Altitude Flashcards
(32 cards)
What level of elevation defines ‘altitude’?
2500 m
Above what altitude is long term habitation impossible.
6000 m
Above what altitude would acute exposure lead to loss of consciousness
5500 m
What’s Everests peak altitude
8848 m
How many people live at altitudes pf more than 2500 m
100 million
List the problems associated with increasing altitude
- Barometric pressure declines exponentially
- Temp declines 1 deg C every 150 m
- Reduced relative humidity (fluid loss)
- Increased solar radiation (reduces cloud cover)
What’s Dalton’s law. Give the equation for PAO2
Dalton’s law states that the total pressure of a mixture of gases is equal to the sum of the partial pressures of the gases in the mixture.
Therefore,
PAO2 = PB x FiO2
So as PB decreases with altitude, PaO2 decreases too.
How is the PaO2 affected by altitude
Alveolar gas equation
PA = FIO2 (PB - PH20) - PaCO2/R
Reduced alveolar PAO2 leads to hypoxic hypoxia
How is saturated vapour pressure changed by altitude?
It remains unchanged –> 6.3 kPa at 37 deg C
PA = FIO2 (PB - PH20) - PaCO2/R
PH20 - saturated vapour pressure of water is unchanged at altitude 6.3 kPa. Therefore it has a relatively greater effect at altitude.
At what altitude are physiological changes observed? Why do physiological changes not occur below this altitude. And which systems are involved
> 2500
At this altitude the PaO2 falls below 8 kPa which is the THRESHOLD FOR ACTIVATION of the PERIPHERAL CHEMORECEPTORS
RSP, CVS, Haem, Renal
Summarise the acute and chronic physiological response to altitude
Acute adaptation aims to increase PaO2 by hyperventilation and is limited by respiratory alkalosis.
Chronic adaptation permits hyperventilation as the kidneys correct the pH disturbance.
What is the ‘Braking effect’ with regard to the acute physiological response to altitude?
Peripheral chemoreceptors sense PaO2 < 8 kPa
–> hyperventilation
Hyperventilation –>
- Low PaCO2
- High pH
Low PaCO2 sensed by central chemoreceptors
–> Limits hyperventilation
High pH sensed by carotid bodies
–> Limits hyperventilation
This limitation on hyperventilation by the central and peripheral chemoreceptors is known as the braking effect
What is the mechanism for chronic physiological adaptation to altitude, i.e. what removes the braking effect
Previously thought:
–> Over a few days, kidneys excrete excess HCO3- reducing alkalosis and permitting more hyperventilation to compensate for low PaO2.
Now:
–> recent studies show that braking effect is decreased before renal HCO3- excretion begins. So now it is believed that the CSF HCO3- is reduced by another mechanism not yet elucidated.
Is there a diffusion limitation at altitude? Describe the mechanism.
Under certain circumstances: with exercise and/or High Altitude Pulmonary Edema
Exercise reduces transit of blood past alveoli. As O2 conc gradient is lower, O2 diffusion may not complete prior to RBC completing pass of alveoli.
HAPE –> Increased interstitial fluid thickens the alveolar-capillary barrier.
Summarise the acute and chronic RESP response to altitude
Low PaO2 < 8.0 –> peripheral chemoreceptor driven hyperventilation + respiratory alkalosis. Low PaCO2 (central chemoreceptors) + High pH (peripheral chemoreceptors) –> braking effect on hyperventilation.
Over time, first BBB (unknown mechanism) and then kidneys excrete additional HCO3- to mitigate the braking effect and allow for further hyperventilation and chronic adaptation to altitude (low PaO2)
Summarise the CVS response to altitude
- Increased HR (SNS response to low PaO@)
- Reduced plasma volume (Hct increases 20%)
- -> low PaO2 –> SNS –> Increase CO and increased GFR (pressure diuresis)
- -> Hyperventilation + Reduced relative humidity –> increased insensible losses. - Increased myocardial work
- -> Increased blood viscosity (Hct 0.6) increases LV work - Hypoxic Pulmonary Vasoconstriction
- -> HAPE (Hydrostatic Pressure increased)
- -> Acute RHF
What are the mechanisms for reduced plasma volume at altitude
Low PaO2 –> SNS –> increased CO –> increased GFR and RPP –> Pressure diuresis
Also
Hyperventilation combined with reduced relative humidity at altitude increases insensible fluid losses from lungs.
Describe the changes to the oxygen haemoglobin dissociation curve that occur at altitude
Initially
P50 shifts to the left due to respiratory alkalosis
Thereafter, (over 7 days)
RBC’s produce increased 2.3 DPG returning P50 rightward
How is the red cell mass affected by altitude
Chronic hypoxia at altitude (over hours) kidney responds by increasing EPO secretion stimulating bone marrow to produce erythrocytes
How does the VTE risk differ at altitude
Thrombosis is more likely at altitude due to increased blood viscosity and hypoxic platelet activation
Describe and classify the body’s response to chronic exposure to a cold environment
Heat conservation
- Peripheral vasoconstriction
- Decreased sweating
- Behavioural change (clothing)
Heat production
- Increased BMR
- Shivering
- Increased brown fat activity
All heat generating mechanism consume O2 at a time of relative hypoxeamia
Summarise the haematological changes to altitude
- OHDC P50 initially left from resp. alk and then right RBCs make more 2.3 DPG (7 days)
- EPO from kidney to low PaO2 – hours
- Increased thrombosis risk (viscosity and plt activation with low PaO2)
Define acute high-altitude illness
Maladaptive physiological response to high altitude, occurring in unacclimatised individuals who ascend too quickly
Define and describe the three high altitude syndromes?
Acute Mountain Sickness (AMS)
- Headache +
—> Nausea / Dizziness / Anorexia / Insomnia
Rx: Remain at same altitude 3 - 4 days
High Altitude Cerebral Edema (HACE) - Headache + ---> Ataxia / Severe Cognitive Impairment (Can result in seizures / coma / death) Rx: Descent
High Altitude Pulmonary Edema (HAPE)
- Exertional dyspnoea and persistent dry cough
–> then haemoptysis and orthopnoea
–> Most serious accounting for most mortality
Rx: Descent
