Hypoxia Flashcards
Hypobaric hypoxia= ?
low pressure hypoxia because even though the proportions are the same the amount of O2 is less
Hypoxia
Describes a specific environment, specifically PO2 in environment
Hypoxaemia
Describes the blood environment, specifically the PaO2
Ischaemia
Describes tissues receiving inadequate oxygen, e.g. forearm ischaemia
As a result of receiving hypoxaemic blood
Relationship between PaO2 and Age
Increase age= decrease PaO2
The O2 cascade describes?
Related to which law?
the decreasing oxygen tension from inspired air to respiring cells
O2 is most abundant when it’s in the air (keeps getting lower throughout the pathway of the body)
Fick’s law of diffusion states that flow rate is proportional to the pressure gradient
Fick’s law
What influences it?
“V Gas”= 𝐴/𝑇∙𝐷∙[𝑃1−𝑃2]
Structural diseases reduce A
Breathing hypoxic gas reduces P1-P2 gradient
Fluid in alveolar sacs increases T
Oxygen cascade summary graph draw (slide 9, lecture 15) Where is biggest proportion of O2 lost? Impact of hyperventilation? Second significant drop? Dotted lines? Why don't O2 and CO2 change by same amount?
Mixing phase is where the biggest proportion of O2 is lost
Hyperventilation (not just breathing fast) increases the partial pressure O2 gradient and CO2 gradient with means more O2 can get in which increases PO2
Second significant drop= by the tissues (but depends on what they’re doing)
Dotted lines- where O2/ CO2 may go down/up during exercise, Amount O2 changes and CO2 changes is not equal because of the sigmoid shaped curve in O2 but linear shaped curve in CO2
Factors that can impede oxygen cascade+ explanation
Alveolar ventilation
V/Q matching
V/Q matching= Ventilation/ Perfusion mismatching, e.g. if there is a blockage in an airway which prevents air from getting there but blood is coming there then it doesn’t matter how much ventilation is occurring because it wont get to the gas exchange surface.
Diffusion capacity
Diffusion capacity: could be to do with gas or membrane (if membrane thickness increases then diffusion rate decreases)
Cardiac output
Cardiac output: heart needs to be good at delivering the blood with a higher conc of o2 to the tissues otherwise the pulmonary circulation is pointless
Impact of high altitude on oxygen cascade draw?
slide 10, lecture 15
smaller bars= at a high altitude, the O2 cascade is much more shallow plus you’re probably physically exerting yourself= harder to maintain homeostasis
Changes of high altitude
Hypoxia: Much less oxygen in the ambient air
Thermal stress: Freezing cold weather (-7 °C per 1000m), High wind-chill factor
Solar radiation: Less atmospheric screening, Reflection off snow
Hydration: Water lost humidifying inspired air, Hypoxia induced diuresis
Dangerous: Windy, unstable terrain, hypoxia-induced confusion and malcoordination
Accommodation and acclimatisation to high altitude
slide 14, lecture 15
PAO2= alveolar oxygen
PaO2= arterial oxygen
Decrease in the above two recognised by peripheral chemoreceptors (usually central chemoreceptors recognise increases in CO2 so this is a different mechanism)
Increases sympathetic activation= increase ventilation= increase alveolar oxygen= increase O2 loading into blood
Sympathetic activation also increases cardiac output through increase in HR+ Stroke Volume (Q) through increases in rate of conduction through the heart
Cardiac output increases throughput in lungs+ delivery to tissues
Ventilation comes at a cost though because PaCO2 decreases= decrease ventilation even though you were solving O2 issue
Loss in CO2=increase pH= changes oxygen dissociation curve to the left which increases affinity of O2 to Hb= decrease O2 unloading
Alkalosis detected by carotid bodies from high pH (same place as peripheral chemoreceptors) leading to kidney increasing H+ and increasing HCO3- excretion, takes longer time to do this but leads to increase O2 unloading.
Low O2 detected= increase erythropoietin secretion= increase RBC production= Increase O2 loading
Other changes= Increase oxidative exzymes= increase aerobic respiration before you move to anaerobic mechanism, also increase mitochondria which both lead to increase 2,3- DPG which gives right shift to ODC because conformational change= increase O2 unloading
Acclimation meaning
Like acclimatisation but stimulated by an artificial environment (e.g. hypobaric chamber or breathing hypoxic gas)
Prophylaxis= ?
Prophylaxis for high altitude
treating something before it happens
Acetazolamide
- Carbonic anhydrase inhibitor – accelerates the slow renal compensation to hypoxia-induced hyperventilation
- directly linked to turning CO2 into H2CO3 , so inhibition reduces initial alkalotic response to low oxygen
Native highlanders have specialised anatomical and physiological adaptations:
‘Barrel chest’ – larger TLC, more alveoli and greater capillarisation, More O2 into the body
Increased haematocrit – greater oxygen 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 oxygen utilisation at cellular level, More O2 utilised
Chronic mountain sickness Causes Pathophysiology Symptoms Consequences Treatment
Causes: unknown
Pathophysiology: secondary polycythaemia (increase RBC number in response) increases blood viscosity, which sludges through systemic capillary beds impeding O2 delivery (despite more than adequate oxygenation)
Symptoms: cyanosis (purple at tips of fingers+ toes because not enough O2), fatigue
Consequences: ischaemic tissue damage, heart failure, eventual death
Treatment: no interventional medical treatment – sufferers are exiled to lower altitudes
Acute mountain sickness Causes Pathophysiology Symptoms Consequences Treatment
Causes: maladaptation to the high-altitude environment. Usually associated with recent ascent - onset within 24 hours and can last more than a week
Pathophysiology: probably associated with a mild cerebral oedema (fluid accumulation in the cranium which causes head compression)
Symptoms: nausea, vomiting, irritability, dizziness, insomnia, fatigue, and dyspnoea – ‘hangover’
Consequences: development into HAPE (High altitude pulmonary odema) or HACE (
Treatment: monitor symptoms, stop ascent, analgesia, fluids, medication (acetazolamide) or hyperbaric (high pressure) O2 therapy symptoms tend to subside after 48 hrs of increased renal compensation
High altitude pulmonary oedema Causes Pathophysiology Symptoms Consequences Treatment
Causes: rapid ascent or inability to acclimatise
Pathophysiology: vasoconstriction of pulmonary vessels in response to hypoxia increased pulmonary pressure, permeability and fluid leakage from capillaries fluid accumulates once production exceeds the maximum rate of lymph drainage
Symptoms: dyspnoea, dry cough, bloody sputum, crackling chest sounds (respiratory symptoms)
Consequences: impaired gas exchange, impaired ventilatory mechanics
Treatment: descent, hyperbaric O2 therapy, nifedipine (CCB), salmeterol (relaxes smooth muscle to help get the air in), sildenafil (viagra) (affects blood pressure)
High altitude cerebral oedema Causes Pathophysiology Symptoms Consequences Treatment
Causes: rapid ascent or inability to acclimatise
Pathophysiology: 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
Symptoms: confusion, ataxia (not able to move very well) , behavioural change, hallucinations, disorientation (Impairs neurological function)
Consequences: irrational behaviour, irreversible neurological damage, coma, death
Treatment: immediate descent, O2 therapy, hyperbaric O2 therapy, dexamethasone
Type I respiratory failure
Boundaries?
Description?
Causes?
Type I: Hypoxic respiratory failure, PaO2 < 8 kPa
PaCO2 = low/normal
Hypoventilation, V/Q mismatch, Diffusion abnormality
Causes: Pulmonary oedema, Pneumonia, Atelectasis
(Diffusion issue, but CO2 is more diffusible so it moves out fine but O2 can’t move in enough)
Not immediate danger but lungs aren’t working properly
Respiratory failure NB
Respiratory failure is fundamentally a failure of pulmonary gas exchange, generally V/Q inequality (Not necessarily disease severity)
Type II respiratory failure
Boundaries?
Description?
Causes?
Type II: Hypercapnic (high CO2) respiratory failure, PaO2< 8 kPa
PaCO2 > 6.7 kPa
Increased CO2 production, Decreased CO2 elimination
Causes: Decreased CNS drive, Increased work of breathing, Pulmonary fibrosis, Neuromuscular disease, Increased physiological dead space, Obesity
Problem of getting the gas there
Because O2 is usually moving down a greater conc gradient, usually means it’s a CO2 issue (can’t clear out as well)
Could also be a V/Q issue (a lot of the pulmonary vessels aren’t receiving blood flow
SBAs at end of lecture 15, slide 26
If explanations needed go to Hypoxia lecture at 51.35
