16. Hypoxia Flashcards by Georgia Leggett

Hypoxia

Describes a low oxygen (PO2) environment

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Hypoxaemia

Describes low blood oxygen levels (PaO2)

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Ischaemia

Describes tissues receiving inadequate O2

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List 3 situations that can put the body under hypoxic stress

Altitude
Exercise (only in a way: before physiological response)
Disease

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How does PAO2 and PaO2 change with age?

DECREASES

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What is the amount of O2 that will bind to haemoglobin dependent on?

Partial pressure (PO2)

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Oxygen cascade

describes the decreasing oxygen tension from inspired air to respiring cells

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What does Fick’s law of diffusion state

flow rate is proportional to the pressure gradient

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How does the partial pressure of oxygen in the alveoli (after mixing) change?

It’ll continue to move down its concentration into the blood until it reaches equilibrium.

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Describe how the partial pressure of oxygen changes from inspired air to the tissues.

3
- –> 20 (conducting airways)
- –> 13.5 (alveoli)
- –> 13.5 (PaO2 immediately past exchange surface)
- –> 13.3 (diluted by return of bronchial circulation)
- –> 5.3 (mixed venous blood)

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Why are changes in O2 and CO2 not equal?

ODC is sigmoid shaped

CO2 dissociation curve is linear

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State 4 factors affecting the oxygen cascade.

V/Q mismatch
Alveolar Ventilation
Diffusion Capacity
Cardiac Output

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State the 5 challenges of altitude.

Hypoxia: much less O2 than ambient air
Solar Radiation: less atmospheric screening, reflection off snow
Thermal stress: freezing cold, high wind-chill factor
Hydration: water lost humidifying inspired air, hypoxia induced diuresis
Dangerous: windy, unstable terrain, hypoxia-induced confusion

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What would immediate exposure to high altitude (hypoxic environment) result in?

1 min: Incapacitation

2 mins: Death

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What is a consequence of the reduction in ambient pressure at high altitude result in?

Completely lowers the gradient of PO2 between air and tissues

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Describe how the body tries to acclimatise to low atmospheric oxygen by increasing oxygen loading

Reduction in alveolar O2 (PAO2)
Reduction in arterial O2 (PaO2): recognised by peripheral chemoreceptors
3.a) Increased sympathetic activation: increased ventilation: increase in PAO2, increase amount of O2 in blood
3.b) Sympathetic outflow increases CO (through SV and HR): increases delivery of O2
3.c) Increases erythropoietin secretion; increased production of RBCs; increases capacity for O2 loading
3.d) Increase oxidative enzymes, Increases rate of aerobic mechanisms, Increased O2 utilisation
3.e) Increase mitochondrial density, More ATP produced, Increased O2 utilisation
3d and 3e cause a slight increase in 2,3 DPG in RBCs, shifts ODC right, increases O2 unloading

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Describe the consequences of the body trying to acclimatise to low atmospheric oxygen

Decrease PaCO2: Interferes with baseline control of breathing, decreases ventilation (counterproductive as decreases O2 loading)
Decrease PaCO2: Rise in pH, shifts ODC to the left, decrease in O2 unloading

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How does the body cope with the consequences of trying to acclimatise to low atmospheric oxygen?

Alkalosis is detected by carotid bodies 
Changes way kidneys react: 
Increase HCO3- excretion 
Increase H+ in blood
Normalises ODC, increases O2 unloading
Initially responses are quick but when kidneys get involved, takes increased time to fix

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Prophylaxis

Treating something before it has happened

Acclimation

Like acclimatisation but stimulated by an artificial environment e.g. hyperbaric chamber

2 prophylactic measures for dealing with low atmospheric oxygen

Acclimation

Acetazolamide (drug)

Describe the effects of Acetazolamide

Carbonic anhydrase inhibitor:
Accelerates the slow renal compensation to hypoxia-induced hyperventilation
If inhibited can reduce initial alkalotic response to low O2

Describe 4 innate/ developmental adaptations to low atmospheric oxygen

‘Barrel chest’: larger TLC, more alveoli and greater capillarisation: More O2 into the body
Increased haematocritL greater O2 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 O2 utilisation at cellular level: More O2 utilised

Onset of chronic mountain sickness

Acclimatised individuals can spontaneously acquire chronic mountain sickness

Pathophysiology of chronic mountain sickness

Secondary polycythaemia increases blood viscosity, which sludges through systemic capillary beds impeding O2 delivery (despite adequate oxygenation)

Symptoms and consequences of chronic mountain sickness

Symptoms: cyanosis, fatigue (due to inadequate O2 supply) Consequences: ischaemic tissue damage, heart failure, eventual death

Treatment of chronic mountain sickness

Descent to lower altitude

Cause of acute mountain sickness

Maladaptation to the high-altitude environment. Usually associated with recent ascent (within 24 hours) Can last > week

Pathophysiology of acute mountain sickness

Associated with a mild cerebral oedema: fluid accumulating inside cranium causing compression in head

Symptoms and consequences of acute mountain sickness

Symptoms: nausea, vomiting, irritability, dizziness, insomnia, fatigue, and dyspnoea Consequences: development into HAPE or HACE

Treatment of acute mountain sickness

Stop ascent Medication (acetazolamide) Hyperbaric O2 therapy

Causes of High altitude pulmonary oedema (HAPE) and High altitude cerebral oedema (HACE)

Rapid ascent | Inability to acclimitise

Pathophysiology of High altitude pulmonary oedema (HAPE)

Vasoconstriction of pulmonary vessels in response to hypoxia Increases pulmonary pressure Permeability and fluid leakage from capillaries Fluid accumulates once production exceeds the max. rate of lymph drainage

Symptoms and consequences of High altitude pulmonary oedema (HAPE)

Symptoms: dyspnoea, dry cough, bloody sputum, crackling chest sounds Consequences: impaired gas exchange, impaired ventilatory mechanics

Treatment of High altitude pulmonary oedema (HAPE)

``` Descent Hyperbaric O2 therapy Nifedipine (CCB) Salmeterol (relaxes airway smooth muscle) Sildenafil (vasodilation) ```

Pathophysiology of High altitude cerebral oedema (HACE)

Vasodilation of vessels in response to hypoxaemia (to increase blood flow) More blood going into the capillaries Increased fluid leakage Cranium is a ‘sealed box’ – no room to expand so intracranial pressure increases

Symptoms and consequences of High altitude cerebral oedema (HACE)

Symptoms: confusion, ataxia, behavioural change, hallucinations, disorientation Consequences: irrational behaviour, irreversible neurological damage, coma, death

Treatment of High altitude cerebral oedema (HACE)

Immediate descent Hyperbaric O2 therapy Dexamethasone

What's the difference between accommodation and acclimatisation?

Accommodation: ACUTE response, rapid physiological change in response to a change in the oxygen environment Acclimatisation = physiology becomes more efficient so that you can get more out of the environment

Respiratory failure

Failure to maintain adequate pulmonary gas exchange

Hypoxic respiratory failure (Type I)

PaO2: < 8kPa PaCO2: low/ normal Diffusion issue O2 moving into body is impaired

3 Causes of Type I respiratory failure

Pulmonary oedema Pneumonia Atelectasis

Hypercapnic respiratory failure (Type II)

``` PaO2: < 8kPa PaCO2: > 6.7 kPa "Getting the gas there" problem Decreased CNS drive Increased work of breathing ```

Broad causes of Type II respiratory failure

May be increased production of CO2 and unable to clear it May be an elimination issue Maybe a combination of both

4 Causes of Type II respiratory failure

Pulmonary fibrosis Neuromuscular disease Increased physiological dead space Obesity

How to remember the differences in type I and type II respiratory failure

Type I: 1 thing wrong (low O2) | Type II: 2 things wrong (low O2, high CO2)