Udara gas-gas (?) Kadar O2 di alam udara : --% Tekanan O2 (pO2) udara alveolus : --- mmHg Breathing Air Breathing Pure Oxygen Arterial Arterial Barometric Po2 in Pco2 in Po2 in Pco2 in Po2 in Altitude Oxygen Oxygen Pressure Air Alveoli Alveoli Alveoli Alveoli (ft) Saturation Saturation (mmHg) (mmHg) (mm Hg) (mm Hg) (mm Hg) (mm Hg) (%) (%)
0 760 159 40 (40) 104 (104) 97 (97) 40 673 100
10,000 523 110 36 (23) 67 (77) 90 (92) 40 436 100
20,000 349 73 24 (10) 40 (53) 73 (85) 40 262 100
30,000 226 47 24 (7) 18 (30) 24 (38) 40 139 99
40,000 141 29 36 58 84
50,000 87 18 24 16 15
Table Effects of Acute Exposure to Low Atmospheric Pressures on Alveolar
Gas Concentrations and Arterial Oxygen Saturation* Figure. Composition of alveolar air in individuals breathing air (0-6100 m) and 100% O2 (6100-13,700 m). The minimal alveolar PO2 that an unacclimatized subject can tolerate without loss of consciousness is about 35-40 mm Hg. Note that with increasing altitude, the alveolar PCO2 drops because of the hyperventilation due to hypoxic stimulation of the carotid and aortic chemoreceptors. The fall in barometric pressure with increasing altitude is not linear, because air is compressible. HYPOXIA Hypoxia is O2 deficiency at the tissue level. Traditionally, hypoxia has been divided into four types. 1. hypoxic hypoxia (anoxic anoxia), 2. anemic hypoxia, 3. stagnant or ischemic hypoxia, 4. histotoxic hypoxia, Acute Effect of Hypoxia The effects of hypoxia depend upon the tissue affected. In hypoxic hypoxia and the other generalized forms of hypoxia, the brain is affected first. A sudden drop in the inspired PO2 to less than 20 mm Hg, which occurs, causes loss of consciousness in 10-20 seconds and death in 4-5 minutes. Less severe hypoxia causes a variety of mental aberrations: impaired judgment, drowsiness, dulled pain sensibility, excitement, disorientation, loss of time sense, and headache. Other symptoms include anorexia, nausea, vomiting, tachycardia, and, when the hypoxia is severe, hypertension. The rate of ventilation is increased in proportion to the severity of the hypoxia of the carotid chemoreceptor cells. Acute Mountain Sickness A small percentage of people who ascend rapidly to high altitudes become acutely sick and can die if not given oxygen or removed to a low altitude. The sickness begins from a few hours up to about 2 days after ascent. Two events frequently occur: Acute cerebral edema. Acute pulmonary edema. Individuals who do not develop mountain sickness have a diuresis at high altitude, and urine volume is decreased in individuals who develop the condition. Chronic Mountain Sickness Occasionally, a person who remains at high altitude too long develops chronic mountain sickness, in which the following effects occur: 1) polycythemia 2) Elevation of the pulmonary arterial pressure 3) Enlargement of the right side of the heart 4) Falling of the peripheral arterial pressure 5) congestive heart failure ensues, and 6) Death. Acclimatization Acclimatization to altitude is due to the operation of a variety of compensatory mechanisms. The principal means by which acclimatization comes about are 1. a great increase in pulmonary ventilation, 2. increased numbers of red blood cells, 3. increased diffusing capacity of the lungs, 4. increased vascularity of the peripheral tissues, 5. increased ability of the tissue cells to use oxygen despite low pO2 Table Potential problems associated with exposure to increased barometric pressure. Lung damage Oxygen toxicity Convulsions Euphoria Nitrogen narcosis Impaired performance High-pressure nervous Tremors syndrome Somnolence Pain Decompression sickness Paralyses Air embolism Sudden death Oxygen Therapy Administration of oxygen-rich gas mixtures is of great benefit in hypoxic hypoxia. Treatment regimes that deliver less than 100% O 2 are of value both acutely and chronically, and administration of O2 24 hours per day for 2 years has been shown to significantly decrease the mortality of chronic obstructive pulmonary disease. When 100% O2 is first inhaled, there may be a slight decrease in respiration in normal individuals. O2 therapy in hypercapnic patients in severe pulmonary failure must be started with care. Hyperbaric O 2 Therapy exposure to 100% O2 at 2-3 atmospheres limited to 5 hours or less seems not showing O2 toxicity. Use in: carbon monoxide poisoning, radiation-induced tissue injury, gas gangrene, very severe blood loss anemia, diabetic leg ulcers and other wounds that are slow to heal, rescue of skin flaps and grafts in which the circulation is marginal. the primary treatment for decompression sickness and air embolism Oxygen Toxicity The extremely high tissue pO2 that occurs when oxygen is breathed at very high alveolar oxygen pressure can be detrimental to many of the body's tissues. For instance, breathing oxygen at 4 atmospheres pressure of oxygen (pO2 = 3040 mm Hg) will cause brain seizures followed by coma in most people within 30 to 60 minutes. The seizures often occur without warning and, for obvious reasons, are likely to be lethal to divers submerged beneath the sea. Other symptoms encountered in acute oxygen poisoning include nausea, muscle twitching, dizziness, disturbances of vision, irritability, and disorientation. Exercise greatly increases the diver's susceptibility to oxygen toxicity, causing symptoms to appear much earlier and with far greater severity than in the resting person. Excessive Intracellular Oxidation as a Cause of Nervous System Oxygen Toxicity-"Oxidizing Free Radicals." Hypercapnia Retention of CO2 in the body (hypercapnia) initially stimulates respiration. Retention of larger amounts produces symptoms due to depression of the central nervous system: confusion, diminished sensory acuity, and, eventually, coma with respiratory depression and death. PCO2 is markedly elevated, there is severe respiratory acidosis, and the plasma HCO3- may exceed 40 meq/L. Hypocapnia Hypocapnia is the result of hyperventilation. Cerebral blood flow may be reduced 30% or more. The cerebral ischemia causes light- headedness, dizziness, and paresthesias.