HIGH ALTITUDEPHYSIOLOGY

What is high altitude?

International Society forMountain Medicinerecognizes three altituderegions that reflect thelowered amount of oxygenin the atmosphere:

High altitude = 1,500–3,500 metres (4,900–11,500 ft)

Very high altitude = 3,500–5,500 metres (11,500–18,000 ft)

Extreme altitude = above 5,500 metres (18,000 ft)

Physiologically Critical

Altitudes Up to 10,000 ft (3,000 m) “safe zone of

rapid ascent” classically defines ‘high

altitude’

At 17,000 ft (5,000 m) upper limit of

permanent human inhabitation

La Rinconada, a mining village of over 7000 people

in southern Peru at an altitude of up to 17000 ft,

Above 20,000 ft (6,000 m) life is endangered

without supplemental oxygen

At 25,000 to30,000 ft O2 supplement has

to be started.

Called Critical Survival Altitude.

From 40,000 ft(12,000 m) Ozone layer starts

Atmospheric pressure at

different altitude

Barometric pressure falls with increasing altitude,

but composition of air remain same.

According to Dalton’s law:

Total Pressure of Air = Sum of Partial Pressure of All

Gases.

P= pO2+pCO2+pN2+pH2O

Alveolar pH2O & pCO2 determined by body so

does not change with altitude.

Only pO2 & pN2 changes.

Mount Everest - 29,028 ft (8848mt)

Atmospheric Pr = 255 mmHg

PO2= 53 mmHg

Inspired PO2 = 44 mmHg

Unacclimatized person ----

Unconscious in 45 seconds

Dead in 4 to 6 minutes

Hypoxia at high altitude

One of the most important effects of hypoxia is

decreased mental proficiency, which decreases

judgment, memory, and performance of

discrete motor movements.

if an unacclimatized person stays at 15,000 feet for 1 hour,

mental proficiency ordinarily falls to about 50 percent of

normal, and after 18 hours at this level it falls to about 20

percent of normal.

In addition to the mental depression caused by

hypoxia, the work capacity of all muscles is

greatly decreased in a state of hypoxia.

Clinical effects of high

altitude

Acute mountain sickness.

• High altitude cerebral edema (HACE)

• High altitude pulmonary edema (HAPE)

Chronic mountain sickness.

Acute mountain sickness

People who ascend rapidly to high altitudes can

become acutely sick and die if not given O2 or

rapidly moved to a low altitude.

The sickness begins from a few hours up to about

2 days after ascent.

Two events frequently occur:

High altitude pulmonary edema (HAPE)

High altitude cerebral edema (HACE)

High Altitude Cerebral Edema (HACE)

A condition in which the brain swells with fluid

because of the physiological effects of traveling

to a high altitude.

Symptom commonly include confusion, loss of

consciousness, fever, ataxia, photophobia, rapid

heart beat and an altered mental state.

If untreated , it may cause— Disorientation,

coma & Finally Death (due to tentorial herniation

of the brain-tissue)

Mechanism of HACE

Hypoxia due to ↓pO2

Cerebral capillary and

arteriolar dilatation

Limit of cerebral

autoregulatory mechanism

are crossed

↑ capillary hydrostatic

pressure

↑ fluid leakage into

brain tissue

Cerebral edema

develops

Management of HACE

HACE is usually fatal within 24 hours if untreated.

Without treatment, the patient will enter a coma

and then die.

Patients with HACE should be brought rapidly to

lower altitudes and provided supplemental

oxygen.

Drug treatment includes dexamethasone and

diuretics

High altitude pulmonary edema(HAPE)

Manifest above 10000 ft.

Seen in

• 75-80% in persons doing heavy physical work in first 3-4 days of accent

• Persons who acclimatized to high altitude, stay at sea levels for > 2wks& again rapidly re-ascend.

► Not develop in gradual ascent & on avoidance of physical exertion during first 3-4 days of exposure

Manifestations of HAPE:

↓ exercise tolerance & slow recovery from exercise.

fatigue, weakness & exertional dyspnoea .

Condition typically worsens at night & tachycardia and tachypnea occur at rest.

Cough, frothy sputum, cyanosis, dyspneaprogressing to severe respiratory distress

low-grade fever, respiratory alkalosis, & leucocytosis

In severe cases-- an altered mental status, hypotension, and ultimately death may result

Mechanism of development of HAPE

The cause of acute pulmonary edema is still not well understood, but one explanation is the following:

Sympathetic activation by physical work,

sympathetic stimulation by hypoxia &cold.

Pulmonary capillary and arteriole

vasoconstriction.

Increase in pulmonary capillary

hydrostatic pressure.(10 to 25mmHg)

Increase in capillary pressure drives

the fluid out of pulmonary capillaries

Pulmonary edema develops

Management of HAPE

Standard & most imp to descend to lower altitude as quickly as possible( preferably by at least 1000 meters) & to take rest.

Oxygen should be given (if possible).

Symptoms tend to quickly improve with descent, but les severe symptoms may continue for several days.

The standard drug treatments includes dexamethasone & CCB’s (like nifedipine).

Chronic Mountain Sickness

Monge’s disease

Occurs in long term residents of high

altitude.

The red blood cell mass and hematocrit

become exceptionally high,

Develop – Polycythemia, cyanosis,

malaise, fatigue & exercise intolerance.

Treatment- return to lower altitude(at sea-levels)

Extreme ↑Hb

levels

Extreme ↑viscosity

of blood

↓ blood

flow to tissues

widespread

pulmonary

vasoconstriction

(hypoxic

response)

Pul. hypertension

Right sided heart

failure

(Cor pulmonale)

Physiological adaptation at

high altitude

Divided into following two---

1. Acute responses (accommodation)

2. Long term responses (acclimatization)

Accomodation

Refers to immediate reflex adjustments of

respiratory and cardiovascular system to hypoxia

Acclimatization

Refers to changes in body tissues in response to

long term exposure to hypoxia

Accommodation at high

altitudeImmediate reflex responses of the body to acute hypoxic exposure.

A. Hyperventilation:

Decrease arterial PO2 stimulation of peripheral chemo receptors increased rate & depth of breathing

B. Tachycardia:

► due stimulation of peripheral chemo receptors

C. Increased 2,3-DPG conc. in RBC:

within hours, ↑deoxy-Hb conc. locally ↑pH ↑2,3-DPG ↓oxygen affinity of Hb tissue O2 delivery maintained at

Acclimatization at high

altitude:

Various physiological readjustments and

compensatory mechanisms in body that reduces

the effects of hypoxia in permanent residents at

high altitude.

It is done by-

1. A great increase in pulmonary ventilation.

exposure to low PO2 stimulates the arterial

chemoreceptors, and this stimulation increases

alveolar ventilation.

Prolonged hyperventilation CO2 wash-

out respiratory alkalosis renal

compensation by reducing H+ ion

excretion and increasing bicarbonate ion

excretion normalization of pH of blood

& CSF withdrawal of central chemo-

mediated respiratory depression net

result is ↑ resting pulmonary ventilation (by

~5 folds )

2. Increase in Red Blood Cell and Hemoglobin

concentration

Hypoxia induced erythropoiesis through increase in

erythropoietin hormone

↑Hb Conc. & RBC count (within a few wks. stay)

the hematocrit rises slowly from a normal value to an

average of about 60,

blood hemoglobin concentration rises from normal

of 15 g/dl to about 20 g/dl.

3. Increased Diffusion Capacity of Lung

Threefold increase in O2 diffusion capacity

happens due to :

increased pulmonary capillary blood volume,

which expands the capillaries and increases the

surface area through which O2 can diffuse.

an increase in lung tidal volume, which expands

the surface area of the alveolar-capillary interface

still more.

an increase in pulmonary arterial blood pressure,

which forces blood into greater numbers of

alveolar capillaries

4. Increased Tissue Capillarity

More capillaries open up in tissues than at sea

level (normal ~50 % open & rest remains as

‘reserve’).

Growth of new circulatory capillaries in non

pulmonary tissues (angiogenesis).

This combined with systemic vasodilatation(also

a hypoxic response) leads to more O2 delivery to

tissues.

5. Increase in Total Lung Capacity (TLC)

Specially seen in the natives highlander

The chest size is greatly increased (barrel shape

chest), whereas the body size is somewhat

decreased, giving a high ratio of ventilatory

capacity to body mass.

6. Cellular acclimatization

Increased mitochondria

Increased Cytochrome Oxidase

Increased Myoglobin

View from the Everest summit