When patients hypoventilate at the end of a case, reanesthetization might occur. (Image source: Thinkstock)

When patients hypoventilate at the end of a case, reanesthetization might occur. (Image source: Thinkstock)

Awakening from inhaled anesthesia is a complicated business. Once the patient is no longer inhaling anesthetic, the concentration of anesthetic in the blood will drop as anesthetic gas is eliminated via the lungs. However, as the concentration in the blood decreases, the partial pressure in the blood will drop below the partial pressure in the tissues, causing anesthetic gas to flow from the tissue to the blood. If the patient is hypoventilating, net flow of anesthesia gas from the tissues to the blood might exceed the net flow from the blood to the expired air. This would increase the anesthetic concentration in the blood, possibly re-anesthetizing the patient. Could this really happen if a patient stops breathing after awakening from anesthesia?

Drs. Stanley Leeson, Russell S. Roberson, and James Philip, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts had just such a patient. The patient developed laryngospasm soon after the endotracheal tube was removed.  They simulated what goes on when patients hypoventilate at the end of a case and whether there’s the potential for reanesthetization using the Gas Man® simulation program. The results of this study are published in this month’s issue of Anesthesia & Analgesia and described in the article titled “Hypoventilation After Inhaled Anesthesia Results in Reanesthetization.”

The authors simulated the anesthetic concentration in the blood following inhalation of isoflurane, sevoflurane, and desflurane at 0.75 MAC, 1 MAC, and 1.5 MAC for durations of 1-, 2-, 4-, and 6-hours. The simulations were performed using the program Gas Man. Alveolar ventilation (VA) was set to 4 L/min, cardiac output (CO) at 5 L/min, and blood flow to VRG, MUS, and FAT was set to be 76%, 18%, and 6% of cardiac output, respectively. At the end of the simulated period of anesthesia, the vaporizer was set to 0 and fresh gas flow from the anesthesia machine was 8 L/min. When the anesthetic concentration in the VRG reached 0.33 MAC (MAC awake), alveolar ventilation was set to 0, 0.1 and 4 L/min for each anesthetic.

Re-anesthetization occurred more quickly after longer anesthetics, an expected result given the greater degree of tissue saturation. If alveolar ventilation was greater than 1.2 L/min, re-anesthetization was not predicted to occur with any of the combinations of drug, MAC, and anesthetic duration.  The source of anesthetic that re-anesthetized was muscle and not fat.

Impaired ventilation prevents the removal of anesthesia. Based on these simulations, it would be wise to be certain that patient ventilation does not drop below 1.2 L/min following emergence from inhaled anesthetic.

We can add this to the very long list of reasons that breathing is good.

(This post and the associated recording was modified to indicate that muscle was the source of re-anesthetization and to indicate the location of the second author)