Hypoxia Flashcards

1
Q

Hypobaric hypoxia= ?

A

low pressure hypoxia because even though the proportions are the same the amount of O2 is less

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2
Q

Hypoxia

A

Describes a specific environment, specifically PO2 in environment

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3
Q

Hypoxaemia

A

Describes the blood environment, specifically the PaO2

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4
Q

Ischaemia

A

Describes tissues receiving inadequate oxygen, e.g. forearm ischaemia

As a result of receiving hypoxaemic blood

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5
Q

Relationship between PaO2 and Age

A

Increase age= decrease PaO2

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6
Q

The O2 cascade describes?

Related to which law?

A

the decreasing oxygen tension from inspired air to respiring cells
O2 is most abundant when it’s in the air (keeps getting lower throughout the pathway of the body)

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

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7
Q

Fick’s law

What influences it?

A

“V Gas”= 𝐴/𝑇∙𝐷∙[𝑃1−𝑃2]

Structural diseases reduce A
Breathing hypoxic gas reduces P1-P2 gradient
Fluid in alveolar sacs increases T

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8
Q
Oxygen cascade summary graph draw
(slide 9, lecture 15)
Where is biggest proportion of O2 lost?
Impact of hyperventilation?
Second significant drop?
Dotted lines? Why don't O2 and CO2 change by same amount?
A

Mixing phase is where the biggest proportion of O2 is lost

Hyperventilation (not just breathing fast) increases the partial pressure O2 gradient and CO2 gradient with means more O2 can get in which increases PO2

Second significant drop= by the tissues (but depends on what they’re doing)

Dotted lines- where O2/ CO2 may go down/up during exercise, Amount O2 changes and CO2 changes is not equal because of the sigmoid shaped curve in O2 but linear shaped curve in CO2

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9
Q

Factors that can impede oxygen cascade+ explanation

A

Alveolar ventilation
V/Q matching
V/Q matching= Ventilation/ Perfusion mismatching, e.g. if there is a blockage in an airway which prevents air from getting there but blood is coming there then it doesn’t matter how much ventilation is occurring because it wont get to the gas exchange surface.

Diffusion capacity
Diffusion capacity: could be to do with gas or membrane (if membrane thickness increases then diffusion rate decreases)

Cardiac output
Cardiac output: heart needs to be good at delivering the blood with a higher conc of o2 to the tissues otherwise the pulmonary circulation is pointless

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10
Q

Impact of high altitude on oxygen cascade draw?

slide 10, lecture 15

A

smaller bars= at a high altitude, the O2 cascade is much more shallow plus you’re probably physically exerting yourself= harder to maintain homeostasis

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11
Q

Changes of high altitude

A

Hypoxia: Much less oxygen in the ambient air

Thermal stress: Freezing cold weather (-7 °C per 1000m), 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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12
Q

Accommodation and acclimatisation to high altitude

slide 14, lecture 15

A

PAO2= alveolar oxygen
PaO2= arterial oxygen
Decrease in the above two recognised by peripheral chemoreceptors (usually central chemoreceptors recognise increases in CO2 so this is a different mechanism)
Increases sympathetic activation= increase ventilation= increase alveolar oxygen= increase O2 loading into blood
Sympathetic activation also increases cardiac output through increase in HR+ Stroke Volume (Q) through increases in rate of conduction through the heart
Cardiac output increases throughput in lungs+ delivery to tissues
Ventilation comes at a cost though because PaCO2 decreases= decrease ventilation even though you were solving O2 issue
Loss in CO2=increase pH= changes oxygen dissociation curve to the left which increases affinity of O2 to Hb= decrease O2 unloading
Alkalosis detected by carotid bodies from high pH (same place as peripheral chemoreceptors) leading to kidney increasing H+ and increasing HCO3- excretion, takes longer time to do this but leads to increase O2 unloading.
Low O2 detected= increase erythropoietin secretion= increase RBC production= Increase O2 loading
Other changes= Increase oxidative exzymes= increase aerobic respiration before you move to anaerobic mechanism, also increase mitochondria which both lead to increase 2,3- DPG which gives right shift to ODC because conformational change= increase O2 unloading

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13
Q

Acclimation meaning

A

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

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14
Q

Prophylaxis= ?

Prophylaxis for high altitude

A

treating something before it happens

Acetazolamide

  • Carbonic anhydrase inhibitor – accelerates the slow renal compensation to hypoxia-induced hyperventilation
  • directly linked to turning CO2 into H2CO3 , so inhibition reduces initial alkalotic response to low oxygen
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15
Q

Native highlanders have specialised anatomical and physiological adaptations:

A

‘Barrel chest’ – larger TLC, more alveoli and greater capillarisation, More O2 into the body

Increased haematocrit – greater oxygen carrying-capacity of the blood, More O2 carried in blood

Larger heart to pump through vasoconstricted pulmonary circulation, Greater pulmonary perfusion

Increased mitochondrial density – greater oxygen utilisation at cellular level, More O2 utilised

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16
Q
Chronic mountain sickness
Causes
Pathophysiology
Symptoms
Consequences
Treatment
A

Causes: unknown

Pathophysiology: secondary polycythaemia (increase RBC number in response) increases blood viscosity, which sludges through systemic capillary beds impeding O2 delivery (despite more than adequate oxygenation)

Symptoms: cyanosis (purple at tips of fingers+ toes because not enough O2), fatigue

Consequences: ischaemic tissue damage, heart failure, eventual death

Treatment: no interventional medical treatment – sufferers are exiled to lower altitudes

17
Q
Acute mountain sickness
Causes
Pathophysiology
Symptoms
Consequences
Treatment
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 accumulation in the cranium which causes head compression)

Symptoms: nausea, vomiting, irritability, dizziness, insomnia, fatigue, and dyspnoea – ‘hangover’

Consequences: development into HAPE (High altitude pulmonary odema) or HACE (
Treatment: monitor symptoms, stop ascent, analgesia, fluids, medication (acetazolamide) or hyperbaric (high pressure) O2 therapy symptoms tend to subside after 48 hrs of increased renal compensation

18
Q
High altitude pulmonary oedema
Causes
Pathophysiology
Symptoms
Consequences
Treatment
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 (respiratory symptoms)

Consequences: impaired gas exchange, impaired ventilatory mechanics

Treatment: descent, hyperbaric O2 therapy, nifedipine (CCB), salmeterol (relaxes smooth muscle to help get the air in), sildenafil (viagra) (affects blood pressure)

19
Q
High altitude cerebral oedema
Causes
Pathophysiology
Symptoms
Consequences
Treatment
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 (not able to move very well) , behavioural change, hallucinations, disorientation (Impairs neurological function)

Consequences: irrational behaviour, irreversible neurological damage, coma, death

Treatment: immediate descent, O2 therapy, hyperbaric O2 therapy, dexamethasone

20
Q

Type I respiratory failure
Boundaries?
Description?
Causes?

A

Type I: Hypoxic respiratory failure, PaO2 < 8 kPa
PaCO2 = low/normal

Hypoventilation, V/Q mismatch, Diffusion abnormality

Causes: Pulmonary oedema, Pneumonia, Atelectasis
(Diffusion issue, but CO2 is more diffusible so it moves out fine but O2 can’t move in enough)

Not immediate danger but lungs aren’t working properly

21
Q

Respiratory failure NB

A

Respiratory failure is fundamentally a failure of pulmonary gas exchange, generally V/Q inequality (Not necessarily disease severity)

22
Q

Type II respiratory failure
Boundaries?
Description?
Causes?

A

Type II: Hypercapnic (high CO2) respiratory failure, PaO2< 8 kPa
PaCO2 > 6.7 kPa

Increased CO2 production, Decreased CO2 elimination

Causes: Decreased CNS drive, Increased work of breathing, Pulmonary fibrosis, Neuromuscular disease, Increased physiological dead space, Obesity

Problem of getting the gas there
Because O2 is usually moving down a greater conc gradient, usually means it’s a CO2 issue (can’t clear out as well)
Could also be a V/Q issue (a lot of the pulmonary vessels aren’t receiving blood flow

23
Q

SBAs at end of lecture 15, slide 26

A

If explanations needed go to Hypoxia lecture at 51.35