PSA Sentinel, Summer Newsletter 2021

Page 10

Changing a Mindset: Opioids as Analgesics, not Anesthetics regimen employed, if the patient is unlikely to have significant pain in the immediate post-operative period, what are we actually treating with that opioid?

Joseph F. Answine, MD, FASA Alternate District Director to the ASA We, as anesthesiologists, know that providing anesthesia involves multiple molecules with multiple mechanisms of action at multiple sites throughout the nervous system. Whether temporarily scrambling lipids within the neuronal cell membrane, binding to neuronal surface proteins, potentiating GABA pre- and post-synaptically, reducing norepinephrine and/or serotonin release presynaptically, blocking NMDA receptors, stimulating opioid receptors, or a myriad of other mechanisms that we do not know exist as yet, we promote unconsciousness, immobility, amnesia, and a loss of pain perception. By doing one, some, or all of these, we induce and maintain anesthesia.

When an afferent nerve is stimulated, it sends signals to the dorsal horn of the spinal cord, then those electrical signals cross over and travel up the spinothalamic tract to the thalamus as the relay station. Then they go to the brain cortices for identification, the reticular activating system for wakefulness, the hypothalamus for the fight or flight response, and the limbic system for an emotion. While under anesthesia, with stimulation, each area is likely at a different anesthetic depth than the others; therefore, the somatosensory cortex may not identify the pain and the limbic system will not provide an emotion, but the reticular activating system may promote movement and the hypothalamus may stimulate a release of catecholamines leading to a change in the heart rate and blood pressure. Therefore, we could just treat those isolated responses. We could administer a paralytic for movement and antihypertensives for the catecholamine release. Not traditional, but balance will be restored.

By using multiple molecules having different mechanisms of action, we achieve our “balanced anesthetic”. I was taught that you require a hypnotic, such as thiopental or propofol, to achieve unconsciousness; a benzodiazepine, such as midazolam, to achieve amnesia; a paralytic, such as rocuronium, to achieve immobility; and a narcotic, such as fentanyl, to achieve analgesia. An inhaled agent assists with all of the above. A lack of any of these components unbalances the balanced anesthetic regimen. That was drilled into me over and over again. Don’t unbalance the balance! Following that mindset, if a patient becomes tachycardic and/or hypertensive while under anesthesia, they are “in pain”. which requires an opioid to be administered. However, if pain is a perceived response by the brain to stimulation of an A-delta or C afferent nerve, and until then, it is nothing more than a nociceptive signal trying to work its way to a cerebral cortex that is not accepting calls, we are actually giving an opioid when there is no pain. So, based on the procedure and the rest of the

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SENTINEL | The Pennsylvania Society of Anesthesiologists Newsletter

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