O2 CO2 and CO

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Classifications of Hypoxia[edit]

  • Low PaO2:
  • Hypoxic hypoxia (low PAO2)
  • Anaemic hypoxia (low O2 carrying capacity),
  • Stagnant hypoxia (poor tissue perfusion)
  • Histotoxic hypoxia (failure of cellular respiration)

Physiological Consequences of Hypoxaemia[edit]

Tissue Level:

  • When tissue hypoxia or histotoxicity is present, the body resorts to anaerobic metabolism - 19 times less efficient than oxidative phosphorylation
  • This results in depletion of high energy phosphates: ATP and phosphocreatine
  • Anaerobic energy production produces H+ ions and lactate
  • This produces localised acidosis - which is even worse in the CNS where these metabolites cannot escape the blood-brain barrier, causing intracellular acidosis and cell death
  • Hypoxia also causes leaking of K+ outwards and Ca2+ inwards, leading to cell death

Systemic Level:

  • Hypoxia detected by peripheral chemoreceptors (carotid & aortic bodies)
  • Hyperventilation when PaO2 is below 55 mmHg, maximal at <30mmHg
  • Secondary hypocapnia due to hyperventilation
  • Hypoxic pulmonary vasoconstriction
  • Increased cardiac output, decreased MAP due to systemic vasodilatation
  • Preferential organ perfusion (especially brain)
  • Acidosis and Hb-O2 curve right shift

Long Term:

  • Increased haemaglobin/haematocrit levels due to erythropoietin

Causes of Hypercapnia/Hypocapnia[edit]


  • Due to four different causes:
  • Increased inspired concentration of CO2
  • Increased CO2 production
  • Hypoventilation
  • Increased dead space


  • Always due to increased alveolar ventilation, and this may be due to:
  • Hypoxaemia (which drives increased ventilation at altitude)
  • Metabolic acidosis compensation
  • Neurological disorders (such as head injuries) and emotional states such as fear

Physiological Consequences of Hypercapnia[edit]

  • Causes acidosis (in blood, ECF and CSF) via carbonic anhydrase


  • Increased cerebral blood flow
  • Increased intracranial pressure
  • Increased brain pH (and metabolic dysfunction)
  • Inert gas narcotic effects - similar to nitrous oxide
  • Convulsant/central depressant at high levels
  • Increased sympathetic outflow & increased sensitivity to parasympathetic tone via ↓ AChE activity in acidosis


  • Hypercapnia detected at central chemoreceptor (80% of sustained response) in the ventral medulla and in peripheral chemoreceptors (rapid response) hyperventilation up to PaCO2 of 100-150 mmHg
  • Increased pulmonary vascular resistance via pulmonary vasoconstriction (weaker effect than hypoxia)
  • Hypoxia (CO2 occupying space in Alv)
  • Acidosis & CO2 shifts Hb-O2 dissociation curve to the right


  • Decreased heart contractility and rate (usually overridden by catecholamine release causing increased contractility and heart rate)
  • Systemic vasodilation
  • Arrhythmogenic


  • Adrenaline release during severe hypercapnia

Renal Effects:

  • Arteriole constriction in severe hypercapnia (anuria)
  • Renal bicarbonate compensation in respiratory acidosis and alkalosis

Physiological Consequences of Hypocapnia[edit]

  • Mainly opposite effects to those of hypercapnia
  • Alkalosis (↓ free Ca2+)


  • Cerebral vasoconstriction: ↓ ICP
  • ↑ neural excitability at low PaCO2


  • Detected at central and peripheral chemoreceptors
  • Reduced respiratory drive (dangerous in labour)
  • Can produce apnoea in anaesthetized patients, but not usually when conscious
  • Pulmonary vasodilation


  • ↑ Peripheral resistance
  • ↓ cardiac output
  • Hb-O2 dissociation curve shifted to the left

Carbon Monoxide Poisoning[edit]

  • Usually due to inhalation but may be due to ingestion of methylene chloride which is metabolised in the liver to CO
  • CO binds to heme with an affinity 240 times that of O2
  • It causes an allosteric change in which greatly inhibits the three other heme binding sites from offloading O2
  • The result is a shift of the O2 dissociation curve to the left


  • Neurological Symptoms - headache, fatigue, dizziness, convulsions, respiratory arrest
  • Cardiovascular Symptoms - tachycardia, hypotension, and cardiac arrhythmia
  • Gastrointestinal Symptom - Nausea
  • CO also inhibits oxidative phosphorylation via cytochrome oxidase like cyanide but to a lesser extent which exacerbates the hypoxia
  • The mechanism of the delayed neurological sequelae is not well understood but may be related to toxic oxygen species generated by xanthine oxidase
  • Treatment is via high flow O2 and HBOT may be indicated.
  • Hyperbaric oxygen therapy - given at 3x atmospheric pressure hastens the dissociation of CO from carboxyhaemoglobin and cytochrome oxidase