see also:

• hypoxia
• arterial and venous blood gases (ABGs/VBGs)
• ventilation

• hypercapnia is an elevated blood carbon dioxide level which may be acute or chronic
• elevated blood carbon dioxide levels result in carbonic acid formation and a respiratory acidosis
  • if persistent, over time the kidneys will attempt to correct this by retaining bicarbonate and hence generating a partly compensatory metabolic alkalosis
• carbon dioxide rapidly crosses the blood-brain barrier, so elevated levels immediately alter brain chemistry and if become excessively high, may result in CO2 narcosis, coma and death

• hypoventilation “type 2 respiratory failure” (see ventilation)
  • impaired CNS respiratory drive
    • sedative medications/substances eg. opiates and opioids
    • intracranial pathology such as stroke (CVA), raised intracranial pressure (ICP), etc
    • loss of hypoxic drive in those with chronic hypercapnia (ie. when given high levels of inspired oxygen in a patient dependent upon hypoxia to drive respiration as hypercapnia is chronic)
  • impaired ventilation due to a respiratory or thoracic pathology
    • eg. severe asthma, pneumothorax, chest trauma, chronic obstructive pulmonary disease (COPD), obstructive sleep apnoea (OSA), phrenic nerve palsy, spinal cord injury, etc
  • compensatory in response to underlying metabolic alkalosis
    • the arterial pH will be high, not low as you would expect in other causes of hypercapnia
• excessive inspired carbon dioxide levels
  • normal carbon dioxide levels in the air are neglible at ~400ppm (up to 1000ppm in occupied rooms, up to 2000ppm in poorly ventilated occupied rooms, maximum allowed workplace levels are ~5000ppm)
  • you normally exhale carbon dioxide at concentrations of 5% (50,000ppm) and this usually gets rapidly diluted into the air you breathe UNLESS it is an enclosed space
  • rising inspired CO2 levels increase end tidal CO2 levels in normal young adults when given as stepwise increases with each level being 12 minutes duration ¹⁾:
    • 2% ⇒ 40-45mmHg end tidal CO2
    • 4% ⇒ 42-47mmHg end tidal CO2 - this level results in headaches which become worse as end tidal CO2 rises
    • 6% ⇒ 51-55mmHg end tidal CO2
    • 8% ⇒ 64-66mmHg end tidal CO2
  • your body at rest usually produces 0.2L/minute of CO2 and this will be exhaled into the enclosed space resulting in a rapid build up
  • breathing closed circuits eg. anaesthetic circuits without a CO2 scavenger
  • enclosed unventilated small spaces eg. sealed small tents, head inside a plastic bag, occupational settings, etc
    • minutely rate of rise in FiCO2 = (CO2 production in L/minute) / (Volume of the space in litres)

• cerebral vasodilation and CNS effects
  • minor transient hypercapnia appears to help glymphatic system of the brain flows and waste removal by creating a vasodilatory pump-like effect
  • headaches
    • often present as dull, throbbing morning headaches on both sides of the head when a person wakes up after episodes of obstructive sleep apnoea (OSA), etc as most episodes of hypercapnia occur during sleep
    • in studies of increasing inspired CO₂, inspired levels of CO₂ above 4% appeared to cause headaches however dosing with 400mg caffeine 1hr prior reduced the headaches at inspired levels up to 8% via increasing respiratory ventilation stimulation ²⁾
  • dizziness
  • impaired cognition
  • as cerebral blood flow increases (due to CO₂ acting as a potent cerebral vasodilator), intracranial pressure rises.
    • this can lead to CO₂ narcosis, a state of profound sedation that may progress to further hypoventilation and respiratory acidosis, stupor, seizures, coma, and respiratory arrest.
• cardiovascular effects:
  • moderate elevations stimulate the sympathetic nervous system, causing tachycardia (rapid heart rate) and increased cardiac output
  • when blood pH drops significantly (eg. below 7.15), the excess acid directly depresses heart muscle contractility. This results in systemic vasodilation, hypotension (dangerously low blood pressure), and a high risk of cardiac arrhythmias
• respiratory effects:
  • the body's primary reflex to hypercapnia is to stimulate the brain's respiratory centers (if they are functional and not excessively sedated such as by a sedative overdose) to increase breathing rate and depth (hyperventilation) to “blow off” the excess CO₂. However, if the underlying cause is a structural or neuromuscular failure (like severe COPD, obstructive sleep apnoea (OSA), or obesity hypoventilation syndrome), the respiratory pump cannot correct it, this may lead to CO₂ narcosis and worsening the CO₂ retention.
• systemic and cellular effects:
  • respiratory acidosis
    • the buildup of CO₂ generates carbonic acid, leading to respiratory acidosis
      • for every 12mmHg rise in arterial pCO2, arterial pH would be expected to rise by ~0.1 if there is no metabolic compensation
    • while the kidneys can slowly compensate in chronic hypercapnia (as in severe COPD) by retaining bicarbonate, acute hypercapnia results in rapid, dangerous drops in blood pH
  • immune suppression:
    • chronic hypercapnia is known to suppress both innate and adaptive immune responses in the lungs, increasing susceptibility to respiratory infections
  • renal and endocrine:
    • hypercapnia stimulates the sympathetic nervous system and the renin-angiotensin-aldosterone system, causing renal vasoconstriction which can decrease blood flow to the kidneys