introduction physiology of altitude acclimatization … · 2014-01-22 · introduction physiology...

沈政翰 2013/1/14

Introduction

Physiology of Altitude Acclimatization

Pathophysiology Acute Mountain Sickness (AMS)

High-Altitude Cerebral Edema (HACE)

High-Altitude Pulmonary Edema (HAPE)

Treatment and Prevention

Mountains cover one-fifth of the earth's surface; 38 million people live permanently at altitudes 2400 m, and 100 million people travel to high-altitude locations each year.

山地、丘陵、平原的比例是 3：4：3丘陵也算是山的話，台灣山岳區的面積可占全台的70％。 3000 公尺的山峰，更高達257 座。

Altitude illness is likely to occur above 2500 m but has been documented even at 1500–2500 m.

High-altitude syndromes are those attributed directly to the hypoxia: acute hypoxia, AMS, pulmonary edema, cerebral edema, retinopathy,

peripheral edema, sleeping problems, and a group of neurologic syndromes.

mountain environment associated illnesses : hypothermia, frostbite, trauma, ultraviolet keratitis, dehydration, and

lightning injury.

西藏(拉薩)— 3650 m

四川九寨溝— 2930 m

祕魯馬丘比丘— 2,430 m

尼泊爾— 1/4>3000公尺

Intermediate altitude (1520 -2440 m):produces decreased exercise performance and increased alveolar ventilation without major impairment in arterial oxygen transport.

2130 - 2440 m : Acute mountain sickness (AMS) occurs at this altitude . Patients chronic obstructive pulmonary disease (COPD) or congestive heart failure (CHF) at low altitude may become more symptomatic.

High altitude (2440 to 4270 m) : is associated with decreased arterial oxygen saturation (SaO2), and marked hypoxemia may occur during exercise and sleep. Most cases of altitude-related medical problems occur in this elevation range, because of the availability of overnight tourist facilities located at these heights.

Very high altitude(4270 to 5490 m) : South America and the Himalayas. Abrupt ascent can be dangerous, and a period of acclimatization is required to prevent illness.

Extreme altitude >5490 m (>18,000 ft): is experienced only by mountain climbers and is accompanied by severe hypoxemia and hypocapnia.

Because hypoxemia is maximal during sleep, the sleeping altitude is the critical altitude to consider

氣壓低

氣體密度隨高度而降低

濕度低

溫度低

PB (mmHg) FIO2 (%) PIO2 (mmHg)

海平面 760 20.95 150

3000 公尺 526 20.95 110

4510 公尺 446 20.95 83

8848 公尺 247 20.95 42

北大武山 3090 M

台南市左鎮二寮日出 168m

Introduction






The primary initial adaptation is maintenance of alveolar PO2 through increased ventilation.

A low hypoxic drive may allow extreme hypoxemia to develop during sleep.

Initial hyperventilation is attenuated quickly by respiratory alkalosis, which acts as a brake on the respiratory center. As renal excretion of bicarbonate compensates for the respiratory alkalosis, pH returns toward normal, and ventilation continues to increase. ( 4-7day )

Within 2 hours of ascent to altitude, erythropoietin level increases and results in increased red cell mass over days to weeks.

Shifts in the oxy-hemoglobin dissociation curve are thought to be minimal at altitude because of balancing physiologic effects.

2,3-diphosphoglyceric acid (DPG) increase and shifts the curve to the right. Respiratory alkalosis shifts the curve to the left.

R→T

V↑

DPG

acetazolamide

Balance

Peripheral venous constriction on ascent to altitude causes an increase in central blood volume that triggers baroreceptors to suppress secretion of antidiuretic hormone (ADH) and aldosterone and induce a diuresis.

Decreased plasma volume and hyperosmolality (serum osmolality of 290 to 300 mOsmol/kg) due to a reset of the osmolar center of the brain.

Antidiuresis is a hallmark of AMS.

Stroke volume decreases initially, and increased heart rate maintains cardiac output. Maximum exercising heart rate declines at altitude proportional to the decrease in maximum oxygen consumption ( O2max).

Cardiac muscle in healthy persons can withstand extreme levels of hypoxemia (PaO2 of

O2max : drops dramatically on ascent to altitude, approximately 10% for each 1000-m altitude gain above 1500 m.

During acclimatization, maximal endurance increases appreciably after 10 days, but O2max does not.

The mechanism of this decrement might be lack of adequate oxygen supply to the muscle cells due to the low driving pressure for diffusion of oxygen from the capillary.

Another theory suggests that the central nervous system (CNS) limits muscle activity to preserve its own oxygenation

Sleep stages III and IV are reduced at altitude, whereas sleep stage I is increased, but with only slightly less rapid eye movement time.

The frequent arousals are a common source of bitter complaints from skiers and others, but they are innocuous and improve with time at altitude.

The typical periodic breathing (Cheyne-Stokes respiration) in those sleeping at >2700 m consists of 6- to 12-second apneic pauses interspersed with cycles of vigorous ventilation. Intervals of apnea of >20 seconds have been observed at extreme altitudes.

The frequent awakenings are not necessarily related to sleep periodic breathing, and neither are they related to AMS. Presumably, the mechanism of the lighter sleep is related to cerebral hypoxia.

Introduction






Evidence

AMS is a neurologic syndrome characterized by headache, GI disturbances, dizziness or light-headedness, and sleep disturbance.

AMS must be distinguished from exhaustion, dehydration, hypothermia, alcoholic hangover.

sleeping altitude 2740m seems to be a threshold for an increase in attack rate.

altitude incidence 2210m 25 % (colorado)

2220~2270m 17~40 %

Nepal on the path to Mount Everest 40 % ( 8% -->HACE & HAPE )

Mount Rainier (4320m) 70 % rapid ascent

Lake louise, Canada 1750 m ~ 1884 m

Age ( Children,

AMS is due to hypobaric hypoxia, but the exact sequence of events leading to illness is unclear.

Vasodilation occurs in the brain and its volume increases in all persons ascending to high altitude because of increased cerebral blood flow and accompanying increased blood volume.

The leaky blood–brain barrier is due either to loss of autoregulation and overperfusion, or to hypoxia-induced increased permeability caused by mediators such as vascular endothelial growth factor or bradykinin, or to a combination of the two processes.

The cerebral edema, interstitial pulmonary edema, peripheral edema, and antidiuresis observed in AMS all point to an abnormality of water handling by the body.

The mechanism is thought to be increases in renin-angiotensin, aldosterone, and ADH in contrast to the normal ADH and aldosterone suppression at high altitude and the usual .

dexamethasone

Three principles: do not proceed to a higher sleeping altitude in the presence of

symptoms. descend if symptoms do not abate or become worse despite treatment. descend and treat immediately in the presence of a change in

consciousness, ataxia, or pulmonary edema.

Mild AMS is self-limited and generally improves with an extra 12 to 36 hours of acclimatization if ascent is halted.

Headache from AMS often dissipates within 10 to 15 minutes with supplemental oxygen administration.

Pharmacologic treatment offers an alternative to descent or oxygen administration in patients with mild to moderately severe AMS.

AMS HACE

HAPE

HACE progressive neurologic deterioration with AMS or HAPE

It is characterized by altered mental status, ataxia, stupor, and progression to coma if untreated.

Headache, nausea, and vomiting are not always present.

Because of raised intracranial pressure, focal neurologic signs, such as third and sixth cranial nerve palsies, may result.

HACE is usually associated with pulmonary edema

HAPE is the most lethal of the altitude illnesses.

Incidence:

Women < men

Heavy exertion

Rapid ascent

Cold

Excessive salt ingestion

Use sleeping medication

HAPE is a noncardiogenic, hydrostatic edema. The culprit in HAPE is high microvascular pressure.

Pulmonary hypertension is an essential component, but not all persons with pulmonary hypertension develop HAPE.

Pulmonary venous constriction and uneven arterial vasoconstriction, which leads to overperfusion of some areas of the lung vasculature.

Inflammation is not present early in the course of HAPE, as measured by the chemical composition of bronchoalveolar lavage fluid, but appears to be a secondary finding later in the illness.

?

AMS : oxygen , descent

HACE : oxygen , descent

HAPE : oxygen , hyperbaric units , descent

↓65%

↓30~50%

AMS headache aspirin 650 mg

acetaminophen 650~1000 mg

ibuprofen 600~800 mg

vomit ondansetron 4~8mg /Q4H~Q6H

migraine sumatriptan 50 mg within 1 hr of ascent

Frequent wakening zolpidem 10 mg HS

zolpidem C.R. 12.5 mg HS

eszopiclone 2~3 mg HS

diphenhydramine 25~50 mg HS

HAPE prevent dexamethasone ↓ 78%

Salmeterol inh. BID ↓ 50%

Objective: The objective of this study is to determine the association between the

duration of high-altitude (>3000 m) pre-exposure and acute mountain sickness (AMS) incidence. Methods: 2 random days each month from 2007/04 ~2008/03 at Paiyun Lodge

(3402 m), Jade Mountain, Taiwan. Demographic data, prior AMS history , symptoms, and scores and the days and times of high-altitude pre-exposure within the preceding 2 months were obtained from lowland (>1500 m) trekkers.

Beidleman et al. reported that the incidence and severity of AMS at 4300 m were reduced immediately after intermittent altitude exposure for 3 weeks.

introduction physiology of altitude acclimatization … · 2014-01-22 · introduction physiology...

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