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Monday 5th February 2018
Systemic Hypoxia
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Systemic hypoxia = low partial pressure (PaO2) of oxygen in arterial blood
Normal PaO2 = 98mmHg
o Normal level of O2 in arterial blood (a means arterial)
Hypoxia – PaO2 < 60mmHg
o When looking at relationship between amount of O2 carried by haemoglobin at
different partial pressures; 60mmHg just about on down slope of O2/haem
dissociation curve
 So this is when things become critical; just a small reduction of O2 in lungs
gives big affect on O2 in blood
When does hypoxia occur?
o High altitude (low atmospheric pressure)
 So there is a low partial pressure of O2 in atmosphere so there’s a low level
of O2 in lungs therefore reduction of O2 in arterial blood
o Low O2 concentration in environment
 Could happen in miners or someone who goes caving (can be occupational
hazard)
o During a long dive
 Long time under water, can’t breathe in air, O2 you use up more & more
depleted
o Respiratory disease (most common!)
 Usually chronic (long term)
 Alternatively, acute means short-lasting event
 Inadequate ventilation (ability to breathe in and out) or exchange of O2
(exchange surfaces thickened)
Sometimes hypoxia occurs during treatment
o When patient is anaesthetised (acute event bc require surgery)
 General anaesthetic (GA) sometimes given w/ sedative  depressed
ventilation
 General anaesthetic may also be given muscle relaxant  relaxes all skeletal
muscles in body (reduce muscle tone)
 Requires pump ventilation
o Relaxing skeletal muscle means relaxing respiratory muscle,
so patient can’t ventilate themselves
 Makes surgery treatment easier e
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relaxes jaw; not tense
 O2 supply may be inadequate during pump ventilation
o Shouldn’t happen but does
o General anaesthetic depresses ventilation so patient may
have higher O2 consumption than usual
o Or something may go wrong; gas supply switched off or
tube gets kinked

Local effects of hypoxia:
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Hypoxic blood has blue tinge to it; known as cyanosis
Cyanosis  lips, mucosal membranes etc become blue tinged

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o Can also be seen in white of eyes and fingers (nail beds)
Easy for dentist to notice these bc they look at lips & mucosal membranes
o Most sensitive markers of hypoxia bc lots of blood vessels very close to surface
Heart
o When hypoxic blood circulation to/through heart it depresses SAN (decreases heart
rate)
o Also depresses force of contraction ; depresses contractility of ventricular muscle
o local effects on pacemaker activity & cardiac muscle cells sensitivity to Ca2+
 so… heart is good indicator of hypoxia
 bradycardia indicates hypoxia
Brain – cerebral circulation
o Blood vessels v sensitive to hypoxia
o When level of blood O2 going to brain decreases (particularly below 60mmHg)
 Vessels dilate (local effect on arterioles)
 Graded w/ severity of hypoxia (if it goes from 60mmHg to 50 to 40; you will
get increasingly pronounced vasodilatation in brain)
 Helpful bc reduction in resistance in cerebral circulation helps
increase O2 in blood flow to brain
o Remember brain critically dependent on O2
o Neuronal tissue can’t undergo anaerobic metabolism
Pulmonary circulation
o In systemic circulation; brain is most sensitive to hypoxia
o But ALL blood from RV (right ventricles) going to lungs  lungs are sensitive to
hypoxia
o Hypoxia makes pulmonary vessels constrict (opposite of what it does in systemic
circulation)
 Arteriolar vasoconstriction
o When localised to PART of the lungs; vasoconstriction = beneficial
 Redistributes blood flow to better ventilated areas

Image: shows 2 schematics of alveoli with air coming in & out
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o Left shows healthy alveoli
o Right shows badly ventilated alveolus
 Maybe mucus in opening
 Maybe fluid in opening

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Not being circulated properly so there is a low O2 level in alveolus bc
not properly ventilated or at ventilated at all
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 Arteriole & venous blood vessels constrict
 Vascular smooth muscle in lungs different to cerebral circulation; it
constricts when local environmental pO2 low
 Consequence is that it raises pulmonary vascular resistance
o Normally much lower than systemic vascular resistance
(about 1/7th of systemic)
o Vasoconstriction throughout lungs pushes resistance of
pulmonary circulation up
 RV blood has nowhere to go except lungs; so
constriction of all lungs pushes pressure ALL through
pulmonary circulation will rise (pulmonary artery,
veins, capillaries etc)
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 Hydrostatic pressure is a force that makes
fluid filter out capillaries
o So widespread vasoconstriction in
hypoxia increases fluid filtration out
of pulmonary capillaries and causes
oedema (accumulation of fluid in
interstitial spaces first then
eventually pushes into alveoli)
o Any expansion of interstitial space
or filling alveoli with fluid is
detrimental to gaseous exchange bc
increases diffusion distances
between air & capillary blood
 Gives person rattling cough
which also makes it harder
to breathe bc trying to
expand an airway that’s
filled w/ water
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Increasing vascular resistance also increases workload of
right ventricle (RV)
 Normally LV wall is thick bc systemic circ has high
resistance; RV usually thin walled bc normally
pumping against low resistance
 So increasing RV work which not built for
 Eventually leads to right ventricular heart
failure
 Long lasting vasoconstriction leads to heart
failure
 Acutely; hypoxic vasoconstriction in a
patient isn’t good bc increases likelihood of
oedema forming;
o If they already have any hypoxia &
you give them GA, you risk hypoxia
getting worse & sending them into
RV heart failure
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Peripheral chemoreceptors stimulated (aka increase in afferent activity) by decrease in PaO2
(basically hypoxia)
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 2 sites to sense O2
Also sensitive to levels of CO2 in arterial blood (increase) & levels of pH (decrease)
o Dr Thomas
When blood hypoxic; increases (NTS) afferent activity up to medulla
o Homeostatically regulate PaO2 by changing respiration
 You would expect… When o2 levels down, increase in respiration to get
more O2 into alveoli therefore blood BUT changes in respiration affect the
CVS so
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Also constricting all tissues in
body therefore reducing amount of O2 to muscles, kidneys,
gut etc
 Conserving their use of O2 so more available to go
up to brain (where sympathetic vasoconstriction is
minimal)
o This superimposed upon local effects of hypoxia;
 Local effects=
 Heart rate goes down
 Depressed contractility
 Cerebral vasodilatation
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Pulmonary constriction
o So actually… reflex & local effects working together;
reducing amount of O2 consumed by heart
 Sympathetic vasoconstriction in body as a whole
making more O2 available for brain where there is
cerebral vasodilatation; helps improve O2 supply to
brain but patient remains hypoxic
 These are helping in situation where can’t
take more O2 onboard
 There will still be pulmonary
vasoconstriction bc nothing to alleviate level
of O2 in lungs bc this person cannot
hyperventilate
Work done by heart is limited by reflex & local effects but pulmonary
vasoconstriction leads to pulmonary oedema
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o Local affects of hypoxia are the same
 HR down
 Depresses contractility

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Cerebral vasodilatation
Pulmonary vasoconstriction

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OVERALL:
o Increase in respiration able to restore PaO2 up towards normoxia (homeostatic/
normal)
 Homeostatic mechanism that chemoreceptors trigger does actually happen
o Blood less hypoxic in someone who can ventilate
o Mechanisms ensure when respiration goes up, HR increases
 HR increase helps increase CO (cardiac output)
 Additional O2 supplied to brain bc sent there by cerebral dilatation
and away from other tissues & organs
o So… reflex effects on heart overcome local effects on heart
o Because person now hyperventilation; pulmonary hypoxic vasoconstriction less
severe bc now bringing more O2 into alveoli
o People who are hypoxic with respiratory disease but can ventilate called PINK
PUFFERS (can keep O2 levels high enough to stay pink but only do it by puffing)

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Blue bloater
o Swollen ankles
o Ascites (abnormal accumulation of fluid in peritoneal/ abdominal cavity)
o Rattily chest bc congestion on lungs
o Blue-ish around mouth
Pink puffer
o Hyperventilating bc ribcage higher
o Pink colour

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