Hypercarbia induces vasoconstriction in all vascular beds but lung and placental. The deleterious effects are most obvious on the neurological system where it results in decreased cerebral perfusion and altered mental status including delirium.
It is generally thought of as a disorder in ventilation. However, there are three factors that play an important role and is summarized best in this formula:
Production of CO2 (VCO2)
CO2 is produced through metabolism. In aerobic metabolism, CO2 is the final low energy state of a previous high energy sugar, protein, or fat moiety. In vitro, each of these energy sources has a different stoichiometry best summarized by the respiratory quotient (CO2 eliminated / O2 consumed. RQ of fat is 0.7, protein is 0.8-0.9, and carbs is 1.0. Hence, utilizing fats over carbs has the theoretical benefit of decreasing PaCO2. Nutritional studies has NOT shown a benefit in feeding increased fats:carbs diets on PaCO2. Nor is there any benefit on CO2 by restricting caloric intake below resting energy expenditure. This makes sense because your body will metabolize a basal amount of glucose/glycogen even if not fed. But it might metabolize more if overfed.
In anaerobic metabolism, hydrogen ions are byproducts which react with native bicarb buffer to produce CO2. This same effect is seen in stress responses which increase the body’s preference for utilizing anaerobic metabolism as well as toxicologic conditions. It is important to realize that treating acidosis with bicarb will worsen hypercarbia. In patients who cannot increase RR accordingly, bicarb infusions are not helpful.
Brainstem respiratory depression
- Drugs (e.g., opiates)
- Obesity-hypoventilation syndrome
- Critical illness polyneuropathy
- Guillain-Barré syndrome
- Critical illness myopathy
- Magnesium depletion
- Myasthenia gravis
Physiologic vs anatomic vs iatrogenic