In this episode, I’ll discuss scenarios where dexmedetomidine & etomidate are better than ketamine.
Strictly referring to therapeutic uses, ketamine is a stylish medication to use and to talk about using. It has been FDA approved for over 45 years, but ketamine’s popularity as measured by published journal articles is at it’s highest level yet.
In episode 16, I discussed the use of ketamine in critical care. And in episode 98, I discussed whether there was a pro-ketamine bias in the #FOAMed community.
Ketamine’s unique dissociative mechanism of action, analgesic effects, and side effect profile are attractive to many clinicians. Anecdotally, some clinicians seem to wear the choice of ketamine as a badge of honor. Dig far enough on twitter, and you’ll get an idea of what I mean.
The usual side effect profile of ketamine includes excessive secretions, laryngeal spasm, positive cardiovascular effects (slight increase in blood pressure and heart rate), and neuropsychological effects such as dysphoria or emergence phenomenon. Each of these effects may be rationalized as easily managed, but they are potential effects nonetheless.
Besides having an analgesic property, benefits of ketamine are often described as:
AND
Except neither of those “benefits” can be taken as absolute statements.
Ketamine is not supposed to cause respiratory depression, but it can. In episode 139 I described an agitated patient that got a low dose of ketamine and developed apnea within 1 minute. One review from 2008 in the American Journal of Emergency Medicine even stated that
a brief period of apnea around the time of injection is common.
Ketamine is not supposed to cause hypotension, but it can. In patients whose catecholamine stores are depleted (such as in severe sepsis), ketamine can have direct negative inotropic effects. One of the more compelling reasons for ketamine use – its’ lack of cardiac depressant effects – isn’t valid in scenarios where it would be most needed. A pediatric review article from 2012 stated:
The evidence regarding ketamine’s support of cardiovascular function is applicable to clinical situations where endogenous catecholamine stores are not likely to be exhausted.
And if that is not enough, Dr. Sergey Motov and colleagues have published a horror-story of a case regarding a 58 year-old female who got ketamine for procedural sedation. In this case, ketamine appeared to cause hypertensive emergency with acute pulmonary edema leading to endotracheal intubation and cardiac arrest with successful resuscitation and stabilization.
The case of ED ketamine use that really shook me up! #FOAMed #ketamine #meded https://t.co/d9W64vJ4t8
— Sergey Motov (@painfreeED) November 1, 2016
In critically ill patients ketamine is frequently considered for:
1. Induction for rapid sequence intubation when hypotension cannot be tolerated
2. Procedural sedation when respiratory depression cannot be tolerated
But given the known side effect profile of ketamine, I’d rather use:
1. Etomidate as induction for rapid sequence intubation when hypotension cannot be tolerated
2. Dexmedetomidine for procedural sedation when respiratory depression cannot be tolerated
Although dexmedetomidine can cause hypotension/bradycardia, there are no reports of apnea when it is used as monotherapy and only 2 cases where dexmedetomidine + opioids likely led to apnea.
There are still plenty of indications such as excited delirium, rescue analgesia, status asthmaticus, and even status epilepticus where ketamine has a favorable risk:benefit analysis.
If you like this post, check out my book – A Pharmacist’s Guide to Inpatient Medical Emergencies: How to respond to code blue, rapid response calls, and other medical emergencies.
Joe,
I’ve had great experience with ketamine in the ED setting. Some things to consider when giving ketamine:
1. A slow IV push administered over 1 minute can prevent the sudden apnea and other side effects such as re-emergence. Rapid IV push has been associated with increase risk of side effects.
2. Pre-emptive zofran administration prior to admin can decrease rates of N/V. I usually tell my doc to give it prior to the slow infusion.
I completely disagree with using Precedex for procedural sedation. Precedex cannot cause a deep enough sedation and although it does not cause respiratory compromise, the hypotension is almost as bad as propofol. Precedex onset of action is also not as fast as other sedatives out there.
I’m with you with etomidate. Apnea is a concern for patient that are obese so we should watch for that.
Thank you for sharing your experiences & opinions!
Your points about dexmedetomidine are certainly true – it has a slower onset and has a risk of hypotension (and even bradycardia) similar to propofol.
The cost of precedex may be too costly. I have thought of using it for dsi. Procedural sedation for oxygenation for dyspneic patient with fever and rapid afib. But no hypotension yet. Pt with pna..not in chf..yet.