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Respiratory System > Hypoxia > Flashcards

Hypoxia Flashcards

1
Q

What is meant by hypoxia

A

Describes a specific
environment
Specifically the PO2 in that environment

Hypoxia is a set of conditions and all the conditions of the person

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2
Q

What is meant by hypoxaemia

A

Describes the blood environment

Specifically the PaO2

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3
Q

What is meant by ischaemia

A

Describes tissues receiving inadequate oxygen

e.g. forearm ischaemia

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4
Q

What factors can put the body under hypoxic stress

A

Hypoxic stress: can be brought on by altitude, exercise and disease e.g. COPD

Transient hypoxic state in exercise is well dealt with in healthy individuals, but may be dangerous in unhealthy individuals.

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5
Q

How can the body respond to hypoxic stress

A

The body can adapt and compensate for hypoxic circumstances to maintain oxygen delivery

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6
Q

How does the PaO2 reaching the tissues change with age

A

It decreases with every decade

Mean PO2 in the alveolar space and in the arterial blood decreases with age as seen in the chart

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7
Q

Summarise oxygen transport

A

§ PO2 drops further into the lungs as mixing and humidification occurs.
§ The bronchial drainage (circulation) adds to the return of blood to the heart making the blood reduce from 100% saturation to 97% saturation.

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8
Q

Summarise the oxygen dissociation curve

A

§ A range of partial pressures at levels of saturation of oxygen in the blood.
§ Blue line represents shifts due to increased metabolism (e.g. exercise).
o Increase acidity, hypercapnia, 2,3-DPG production etc.
§ P50 line indicates how much loading/unloading is occurring in the haemoglobin on different curves.

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9
Q

What does the oxygen cascade describe

A

The O2 cascade describes the decreasing oxygen tension from inspired air to respiring cells

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10
Q

What does Fick’s law of diffusion state

A

Fick’s law of diffusion states that flow rate is proportional to the pressure gradient

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11
Q

What can impact Fick’s law in the lungs

A

Structural disease reduces this area
Fluid in the alveolar sacks increases this thickness
Breathing hypoxic gas reduces this gradient
All reducing the oxygen gradient

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12
Q

Describe the oxygen cascade

A

You start with 21.3kPa of oxygen at atmospheric pressure and as you go down the levels, the kPa reduces
humidification reduces the partial pressure to 20.0kPa in the upper airways
mixing reduces the partial pressure to 13.5kPa
There is then NO CHANGE between the alveolar air and post-alveolar capillaries.
Partial pressure decreases to 13.3kPa in the arteries due to bronchial drainage
the oxygen is then utilised (a-vO2 difference)
partial pressure decreases to 5.3kPa in tissues and veins

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13
Q

Describe what can alter the oxygen cascade

A

O2 therapy increases the partial pressure of oxygen in the ambient air, humid air decreases this
Hyperventilation increases the partial pressure in the alveoli, hypoventilation reduces this pressure
Partial pressure in the post-alveolar capillaries can decrease if there is a diffusion defect (Fick’s law)- less efficient diffusion
exercise decreases the partial pressure of oxygen and veins (as it is respired more) and thus the difference between arterial and venous PO2 increases and more oxygen is delivered to the tissues.

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14
Q

Describe the challenges to the oxygen cascade

A

Alveolar ventilation: Hyperventilation increases partial pressure in alveoli- increasing diffusion. Hypoventilation reduces this

V/Q matching- blockage in the respiratory tree- no air, but blood there, then no diffusion, lower PO2 in blood. If heart is working with the lungs it will send less blood to areas where no ventilation is taking place

Diffusion capacity (see factors affecting Fick’s law)

Cardiac output- adequate Q to move blood to the tissues- if not high enough, less blood delivered to tissues- lower pressure gradient

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15
Q

What is the role of unbound oxygen

A

The unbound oxygen (dissolved, not bound to iron) doesn’t deliver oxygen but conducts responses to hypoxaemia.

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16
Q

What happens when you breathe hypoxic air

A

If you are breathing hypoxic air, all the levels simply reduce
harder to maintain homeostasis

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17
Q

Describe consequences of a changing environment

A

Originally thought to be impossible to reach the summit of Everest without supplemental oxygen.
We now know this is just about our limit

Even breathing unpressurised 100% O2 is inadequate to maintain arterial saturation

Airplanes are pressurised to about 2000 m
‘Oxygen masks will fall in case of depressurisation

Boiling point is inversely proportional to altitude. ‘You can’t make a good cup of tea on Everest’

Eustace and Baumgarter wore pressurised suits to allow them to breathe (provided a viable pressure gradient) and to stop their bodily fluids from boiling

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18
Q

What is the Armstrong limit

A 
Armstrong limit (H2O boils at 37°C)
Boiling point is inversely proportional to altitude 
Around 20000m
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19
Q

Describe the challenges of high altitude

A

Hypoxia
Much less oxygen in the ambient air

Thermal stress
Freezing cold weather (-7 °C per 1000 m)
High wind-chill factor

Solar radiation
Less atmospheric screening
Reflection off snow

Hydration
Water lost humidifying inspired air
Hypoxia induced diuresis

Dangerous
Windy, unstable terrain, hypoxia-induced confusion and malcoordination

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20
Q

Outline the response to high altitude

A

Still 21% O2 but the partial pressure of oxygen decreases in the alveoli and arteries (stimulating erythropoiesis, increasing O2 loading)
this activates peripheral chemoreceptors (as opposed to central control using CO2)

increased SNS outflow increases ventilation to increase alveolar oxygen and oxygen loading, as well as increasing HR and Q- also increasing O2 loading

Hyperventilation leads to hypocapnia, reducing central drive to breathe, reducing ventilation and hence oxygen loading
pH increases, shifting the ODC to the left (less O2 unloading- opposite of bohr shift)

Alkalosis produced by increased pH detected by carotid bodies, increasing bicarbonate secretion (and causing kidneys recover/save/manufacture acid) to normalise ODC and increasing oxygen unloading (H+ increases)

21
Q

What are the other responses to high altitude

A

oxidative enzyme/mitochondrial numbers increase to allow for greater oxygen utilisation to produce energy; small 2,3-DPG increase, causing shift to right and increased oxygen unloading

22
Q

What is meant by accommodation

A

acute responses involving a rapid physiological change in response to a change in the oxygen environment.

23
Q

What is meant by acclimatisaiton

A

physiology becomes more efficient to get as much O2 out of the air as possible (a more gradual change).
o PaO2 increases while PaCO2 falls.

24
Q

What is meant by acclimation

A

Like acclimatisation but stimulated by an artificial environment (e.g. hypobaric chamber or breathing hypoxic gas

25
Q

What is meant by hypobaric hypoxia

A

Low PaO2 stimulates ventilation to increase PaO2 which is called hypobaric hypoxia.

26
Q

What is the role of acetazolamide

A

Carbonic anhydrase inhibitor – accelerates the slow renal compensation to hypoxia-induced hyperventilation

27
Q

Describe prophylactic treatments for altitude

A

rophylaxis treatments include:
o Acclimation – artificial acclimatisation (e.g. hypobaric chamber).
o Acetazolamide – carbonic anhydrase inhibitor which will accelerate renal compensation to hypoxia-induced hyperventilation.

28
Q

Describe the innate/developmental adaptations to high altitude seen in native highlanders

A

‘Barrel chest’ – larger TLC, more alveoli and greater capillarisation- get more oxygen in

Increased haematocrit – greater oxygen carrying-capacity of the blood- more oxygen carried

Larger heart to pump through vasoconstricted pulmonary circulation- greater pulmonary perfusion

Increased mitochondrial density – greater oxygen utilisation at cellular level

29
Q

Are these adaptations universally seen

A

These are general adaptations and not necessarily displayed in all high-altitude populations – ethnic/genetic differences?

30
Q

Essentially, what happens in chronic mountain sickness

A

The mechanisms that help individuals to adapt to high altitudes become overactive- impossible to survive at that altitude.
Acclimatised individuals can spontaneously acquire chronic mountain sickness (Monge’s disease)

31
Q

Summarise chronic mountain sickness

A

Causes: unknown
Pathophysiology: secondary polycythaemia increases blood viscosity, which sludges through systemic capillary beds impeding O2 delivery (despite more than adequate oxygenation- it is harder to pump more viscous blood at a higher pressure to get it to reach capillary beds)
Symptoms: cyanosis, fatigue- oxygen supply issue
Consequences: ischaemic tissue damage, heart failure, eventual death
Treatment: no interventional medical treatment – sufferers are exiled to lower altitudes

32
Q

Summarise acute mountain sickness

A

Causes: maladaptation to the high-altitude environment. Usually associated with recent ascent - onset within 24 hours and can last more than a week
Pathophysiology: probably associated with a mild cerebral oedema (fluid builds up- compressing the cranium)
Symptoms: nausea, vomiting, irritability, dizziness, insomnia, fatigue, and dyspnoea – ‘hangover’
Consequences: development into HAPE or HACE
Treatment: monitor symptoms, stop ascent, analgesia, fluids, medication (acetazolamide) or hyperbaric O2 therapy symptoms tend to subside after 48 hrs of increased renal compensation

33
Q

How can acute mountain sickness be prevented

A

Slower ascent- to allow physiological responses to high altitude to develop.

34
Q

What happens in High altitude pulmonary oedema

A

Pulmonary arterioles vasoconstrict in response to hypoxia- unlike vasodilation in the rest of the body
Higher hydrostatic pressure- more fluid leakage

35
Q

Summarise high altitude pulmonary oedema

A

Causes: rapid ascent or inability to acclimatise
Pathophysiology: vasoconstriction of pulmonary vessels in response to hypoxia increased pulmonary pressure, permeability and fluid leakage from capillaries fluid accumulates once production exceeds the maximum rate of lymph drainage
Symptoms: dyspnoea, dry cough, bloody sputum, crackling chest sounds
Consequences: impaired gas exchange, impaired ventilatory mechanics
Treatment: descent, hyperbaric O2 therapy, nifedipine (CCB), salmeterol (dilate the airways, more air in), sildenafil ( Viagra, reduces BP)
All cause vasodilation by a viariet of mechanisms- increasing the chance of a successful outcome

36
Q

What is key to remember about HACE

A

Easier to observe from the 3rd person

Denial is the first symptom.

37
Q

Summarise HACE

A

Causes: rapid ascent or inability to acclimatise
Pathophysiology: vasodilation of vessels in response to hypoxaemia (to increase blood flow) more blood going into the capillaries increases fluid leakage cranium is a ‘sealed box’ – no room to expand so intracranial pressure increases
Symptoms: confusion, ataxia, behavioural change, hallucinations, disorientation
Consequences: irrational behaviour, irreversible neurological damage, coma, death
Treatment: immediate descent (sometimes not feasible), O2 therapy, hyperbaric O2 therapy, dexamethasone (anti-inflammatory)

38
Q

Describe the dive reflex

A

Cold water hitting face

reduces heart rate and oxygen consumption

39
Q

What happens with hyperventilation at 10% oxygen

A

Threshold for CO2 increases (can hold breath longer before fainting)
but O2 threshold for blackout decreases

40
Q

How many types of respiratory failure are there

A

3

41
Q

What is meant by respiratory failure

A

Respiratory failure is fundamentally a failure of pulmonary gas exchange, generally V/Q inequality (Not necessarily disease severity)
PaO2< 8kPa- subdivided into type 1 or 2 depending on PaCO2 level
Rarely occurs in isolation
In initial stages of lung disease- body maintains adequate oxygenation by adapting to increased ventilatory demand
However, as the underlying disease progresses, ventilatory workload can become excessive- resulting in failure to oxygenate blood adequately and to remove CO2.

42
Q

Describe Type 1 respiratory failure

A

Hypoxic
respiratory failure PaO2 < 8 kPa
PaCO2 = low/normal (CO2 more diffusible and so is fine)

Due to:
Hypoventilation
V/Q mismatch
Diffusion abnormality- fluid in lungs- O2 moves less

Caused by: 
Pulmonary oedema
Pneumonia
Atelectasis (partial collapse or incomplete inflation)
P.E
43
Q

Describe type 2 respiratory failure

A

Getting the gas there problem, could be a V/Q mismatch- no blood flow- no gas getting into blood

Hypercapnic respiratory failure PaO2 < 8 kPa
PaCO2 > 6.7 kPa

Increased CO2 production- lungs don’t respond to exercise
Decreased CO2 elimination

Decreased CNS drive
Increased work of breathing
Pulmonary fibrosis
Neuromuscular disease
Increased physiological dead space
Obesity
44
Q

What happens in T2RF

A

Ventillatory drive is insufficient
The work of breathing is excessive
The lungs cannot pump air in or out effectively

Often an acute exacerbation of COPD- increases the work of breathing (when they are already hypercapnic and hypoxaemic)
acute on chronic respiratory failure.

45
Q

Why is breathing high pressure oxygen for a sustained period not advisable

A

Central drive to breathe is reduced
Despite hyperbaric oxygen reducing the sensitivity of peripheral chemoreceptors, it is unlikely to affect the central proton-sensitive mechanisms.

46
Q

What can decrease SvO2

A

Cold weather
Reduces O2 requirement (after non-shivering thermogenesis has stopped leading to hypothermia)
therefore less oxygen is extracted from blood

47
Q

What is routinely used as an index of tissue perfusion in ventilated critical patients

A

SvO2

Used as a reliable index of O2 extraction- assuming O2 delivery is adequate

48
Q

What is the most sensitive indicator of ischaemia

A

plasma lactate

produced during anaerobic respiration- which only occurs in tissues receiving inadequate blood supply.

Respiratory System (23 decks)

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