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How is sustained Hyperventilation possible at altitude?
- HCO3 - actively removed from CSF to reduce pH
- Glomus cells in carotid bodies become more sensitive to PO2
- Kidneys excrete more HCO3 - , lowering plasma pH
What are short/intermediate term responses to high altitude?
- Hb-O2 dissociation
- BMR increases to ~20%
- VO2max decreases by ~25%
how do Tibetans and Andean Aymara respond to high altitude conditions?
- Same BMR as would be expected for age, sex, and weight
- Same VO2max as expected for level of training
- Both have increased vital capacity (biggest breath possible)
- Tibetans have lower Arterial O2 content than the sea level mean
- Andeans have a higher Arterial O2 content than the sea level mean
- Both have elevated hemoglobin conc. - andeans have higher than tibetans
- Andeans have a much higher erytropoietin levels
- Tibetans have chronically increased ventilation but still have reduced arterial O2 relative to low landers. they compensate with increased blood flow in part due to reduced pulmonary pressure, and increased capacity for the tissues to "grab" oxygen (increased capillary density)
- Andeans have slightly increased ventilation, and increased Hb conc. and saturation, resulting in increased arterial O2 relative to lowlanders They have limited cardiovascular responses and suffer from pulmonary hypertension.
What are AMS, HAPE, and HACE and how can they best be treated
- AMS aka altitude sickness (acute mountain sickness)
- HAPE (high-altitude pulmonary edema)
- Hypoxia-induced pulmonary hypertension:
- locally low pulmonary PO2 triggers vasoconstriction
- hypertension leads to leakage across capillaries
- lungs fill with blood and waterdexamethasone
- HACE (High-altitude cerebral edema)leakage across blood-brain barrier leads to edema
- All of these are best treated by getting down the mountain