special situation - high altitude Flashcards
which values both drop with increasing altitude?
- atmospheric pressure
- PI02
what is the acute response to altitude ?
- Low P02 stimulates peripheral chemoR exciting the carotid Bodies
- leads to hyperventilation
- hypocapnic and rise in pH
- respiratory alkalosis
what effects does a respiratory alkalosis have?
- slight fall in VE and the drive to breathe is reduced
what does a lower PaCO2 mean?
- reduced drive to breathe
- shifts 02 dissociation curve to the left increasing affinity for Hb reduced unloading
- drives periodic breathing (cheynes-strokes respiration)
- periods of apnoea
- it is the hypoxia In combination with hypocapnia which leads to this pattern
why is hyperventilation important?
- explained via alveolar gas equation
- x2 it reduces the PAco2 by a half
- also reduces the PaCo2
- increased PA02 from 6.75–> 10kpa
- increased PA02 whilst not changing the PI02
- increased diffusion gradient
what are the cardiovascular responses to acute hypoxia?
- tachycardia graded
- suppression of vagal tone
- dilatation of vessels to increase flow to vascular beds
- raised tissue perfusion –> splanchnic and coronary arteries
what occurs at cerebral vascular beds ?
- vasoconstriction to hypocapnia
- altitude induced hyperventilation
- very responsive to Pac02
what are cerebral vessels less responsive to?
- arterial levels of 02
- moderate hypoxia–> little change
- severe–> vasodilation (release of K, NO, adenosine)
what occurs at the lungs during acute hypoxia ?
- hypoxic vasoconstriction of pulmonary vessels (HPV)
- intrinsic mechanisms and endothelial control
- diversion of blood from areas of lower VE to those richer in 02
- ensures matching of V/Q
- widespread HPV
- chronic HPV is related to endothelial effects
what are the symptoms ton acute mountain sickness ?
· Headache above 2500m and one of the following
- Dizziness
- Irritability
- Vomiting
- Nausea
- Breathlessness
- Insomnia
- Fatigue
what is AMS brought on by ?
1) Cerebral oedema
Dilation of cerebral arterioles in severe hypoxia (increases capillary filtration pressure), hypoxia-induced increased permeability of capillaries
2) Pulmonary oedema / in alveoli
Uneven hypoxic vasoconstriction of P vessels (HPV), increased cap permeability –> protein leakage
what are the chronic responses to exposure ?
- adaptive and acclimatization phases
- body compensates for low Pa02 and improves 02 delivery to tissues
- hyperventilation increases again (VAH)
why does VAH occur again?
- altered Ph (hypocapnic alkalosis is restored)
- peripheral chemoreceptor sensitivity and NT releases increases with chronic exposure to hypoxia
- carotid bodies increase in size
how is pH restored?
· Cerebral Ph is restored, pH of CSF decreases (central chemoreceptors become activated again, so brake removed)
· Decreased reabsorption of HC03- and decreased H+ secretion in urine restores plasma pH (again increases responsiveness of central CR)
- Metabolic compensation for resp alkalosis is 2-3 weeks
- this counteracts the R alkalosis and offsets inhibition of central and peripheral chemoR
what does increasing 2,3-DPG production do?
- allows us to increase 02 delivery around the body
- right shift on the 02 dissociation curve
- increased delivery to peripheral respiring tissues
- decreased 02 affinity and therefore a greater proportion of 02 in blood
what are the effects of HIF activation ?
- increased angiogenesis
- EPO synthesis
- increased carotid body sensitivity
- hyperplasia, hypertrophy and more NT from carotid bodies
- neovascularization
- cell proliferate
- glucose metabolism
what are the effects of HIF on blood?
- increased EPO from kidney
- increased RBC (polycythaemia)
- period of chronic hypoxia
- increase in Hb
- increased o2 carrying capacity
- carrying more 02 for that lower pa02
- increased HCT
- 02 content restored to normal
what is the consequence of increasing HCT?
- leads to increased TPR and increases work load on the heart
what happens to pulmonary diffusing capacity ?
· Increases by up to 3x
· More pulmonary capillaries are open–> more taking part in GE
· High capacity circulation
· Increased P capillary blood volume (mobilization)
· Greater SA ensuring all alveoli involved in GE
what happens to ECV?
- decreases
- fall in blood flow
- redistribution in flow
- reflex actions occurs due effect of Chemoreceptors -
- kidneys -> increased salt and water excretion
what is the tissue function during chronic hypoxia?
· Redistribute blood where it needs to be even at lower ABP
· Hypoxia stimulates increased capillarity (angiogenesis)
· Improves 02 transfer
· Increased cytochrome oxidase activty
· Mitochondria utilize o2 more effectively
· Increased myoglobin content in skeletal muscle
· Raises reserve store of 02, HIF mediated
what are the consequences of chronic mountain sickness ?
· Prolonged stay at alt
· Compensatory responses start to fail
· VE falls again -> dyspnoea and cyanosis
· CVS cant keep up with delivery of 02 to tissue
· Further increases in pulmonary pressure over time
· Big increase in HCT . 60% –> congestive right sided heart failure -> increased pulmonary pressure and after-load / left sided? Due to HCT too.
