Moderate/Severe
Rest and stop ascent Descend 100m
Descend if not Acetazolamide
improved after 24 Dexamethasone
hours Hyperbaric O2
Drink fluids
Simple analgesics
Prevention
Following acclimatization
Resolves 1-3 days protocols
Medications
26 July 2017 62
Progression of Acute Mountain
Sickness

If ascent is continued or accelerated

by a patient with untreated AMS, HAPE
or HACE may occur and death may
result
 Usually get AMS before HACE
Mental status changes +/ ataxia
Confusion, ataxia, stupor
focal neurologic signs
May lead to coma, irreversible neurological
damage or death
Incidence 0.53% - 1.25%
 Other causes of encephalopathy
CO poisoning
Hypertensive crisis
Hypoxia
Meningitis
Hypoglycemia
Hypothermia
 Ataxia (e.g. poor heel toe walking)
Focal neurological signs
Papilloedema & retinal
haemorrhages
 IMMEDIATE DESCENT
Do NOT wait until morning if HACE occurs at
night
Oxygen
Hyperbaric bag (to facilitate descent if
necessary NOT replace it)
Dexamethasone
 Commonest cause (54%)of Hospital admission due
to HAA related illnesses
Most common cause of death from high altitude
illness.
Until 1960 Pneumonia
1960 - Pulmonary edema (Houston)

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Non cardiogenic pulmonary edema
Manifests within 2-4 days of ascent >2400m
(8000 feet)
2nd night
 Pulmonary hypertension
Exaggerated Hypoxic Pulmonary vasoconstriction
High levels of ET1
Increased sympathetic tone
Lower levels of NO
Uneven hypoxic vasoconstriction
Pulmonary Endothelium Fragility
Abnormal alveolar fluid resorption
 Signs: better than expected
Symptoms: AMS Tachycardia
Reduced exercise Tachypnoea
tolerance Low grade fever
Dry cough Pallor
Cyanosis
Dyspnea at rest Crackles
Blood stained sputum Signs of RV strain
Mental changes RV heave, Loud P2
 Pneumonia
Pulm embolism
MI
Asthma
Pulm Infarction

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General Specific
Hyperbaric chamber
Descent
Oxygen - CPAP
Rest carry the patient
Drug therapy
Hydration
Nifedipine
Tadalafil/ sildenafil

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 Acclamatisation
Drugs
Nifedipine
Salmetrol
Tadalafil
Dexamethasone
26 July 2017 76
26 July 2017 77
26 July 2017 78
Avalanche

50 to 100 miles per hour

Can be as fast as 200 miles per
hour
Can generate impact pressures
> 150 lbs/square inch
(can destroy even concrete
structures)
Occur with greatest frequency
on slopes of 30 to 45 degrees
Causes of death in avalanche

Direct impact trauma of snow blocks or ice

Indirect trauma of hitting against objects
such as trees or rocks
Hypoxia from encasement in snow
Hypothermia
Restrictive chest compression
Radiation Exposure

High altitude retinopathy

UV keratitis
pain, photophobia, tearing,
erythema, chemosis, eyelid
swelling
24 h to heal, analgesics and cold
comp.
Wear sunglasses
UV dermatitis
 Miscellaneous Altitude Related
Medical Problems

Immune suppression
probably related to tissue hypoxia
wounds slower to heal & more likely to get infected
wound infections can show antibiotic resistance
Prothrombotic state leading to various Thrombosis
High altitude peripheral edema
 Khumbu cough
Purulent bronchitis and painful throat near
universal at very high altitude
respiratory heat loss, bronchospasm and mucosal
cracking (dry and cold effects)
coughing can lead to rib #s
Antibiotics no use
wear your balaclava there are face masks that
act as HME
 1. Chronic mountain sickness- due to
excessive erythrocytosis
Described in 1928 Monges disease
Young and middle aged men
Low Landers who ascend to HA
High Landers with / without respiratory disease
Increased blood volume, PAH, haematocrit >60%
CNS symptoms dominate
Plethoric florid faces, dark red conjunctiva, haemorrage below nail

2. High altitude pulmonary hypertension

Without polycythemia
 Non Freezing
Chilblain
Trench foot
Freezing
Frost bite
Chilblains