16. Hypoxia Flashcards
Hypoxia
Describes a low oxygen (PO2) environment
Hypoxaemia
Describes low blood oxygen levels (PaO2)
Ischaemia
Describes tissues receiving inadequate O2
List 3 situations that can put the body under hypoxic stress
Altitude
Exercise (only in a way: before physiological response)
Disease
How does PAO2 and PaO2 change with age?
DECREASES
What is the amount of O2 that will bind to haemoglobin dependent on?
Partial pressure (PO2)
Oxygen cascade
describes the decreasing oxygen tension from inspired air to respiring cells
What does Fick’s law of diffusion state
flow rate is proportional to the pressure gradient
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.
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)
Why are changes in O2 and CO2 not equal?
ODC is sigmoid shaped
CO2 dissociation curve is linear
State 4 factors affecting the oxygen cascade.
V/Q mismatch
Alveolar Ventilation
Diffusion Capacity
Cardiac Output
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
What would immediate exposure to high altitude (hypoxic environment) result in?
1 min: Incapacitation
2 mins: Death
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
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
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
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
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)
