Hypoxia Flashcards

1
Q

What is hypoxaemia?

A

Describes the blood environment - below 8 kPa can be considered to be hypoxaemia

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2
Q

What is hypoxia?

A

Describes the environment - PO2 in envrionment

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3
Q

What factors put the body under hypoxic stress?

A

Altitude - air has less o2 so starting point of oxygen cascade is lower
Disease
Exercise? - very short amount of time

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4
Q

What is barometric pressure?

A

Atmospheric pressure at a particular place

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5
Q

As altitude increases, what happens to the atmospheric (barometric) pressure?

A

As altitude increases, atmospheric pressure decreases.

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6
Q

What is the saturation and partial pressure of oxygen in the blood at the exchange surface?

A

75%

Partial pressure - 5.3kPa

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7
Q

What happens to the mean PO2 in alveolar space and arterial blood with age?

A

Decreases

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8
Q

What is the oxygen cascade?

A

The decreasing oxygen tension from inspired air to the respiring cells

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9
Q

What is the amount of gas that diffuses across a surface proportional to?

A
  • Surface area
  • Diffusion constant - e.g. CO2 diffuses faster than O2
  • Diffusion gradient
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10
Q

Describe the oxygen cascade - how does oxygen in the air/blood change along the circuit?

A
  • Start with 21.3 kPa of oxygen at atmospheric pressure
  • Oxygen displaced when air is humidified
  • Further down the airways air mixes with that which is preexisiting - bar can be moved UP (hyperventilation) or DOWN (hypoventilation)
  • No change between the alveolar air and the post-alveolar capillaries
  • Slight decrease between post-alveolar capillaries and arteries because of the bronchial drainage
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11
Q

How is oxygen transported in the blood?

A

free - 2%

bound to Hb - 98%

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12
Q

What factors affect the oxygen cascade?

A

1) Alveolar Ventilation
2) Ventilation/Perfusion Matching - if you are ventilating airways that are not perfused or hyper-perfused, you won’t achieve efficient gas exchange.
3) Diffusion Capacity - some disease can affect the parenchyma (the functional subunits - the alveolar capillary membranes) can become thickened and less exchange
4) Cardiac Output - if you increase cardiac output then you increase the amount of blood flowing through and getting the opportunity to oxygenate hence increasing oxygen delivery

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13
Q

What are the five challenges of altitude?

A
  • Hypoxia
  • Thermal stress: freezing cold and high-wind chill factor
  • Solar radiation: less atmospheric screening and reflection off snow
  • Hydration: water lost humidifying inhaled air and hypoxia induced diuresis
  • Dangerous: windy, unstable etc.
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14
Q

What are some innate/developmental adaptations to high altitude?

A
  • barrel chest: larger chest and bigger lungs, larger TLC, more alveoli and more capillaries
  • increased haematocrit: more RBCs due to chronic secretion of erythropoietin
  • larger heart: pulmonary vasculature constricts in response to hypoxia so you need a stronger right side of the heart to push blood through the increased resistance
  • increased mitochondrial density
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15
Q

What is chronic mountain sickness - cause, pathophysiology, symptoms, consequences and treatment?

A
  • LT adaptation in acclimatised individuals can cause CMS (Monge’s disease)
  • unknown cause
  • pathophysiology: secondary polycythaemia in response to hypoxia. RBCs are overproduced so increased haematocrit. Hence the viscosity of the blood increases.
  • symptoms: cyanosis
  • consequences: heart failure, death
  • treatment: move to lower altitude
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16
Q

What happens to barometric pressure as altitude increases and what does this mean?

A

Barometric pressure decreases with increasing altitude so there is a smaller PO2 and so the O2 cascade gradient is more shallow

17
Q

What is high altitude cerebral oedema - cause, pathophysiology, symptoms, consequences and treatment?

A
  • cause: rapid ascent or inability to acclimatise
  • pathophysiology: vasodilation of vessels in response to hypoxaemia. More blood to capillaries causes more fluid leakage. No space to cerebrum to expand and pressure in cranium increases
  • symptoms: confusion, ataxia, behavioural change, hallucinations and disorientation
  • consequences: irrational behaviour, irreversible neurological damage, coma and death
  • treatment: immediate descent, o2 therapy, hyperbaric o2 therapy, dexamethasone (corticosteroid)
18
Q

What is high altitude pulmonary oedema - cause, pathophysiology, symptoms, consequences and treatment?

A
  • causes: rapid ascent or inability to acclimatise
  • pathophysiology: vasoconstriction of pulmonary vessels in response to hypoxia which causes increased pulmonary pressure/permeability and more fluid leakage. This accumulates and it exceeds max rate of lymph drainage
  • symptoms: dyspnoea, dry cough, bloody sputum, crackling chest sounds
  • consequences: impaired gas exchange, impaired ventilation
  • treatment: descent, hyperbaric o2 therapy, nifedepine, salmeterol, slidenafil
19
Q

What is respiratory failure and what are the two main types?

A

Ineffective exchange of gas between lungs and blood.

1) Type 1: hypoxic respiratory failure. Aterial oxygen partial pressure less than 8
2) Type 2: Hypercapnic respiratory failure. Aterial carbon dioxide partial pressure greater than 6.7
3) Mixed respiratory failure (mixture of 1 and 2)

20
Q

What happens in type 1 and type 2 respiratory failure?

A

Type 1 - ventilation/perfusion mismatch in the lungs

Type 2 - hypoventilated lungs, inadequate gas exchange as alveolar air stagnate and concentration gradient is poor

21
Q

What problems can lead to Type 1 respiratory failure?

A

Pulmonary oedema
Pneumonia
Atelectasis

22
Q

What problems can lead to Type 2 respiratory failure?

A

Pulmonary fibrosis
Neuromuscular disease
Obesity
Increased physiological dead space

23
Q

What is acclimation?

A

Like acclimatisation but stimulated by an artificial environment e.g. breathing hypoxic gas. Recreational climbers for example take Acetazolamide - carbonic anhydrase inhibitor to accelerates slow renal compensation to hypoxic induced hyperventilation

24
Q

What is accommodation?

A

Rapid physiological change in response to a change in the oxygen environment

25
Q

What is acclimatisation?

A

Physiology becoming more efficient so you can obtain as much from the air as possible. PaO2 increases and PaCO2 decreases.

26
Q

What is hypobaric hypoxia?

A

When the body doesn’t have enough oxygen from the air and so tissues are not supplied with enough.

27
Q

What is the process of accomodation and acclimatisation?

A
  • Decrease in atmospheric O2 (hypobaric hypoxia)
  • Reduction in alveolar PO2
  • Less arterial PO2
    (- low arterial oxygen sensed in kidney so more erythropoetin and more RBC made and more oxygen loading)
  • Peripheral chemoreceptors activated
  • increase sympathetic activity
  • Hyperventilation
  • Increase alveolar PO2 and more loading
  • Increase in HR, contraction and CO (by sympathetic)
  • More ventilation means PACO2 decreases
  • Decrease in central drive to breathe (less in CSF)
  • less ventilation so less oxygen loading
  • higher pH so ODC shifts to the left
  • Less oxygen unloading
  • Alkalosis detected
  • Kidneys can correct this by secreting more HCO3- and H+.
  • ODC normalises
  • Oxygen loading increases
28
Q

What happens at a cellular levels when the oxygen loading is high (part of acclimatisation/accomodation)?

A
  • more oxidative enzymes
  • higher mitochondrial density
  • higher 2,3-DPG in RBC so ODC shifts to the right
29
Q

How does exercise lead to increased ventilation rate?

A

During exercise the amount of carbon dioxide produced increases. This leads to pH reduction. This mild acidosis and hypercapnia shift the ODC to the
right to improve oxygen unloading at the tissues. The increased PCO2 is detected by central chemoreceptors in the medulla that
increase the ventilation rate.

30
Q

Why is it important during ascent to slowly ascend?

A

To give

the body time to acclimatise

31
Q

What are the two initial physiological responses to hypobaric
hypoxia?

A
  • Renal compensation: bicarbonate excretion helps pH to return to normal and shifts the ODC into its normal
    position
  • Increased production of 2,3-DPG to improve oxygen unloading at the tissues
32
Q

What is a longer term adaptation to hypoxia?

A

Secondary erythrocytosis - chronic hypoxia is detected by cells in the kidneys and erythropoietin is secreted, so more RBCs Hence the oxygen-carrying capacity of the blood is also increased.

33
Q

What is VO2 max?

A

The total capacity to deliver oxygen to tissues.