SUPPRESSION OF VENTILATION AND CO2 TOXICITY IN COPD PATIENT
By: Kristal Rubio, Student 2005
COPD patients’ bodies learn to live in a state of elevated pCO2 levels due to their oxygenation-perfusion mis-match. Their bodies accept the higher level and adjust, making a new “balance” for themselves.
Patients with COPD have a stimulus for respiration which is driven by the decrease in blood oxygenation, rather than an increase in CO2 levels as seen in a patient with no respiratory problems.
Administration of a high amount of oxygen (over 2 L/ min) to a COPD patient causes in increased oxygenation in the blood, but blocks their breathing stimulus (respiratory drive). While the higher level of oxygen helps the patient very briefly in the short term (by bringing up their O2 levels), it causes the patient to breathe at a slower rate, causing a buildup of CO2 in the blood stream. Add this buildup to the already increased CO2 level that the patient’s body is already accustomed to and the patient will very rapidly develop carbon dioxide narcosis (CO2 toxicity) which will ultimately lead to the patient’s death.
Oxygen- induced hypoventilation is prevented by administering oxygen at low rates (1 to 2 L/ min). (PG 601, Bruner & Suddarth).
Ex. (With hypothetical numbers):
Patient has the following levels prior to oxygen administration:
pCO2 - 30 pO2 - 32 R Rate - 20
Oxygen is administered at 3L/min.
Due to the low O2 concentration, the patient’s respiratory drive is activated and the respirations increase to 26.
The patient’s levels change. The O2 increases to 45, and the CO2 decreases a little to 28 ( still above average, but closer to normal).
But, since the O2 level is now up, the patient’s respiratory drive is shut off and the respirations now decrease to 17.
The patients O2 level stays at a normal range because the oxygen is still being supplied at 3L/min; however, since the patient’s respirations have now decreased to a lower level, patient is not blowing off the CO2 at as high of a rate as he previously was. The CO2 is now building up in the blood stream even higher (on top of the already elevated level of 28). This causes the patient to develop carbon dioxide toxicity or narcosis, even though his oxygen saturation is at a good level.