see also:

• oxygen
• arterial and venous blood gases (ABGs/VBGs)
• home oxygen
• respiratory medicine

• hypoxic hypoxia can be arbitrarily defined as arterial oxygen partial pressure of less than 80mmHg in room air
• an arterial PO2 < 60mmHg indicates respiratory failure as, at oxygen levels below this, the Hb-oxygen dissociation curve is steep which means that the ability for Hb to carry much oxygen to the tissues is markedly diminished, as it evolved to be off-loading oxygen to the tissues at these pressures.
  • pO2 of 60mmHg equates to an oxygen saturation of less than 90% (see Hb-oxygen dissociation curve - see wikipedia)
• other causes of “hypoxia” or insufficient cellular oxygen usage include:
  • anaemic hypoxia - insufficient haemoglobin to carry the oxygen in the blood
  • impaired oxygen delivery due to carbon monoxide poisoning or methaemoglobinaemia
  • ischaemic hypoxia due to impaired blood flow such as from either blockages, vasoconstriction or venous stagnation
  • histotoxic hypoxia due to impaired cellular utilisation of oxygen such as with cyanide poisoning
• the following assumes we are discussing hypoxic hypoxia

• an understanding of this equation if critical in emergency medicine
• each minute, a human at rest consumes ~4ml oxygen per kg body weight and produces ~3ml carbon dioxide per kg body weight
• the ratio of CO2 produced to oxygen used is the “respiratory quotient”
• normal alveolar ventilation = 5L/min in adults with a tidal volume approx. 500ml (7ml/kg)
• FiO2 = fraction of oxygen in inspired gas
  • for room air, this is 0.21, for 100% oxygen, this is 1.00
• Patm = atmospheric pressure = 760mmHg at sea level (approx) = 101kPa = 12.8 psi
• Pwater = saturated water vapour pressure at body temperature and at prevailing atmospheric pressure = 47mmHg
• PaCO2 = arterial carbon dioxide partial pressure in mmHg (normal ventilation = 40mmHg)
• RQ = respiratory quotient = 0.8 for most people
• if FiO2 is low, the equation can be simplified by approximating FiO2 x (1-RQ) = 0

• another essential concept to understand in emergency medicine
• an increased A-a gradient suggests their is a pulmonary oxygen transfer aetiology to hypoxia such as impaired diffusion, V/Q mismatch, or right-to-left shunt
• normal range is 5-20mmHg, increasing by 1mmHg for every decade in age
• see medcalc3000 A-a gradient calculator

• the body normal maintains alveolar ventilation to give a relatively constant PaCO₂ of 40mmHg by adjusting respiratory rate and tidal volume
  • this level will be lowered in hyperventilation which will result in respiratory alkalosis
  • this level will rise in hypoventilation which will result in respiratory acidosis

alveolar ventilation = (tidal volume - physiologic dead space) x respiratory rate

NB. physiologic dead space is usually ~150mL

PaCO₂ = (rate of CO₂ production (usually 200mL/min) x conversion constant (usually 0.863) / alveolar ventilation) + PiCO₂

inspired CO₂ in mmHg = PiCO₂ = FiCO₂ x (Patm - water vapour pressure)

where FiCO₂ = fractional amount of CO₂ in inspired air, Patm is usually ~760mmHg, and the water vapour pressure is usually ~47mmHg

NB. 1% = 0.01 fractional, to get fractional from PPM, divide PPM by 1 million;

the industrial standard for max safe level of FiCO₂ = 5000ppm or 0.5% while hypercapnia level is 3% and severe toxicity level 5%

in normal circumstances, ETCO₂ of exhaled air = 5% or 50,000 ppm at a usual minute volume of 5L/min

• minutely rate of rise in FiCO₂ = (CO₂ production in L/minute) / (Volume of the space in litres)
• this is why people suffocate when placing their head inside a sealed plastic bag - it doesn't take long for CO₂ levels to rise to dangerous levels
  • eg. 5L bag will rise in 0.2L/min / 5L = 0.04 = a rise of 40,000ppm within 1 minute which would cause CO₂ narcosis, severe hypoxia and death
  • eg. sleeping in a sealed 2P tent of volume 2700L would result in a rise of FiCO₂ = 0.2L/min / 2700 = 74ppm per minute and time to 3% would be 400 minutes (ie. 6.75hrs)
    • fortunately inner tents for sleeping are made of breathable fabrics (ie not for waterproofing) and these will not allow CO₂ levels to rise significantly as they have higher gas diffusion rates through the weaves

• high altitude
• enclosed spaces

• in this case there is a rise in arterial PCO2 levels
• obstructed airway
• decreased conscious state - eg. stroke (CVA), toxicology, CO₂ narcosis
• exhaustion from work of breathing
• painful breathing - shingles, pleurisy, fractured ribs, etc
• muscle paralysis - toxinology, neuro-muscular blockers, neuropathies
• chest wall pathology or injury

• pneumothorax
• pneumonia
• asthma
• pulmonary embolism (PE)
• chronic obstructive pulmonary disease (COPD)
• acute pulmonary oedema (APO)
• Acute Respiratory Distress Syndrome (ARDS)
• pleural effusion
• pulmonary fibrosis
• congenital heart disease with right to left shunt
• other pulmonary pathology

• ensure adequate airway and ventilation
  • may require positive pressure ventilation such as BiPAP or via intubation
• increase FiO2 as needed
• improve lung function
  • Rx the cause where possible
• in suitable patients, when severe hypoxic hypoxia persists despite the above:
  • consider ECMO
  • in the future, whilst awaiting ECMO, we may be able to give an immediate iv infusion of John Kheir's idea of oxygen filled nanoparticles which seem to work in preliminary testing