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Respiratory System > 15. Hypoxia > Flashcards

15. Hypoxia Flashcards

1
Q

What is the difference between hypoxia, hypoxaemia and ischaemia?

A
  • Hypoxia - low PO2 in a specific environment
  • Hypoxaemia - low PO2 in blood (below 8 kPa)
  • Ischaemia - tissues receiving inadequate oxygen
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2
Q

Which 2 factors can put your body under hypoxic stress?

A
  • Disease e.g. COPD

* Altitude

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3
Q

What is ambient air?

A

(• atmospheric air in its natural state)
• 21.3 kPa
• 20.9% of total atmospheric pressure

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4
Q

As altitude increases, what happens to barometric and partial pressure?

A
  • Barometric pressure - decreases
  • Partial pressure - decreases

(due to Dalton’s Law)

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5
Q

What is polycythaemia?

A
  • Abnormally increased concentration of haemoglobin in the blood
  • Due to reduction in plasma volume or increase in red cell numbers
  • Increases the ODC
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6
Q

What is the oxygen cascade?

A

• Describes decreasing oxygen tension from inspired air to respiring cells
• Start with 21.3 kPa - ambient air
• Lost of oxygen during:
- humidification
- mixing in alveoli (or gain in hyperventilation)
- dilution by bronchial drainage in the arteries
- tissues
• Alveolar air = post-alveolar capilaries

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7
Q

What 3 factors is the diffusion of gas across a membrane proportional to?

A
  • SA
  • Diffusion constant (CO2 diffuses faster than O2)
  • Diffusion gradient
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8
Q

What is the artery and vein PO2?

A
  • Artery - 13.3 kPa

* Vein - 5.3 kPa

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9
Q

What is the drop in PaO2 from the arteries to the tissues associated with?

A

• Not directly keeping you alive
• Associated with a big unloading of haemoglobin
- which is associated with a lot more oxygen
• Therefore, the change in PaO2 is needed to facilitate the unloading of haemoglobin

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10
Q

What 4 factors influence the oxygen cascade?

A
  • Alveolar Ventilation
  • Ventilation/perfusion matching - for efficient gas exchange
  • Diffusion capacity - some diseases can thicken the parenchyma
  • Cardiac output - increased CO, more blood oxygenated
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11
Q

What does the oxygen cascade look like if you’re breathing hypoxic air?

A
  • PO2 of ambient air is much lower

* Therefore ever other section is lower, reducing exercise capacity

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12
Q

Describe the graph showing the proportion of energy source for performing maximal exercise for a given amount of time

A
  • Logarithmic time scale
  • 10 seconds uses ATP and ATP-Phosphocreatine
  • Lactic acid peaks before 60 seconds
  • Longer than 60 seconds - aerobic
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13
Q

What is VO2 max?

A
  • Total capacity to deliver oxygen to tissues

* Dependent on ventilation and cardiac output

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14
Q

Why is prolonged anaerobic respiration bad?

A
  • Produces lactic acid
  • Dissociates into lactate- and H+
  • Lower pH
  • Active site on enzymes affected
  • Impedes glycolytic enzymes for aerobic energy production
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15
Q

Describe the ventilation-time graph during exercise?

A
  • Need 40L/min to meet metabolic demand
  • Lag - body doesn’t achieve this straight away (oxygen deficit)
  • Rapid rise => steady rise => supply matches demand
  • Finished exercise - continue to breathe at a greater rate to repay the oxygen debt (excess post-exercise oxygen consumption)
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16
Q

Apart from heavy breathing, where else does the energy come from after exercise to repay oxygen debt?

A

• Stored energy

  • intramuscular ATP
  • phosphocreatine
  • myoglobin (holding onto O2, ready to release it)
17
Q

How does breathing change during exercise?

A

• Breathing rate increases from 12-20
• Ventilation increases, then becomes stable - increasing tidal VOLUME is more efficient at increasing ventilation than increasing respiratory RATE
• Tidal volume reaches a limit (can’t match vital capacity)
- respiratory rate starts to increase
- due to energy efficiency

18
Q

What are the 5 challenges of altitude?

A
  • Hypoxia
  • Thermal stress
  • Solar radiation
  • Hydration (water used to humidify air, hypoxia induced diuresis)
  • Dangerous (hypoxia-induced confusion)
19
Q

What is accommodation and acclimatisation?

A
  • Accommodation - (acute) physiological change in response to a change in the oxygen environment
  • Acclimatisation - physiology becomes more efficient in a changed environment
20
Q

What happens to the blood gases during acclimatisation?

A

• PaO2 increases
• PaCO2 falls
• Attributed to:
- renal compensation for respiratory alkalaemia
- slow increasing ventilatory sensitivity to hypoxia

21
Q

Where is erythropoietin mainly secreted from?

A

Renal cortex

22
Q

What is hypobaric hypoxia and how is it overcome?

A
  • Low PaO2 (due to low air pressure and air density)
  • Ventilation stimulated to increase PAO2
  • Increased diffusion gradient to allow more oxygen into the blood
23
Q

What is the prophylaxis for high altitude?

A

(Action taken to prevent disease)
• Acetazolamide (carbonic anhydrase inhibitor)
- less bicarbonate to accept protons
- triggers an increase in the slow renal response (compensation to hypoxia-induced hyperventilation)

24
Q

What is acclimation?

A
  • Like acclimatisation

* Stimulated by an artificial environment

25
Q

What are 4 of the innate/developmental adaptations to high altitudes?

A
  • Barrel chest - increased lung SA, larger TLC
  • Increase haematocrit - chronic secretion of erythropoietin
  • Larger heart (right ventricular hypertrophy) - due to the constriction of pulmonary vasculature from hypoxia (stronger heart needed to increase pulmonary perfusion)
  • Increased mitochondrial density - more O2 utilised
26
Q

What is the pathophysiology of chronic mountain sickness (Monge’s disease)?

A

• Secondary polycythaemia, which increases blood viscosity

  • impedes O2 delivery
  • despite adequate oxygenation
27
Q

What are the symptoms, consequences and treatments for chronic mountain sickness?

A

Symptoms
• Cyanosis
• Fatigue (from decreased capillary confusion)

Consequences
• Ischaemic tissue damage
• Heart failure
• Eventual death

Treatment
• Sufferers exiled to lower altitudes

28
Q

What is the cause and pathophysiology of acute mountain sickness?

A

Cause
• Maladaptation to the high-altitude environment
• Associated with recent ascent

Pathophysiology
• Probably associated with a mild cerebral oedema

29
Q

What are the symptoms, consequences and treatments for acute mountain sickness?

A

Symptoms
• Nausea, vomiting, dizziness, insomnia, dyspnoea

Consequences
• High-altitude cerebral oedema (HACE)
• High-altitude pulmonary oedema (HAPE)

Treatment
• Stop ascent
• Analgesia (painkiller)
• Fluids
• Acetazolamide
• Hyperbaric O2 therapy
30
Q

When do symptoms subside for acute mountain sickness?

A
  • Onset within 24 hours
  • Tend to subside after 48 hours of increased renal compensation
  • Can last more than a week
31
Q

What is ataxia?

A

Impaired ability to coordinate movement

32
Q

What is the cause and pathophysiology of High-Altitude Cerebral oedema (HACE)

A

Cause
• Rapid ascent
• Inability to acclimatise

Pathophysiology
• Vasodilation of vessels in response to hypoxaemia
• More blood - increased fluid leakage
• Sealed cranium - increased intracranial pressure

33
Q

What are the symptoms, consequences and treatments for High-Altitude Cerebral oedema (HACE)

A 
Symptoms
• Confusion
• Ataxia
• Behavioural change
• Hallucinations

Consequences
• Irreversible neurological damage
• Coma
• Death

Treatments
• Immediate descent
• O2 therapy
• Hyperbaric O2 therapy
• Dexamethasone (corticosteroid to reduce pressure)
• Mannitol (osmotic diuretic)
34
Q

What is the cause and pathophysiology of High-Altitude Pulmonary oedema (HAPE)

A

Cause
• Rapid ascent
• Inability to acclimatise

Pathophysiology
• Vasoconstriction of pulmonary vessels in response to hypoxia
- redirection of blood from poorly to well-ventilated areas of the lung (ventilation/perfusion matching)
• Increased pulmonary pressure, permeability and fluid leakage

35
Q

What are the symptoms, consequences and treatments for High-Altitude Pulmonary oedema (HAPE)?

A 
Symptoms
• Dyspnoea
• Dry cough
• Bloody sputum
• Crackling chest sounds

Consequences
• Impaired gas exchange
• Impaired ventilatory mechanics

Treatments
• Descent
• Hyperbaric O2 therapy
• Nifedipine (CCB - vasodilation)
• Salmeterol
• Sildenafil
36
Q

What is Type I respiratory failure?

A
  • Hypoxic
  • Ventilation/perfusion mismatch
  • Perfused alveoli are hypoventilated or ventilated alveoli are hypoperfused
  • CO2 can diffuse easily out of blood - normal level
  • O2 cannot move into blood - low PaO2
  • Pulmonary oedema
  • Pneumonia
  • Atelectasis
37
Q

What is Type II respiratory failure?

A
  • Hypercapnic
  • Hypoventilated lungs
  • Alveolar air stagnates - poor gradient
  • PaO2 is low, PaCO2 is high
  • Decreased CNS drive
  • Increased work of breathing
  • Pulmonary fibrosis
  • Increased physiological dead space
38
Q

What is Type III respiratory failure?

A
  • Doesn’t exist
  • Simply known as mixed respiratory failure
  • Combination of Type I and II

Respiratory System (18 decks)

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