|
Adaptive physiological responses, as well as disease, are
associated with both living and travel at high altitudes.
From a
physiological standpoint, altitudes are separated into three categories :
Below 2500 meters ; 2500 to 4000 meters ; and above 4000 meters.
High altitude
illness is rare, mainly because of the
acclimatization of mountain
climbers before extreme altitudes are achieved.
However, there is an
altitude limit beyond which human life cannot be sustained for prolonged
periods.
Communities in the Andes succeed at 4000 to 4300 meters. The
indigenous people adapt to the decreased pressure and availability of
oxygen by developing elevated hematocrits and large "barrel" chests with
increased lung volume.
Even those who live in this zone do not survive at elevations above 5500
to 6000 meters.
Prolonged stays at this altitude result in weight loss, difficulty in
sleeping, and lethargy, perhaps because of the redirection of cellular
energy simply for survival.
For example, of the oxygen obtained per inhalation at 6000 meters, 75% to
90% is utilized for the effort of inspiration alone.
The modification induced by high altitude are
related to a decreased atmospheric pressure and ,therefore, to decreased
oxygen availability.
It has been suggested that the decreased oxygen
tension and the limited ability of the lungs to extract oxygen at lower
pressures produce the hypoxia that is probably the most important factor in
causing high-altitude illness.
The narrow reserve is illustrated by the observation that physical
activity at these heights leads to a decrease in the partial pressure of
arterial oxygen, where as comparable physical activity at sea level does
not change oxygen saturation. At sea level, cardiac output limits
exercise, where as at high altitudes the diffusing capacity of lung for
oxygen seems to be the determinant.
Acclimatization to
chronic hypoxia at high altitudes results in a reduced ventilatory drive.
Acclimatized individuals have
- An increased number of capillaries per unit of
brain, muscle, and myocardium ; Increased amount of myoglobin within
tissues ; Increased mitochondria per cell and ; An increased hematocrit.
An
increase in erythrocyte levels of 2'3'diphosphoglycerate, which enhances
oxygen delivery to tissues, occurs within hours, but the induction of polycythemia
requires months.
Some of the minor effects of high altitude are systemic edema, retinal
hemorrhages, and flatus expulsion.
The more serious nonfatal diseases are acute and chronic mountain sickness
and high altitude deterioration.
Fatal disease can develop in the form of high-altitude pulmonary edema and
high-altitude encephalopathy.
High-Altitude Systemic Edema:
High-altitude systemic edema results from an
asymptomic modification of vascular permeability, particularly in the
hands, face, and feet and most often occurs at elevations over 3000
meters.
It is reflected only in weight gain.
Upon return to lower
altitude, a diuresis causes the edema to disappear.
This disorder is twice as common in women as in men.
The cause of this peculiar condition is not known. An endothelial response
to hypoxia provides only a partial explanation.
High-Altitude Retinal Hemorrhage:
A critical analysis by funduscopic
examination revealed that 30% to 60% of those sleeping above 5000 meters
had retinal hemorrhage.
The initial effect includes retinal vascular engorgement and tortuousness.
Optic disc hyperemia is also noted, and multiple flame-shaped hemorrhages
subsequently occur. These changes are reversible.
High-Altitude Flatus:
Changes in external pressure and the production of intestinal gas provide
for expansion of the luminal contents of the intestine and increased
flatus at altitudes above 3500 meters.
No specific physical disease has been associated with these changes,
although social problems have been encountered.
Acute Mountain Sickness:
Acute mountain sickness is rare below 2500 meters,
but is present to some degree in nearly everyone at 3000 to 3600 meters.
The initial presentation includes headache, lassitude, anorexia, weakness
and difficulty in sleeping.
The pathophysiological mechanism that
underlies this disease is in part related to hypoxia and a shift in plasma
fluid to the interstitial space.
Adaptation through a modification of pulmonary function (increased
respiratory rate) may lead to some improvement.
Descent to lower altitudes is certainly indicated.
Chronic
or subacute exacerbation of this disease also occurs, frequently at lower
altitudes, and the symptoms may be severe. The basis of the disease is not
known.
High-Altitude Deterioration:
High-altitude deterioration, generally occurring at
higher elevations (5500 meters or more), presents as a decrease in
physical and mental performance.
The combination of chronic hypoxia,
inadequate fluid intake, and inadequate nutrition, together with decreased
plasma volume and hemoconcentration, are aggravating factors.
High-Altitude Pulmonary Edema and Cerebral Edema
:
Serious high-altitude problems, including pulmonary edema and cerebral
edema, can occur with a rapid ascent to heights over 2500 meters,
particularly in susceptible individuals who are unable to tolerate
sleeping at higher altitudes.
Tachycardia, right ventricular overload, and
a marked reduction in arterial oxygen pressure, are seen, but there is no
change in pH or carbon dioxide retention.
A characteristic patchy
pulmonary infiltrate is seen radiographically.
Pulmonary hypertension due
to increased resistance is common in patients with high-altitude pulmonary
edema.
Hypoxic vasoconstriction and intravascular thrombosis have been
proposed as causes of pulmonary hypertension.
Eventually, cardiac output
is decreased and systemic blood pressure falls.
The precapillary
arterioles become dilated, increasing capillary bed pressure and inducing
interstitial and alveolar edema.
Autopsy findings include severe confluent
pulmonary edema, proteinaceous alveolar exudates, and hyaline membrane
formation.
Capillary obstruction by thrombi has been noted. A dilated heart and
enlarged pulmonary arteries are commonly found.
High-altitude encephalopathy is characterized by
confusion, stupor, and coma.
Autopsies have consistently revealed cerebral edema and vascular
congestion.
A proposed mechanism is severe cerebral hypoxia, with inhibition of the
sodium pump and resultant intracellular edema.
Environmental Pathology - Physical Agents :
click here
Environmental Pathology-Thermal Regulatory
Dysfunction: click here
Environmental Pathology - Hypothermia:
click here
Environmental Pathology - Hyperthermia:
click here
Environmental Pathology- Electrical Burns: click
here
Environmental Pathology - Physical Injuries: click
here
|
