F8iii / 22A19: Describe the physiological factors that affect PaCO2

22A19: Exam Report

Describe the physiological factors that affect PaCO2

33% of candidates passed this question.

Candidates who scored well generally defined PaCO2 and proceeded to describe factors in terms of those related to production and elimination.

Good answers described the key production factor as being rate of production through aerobic metabolism which is in turn influenced by substrate and BMR.

Those who scored well described elimination as being dependent upon minute ventilation, which in turn is influenced by CO2 detection by chemoreceptors, specifically detailing the difference between peripheral and central.

Many candidates detailed pathophysiological factors which unfortunately did not gain any marks.

F8iii / 22A19: Describe the physiological factors that affect PaCO2


  • PaCO2 = partial pressure of CO2 in the arterial blood
  • Normal value ~ 40mmHg
  • Normally PaCO2 controlled by alveolar ventilation (negative feedback loop)
  • CO2 ~10x more soluble than O2 -> less pressure for a given content (Henry Law)

Factors affecting CO2 production

  • CO2 is produced via Krebs cycle (final destination of carbons from energy sources, such as carbohydrates)
  • Krebs cycle is dependent (share same intermediates – NADH, etc) to oxidative phosphorylation Hence, increased aerobic consumption increases CO2 -> PaCO2
  • Factors that increase MVO2:
    • Hyperthermia
    • Sepsis
    • Exercise
    • Thyroid hormones
    • Increased muscle mass
    • Younger age
    • Pregnancy
  • RQ ratio = ratio of CO2 production for each o2 consumed 1 for CHO, 0.8 for fat, 0.7 proteins

Factors affecting Alveolar Ventilation

  • CO2 clearance is ventilation-limited (due to continuous perfusion, high permeability)
  • Often MV determined by PaCO2 (via peripheral and chemoreceptors), but factors independently altering MV can affect PaCO2 (a rectangular hyperbola relationship)
  • Peripheral Chemo = on aortic and carotid bodies = sense PaCO2 and pH = High PaCO2
  • High MV
  • Central Chemo = on medulla = sense pH of CSF/interstitial = determined by CO2 diffusion and conversion to H2CO3 via anhydrase carbonic (high content in CSF).
  • Note: CSF has low buffering capacity
  • High MV -> higher excretion -> Lower PaCO2
  • High MV:
    • Pain
    • Metabolic acidosis
    • Iatrogenic (mechanical vent.)
    • Hypoxia
    • Progesterone
  • Low MV:
    • Opioids
    • Muscular-skeletal disease
    • Alkalosis
    • CNS issues -> Higher PaCO2
  • Alveolar vent = VT – Dead space (VD)
  • Higher Dead Space = lower Alv Vent = High PaCO2 (body would compensate with increasing MV/RR if allowed: not paralysed or GA)
  • Increases VD
  • Apparatus: e.g. long tubing distal to Y piece
  • Anatomical: reasonably fixed
  • Alveolar: (i.e. West zone 1)
    • ↑ Alveolar pressure: positive pressure ventilation, PEEP
    • ↓ Pulmonary arterial pressure: e.g. haemorrhage
  • Obstructive diseases (COPD/Asthma)
  • Shunt has a lesser effect on PaCO2 -> PaCO2 approaches PvO2 (45mmHg)

Factors affecting PaCO2 : CaCO2 (temp and Haldane)

  • Temperature affects the equilibrium constant for the solvation process (k): the solubility of O2 and CO2 is increased at low temperatures. Thus at low temperatures, there will be a lower partial pressure for a higher dissolved concentration of gas
  • Oxygen and carbon dioxide increase in solubility as water temperature decreases, so their partial pressures will be less
  • Haldane effect
    •  ↓ PaO2/SaO2 -> ↑Hb affinity for CO2 -> ↓ PaCO2:CaCO2
    •  70% of increment due to ↑carbamino formation
    •  30% of increment due to ↑pKa imidazoles 6.8 to 7.9 hence better buffer

Author: Henrique Mendes