In November 2016, the full article will appear in JEMS magazine, both on their website – JEMS.com – and in magazine publication. How much do you think you know? Before you read the article, take this quiz to see how much you really know about how to use ketamine in emergency situations.
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At 0300 hrs you are toned out to a single vehicle accident with one passenger who slid off the road and wrapped his car around a light pole. A 44 year old male is alert, rates his pain a 13 on a 1-10 scale, and reports that he has asthma. Vital signs are: heart rate 70, blood pressure 90/60, and respirations of 25. Extrication will be at least 30 minutes and the patient has multiple fractures. What drug will you consider that can manage this patient’s pain, improve his cardiovascular state, and sedate him for extrication? Have you considered ketamine?
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You’ll also note the chart: the information enclosed was not published with the article due to space restrictions. Ketamine is a dissociative molecule meaning the drug breaks apart (or dissociates) and attaches to many different receptors. This binding results in either the turning on of receptors (upregulation) or turning them off (down regulation) causing various effects. In this case, we focus specifically on 3 major channels and receptors that provide the desired effects of ketamine for field use: sedation, hypnosis, analgesia, and bronchodilation/vasoconstriction. Note that many other channels and receptors are effected by ketamine molecules.
| Molecular Systems affected by Ketamine | ACTION | ALTERATION BY KETAMINE |
| NMDA | “Turned on” by glutamate. NMDA is an excitatory receptor for locomotion, breathing, behavior, learning, & memory. | Temporarily blocks glutamate, resulting in sedation of locomotion, relaxation of breathing, sedation, disruption of memory. |
| HCN-1 | Contributes to cortical and cardiac rhythms. | Promotes cortical synchronization and rhythms, contributing to hypnosis . |
| Nicotinic acetyl-choline ion channels | Modulates regulation of dopamine, serotonin, and dopamine. | Inhibits glutamate causing downregulation contributing to analgesia . |
| L-type Ca2+ channels | Excitation-contraction of skeletal, cardiac, and smooth muscles. | Inhibits channels resulting in vasodilation and bronchodilation |
Fig 1. Summary of receptors affected by ketamine that are pertinent to EMS use. Demonstrates the pathophysiology and dissociative pharmacology of ketamine. NMDA= n-Methyl-d-Aspartate. HCN-1= hyperpolarisation-activated cyclic nucleotide channels.
References for Figure 1
- Sleigh J, Harvey M, Voss L, et al. Ketamine-more mechanisms of action than just NMDA blockade. Trends in Anesthesia and Critical Care. 2014; 4. 76-81.
- Blanke M, VanDongen A. Biology of the NMDA Receptor. CRC Publishing: Boca Raton, pp 283-312,2009.
- Chen X, Shu S, Bayliss D. HCN1 channel subunits are a molecular substrate for hypnotic actions of ketamine.The Journal of Neuroscience. 2009;29. 600-609.
- Tassonyi E, Charpantier E, Muller D. The role of nicotinic acetylcholine receptors in the mechanisms of anesthesia. Brain Bulletin. 2002;15. 133-150.
- Corringer JP, Changeux PJ. 2008. Nicotinic Acetylcholine Receptors. Scholarpedia.Retrieved August 8, 2016 from http://www.scholarpedia.org/article/Nicotinic_acetylcholine_receptors
- Kaye A, Bannister R, Anwar M, et al. Pulmonary vasodilation is mediated in part by L-type calcium channels. Anesthesia and Analgesia. 1998;87. 956-962
For the in depth article, go to JEMS.COM starting November first.
This post, the quiz, and the table are Copyright 2016, Dr. Lindsay Henderson, M. D. If you wish to use or replicate any of the above information, please contact me.