Carbon Dioxide Basics
Comparison: Oxidative Metabolism v. Glycolytic Metabolic
Promoters of Efficient v. Inefficient Metabolism
Altitude Sickness: Therapeutic Effects of Acetazolamide and Carbon Dioxide
Low CO2 in Hypothyroidism
Lactate Paradox: High Altitude and Exercise
Altitude Improves T3 Levels
Protective Carbon Dioxide, Exercise, and Performance
Synergistic Effect of Creatine and Baking Soda on Performance
Ray Peat, PhD on Carbon Dioxide, Longevity, and Regeneration
Mitochondria & Mortality
Altitude and Mortality
“Low thyroid leads to low production of carbon dioxide and wastage of glucose.” -Ray Peat, PhD
When carbon dioxide production is low, because of hypothyroidism, there will usually be some lactate entering the blood even at rest, because adrenalin and noradrenalin are produced in large amounts to compensate for hypothyroidism, and the adrenergic stimulation, besides mobilizing glucose from the glycogen stores, stimulates the production of lactate. The excess production of lactate displaces carbon dioxide from the blood, partly as a compensation for acidity. The increased impulse to breath (“ventilatory drive”) produced by adrenalin makes the problem worse, and lactate can promote the adrenergic response, in a vicious circle. -Ray Peat, PhD
The low carbon dioxide production of hypothyroidism (e.g., Lee and Levine, 1999), and the respiratory alkalosis of estrogen excess, are often overlooked. An adequate supply of calcium, and sometimes supplementation of salt and baking soda, can increase the tissue content of CO2. -Ray Peat, PhD
Calcitonin, vitamin D-active metabolite, and estrogen-”HRT” treaments can cause respiratory alkalosis (relative hyperventilation), and hypothyroidism produces a predisposition to hyperventilation. Hyperventilation tends to cause calcium loss. In respiratory alkalolis, CO2 (and sometimes bicarbonate) are decreased, impairing calcium retention, and in “metabolic alkalosis,” with increased bicarbonate, calcium is retained more efficiently and bone formation is stimulated, and its dissolution is suppressed. -Ray Peat, PhD
Can J Anaesth. 1999 Feb;46(2):185-9.
Acute respiratory alkalosis associated with low minute ventilation in a patient with severe hypothyroidism.
Lee HT, Levine M.
Patients with severe hypothyroidism present unique challenges to anesthesiologists and demonstrate much increased perioperative risks. Overall, they display increased sensitivity to anesthetics, higher incidence of perioperative cardiovascular morbidity, increased risks for postoperative ventilatory failure and other physiological derangements. The previously described physiological basis for the increased incidence of postoperative ventilatory failure in hypothyroid patients includes decreased central and peripheral ventilatory responses to hypercarbia and hypoxia, muscle weakness, depressed central respiratory drive, and resultant alveolar hypoventilation. These ventilatory failures are associated most frequently with severe hypoxia and carbon dioxide (CO2) retention. The purpose of this clinical report is to discuss an interesting and unique anesthetic presentation of a patient with severe hypothyroidism.
We describe an unique presentation of ventilatory failure in a 58 yr old man with severe hypothyroidism. He had exceedingly low perioperative respiratory rate (3-4 bpm) and minute ventilation volume, and at the same time developed primary acute respiratory alkalosis and associated hypocarbia (P(ET)CO2 approximately 320-22 mmHg).
Our patient’s ventilatory failure was based on unacceptably low minute ventilation and respiratory rate that was unable to sustain adequate oxygenation. His profoundly lowered basal metabolic rate and decreased CO2 production, resulting probably from severe hypothyroidism, may have resulted in development of acute respiratory alkalosis in spite of concurrently diminished minute ventilation.