15 Hypoxia Flashcards

1
Q

Q: What is the difference between hypoxia and hypoxaemia? What does ischaemia describe?

A

A: hypoxia describes a specific environment (Specifically the PO2 in that environment) eg less than 8kPa

hypoxaemia describes the blood environment (Specifically the PaO2)

Describes tissues receiving inadequate oxygen e.g. forearm ischaemia

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2
Q

Q: What factors can put the body under hypoxic stress? (2) What can the body do in hypoxic circumstances? why?

A

A: -altitude
-disease
(-exercise can make us transiently hypoxic but body really quickly handles it- get oxygen debt)

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

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3
Q

Q: How will the oxygen dissociation curve change with increasing or decreasing the number of red blood vessels available? What can change it in a different way?

A

A: stretch graph up and down (if stretch up= get same saturation with less oxygen content)

side to side is changed by affinity changes

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4
Q

Q: What’s the oxygen cascade? What does a law state? 3 factors? Eqn?

A

A: describes the decreasing oxygen tension from inspired air to respiring cells

Ficks law of diffusion states that flow rate is proportional to the pressure gradient

  • Hypoxic stress/Inspiring hypoxic gas = – diffusion gradient ([P1 - P2])
  • Structural disease = – area (A)
  • Fluid in the alveolar sacks increases this thickness (T)

……………A
Vgas = — x D x [P1 - P2]
…………….T

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5
Q
Q: O2 cascade. What can affect ambient air? (2) 
Upper airway air? 
Alveolar air? (3)
Post alveolar capillaries?
Arteries?
Tissues? (2)
Veins? (2)
A

A: -humid air will decrease pO2
-O2 therapy will increase => 21.3kPa

-as it’s breathed in, mixed with water (humidification -> decrease pO2 slightly) => 20Kpa

  • mixes with air already there so pO2 decreases
  • hypoventilation would decrease more
  • hyperventilation would increase pO2 => 13.5kPa
  • same pO2 unless diffusion defect = causes decreases value (eg increased thickness or less SA)
  • following bronchial drainage (keeps airways alive) => 13.3kPa
  • oxygen utilisation and diffusion so pO2 decreases
  • more decrease with exercise

-could be 5.3 or 1.3kPa

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6
Q

Q: What are the 4 main factors of the oxygen cascade?

A

A: Alveolar ventilation
V/Q matching (ventilation/perfusion- are parts of lung ventilated also perfused)
Diffusion capacity
Cardiac output

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7
Q

Q: How is the oxygen cascade affected if you were on everest? What is the big change that everest gives? 2 other examples.

A

A: big hit on the pO2 actually available in first place

increase in pressure

  1. Eustace and Baumgarter wore pressurised suits to allow them to breathe (provided a viable pressure gradient) and to stop their bodily fluids from boiling
  2. Airplanes are pressurised to about 2000 m
    ‘Oxygen masks will fall in case of depressurisation’
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8
Q

Q: What changes with increasing altitude? therefore? (2)

A

A: Barometric pressure decreases with increasing altitude

Therefore a smaller P(I)O2 (inspired) and hence a shallower O2 cascade gradient

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9
Q

Q: Imagine that we built a teleportation device that could transport us to the summit of Everest. Assuming we had some warm clothing, what would happen to us if we went directly there in less than a second? (2)

What do climbers need?

A

A: Within one minute we’d be unconscious due to hypoxia
Within two minutes we’d be dead from oxygen starvation

Climbers will often use supplemental oxygen to make the ascent easier (not easy)

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10
Q

Q: What are the 5 changes of high altitude?

A

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 protection from it)
Less atmospheric screening
Reflection off snow

Hydration (we get dehydrated)
Water lost humidifying inspired air so we don’t damage our lungs
Hypoxia induced diuresis

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

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11
Q

Q:

A

A: 1. decreased atmospheric O2 due to hypobaric hypoxia
2. less P(A)O2 (alveolar) -> less P(a)O2 (arterial)

  1. activates peripheral chemoreceptors (in carotid bodies and aortic arch) -> increases activity of SNS
  2. more SNS activity-> increases ventilation -> increase P(A)PO2 and O2 increase loading
  3. more SNS activity-> increase HR and increase force of contraction -> increases CO -> increase O2 loading
  4. more ventilation (hyperv) from more SNS activity -> decreases P(a)CO2 -> less CO2 in CSF-> decreased central drive to breathe -> decreases ventilation -> decreases O2 loading
  5. decrease in P(a)CO2 -> lose acid from body -> increase pH -> leftwards shift of ODC= increases affinity of Hb to oxygen = decreases O2 loading
  6. alkalosis is detected by carotid bodies -> increased HCO3- excretion -> increases H+ in blood -> corrects ODC -> increases O2 loading

from 2 -> 9. kidneys detect -> increases erythropoeitin amount -> increase RBC production/maturation by bone marrow -> increase haematocrit-> increase O2 loading

CELLULAR LEVEL

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12
Q

Q:

A

A: at cellular level

  • increased oxidative E -> increases O2 utilisation
  • increased mitochondrial density -> increases O2 utilisation
  • small increase in 2,3-DPG-> rightwards shift of ODC-> increased O2 unloading
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13
Q

Q: Prophylaxis of going to high altitudes. (2)

A

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

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

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14
Q

Q: How does Acetazolamide work?

A

A: CO2 via carbonic anhydrase -> increased HCO3- -> binds with free H+ -> causes pH to rise

said drug = carbonic anhydrase inhibitor -> slows down that process-> accelerates the slow renal compensation to hypoxia-induced hyperventilation

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15
Q

Q: Innate development adaptations. Who has them? List 4. Include the consequence of each one.

A

A: Native highlanders

‘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

Q: What is chronic mountain sickness? Cause? Pathophysiology? Symptoms? (2) Consequences? (3) Treatment?

A

A: (Sometimes these long-term adaptations can become problematic)

Acclimatised individuals can spontaneously acquire chronic mountain sinckness (Monge’s disease)

Causes: unknown

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

Symptoms: cyanosis, fatigue

Consequences: ischaemic tissue damage, heart failure, eventual death

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

17
Q

Q: Define polycythaemia.

A

A: abnormally increased concentration of haemoglobin in the blood, either through reduction of plasma volume or increase in red cell numbers

18
Q

Q: What can cause acute mountain sickness AMS? Usually associated with? Pathophysiology? Symptoms? Consequences?

A

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

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

Consequences: development into HAPE or HACE (high altitude cerebral or pulmonary oedema)

19
Q

Q: What’s the treatment for acute mountain sickness? When do symptoms subside?

A

A: Treatment: monitor symptoms, stop ascent, analgesia (pain relief), fluids, medication (acetazolamide) or hyperbaric O2 therapy (breathing high concentration O2 under pressure)

symptoms tend to subside after 48 hrs of increased renal compensation

20
Q

Q: What is HACE? Cause? (2) Pathophysiology? Consequences?

A

A: High altitude cerebral oedema

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 and since cranium is a ‘sealed box’ – no room to expand so intracranial pressure increases

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

21
Q

Q: What are the symptoms of HACE? Treatment?

A

A: Symptoms: confusion, ataxia, behavioural change, hallucinations, disorientation

Treatment: immediate descent, O2 therapy, hyperbaric O2 therapy, dexamethasone (corticosteroid-> help alleviate some pressure in head), osmotic diuretic eg manitol

22
Q

Q: What is HAPE? Cause? (2) Pathophysiology? Consequences?

A

A: high altitude pulmonary oedema

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

Consequences: impaired gas exchange, impaired ventilatory mechanics

23
Q

Q: HAPE symptoms? Treatment?

A

A: Symptoms: dyspnoea, dry cough, bloody sputum, crackling chest sounds

Treatment: descent, hyperbaric O2 therapy, nifedipine (Calc Channel Blocker-> aids vasodilation), salmeterol, sildenafil

24
Q

Q: Compare HAPE and HACE.

A

A: HACE is to do with increasing constriction (related to pressure) while HAPE is to do with leakiness (less to do with pressure)

25
Q

Q: Define respiratory failure. Not necessarily? Types?

A

A: fundamentally a failure of pulmonary gas exchange, generally V/Q inequality (ventilation/perfusion) (Not necessarily disease severity)

type I (hypoxic) and II (hypercapnic)

26
Q

Q: Type I respiratory failure. What is it related to? PaO2? PaCO2? Pathophysiology. (4) 3 causes.

A

A: Hypoxic respiratory failure (related to movement from gas airways into blood: alveocapillary border- difficulty moving O2 in)

PaO2 < 8 kPa
PaCO2 = low/normal (no issues in its movement)

could be caused by air way or vessel block
Hypoventilation
V/Q mismatch
Diffusion abnormality

Pulmonary oedema
Pneumonia- fluid in lungs
Atelectasis- collapse of lung

27
Q

Q: Type II respiratory failure. PaO2? PaCO2? Pathophysiology? (2) Causes. (7)

A

A: Hypercapnic respiratory failure (ventilation issue)
PaO2 < 8 kPa = low
PaCO2 > 6.7 kPa = high

Increased CO2 production
Decreased CO2 elimination

Decreased CNS drive
Increased work of breathing
Pulmonary fibrosis
Neuromuscular disease
Increased physiological dead space
Obesity- lots of excess tissue and weight-> difficult for respiratory muscles to work
bronchoconstriction