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Correspondence  |   November 2017
A Deeper Look at Anesthesia Depth
Author Notes
  • Tufts University School of Medicine, Tufts Medical Center, Boston, Massachusetts. rknapp@tuftsmedicalcenter.org
  • This letter was sent to the author of the original article referenced above, who declined to respond.—Evan D. Kharasch, M.D., Ph.D., Editor-in-Chief.
    This letter was sent to the author of the original article referenced above, who declined to respond.—Evan D. Kharasch, M.D., Ph.D., Editor-in-Chief.×
  • (Accepted for publication July 26, 2017)
    (Accepted for publication July 26, 2017)×
Article Information
Correspondence
Correspondence   |   November 2017
A Deeper Look at Anesthesia Depth
Anesthesiology 11 2017, Vol.127, 904-905. doi:10.1097/ALN.0000000000001849
Anesthesiology 11 2017, Vol.127, 904-905. doi:10.1097/ALN.0000000000001849
To the Editor:
The editorial by Garcia and Sleigh1  provided an outstanding discussion of ketamine’s complexities. Their conclusion, that we use a flawed concept of anesthesia depth, was insightful and provides a reason as well as an opportunity to suggest something more meaningful.
Anesthetic “depth” is one of our profession’s oldest and most used metaphors. As a metaphor, greater depth has long held connotations of an increased anesthetic dose and a traditionally strong connection to our observations of deep sleep.
In the past, this did not pose a particular problem, but now it does. Connecting greater depth to deeper sleep tends to push our thinking toward a unitary concept of anesthetic action, even though the unitary concept has been discredited. In this way, our most common metaphor actually hampers our using more appropriate concepts of anesthetic actions and interactions.
But shifting the depth connection away from sleep and toward anatomy can resolve this problem. The key to this is that increased depth is synonymous with higher minimum alveolar concentration (MAC) values. When these MAC values are aligned with the relevant neuroanatomy, a connection between depth and anatomy arises that is far more functional than the connection between depth and sleep.
To see this, consider some specific anesthetic effects associated with specific MAC values. Loss of movement results from the equipotent dose of the γ-aminobutyric acid–enhancing anesthetics known as 1 MAC. Loss of consciousness occurs at approximately 0.3 MAC (MAC-Awake)2  and 1.3 MAC produces suppression of the sympathetic nervous system (MAC-BAR).3 
These three functions—consciousness, movement, and sympathetic suppression—can be attributed to three more or less distinct regions of the nervous system. Consciousness is associated with the cerebral cortex, movement goes with the spinal cord, and a significant component of sympathetic suppression occurs outward from the spinal cord.4,5  When you match these locations to the appropriate MAC values, you find that an increasing anesthetic dose, or increasing depth, produces effects first in the cortex (0.3 MAC), then down the spinal cord (1 MAC), and then finally further out toward the periphery (1.3 MAC).
This gives the metaphor of depth an actual, if coincidental, anatomic correlation. Increased doses of anesthetic produce effects first in the “uppermost” region of the nervous system, then further “down,” and finally further “out.” In other words, “depth” is a descent down the nervous system as anesthetic dosage increases, and an ascent back up as the dosage level is reversed.
This makes increasing anesthetic depth a metaphor for anesthetic affect on an increasingly larger number of neural subsystems, instead of limiting depth to describing an observed state as somehow more profound in an ill-defined manner. Of course, this is based on an enormous simplification of the nervous system. But even at that, it allows the concept of depth to provide a much more meaningful context for the complexities described by Garcia and Sleigh. It also encourages us to view anesthesia not as a unitary phenomenon, but rather as a suite of altered neurologic functions roughly affiliated with a suite of neurologic regions. And it is this suite of regions, and their interconnections, that provides a substrate of sufficient complexity to encompass all the alterations caused by anesthetics.
Competing Interests
The author declares no competing interests.
Robert M. Knapp, D.O., J.D., Tufts University School of Medicine, Tufts Medical Center, Boston, Massachusetts. rknapp@tuftsmedicalcenter.org
References
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Daniel, M, Weiskopf, RB, Noorani, M, Eger, EIII . Fentanyl augments the blockade of the sympathetic response to incision (MAC-BAR) produced by desflurane and isoflurane: Desflurane and isoflurane MAC-BAR without and with fentanyl. Anesthesiology 1998; 88:43–9 [Article] [PubMed]
Wang, L, Spary, E, Deuchars, J, Deuchars, SA . Tonic GABAergic inhibition of sympathetic preganglionic neurons: A novel substrate for sympathetic control. J Neurosci 2008; 28:12445–52 [Article] [PubMed]
Ebert, TJ . Sympathetic and hemodynamic effects of moderate and deep sedation with propofol in humans. Anesthesiology 2005; 103:20–4 [Article] [PubMed]