Physiology of high altitude Flashcards
Describe the ventilatory response associated with hypoxia.
Hypoxia = increased ventilation (due to hypoxia detectors in carotid bodies)
- hypoxia-driven hyperventilation is partially antagonised by the more powerful depression of ventilation –> due to excess blow-off of CO2 which therefore leads to alkalosis at chemoreceptors
- the ventilatory response is inadequate to cope with low pO2 and a degree of hypoxaemia and hypoxia results
- hypoxic drive is only significant with low pO2 (~60mmHg) together with high pCO2
Why can rapid ascent (when climbing) worsen hypoxaemia and lead to pulmonary arterial hypertension?
Rapid ascent = stimulation of sympathetic NS
- results in increased HR, CO and BP
- ppO2 is alveoli is low therefore pulmonary circulation reacts to hypoxia with vasoconstriction
- this worsens hypoxaemia and increases pulmonary resistance which leads to pulmonary arterial hypertension
How long does it take to acclimatise to:
a. 2000m
b. 2000-6000m
a. rapid (1-2 days)
b. few weeks (if no resp. disease)
How would an individual feel at:
a. 6000m
b. >7000m
c. >7500m
a. feel well, reasonable appetite, normal sleep, can carry 20-25kg
b. significant hypoxia, increased tiredness, continuous exercise is impossible
c. DEATH ZONE: severe hypoxia, will last 2-3 days
Explain the mechanism of acclimatisation.
- Metabolic acidosis: retention of acid and increased excretion of HCO3-
- increased erythrocyte number (haematocrit)
- Reduced pulmonary vascular resistance
Describe the physiological changes that occur during acclimatisation.
- Low pO2: increased rate + depth of breathing –> blow off excess CO2
- results in respiratory alkalosis
- high pH inhibits central chemoreceptors leading to reduced breathing rate = hypoxaemia - Kidneys increase the excretion of HCO3- + acid retention leading to metabolic acidosis
- this counteracts the respiratory alkalosis
- restoration of pH and therefore drive to central chemoreceptors is restored
- sustained increase in rate and depth of breathing - Hypoxaemia stimulates interstitial cells in the kidney leading to increased EPO
- increased haematocrit and O2 carrying capacity of the blood
- increased haematocrit = increased viscosity = increased pulmonary vascular resistance = pulmonary arterial hypertension and right heart failure - reduced hypoxic vasoconstriction and collateral circulations (due to NO production) = reduced pulmonary vascular resistance
What illnesses/conditions can occur with high altitudes?
- Acute mountain sickness (AMS) - 1st sign something is wrong
- High altitude cerebral oedema (HACE) - follows AMs if not treated
- High altitude pulmonary oedema (HAPE) - pulmonary condition that follows AMS
What are the S+S of AMS?
- headache (essential component)
- poor sleep
- N+V
- dizziness
- tiredness
Socred 0-3 by severity; >3 = AMS; occurs around 5000m (can occur at 2500m)
What is the treatment for AMS?
Mild = rest (no further ascent) More severe: 1. immediate descent 2. O2 3. Acetazolamide (250mg x 3 daily) 4. Dexamethasone (4mg x4 daily) - oral/IV
How can AMS be prevented?
- slow ascent
- avoid unnecessary exercise
- acetazolamide (250mg x 2 daily)
Explain the MOA of acetazolamide/diamox.
- CA inhibitor
- increases HCO3- excretion = metabolic acidosis
- will counteract/compensate for respiratory alkalosis
- speeds up acclimatisation
NET EFFECT of diamox/acetazolamide:
- HCO3- and Na+ lost in the urine
- urine is alkaline and blood is more acidic
- can also inhibit Ca in RBCs –> reduced CO2 in lungs –> reduced loss of CO2 = counteracts excessive CO2 loss from hyperventilation
Explain how bicarbonate is reabsorbed by the kidneys.
- Blood —CO2—> PCT cells
(HCO3- + H+ CO2 + H2O) - H+ are ejected into tubular lumen by Na+/H+ exchange ATPase
- -> Na+ reabsorbed from tubular fluid + H+ ejected; HCO3- collects in cells - Excreted H+ reacts with HCO3- (HCO3- + H+ CO2 + H2O)
- CO2 diffuses back into tubule cells (converted to carbonic acid)
- -> HCO3- is reabsorbed from the tubular lumen into tubular cells - H2CO3- –CA–> HCO3- + H+ (inside tubular cell)
- -> H+ is pumped OUT - continue reabsorption cycle
- -> HCO3- moves from tubular cells into the blood
What are the S+S of HACE?
- Ataxia
- N+V
- Hallucination/disorientation
- Reduced consciousness
- Coma
- Confusion
How can HACE be treated?
- Descent and O2 (2-4 L/min)
- 48mg of dexamethasone (1st dose) and then 4mg every 6 hours
- Hyperbaric/portable altitude chamber (increase ppO2 to improve oxygenation and reduce vasoconstriction)
- Acetazolamide (reduce CSF formation and reduced ICP)
- -> every 12 hours
What are the S+S of HAPE?
- reduced exercise tolerance
- blood stained sputum
- crackles on auscultation of chest
- dry cough
- dyspnoea
