special situation - high altitude Flashcards

1
Q

which values both drop with increasing altitude?

A
  • atmospheric pressure

- PI02

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2
Q

what is the acute response to altitude ?

A
  • Low P02 stimulates peripheral chemoR exciting the carotid Bodies
  • leads to hyperventilation
  • hypocapnic and rise in pH
  • respiratory alkalosis
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3
Q

what effects does a respiratory alkalosis have?

A
  • slight fall in VE and the drive to breathe is reduced
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4
Q

what does a lower PaCO2 mean?

A
  • 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
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5
Q

why is hyperventilation important?

A
  • 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
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6
Q

what are the cardiovascular responses to acute hypoxia?

A
  • tachycardia graded
  • suppression of vagal tone
  • dilatation of vessels to increase flow to vascular beds
  • raised tissue perfusion –> splanchnic and coronary arteries
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7
Q

what occurs at cerebral vascular beds ?

A
  • vasoconstriction to hypocapnia
  • altitude induced hyperventilation
  • very responsive to Pac02
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8
Q

what are cerebral vessels less responsive to?

A
  • arterial levels of 02
  • moderate hypoxia–> little change
  • severe–> vasodilation (release of K, NO, adenosine)
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9
Q

what occurs at the lungs during acute hypoxia ?

A
  • 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
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10
Q

what are the symptoms ton acute mountain sickness ?

A

· Headache above 2500m and one of the following

  • Dizziness
  • Irritability
  • Vomiting
  • Nausea
  • Breathlessness
  • Insomnia
  • Fatigue
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11
Q

what is AMS brought on by ?

A

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

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12
Q

what are the chronic responses to exposure ?

A
  • adaptive and acclimatization phases
  • body compensates for low Pa02 and improves 02 delivery to tissues
  • hyperventilation increases again (VAH)
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13
Q

why does VAH occur again?

A
  • altered Ph (hypocapnic alkalosis is restored)
  • peripheral chemoreceptor sensitivity and NT releases increases with chronic exposure to hypoxia
  • carotid bodies increase in size
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14
Q

how is pH restored?

A

· 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
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15
Q

what does increasing 2,3-DPG production do?

A
  • 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
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16
Q

what are the effects of HIF activation ?

A
  • increased angiogenesis
  • EPO synthesis
  • increased carotid body sensitivity
  • hyperplasia, hypertrophy and more NT from carotid bodies
  • neovascularization
  • cell proliferate
  • glucose metabolism
17
Q

what are the effects of HIF on blood?

A
  • 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
18
Q

what is the consequence of increasing HCT?

A
  • leads to increased TPR and increases work load on the heart
19
Q

what happens to pulmonary diffusing capacity ?

A

· 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

20
Q

what happens to ECV?

A
  • decreases
  • fall in blood flow
  • redistribution in flow
  • reflex actions occurs due effect of Chemoreceptors -
  • kidneys -> increased salt and water excretion
21
Q

what is the tissue function during chronic hypoxia?

A

· 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

22
Q

what are the consequences of chronic mountain sickness ?

A

· 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.