hypoxia Flashcards

1
Q

hypoxia

A

specific env and ste of conditions

specifically PO2 in the env

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2
Q

hypoxaemia

A

describes the blood env

PaO2

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3
Q

Ischemia

A

tissue receiving inadequate oxygen eg forearm ischemia

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4
Q

Factors that cause hypoxic stress on the body

A

altitude
exercise - but physiological response is efficient so not experienced- more O2 is supplied
disease - COPD

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5
Q

what is the O2 cascade

A

describes the decreasing O2 tension from inspired air to respiring cells ]
ambient air - highest PO2
reduction in upper airway - humidification
biggest loss in alveoli - mixing - have tio ventilate
small loss in arteries for bronchiole drainage
big loss in tissues - O2 diffusion
vol perfusion matching
cardiac output
thickness of membrane

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6
Q

factors affecting the O2 cascade

A

o2 therapy increase start PO2
breathing inhaled air decrease start
hyperventilation - reduce affect of mixing - faster
hypoventilation exacerbate mixing
diffusioin affect reduce PO2 in post alv cap
exercise reduce PO2 in tissue - diffusion, increase PCO2

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7
Q

PCO2 and PO2 in O2 cascade

A

changes are not same
O2 - sigmoid shape
CO2 - linear change

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8
Q

Oxygen cascade on Everest

A

lower starting PO2

gradient less to work with

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9
Q

Fick’s law

A
of diffusion 
flow rate proportional to pressure grad 
Vgas = area/thickness * diffusibility * PP grad 
structural disease reduce area
fluid in alveoli - increase thickness
hypoxic gas reduce PP grad 
hyperoxic gas increase PP grad
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10
Q

Gas transport change at altitude

A

boiling point inversely proportional to altitude
need pressurised suit at high altitude - allow breathe and stop body fluids evaporating
hypoxia - less O2 in the air
thermal stress: -7degrees for 1000m, wind chill
solar radiation- sun and reflection
hydration - water lost humidifying inspired air - hypoxia induced diuresis - breathe dry air
hypoxia induced confusion and miscoordination

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11
Q

Oxygen dissociation curve

A

how much O2 bidn is dependant on PP

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12
Q

Type 1 resp failure

A
failure of pul gas exchange 
V/Q inequality
hypoxic 
O2 into blood impaired
CO2 out - fine because it is more diffusible 
PaO2<8KPa 
PaCO2 - low/normal 
hypoventilation 
diffusion abnormality 
pul oedema 
pneumonia 
atelectasis - collapse or closure of the lung - worse GE
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13
Q

Type 2 resp failure

A
hypercapnic resp failure 
getting gas there problem
V/Q problem 
PaO2<8KPa - low but not really the problem - O2 down greater conc grad so fine 
PaCO2 >6.7KPa 
increased CO2 production 
decreased VCO2 elimination 
decreased CNS drive 
increased work of breathing 
pul fibrosis 
neuromuscular disease 
increased physiological dead space
obesity
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14
Q

good Physiological response to high altitude

A
low atm O2 
reduced PAO2 
reduced PaO2 
activation peripheral chemoreceptors - carotid bodies 
increase sympathetic outflow 
increase vent 
reduce PaCO2 
increase PH 
alkalosis detected by carotid body 
increase HCO3 excretion 
ODC normalises 
increased O2 unloading
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15
Q

good ‘side effects’ of physiological response to attitude

A

increased symp outflow =
increased HR and Flow
increased O2 loading

increased vent =
increased PAO2
increased O2 loading

decreased PaO2 = 
increased erythropoietin 
increased erythropoiesis 
increased O2 loading 
increased ox loading
increase oxidsative enzymes
small increase in 2,3-DPG in RBC 
right shift ODC 
increase O2 unloading 
increase O2 utilisation
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16
Q

bad ‘side effects’ of physiological response to altitude

A

reduced PaCO2 =
loss of central drive to breathe
reduced vent
reduced O2 loading

increased pH =
left shift ODC
decrease O2 unloading

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17
Q

Prophylaxis of altitude treatment

A

acclimation - from artificial exposure to the environment
acetazolamide - carbonic anhydrase inhibitor, accelerate the slow renal compensation to hypoxia induced ventilation - reduce initial alkolytic response

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18
Q

Innate developments to prevent altitude sickness

A

barrel chest - larger TLC and capillarisation - more O2 in
increased haematocrit (vol % RBC in blood) - greater O2 carrying capacity - more O2 carried
larger heart to pump through vasoconstricted circulation - greater perfusion
increased mitochondrial density - greater oxygen utilisation at cellular level - more O2 used
because of exposure through childhood and genetics
not all expressed in all populations

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19
Q

Chronic mountain sickness

A

Monge’s disease
acclimatised people spontaneously acquire chronic mountain sickness
cause unknown

20
Q

pathophysiology of chronic mountain sickness

A

secondary polycythaemia - increase blood viscosity (haematocrit is increased)
sludge through cap beds- impede O2 delivery

21
Q

symptoms of c nmountain sickness

A

cyanosis

fatigue

22
Q

consequences of c mountain sickness

A

ischemic tissue damage
heart failure
eventual death

23
Q

treatment

A

no interventional treatment

forced to go down the hill

24
Q

causes of acute mountain sickness

A

maladaptation to high altitude env

recent ascent- onset in 24 hours - last a week

25
pathophysiology of a mountain sickness
associated with mild cerebral oedema | fluid accumulate in the cranium
26
symptoms of a mountain sickness
``` nausea vomiting irritability dizziness insomnia fatigue dyspnoea disappear after 48hours of increased kidney compensation ```
27
consequences of a mountain sickness
development to high altitude pul oedema | development to high altitude cerebral oedema
28
treatment of a mountain sickness
``` monitor symptoms stop ascent analgesia - pain killer acetazolamide hyperbaric O2 therapy ```
29
cause of High altitude pulmonary oedema
rapid ascent | inability to acclimatise
30
pathophysiology of high alt oedema
vasoconstriction pul vessels -response to hypoxia increased pul pressure increased fluid leakage from caps fluid accumulates - when exceed max lymph drainage
31
symptom of high alt oedema
dyspnoea dry cough bloody sputum crackling chest sounds
32
consequences of high alt pul oedema
impaired GE and ventilatory mechanics
33
treatment of high alt pul oedema
``` descent hyperbariac O2 therapy nifedipine - Ca channel blocker - vasodilate pul cic salmeterol - relax airway sm sildenafil - affect Bp ```
34
cause of high altitude cerebral oedema
rapid ascent | inability to acclimatise
35
pathophysiology of high alt cer oedema
vasodilation of vessels - hypoxia more blood to cap - increased leakage cranium in sealed box -cant expand intracranial pressure increases
36
symptoms of high alt cer oedema
``` confusion ataxia - stumbling behaviourala change hallucinations disorientation - confusion - middle ear ```
37
consequences of hugh alt cer oedema
irrational behaviour irreversible neuro damage coma death
38
treatment of high alt cer oedema
immediate decent O2 therapy hyperbaric O2 therapy dexamethasone
39
H0w can we hold our breath for along time
wet suit - protect form the cold external environment hyperventilate with O2 - move the blackout and CO2 threshold cold water over face - slows breathing and heart rate
40
how do you calculate a persons total blood vol
``` 5l/70kg = 71ml/kg 71*weight = vol of blood ```
41
how do you calculate the amount of Hb in the blood
multiply Hb conc in g/L against blood vol in L
42
how do you calculate cardiac output from ESV and ejection fraction
ESV/(100-EF) = SV | SV - ESV
43
stages of acclimatisation to high altitude
``` low atmospheric O2 reduced PAO2 reduced PaO2 hypoxia detected by carotid bodies increased vent increased PAO2 reduced PACO2 increased PaO2 reduced PaCO2 reduced [H+] increased pH pH imbalance detected by carotid bodies increased HCO3- excretion via the kidneys increased H+ and reduced pH ```
44
blood gases after 2 weeks at altitude
pH - unchanged- kidneys will have compensated by now PCO2 - low - reduced because of increased ventilation BE low PO2 low
45
maximum altitude for permanent human residence
5500m
46
oxygen transport - partial pressure
age related decline in lung func | tissue use a lot of O2 - PP wise