15. Hypoxia Flashcards
What is the difference between hypoxia, hypoxaemia and ischaemia?
- Hypoxia - low PO2 in a specific environment
- Hypoxaemia - low PO2 in blood (below 8 kPa)
- Ischaemia - tissues receiving inadequate oxygen
Which 2 factors can put your body under hypoxic stress?
- Disease e.g. COPD
* Altitude
What is ambient air?
(• atmospheric air in its natural state)
• 21.3 kPa
• 20.9% of total atmospheric pressure
As altitude increases, what happens to barometric and partial pressure?
- Barometric pressure - decreases
- Partial pressure - decreases
(due to Dalton’s Law)
What is polycythaemia?
- Abnormally increased concentration of haemoglobin in the blood
- Due to reduction in plasma volume or increase in red cell numbers
- Increases the ODC
What is the oxygen cascade?
• 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
What 3 factors is the diffusion of gas across a membrane proportional to?
- SA
- Diffusion constant (CO2 diffuses faster than O2)
- Diffusion gradient
What is the artery and vein PO2?
- Artery - 13.3 kPa
* Vein - 5.3 kPa
What is the drop in PaO2 from the arteries to the tissues associated with?
• 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
What 4 factors influence the oxygen cascade?
- Alveolar Ventilation
- Ventilation/perfusion matching - for efficient gas exchange
- Diffusion capacity - some diseases can thicken the parenchyma
- Cardiac output - increased CO, more blood oxygenated
What does the oxygen cascade look like if you’re breathing hypoxic air?
- PO2 of ambient air is much lower
* Therefore ever other section is lower, reducing exercise capacity
Describe the graph showing the proportion of energy source for performing maximal exercise for a given amount of time
- Logarithmic time scale
- 10 seconds uses ATP and ATP-Phosphocreatine
- Lactic acid peaks before 60 seconds
- Longer than 60 seconds - aerobic
What is VO2 max?
- Total capacity to deliver oxygen to tissues
* Dependent on ventilation and cardiac output
Why is prolonged anaerobic respiration bad?
- Produces lactic acid
- Dissociates into lactate- and H+
- Lower pH
- Active site on enzymes affected
- Impedes glycolytic enzymes for aerobic energy production
Describe the ventilation-time graph during exercise?
- 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)
Apart from heavy breathing, where else does the energy come from after exercise to repay oxygen debt?
• Stored energy
- intramuscular ATP
- phosphocreatine
- myoglobin (holding onto O2, ready to release it)
How does breathing change during exercise?
• 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
What are the 5 challenges of altitude?
- Hypoxia
- Thermal stress
- Solar radiation
- Hydration (water used to humidify air, hypoxia induced diuresis)
- Dangerous (hypoxia-induced confusion)
What is accommodation and acclimatisation?
- Accommodation - (acute) physiological change in response to a change in the oxygen environment
- Acclimatisation - physiology becomes more efficient in a changed environment
What happens to the blood gases during acclimatisation?
• PaO2 increases
• PaCO2 falls
• Attributed to:
- renal compensation for respiratory alkalaemia
- slow increasing ventilatory sensitivity to hypoxia
Where is erythropoietin mainly secreted from?
Renal cortex
What is hypobaric hypoxia and how is it overcome?
- 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
What is the prophylaxis for high altitude?
(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)
What is acclimation?
- Like acclimatisation
* Stimulated by an artificial environment
What are 4 of the innate/developmental adaptations to high altitudes?
- 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
What is the pathophysiology of chronic mountain sickness (Monge’s disease)?
• Secondary polycythaemia, which increases blood viscosity
- impedes O2 delivery
- despite adequate oxygenation
What are the symptoms, consequences and treatments for chronic mountain sickness?
Symptoms
• Cyanosis
• Fatigue (from decreased capillary confusion)
Consequences
• Ischaemic tissue damage
• Heart failure
• Eventual death
Treatment
• Sufferers exiled to lower altitudes
What is the cause and pathophysiology of acute mountain sickness?
Cause
• Maladaptation to the high-altitude environment
• Associated with recent ascent
Pathophysiology
• Probably associated with a mild cerebral oedema
What are the symptoms, consequences and treatments for acute mountain sickness?
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
When do symptoms subside for acute mountain sickness?
- Onset within 24 hours
- Tend to subside after 48 hours of increased renal compensation
- Can last more than a week
What is ataxia?
Impaired ability to coordinate movement
What is the cause and pathophysiology of High-Altitude Cerebral oedema (HACE)
Cause
• Rapid ascent
• Inability to acclimatise
Pathophysiology
• Vasodilation of vessels in response to hypoxaemia
• More blood - increased fluid leakage
• Sealed cranium - increased intracranial pressure
What are the symptoms, consequences and treatments for High-Altitude Cerebral oedema (HACE)
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)
What is the cause and pathophysiology of High-Altitude Pulmonary oedema (HAPE)
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
What are the symptoms, consequences and treatments for High-Altitude Pulmonary oedema (HAPE)?
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
What is Type I respiratory failure?
- 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
What is Type II respiratory failure?
- 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
What is Type III respiratory failure?
- Doesn’t exist
- Simply known as mixed respiratory failure
- Combination of Type I and II
