15 Hypoxia Flashcards
Define oxygen cascade
It is the decreasing oxygen tension from inspired air to respiring tissues
Summarise oxygen cascade
- Atmosphere: 21 kPa
- Upper airway: 20 kPa (due to humidification)
- Alveoli: 13.5 kPa (due to mixing and is variable to hyper- or hypo- ventilation)
- Post-alveolar capillaries: 13.5 kPa (can be reduced by reduced diffusion capacity)
- Arteries: 13.3 kPa (due to mixing from bronchial circulation)
- Veins: 5.3 kPa (variable)
What are the 4 factors that can affect oxygen cascade
Ventilation
Cardiac output
Diffusion capacity
V/Q mismatch
What are the challenges to altitude
Hypoxia Thermoregulation Radiation Dehydration Danger (eg wind, hypoxia induced confusion)
List advantageous and disadvantageous physiological response to acclimatisation to high altitude
Advantageous:
- Sympathetic activation to increase HR and flow
- Increase ventilation to take in more oxygen
- Renal excretion of excess HCO3- and retain H+
- Erythropoietin
- Increase in oxidative enzymes, mitochondrial density and 2,3 DPG in RBC
Disadvantageous
- Decrease in PaCO2 to prevent breathing
- Increase pH to shift ODC to the left
What are possible prophylaxis to high altitude
Acclimatisation: artificial environment (hypobaric chamber)
Medication: acetazolamide (carbonic anhydrase)
State the developmental changes/adaptations to high altitude
Barrel chest
Enlarged heart
Increased haeatocrit
Increased mitochondrial density
Explain chronic mountain sickness in terms of causes, pathophysiology, symptoms, consequences and treatment
- Causes: unknown
- Pathophysiology: secondary polycythaemia increases blood viscosity, which sludges through systemic capillary beds impeding O2 delivery (despite more than adequate oxygenation)
- Symptoms: cyanosis, fatigue
- Consequences: ischaemic tissue damage, heart failure, eventual death
- Treatment: no interventional medical treatment – sufferers are exiled to lower altitudes
Explain acute mountain sickness in terms of causes, pathophysiology, symptoms, consequences and 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
- Symptoms: nausea, vomiting, irritability, dizziness, insomnia, fatigue, and dyspnoea – ‘hangover’
- Consequences: development into HAPE or HACE
- Treatment: monitor symptoms, stop ascent, analgesia, fluids, medication (acetazolamide) or hyperbaric O2 therapy. Symptoms tend to subside after 48 hrs of increased renal compensation
Explain high altitude cerebral oedema in terms of causes, pathophysiology, symptoms, consequences and 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, behavioural change, hallucinations, disorientation
- Consequences: irrational behaviour, irreversibal neurological damage, coma, death
- Treatment: immediate descent, O2 therapy, hyperbaric O2 therapy, dexamethasone
Explain high altitude pulmonary oedema in terms of causes, pathophysiology, symptoms, consequences and 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
- Consequences: impaired gas exchange, impaired ventilatory mechanics
- Treatment: descent, hyperbaric O2 therapy, nifedipine (CCB), salmeterol, sildenafil
Explain Type I Respiratory Failure
Respiratory failure is usually failure of pulmonary gas exchange, generally V/Q inequality
Involved in hypoxia but no hypercapnia
Causes: hypoventilation, V/Q mismatch, diffusion abnormality
eg. Pulmonary oedema, Pneumonia, Atelectasis
Explain Type II Respiratory Failure
Respiratory failure is usually failure of pulmonary gas exchange, generally V/Q inequality
Involved in hypoxia and hypercapnia ( > 6.7 kPa)
Causes: Increased CO2 production or decreased CO2 elimination due to decreased CNS drive and/or increased work of breathing
eg. Pulmonary fibrosis, Neuromuscular disease, Increased physiological dead space, Obesity
