Respiratory Systems 13 - Hypoxia Flashcards

1
Q

Define hypoxia

A

A specific environment with low O2

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2
Q

Define hypoxaemia

A

A description of the PaO2 in the bloodstream

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3
Q

Define ischaemia

A

Tissuesrecieving inadequate oxygen

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4
Q

Define the oxygen cascade

A
  • The decreasing oxygen tension from inspired air to respiring cells
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5
Q

Summarise the oxygen cascade

A
  • PO2 decreases as gas moves from the ambient air to alveoli to the arteries, tissues and veins
  • The greatest differences in PO2 are between upper airway and alveoli, and between arteries and veins due to exchange at tissues
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6
Q

Why does the oxygen cascade occur? What affects it?

A
  • Due to diffusion capacity of the tissue

- Affected by hyper- and hypoventillation

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7
Q

How does CO2 change throughout the oxygen cascade?

A
  • There is little difference in PCO2 levels from upper airway to the arteries
  • increase in tissues and in air
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8
Q

How does the oxygen cascade change in exercise?

A

The PO2 is lower in each location

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9
Q

List the challenges of high altitude.

A
  • Hypoxia
  • Thermal stress (wind chill factor)
  • Solar radiation (reflection off snow and less atmospheric screening)
  • Hydration (water is lost humidifying inspired air, with induced diuresis)
  • Dangerous (windy, confusion due to hypoxia)
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10
Q

Describe the process of accommodation and acclimatisation at high altitude

A
  • Low PAO2 and PaO2 activates peripheral chemoreceptors to increase sympathetic outflow (increased heart rate/blood flow leads to increased O2 loading)
  • Also increased erythropoietin production and RBC production
  • Increased ventillation, PaCO2 decreases. pH increases
  • Alkalosis detected by carotid bodies, resulting in increased H+ in blood and increased HCO2- excretion
  • ODC normalises
  • High pH causes leftwards shift of ODC so haemoglobin holds on to O2
  • As PaCO2 decreases, central drive to breathe decreases and there is less O2 loading
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11
Q

Define prophylaxis

A

Treatment given or action taken to prevent disease

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12
Q

Define acclimation

A

This is similar to acclimatisation but is stimulated by an artificial environment

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13
Q

What drugs can be used to treat altitude sickness?

A

Acetazolamide, a carbonic anhydrase inhibitor which accelerates slow renal compensation to hypoxia induced hyperventilation

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14
Q

What innate adaptations do native highlanders have?

A
  • Barrel chest (larger TLC, more alveoli more capillaries)
  • Increased haematocrit
  • Larger heart
  • Increased mitochondrial density (greater oxygen utilisation at cellular level)
  • Not present in all high-altitude populations
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15
Q

What is chronic mountain sickness? Describe the pathophysiology and symptoms

A
  • Where acclimatised individuals spontaneously acquire mountain sickness
  • Due to secondary polycythaemia increasing blood viscosity which impedes O2 delivery
  • Symptoms include cyanosis and fatigue
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16
Q

List the consequences of chronic mountain sickness.

A

Ischaemic tissue damage, heart failure, death

17
Q

List the possible treatments for mountain sickness

A

No medical treatment - people must descend to lower altitudes

18
Q

Describe the cause of acute mountain sickness

A
  • Caused by maladaptation to the high-altitude environment, associated with recent ascent
  • Occurs within 24 hours and can last over a week.
19
Q

Describe the pathophysiology of acute mountain sickness

A

Associated with mild cerebral oedema

20
Q

List the symptoms of acute mountain sickness

A
  • Nausea
  • Vomiting
  • Irritability
  • Dizziness
  • Fatigue
  • Dyspnoea
21
Q

List the consequences of acute mountain sickness

A

Development into high altitude pulmonary oedema or high altitude cerebral oedema

22
Q

List the treatments for acute mountain sickness

A
  • Monitor symptoms
  • Stop ascent
  • Analgesia (medication to reduce pain)
  • Azetazolamide or hyperbaric O2 therapy
23
Q

List the causes of high altitude pulmonary oedema

A

Rapid ascent or inability to acclimatise

24
Q

Describe the pathophysiology of high altitude pulmonary oedema

A
  • Vasoconstriction of pulmonary vessels in response to hypoxia
  • Increased pulmonary pressure, permiability and fluid leakage from capillaries
  • Fluid accumulates when lymph production exceeds maximum rate of lymph drainage
25
Q

List the symptoms of high altitude pulmonary oedema

A
  • Dyspnoea
  • Dry cough
  • Bloody sputum
  • Crackling chest sounds
26
Q

List the consequences of high altitude pulmonary oedema

A
  • Impaired gas exchange

- Impaired ventilatory mechanics

27
Q

List the treatments for high altitude pulmonary oedema

A
  • Descent
  • Hyperbaric O2 therapy
  • Nifedipine
  • Salmeterol
  • Sildenafil (viagra)
28
Q

List the causes of high altitude cerebral oedema

A

Rapid ascent/inability to acclimatise

29
Q

Describe the pathophysiology of high altitude cerebral oedema

A
  • 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
30
Q

List the symptoms of high altitude cerebral oedema

A
  • Confusion
  • Ataxia
  • Behavioural change
  • Hallucinations
  • Disorientation
31
Q

List the consequences of high altitude cerebral oedema

A
  • Irrational behaviour
  • Irreversible neurological damage
  • Coma
  • Death
32
Q

List the treatments for high altitude cerebral oedema

A
  • Immediate descent
  • O2 therapy
  • Hyperbaric O2 therapy
  • Dexamethasone
33
Q

Define respiratory failure

A

A failure of pulmonary gas exchange, generally a V/Q inequality

34
Q

What is type 1 respiratory failure?

A
  • Hypoxic respiratory failure
  • PaO2 < 8kPa
  • PaCO2 is low/normal
35
Q

List the causes of type 1 respiratory failure

A
  • Hypoventilation
  • Diffusion abnormality
  • Pulmonary oedema
  • Pneumonia
  • Atelactasis
  • Mismatching V/Q
36
Q

What is type 2 respiratory failure?

A
  • Hypercapnic respiratory failure
  • PaO2 < 8 kPa
  • PaCO2 > 6.7 kPa
37
Q

List the causes of type 2 respiratory failure.

A
  • Increased CO2 production and decreased CO2 elimination
  • Decreased CNS drive
  • Increased work of breathing
  • Pulmonary fibrosis
  • Neuromuscular disease
  • Increased physiological dead space
  • Obesity