altitude and diving Flashcards
what happens to O2 tension at altitude?
At increasing altitude to % of O2 in the air remains constant at 21 %
However the ambient pressure drops exponential with rise in altitude.
5500m (18000ft) is roughly 50kpa (half the ambient pressure)
hence the pp also drops as 21% of 50 is now 11kpa
calculate O2 tension at sea level when 100% saturated with water vapour…
compare this to at 5500 meters (18000ft)
PO2 = (Atm - SVP)x 21%
at sea level = 101-6.3 x 21% = 19.9kpa
at 50kpa = 50-6.3 x 21% = 9.2 kpa
what happens at 63000 ft?
at 63000 ft the pressure of air = 6.25
if fully saturated
6.25 -6.3 = 0 kpa
hence PPO2 is 0
also blood would boil at this temp as SVP of water equals the pressure hence boiling point.
describe the physiological effects of high altitude during gradual accent
following accent, acclimatisation occurs over days to weeks.
- hyperventilation…
- hypoxia - increase in MV - drops CO2
- slow ascent allows pH of the CSF to be corrected such that the central chemoreceptors dont slow down MV with the drop in CO2.
This occurs through removal of HCO3 from CSF and subsequently the kidneys. lower paCO2 in blood means increase in alveolar O2 as per alveolar gas equation so this helps to partly compensate.
drop in CO2 also results in an alkalosis which again would promote peripheral chemoreceptors to drop MV but again with slow ascent gives time for kidneys to remove HCO3 and normalise pH - Oxy Hb dissociation curve
with slow ascent , increase in 2,3 DPG which shifts curve to right and promotes unloading of O2. at high altitude the respiratory alkalosis overrides this and causes left shift. - sympathetic NS stimulation
hypoxia stimulates sympathetic NS , icreases HR and CO to improve DO2. this however increases myocardial O2 consumption. - hypoxic pulmonary vasoconstriction - not beneficial at atitude however normal mechanism causes increase PVR and can promote pulmonary oedema
- longer term changes
- polycytheamia - EPO and erythrocytosis
- increased capilary density
what happens if a person ascends to altitude too quickly?
hypoxia initially stimulates increase MV via peripheral chemoreceptors.
this lowers PaCO2
less CO2 crosses BBB
less H2CO3 made, increase pH of CSF
causes reduction in MV via central chemoreceptors
this is known as the braking effect and will result in hypoxia and unconsciousnes if ascent isnt slowed.
no time for 2,3 DPG or normalisation of blood pH so alkalosis causes shift in dissociation curve to the left. reduces O2 unloading.
no time for EPO/polycythaemia, angiogenesis.
what is the difference between adaptation and acclimitisation?
acclimitisation - changes in an individual to maintain homeostasis with changing environmental conditions e.g. increase 2,3 DPG with altitude, polycythaemia
adaption - changes within a population overtime. secondary to evolution. e.g. population living at high altitude may have changes to Hb subunits to shift dissociation curve to right.
what is high altitude sickness..
a physiological response to high altitude resulting from too quick ascent and no time for acclimatisation
encompases 3 syndromes
- acute mountain sickness - very common and occurs above 3000m during the acclimatisation process. includes nausea, headaches, sob , sleep disturbances
- high altitude cerebral oedema - unknown mechanism of cerebral oedema resulting in confusion, ataxia, seixures, coma
- high altitude pulmonary oedema - secon to pulmonary vasoconstriction increased PVR and pulmonary BP. results in fluid accumulation secondary to starlings forces. major contributor of mortality with altitude.
other issues - hypothermia with altitude
what is the treatment for high altitude sickness
main treatment is descent
can mimic descent via hyperbaric chamber - increases pressure
can improve FiO2 by giving 100% O2
other treatments
- acetazolamide - inhibits carbonic anhydrase. Less HCO3 production hence metabolic acidosis to counter the alkalosis. hence helps maintain MV and right shift of dissociation curve
- HACO - dexamethasone reduces brain swelling
- HAPO - furosemide, nifedipine (reduce vasoconstriction)
what are the symptoms of chronic mountain sickness?
clubbing
polycythaemia - thrombosis due to high viscosity.
how is anaesthetic equipment effected by altitude?
plenum vapourisers - no effect because PP of vapour remains the same. SVP doesnt change with pressure (only temp) so SVP of sevo still 22 kpa at altitude
des vapouriser - Tec 6 - does change. the pp of desflurane will be reduced at lower pressures
flow meters - air will be less dense at altitude so less upward force so will under read . calibrated at sea level. however the molecules of O2 present will be same so no effect overall
cuff pressures - as pressure drops, volume will increase in the cuff and can result in injury to mucosa of trachea
how does pressure change with descent under water?
for every 10meters descent there is an increase in 1atm
e.g. at 20meters deep 1atm +2atm = 3atm pressure
what gas mixtures can be used by scuba divers and why?
most recreational divers use normal air
this is possible up to 50m
after 50meters, the amount N2 dissolved in blood can have anaesthetic affect and cause narcosis / anaesthesia under water.
below this level heliox is used because helium is less soluble in blood and doesnt have narcotic effects.
what is the limit for subadiving?
330 meters
why cant a person descend deep with a snorkle connected to surface of water i.e more than 1m deep/ long snorkle?
dead space within snorkle - rebreathing of CO2
pulmonary oedema - the lungs are in contact with low pressure atmosphere but blood / vasculature is under high pressure. hence by starlings forces, water moves out into the lungs.
what adaptations do free divers have?
can breath hold for longer periods of time
due to ability to become bradycardic to reduce O2 consumption, vasoconstriction to divert blood only to vital organs
