Answers to Quiz 109 · Physiological Changes at High Altitude
Hypoxia-induced hyperventilation becomes significant only when alveolar PO₂ falls below:
Answer: 60 mmHg
The hypoxic drive stays silent until alveolar PO₂ drops below 60 mmHg, which happens at an altitude of about 4500 m (14000 feet). Revise acclimatization to high altitude
The hyperventilation of the first stage of compensation at high altitude is mainly due to stimulation of:
Answer: The carotid bodies
Acute hypoxia acts on the peripheral chemoreceptors, chiefly the carotid bodies. Central chemoreceptors respond to CO₂ and H⁺, which actually fall at altitude. Revise acclimatization to high altitude
Why is the rise in ventilation small during the first stage of compensation at high altitude?
Answer: Falling arterial PCO₂ and alkalosis blunt the hypoxic response
Hyperventilation washes out CO₂, so arterial PCO₂ falls and pH rises; low PCO₂ and alkalosis together oppose the hypoxic drive. Revise acclimatization to high altitude
The renal mechanism of ventilatory acclimatization brings blood pH back toward normal in about:
Answer: 3 days
The kidney excretes more bicarbonate, correcting the alkalosis in roughly 3 days, so urine becomes alkaline and the hypoxic drive is free to raise ventilation further. Ventilation itself climbs over 8 to 10 hours and plateaus after about 2 weeks. Revise acclimatization to high altitude
The maximum height up to which a person can adapt, beyond which O₂ inhalation is needed for survival, is:
Answer: 18000 feet
Adaptation is possible up to 18000 feet. 14000 feet is where alveolar PO₂ reaches 60 mmHg and hypoxic hyperventilation begins. Revise acclimatization to high altitude
The rise in red-cell 2,3-DPG during acclimatization helps the tissues because it:
Answer: Shifts the O₂–Hb dissociation curve to the right
More 2,3-DPG shifts the curve right, so Hb releases O₂ more readily in the tissues. Early on, the alkalosis of hyperventilation shifts the curve left instead. Revise acclimatization to high altitude
Erythropoietin-driven erythropoiesis at high altitude begins in about:
Answer: 3 days
Hypoxia stimulates erythropoietin, and erythropoiesis starts in roughly 3 days and continues for as long as the person stays at altitude. Revise acclimatization to high altitude
Which of these is NOT among the tissue changes of acclimatization to high altitude?
Answer: Fall in myoglobin content
Myoglobin content rises, it does not fall. The other three, with angiogenesis, make up the tissue changes seen mainly in skeletal muscle. Revise acclimatization to high altitude
Cardiac hypertrophy in a long-term high altitude resident is best explained by:
Answer: Polycythemia raising blood viscosity and cardiac workload
A markedly raised hematocrit thickens the blood, so the heart works harder and hypertrophies. Hypoxic systemic vasodilation instead helps tissue blood flow. Revise acclimatization to high altitude
The ventilatory equivalent (VE), the preferred index of the ventilatory response to altitude, is the ratio of:
Answer: Expired minute volume to O₂ consumption
VE is expired minute volume divided by O₂ consumption, and it rises as altitude rises. CO₂ output over O₂ consumption is the respiratory quotient. Revise acclimatization to high altitude
The symptoms of acute mountain sickness typically appear after arrival at high altitude within:
Answer: 4 to 8 hours
They begin within 4 to 8 hours and may last several days. A picture developing over long residence at altitude is chronic mountain sickness instead. Revise high altitude illness
Which of these is NOT a feature of chronic mountain sickness (Monge's disease)?
Answer: Hypovolemia
Monge's disease features hypervolemia, not hypovolemia, along with polycythemia, malaise, fatigue, exercise intolerance, pulmonary hypertension, right ventricular hypertrophy and heart failure. Revise high altitude illness
In chronic hypoxia at altitude, narrowing of the pulmonary arterial lumen is caused by:
Answer: Hypertrophy and hyperplasia of pulmonary arterial smooth muscle
Sustained alveolar hypoxia first constricts the vessels, then remodels them: the smooth muscle hypertrophies and proliferates, fixing the resistance high. Revise high altitude illness
A climber at high altitude becomes disoriented and ataxic and then lapses into coma. The coma is due to:
Answer: Herniation of the brain through the tentorium
Leaky cerebral capillaries produce high altitude cerebral edema; the climber is first disoriented and ataxic, and coma follows once the brain herniates through the tentorium. Revise high altitude illness
Acetazolamide is the diuretic of choice in high altitude illness because it:
Answer: Inhibits carbonic anhydrase, increases bicarbonate excretion and reduces CSF formation
Carbonic anhydrase inhibition dumps bicarbonate, cutting the alkali load, and it also lowers CSF formation. Blocking pulmonary calcium channels is nifedipine's action. Revise high altitude illness
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