In the sedation of the COPD patient, does your sedation change if the patient is very hard to ventilate? Is this a case where you'd consider a ketamine infusion until the COPD is better controlled and the vent settings come into a tolerable range, and then switch over to a more traditional fentanyl and propofol sedation package?
I am unimpressed with the bronchodilatory power of ketamine and would not choose it preferentially over propofol which also has bronchodilatory properties, albeit prob. just as minor as the ketamine
Question in regard to post intubation sedation for bleeding trauma patients that require transfer. Is there any concern for sending these patients out on a ketamine drip, or frequent ketamine dosing? Often these patients are very tachycardic, and I'm wondering if it would put these patients at increased risk for catecholamine surge and heart failure. Would dex be a better option in this scenario?
We often hear concerns about tachycardia and hypertension with ketamine but in the sick patient, they're likely unfounded worries. Ketamine leads to endogenous catecholamine release but in sick patients (trauma or otherwise) the patient has likely used up all their catecholamines already or has maximal surge already from the illness. Ketamine is unlikely to change this. The problem I see with dex is that it needs time to take effect and titrate which you're unlikely to want to take when you're transferring for definitive care. Many prehospital systems and systems with long transport times rely on ketamine for this indication. I'll forward along to Scott as well and see his thoughts
You mention using pressors like norepi when dealing with post-intubation hypotension (whether that's from the intubation itself, or the patient's underlying pathological process.) Are you obtaining central venous access in all of these patients to whom you are administering pressors, or just a solid peripheral line? I find myself placing fewer central lines these days with CLABSI and other potential complications being so scrutinized, as well as the time sink that central venous access has become. But, with your aggressive analgesia+sedative+early pressor strategy, perhaps you advocate for early CVL placement as well? Some post-intubation hypotension is fairly short-lived, and pressors can likely be discontinued relatively quickly, but much of the time I don't have a crystal ball and can't tell who will need longer-term vasopressor therapy to maintain BP in the setting of adequate analgesia and sedation. What are your recommendations?
I do less and less central lines in the ED as well. I'm running the pressors peripherally most of the time to start. I'll place the CVL if the patient has poor peripheral access or I need multiple infusions. Another option is to place a midline which is fairly easy as long as you have the kit. Also, important to note that femoral CVL placement is fine as well. We often shy away from them but best evidence (Parienti 2015 https://www.ncbi.nlm.nih.gov/pubmed/26398070) showed similar infection rates with femoral lines and IJs. I find non-intubated patients often tolerate femoral placement a bit better and, I still think they're faster to place but that may be operator related.
The risk of Propofol Infusion Syndrome is suspected to be increased with the simultaneous administration of propofol and catecholamines (vasopressors). Have you noticed any cases of PRIS with this propofol + norepinephrine strategy?
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Joel R. - April 1, 2019 11:01 PM
In the sedation of the COPD patient, does your sedation change if the patient is very hard to ventilate? Is this a case where you'd consider a ketamine infusion until the COPD is better controlled and the vent settings come into a tolerable range, and then switch over to a more traditional fentanyl and propofol sedation package?
EMCrit - April 2, 2019 7:12 AM
I am unimpressed with the bronchodilatory power of ketamine and would not choose it preferentially over propofol which also has bronchodilatory properties, albeit prob. just as minor as the ketamine
Aaron C. - April 4, 2019 12:01 PM
Question in regard to post intubation sedation for bleeding trauma patients that require transfer. Is there any concern for sending these patients out on a ketamine drip, or frequent ketamine dosing? Often these patients are very tachycardic, and I'm wondering if it would put these patients at increased risk for catecholamine surge and heart failure. Would dex be a better option in this scenario?
Anand S. - April 4, 2019 12:12 PM
We often hear concerns about tachycardia and hypertension with ketamine but in the sick patient, they're likely unfounded worries. Ketamine leads to endogenous catecholamine release but in sick patients (trauma or otherwise) the patient has likely used up all their catecholamines already or has maximal surge already from the illness. Ketamine is unlikely to change this.
The problem I see with dex is that it needs time to take effect and titrate which you're unlikely to want to take when you're transferring for definitive care.
Many prehospital systems and systems with long transport times rely on ketamine for this indication.
I'll forward along to Scott as well and see his thoughts
EMCrit - April 4, 2019 1:56 PM
ditto what Swami said
Shannon G. - April 7, 2019 5:34 AM
You mention using pressors like norepi when dealing with post-intubation hypotension (whether that's from the intubation itself, or the patient's underlying pathological process.) Are you obtaining central venous access in all of these patients to whom you are administering pressors, or just a solid peripheral line? I find myself placing fewer central lines these days with CLABSI and other potential complications being so scrutinized, as well as the time sink that central venous access has become. But, with your aggressive analgesia+sedative+early pressor strategy, perhaps you advocate for early CVL placement as well? Some post-intubation hypotension is fairly short-lived, and pressors can likely be discontinued relatively quickly, but much of the time I don't have a crystal ball and can't tell who will need longer-term vasopressor therapy to maintain BP in the setting of adequate analgesia and sedation. What are your recommendations?
Anand S. - April 7, 2019 6:01 AM
I do less and less central lines in the ED as well. I'm running the pressors peripherally most of the time to start. I'll place the CVL if the patient has poor peripheral access or I need multiple infusions. Another option is to place a midline which is fairly easy as long as you have the kit.
Also, important to note that femoral CVL placement is fine as well. We often shy away from them but best evidence (Parienti 2015 https://www.ncbi.nlm.nih.gov/pubmed/26398070) showed similar infection rates with femoral lines and IJs. I find non-intubated patients often tolerate femoral placement a bit better and, I still think they're faster to place but that may be operator related.
SHIH-CHIN C. - May 18, 2019 1:47 PM
The risk of Propofol Infusion Syndrome is suspected to be increased with the simultaneous administration of propofol and catecholamines (vasopressors). Have you noticed any cases of PRIS with this propofol + norepinephrine strategy?