Hypobaric Flashcards
as you go up atmospheric pressure
decreases. (pp of oxygen also drops)
every 5500m the barometric (atmospheric pressure) falls by
half
big issue with altitude
reduction in oxygen availability
when you breath in you hudifiy the air the effect this has on oxygen partial pressure
reduces it (160-150mmHg)
inspired oxygen levels and alveoli oxygen levels
alveoli levels less as air already in lungs so fresh air is diluted
at higher altitudes you increase your
ventilation rate =
-so difference between alveoli and fresh air is lower
-
hypoxic
deficiency in amount of oxygen reaching tissues
pp of oxygen change around the body is around at sea level
60mmHg
100–>40 when it comes back to be reoxygenised at the lungs
at sea level at rest: Hb is ___ saturated with oxygen, when venous blood returns to the heart and enters pulmonary circulation Hb is __ saturated
97.5% –> 75%
So at rest body consumes 22.5% of the oxygen carried by Hb
At sea level: So at rest body consumes__% of the oxygen carried by Hb
22.5%
at 3000m at rest: alveolar pp of oxygen is ~60-65mmHg, Hb is __% saturated with Oxygen.
when venous blood returns to the heart and enters pulmonary circulation Hb is __ saturated
88% –> 65.5%
this equates to change of pp of oxygen of 60-33mmHg =27 mmHg
pp of oxygen change around the body is around at 3000m
60 -> 33 = 27 mmHg
the shape of oxygen-Hb curve helps _____ cals in arteriole Po2 at high altitude
minimise
early compensation and acclimatisation at high altitudes:
reduction in arteriol PO2–> stimulates peripheral chemoreceptors –> stimulates ventilation THIS HAS 3 IMMEDIATE EFFECTS
-over a few days -weeks acclimatisation takes places
stimulation of peripheral chemoreceptors –> stimulates ventilation;; 3 immediate effects:
- minimises difference in alveolar PO2 and atmospheric PO2
- hyperventilation leads to respiratory alkalosis (reduces effect on ventilation)
- increase in cardiac output
short term acclimatisation takes places at high altitudes =
- sustained higher ventilation rate (further reduction between alveolar and atmospheric PO2 and fall in PCO2)
- linked to decrease in pH (plasma back to 7.4) of cerebrospinal fluid & changes in sensitivity of peripheral chemoreceptors to hypoxia
- renal (kidney) compensations - reduced acid secretion, compensation for alkalosis
what does the renal compensation of early acclimatisation lead to
bicarbonate loss in the urine and diuresis. Correction of the alkalosis further stimulates ventilation
long term changes (acclimatisation)
- INCREASE IN HAEMATOCRIT
- -long term hypoxia leads to increase in the release of erythropoietin
- -stimulation of RBC production in bone marrow
- PULMONARY DIFFUSION CAPACITY
- increased capillary blood volume (increase SA of capillaries in lungs)
- -increase perfusion to upper regions of the lungs
- INCREASE IN TISSUE CAPILLARY DENSITY
- -angiogenesis in tissues, increasing SA for diffusion
- OXIDATIVE ENZYMES
- -stimualtion oxidative enzymes in mitochondria
problems with increasing haematocrit
increase viscosity of blood, its thicker
molecular basis of acclimatisation changes:
linked to stimulation of Hypoxia Induced Factors
- HIF-1alpha
- HIF-1beta
Acute mountain sickness linked to
-linked to rapid ascent in altitude
Acute mountain sickness: symptoms
- headache, nausea, anorexia, malaise, lack of energy, disturbed sleep, occasionally vomiting
- symptoms usually subside after 2-3 days
Acute mountain sickness: CAUSES
- increases in intracranial pressure
- -opposing effect–> hypoxia will increase cerebral blood flow, hypocapnia (lack of CO2) will reduce cerebral flow (balance)
- increase microvascular permeability linked to elevated plasma eicosanoids
Acute mountain sickness: Prevention
slow ascent to high altitude
- if altitude above 3000m u ascend 300m/day with rest days every 2/3 days
- use of acetazolamide (inhibit/reduce bicarbonate reabsorpment by the kidney)
Acute mountain sickness: TREATMENT
- descend from altitude
- take oxygen
- many remain at altitude for 2/3 days to see if symptoms subside
High altitude pulmonary oedema
- increase in blood pressure in the lungs due to excess water
- potentially lethal
High altitude pulmonary oedema: symptoms
someone who has had AMS symptoms for a few days 1 in 200 people
- -become breathless
- cough - dry then ‘frothy’ contains blood (damage of alveoli)
-tachycardia (abnormal HR)
High altitude pulmonary oedema causes:
increase in pulmonary arterial pressures, linked to pulmonary vasoconstriction
High altitude pulmonary oedema treatment
rapid descent from altitude
- adminitset oxygen
- possibly use nidefipine or phosphodiesterase inhibitors
High altitude cerebral oedema
-potentally lethal
-begins as severe AMS
-develops headaches and malaise progressing to ataxia, confusion, alters consciousness, coma
Cause: cerebral oedema (swelling in brain)
-treatment rapid descent
administer Oxygen
Genetic changes: Tibetans
mutations help prevent CMS and help adapt to high altitudes
Genetic changes: Tibetans 2 genes involved
- EPAS1 encodes HIF2𝛂 - Stimulates erythropoiesis alters iron homeostasis, metabolism and vascular permeability
- EGLN1 encodes prolyl hydroxylase domain-containing protein 2 (PHD2) – activity is dependent on oxygen levels.
Genetic changes: Tibetans genes at normal oxygen
PHD2 acts to breakdown HIF2𝛂 and prevents overproduction of haemoglobin
Genetic changes: Tibetans genes at hypoxia
PHD2 is inhibited, and then HIF2𝛂 levels rise and activates downstream responses.
