In a person who is acclimatized to high altitude for a long time, which of the following changes is seen?
Ans: C (Pulmonary arterial hypertension) Ref: Ganong's Review of Medical Physiology, 21st ed, and Medical Physiology: Principles for Clinical Medicine by Rhoades RA 4th edition, pg 396 Explanation: "Although the body undergoes many beneficial changes that allow acclimatization to high altitude, there are some undesirable effects. One of these is pulmonary hypertension (abnormally high pulmonary arterial blood pressure). Alveolar hypoxia causes pulmonary vasoconstriction. Remember that regional hypoxia redirects blood away from poorly ventilated regions in the lung without any change in pulmonary pressure. However, with generalized hypoxia, pulmonary pressure rises because all the preafveolar vessels constrict. In addition, prolonged hypoxia causes vascular remodeling in which pulmonary arterial smooth muscle cells undergo hypertrophy and hyperplasia. The vascular remodeling results in narrowing of the small pulmonary arteries and increases pulmonary vascular resistance, leading to a further significant increase in pulmonary vascular hypertension.'' Ref: Medical Physiology: Principles for Clinical Medicine by Rhoades RA, 4th edition, pg 396 Changes Seen in High Altitude Acclimatization Respiratory alkalosis produced by the hyperventilation shifts the oxygen-hemoglobin dissociation curve to the left, but there is a concomitant. Increase in red blood cell 2, 3-DPG, which tends to decrease the O2 affinity of hemoglobin. The net effect is a small increase in P50. Erythropoietin secretion increases promptly on ascent to high altitude and then falls somewhat over the following 4 days as the ventilatory response increases and the arterial PO2 rises. The increase in circulating RBCs triggered by the erythropoietin begins in 2-3 days and is sustained. | Alveolar PO2 | Hematocrit (Polycythemia) - | MCV and | MCHC. | RBC mass. | Concentration of capillaries in skeletal muscle tissue. | Myoglobin (Facilitates movement of O2 in tissues) | Mitochondria (the site of oxidative reactions). | Tissue cytochrome oxidase. | Aerobic enzyme concentration. | 2,3-BPG. Hypoxic pulmonary vasoconstriction leading to pulmonary arterial hypertension, Right ventricular hypertrophy. Also Note: Hypoxic hypoxia is a problem in normal individuals at high altitudes In high altitudes, the composition of air stays the same, but the total barometric pressure falls with increasing altitude. Therefore, the PO2 also falls. At 3000 m (approximately 10,000 ft) above sea level, the alveolar PO2 is about 60 mmHg and there is enough hypoxic stimulation of the chemoreceptors to definitely increase ventilation. As one ascends higher, the alveolar PO2 falls less rapidly and the alveolar PCO2 declines somewhat because of the hyperventilation. The resulting fall in arterial PCO2 produces respiratory alkalosis. Manifestations in unacclimatized subjects: o c At 3700 m - Mental symptoms o At 5500 m - Hypoxic symptoms o At above 6100 m (20,000 ft) - Unconsciousness and death. Acute "Transient" Mountain Sickness Occurs when unacclimatized persons first arrive at a high altitude. This syndrome develops 8-24 hours after arrival and lasts 4-8 days. It is characterized by headache, irritability, insomnia, breathlessness, and nausea and vomiting. Associated with cerebral edema. The low PO2 at high altitude causes arteriolar dilation, and if cerebral auto regulation does not compensate, there is an increase in capillary pressure that favors increased transudetion of fluid into brain tissue. Decreased urine output (Normally diuresis is seen at high altitude). High-altitude cerebral edema The capillary leakage in mountain sickness progresses to frank brain swelling, with ataxia, disorientation, and in some cases coma and death due to herniation of the brain through the tentorium. High-altitude pulmonary edema. It is a patchy edema of the lungs that is related to the marked pulmonary hypertension that develops at high altitude. Treatment of High Altitude illness All forms of high-altitude illness are benefited by: Descent to a lower altitude. Diuretic acetazolamide - This drug inhibits carbonic anhydrase. producing increased HCO3- excretion in the urine, stimulating respiration, increasing PaCO2. and reducing CSF formation. Oxygen supplementation / Hyperbaric chamber (Pulmonary edema). Glucocorticoids (Cerebral edema). Nifedipine can lower pulmonary artery pressure. Chronic Mountain Sickness (Monge's Disease) Due to aberration of normal physiological response to high altitude. Extremely increased hemoglobin levels. Pulmonary hypertension. Right ventricular failure. Treatment: Return to lower altitudes.
Increased MCHC
Irregular respiration
Pulmonary arterial hypertension
Increased airway resistance