Very interesting case you started with. Don't see with calling EP lab and them being aware of the case that you had done anything wrong. Frustrating that it took so long to get your patient to the necessary procedure. I was not aware that a Bradycardia would degenerate into the tachydysrythmia. Is that the normal progression? Thought they just went into asystole. Thank you.
Fredrick - thanks. Not really blame as much as I simply could have (and should have) done better. I don't know if this is the normal progression. May have to get Amal's thoughts on this. For this particular patient, severe brady and prolonged QT possibly led to the torsades.
Back in the early 70's we'd handle this with atropine and an isoproteronol infusion. But, the frequency of tachydysrhythmias generated interested in ERP's (there were 10 or 12 of us back then) placing emergent temporary transvenous pacers - to get away from the "dangers" of Isuprel. That became the standard paradigm in the US. About 5 years ago, while working in Tasmania (no, it's not near Romania - it's a state of Oz - and, for reasons that escape me, I saw more severely symptomatic bradycardias in 6 months there than I had in 5 years in the US), the paradigm was to avoid the "dangers" and complication rate of emergent pacer insertion by relatively inexperienced ER Docs, and maintain these patients with atropine plus, if needed, an epinephrine drip. Even after the cardiologists had seen and admitted the patients, they'd just keep the drip going overnight and do the pacer insertion the following morning (with the fallback of emergent pacer only if the epi drip didn't work adequately - and, that didn't happen during my time there). I was quite impressed at how well this worked, and how much less stressful it was for someone like me who put in an emergent pacer less than once every couple years.
I'm not sure if the Tasmanian paradigm holds in the rest of Australia, but for those of us in the US who have perhaps not placed a transvenous pacer with enough frequency to be really adept at it, the atropine plus epi drip might me a really nice alternative. Even for our friends.
Hi folks, Regarding the recent article on the use of ketamine for management of agitation it's worth noting that our own ACEP guidelines list "known or suspected schizophrenia" as an absolute contraindication to its use. Food for thought considering the population of patients for whom we'll be considering this sedation strategy. -Mo
Thank you for simplifying the cricon algorithm. Could you please describe how you secure an endotracheal tube if that is what you use for your cric? Thanks, Jen
Hi Michelle, Great segment on pre-charging the defibrillator. Many of us made this change a few years ago in EMS, but hospitals and ED have been slow to adopt. While not a great deal of evidence, this is really a response to the evidence in decreasing pre and/or peri-shock pause.
We also do not use the 2 minute cycle. It is difficult to time a resuscitation in the pre-hospital environment and I don't think we are great at this in the hospital. We use 200 compression cycles as this requires no timing and prevents compressor fatigue. The compressor can only perform 200 compressions and counts aloud every 20th compression. When reaching 180, two things occur: 1. a new compressor moves into position with hands hovering over the chest and; 2. the defibrillator is charged. When reaching the 200th compression the team leader has some choices that must occur in less than 5 seconds. First, if it is a shockable rhythm - shock it. Second, if non-shockable, move on. Third, if unsure, shock it and move on. In all cases hands go back on the chest immediately. This can decrease your pre and peri-shock pause to less than 5 seconds.
A pulse check can occur, but once you have an advanced airway, then EtCO2 is placed and pulse checks no longer occur unless you have a spike in EtCO2, which can also aid in decreasing peri-shock pause with no time dedicated to the insensitive pulse check. Pulse checks would then only occur at the end of a 200 cycle.
Hands-on defibrillation is cool, but I don't think particularly advantageous. I worry that this would empower the compressor to continue too long and introduce fatigue and poor quality CPR. Having a very specific timing sequence to change the compressor and deliver a very rapid shock, if needed, has more utility. With a bi-phasic defibrillator the chance of injury is almost zero, unless you also fall down. Mono-phasic is a different story - ouch!
Team focused or high-performance CPR is great, but in NC we like to draw on our NASCAR roots and use the term pitcrew CPR. Having specific assignments is only the first step, each assignment must also have very specific, timed tasks to complete. This will likely become even more important as EMS continues to embrace termination on scene and the ED sees less cardiac resuscitations - we will get rusty. We already see the impact on our residents as they do not have the opportunity to run a great deal of codes because our surrounding EMS agencies only transport with ROSC. Team training and specific assignments with specific assignment tasks will become even more necessary for the ED.
This technique really keeps you on track with near continous compressions with minimal interruptions. In the ED and hospital it seems we look for any and every excuse to stop compressions. Happy to share our EMS Pitcrew CPR Protocols to anyone interested - easily adopted to ED use. robnelso@wakehealth.edu Thanks, Darrell
To join the conversation, you need to subscribe.
Sign up today for full access to all episodes and to join the conversation.
Frederick R. - November 1, 2016 4:28 PM
Hey Swami,
Very interesting case you started with. Don't see with calling EP lab and them being aware of the case that you had done anything wrong. Frustrating that it took so long to get your patient to the necessary procedure. I was not aware that a Bradycardia would degenerate into the tachydysrythmia. Is that the normal progression? Thought they just went into asystole. Thank you.
Fritz
Anand S. - November 1, 2016 5:13 PM
Fredrick - thanks. Not really blame as much as I simply could have (and should have) done better. I don't know if this is the normal progression. May have to get Amal's thoughts on this. For this particular patient, severe brady and prolonged QT possibly led to the torsades.
Rabbott - November 3, 2016 10:54 AM
Back in the early 70's we'd handle this with atropine and an isoproteronol infusion. But, the frequency of tachydysrhythmias generated interested in ERP's (there were 10 or 12 of us back then) placing emergent temporary transvenous pacers - to get away from the "dangers" of Isuprel. That became the standard paradigm in the US. About 5 years ago, while working in Tasmania (no, it's not near Romania - it's a state of Oz - and, for reasons that escape me, I saw more severely symptomatic bradycardias in 6 months there than I had in 5 years in the US), the paradigm was to avoid the "dangers" and complication rate of emergent pacer insertion by relatively inexperienced ER Docs, and maintain these patients with atropine plus, if needed, an epinephrine drip. Even after the cardiologists had seen and admitted the patients, they'd just keep the drip going overnight and do the pacer insertion the following morning (with the fallback of emergent pacer only if the epi drip didn't work adequately - and, that didn't happen during my time there). I was quite impressed at how well this worked, and how much less stressful it was for someone like me who put in an emergent pacer less than once every couple years.
I'm not sure if the Tasmanian paradigm holds in the rest of Australia, but for those of us in the US who have perhaps not placed a transvenous pacer with enough frequency to be really adept at it, the atropine plus epi drip might me a really nice alternative. Even for our friends.
paul f. - November 9, 2016 7:53 AM
What was the rational for magnesium infusion? Magnesium can slow the Heart rate also. He was not having Torsades before this was given was he?
Morris R., MD - November 10, 2016 9:39 AM
Hi folks,
Regarding the recent article on the use of ketamine for management of agitation it's worth noting that our own ACEP guidelines list "known or suspected schizophrenia" as an absolute contraindication to its use. Food for thought considering the population of patients for whom we'll be considering this sedation strategy.
-Mo
jdoubleu - November 25, 2016 12:22 PM
Hi Scott,
Thank you for simplifying the cricon algorithm. Could you please describe how you secure an endotracheal tube if that is what you use for your cric?
Thanks,
Jen
Rob O - December 1, 2016 3:26 PM
Hi Jen,
We will have a whole critical care mailbag devoted to your very question this spring
Robert N. - November 26, 2016 11:09 AM
Hi Michelle,
Great segment on pre-charging the defibrillator. Many of us made this change a few years ago in EMS, but hospitals and ED have been slow to adopt. While not a great deal of evidence, this is really a response to the evidence in decreasing pre and/or peri-shock pause.
We also do not use the 2 minute cycle. It is difficult to time a resuscitation in the pre-hospital environment and I don't think we are great at this in the hospital. We use 200 compression cycles as this requires no timing and prevents compressor fatigue. The compressor can only perform 200 compressions and counts aloud every 20th compression. When reaching 180, two things occur: 1. a new compressor moves into position with hands hovering over the chest and; 2. the defibrillator is charged. When reaching the 200th compression the team leader has some choices that must occur in less than 5 seconds. First, if it is a shockable rhythm - shock it. Second, if non-shockable, move on. Third, if unsure, shock it and move on. In all cases hands go back on the chest immediately. This can decrease your pre and peri-shock pause to less than 5 seconds.
A pulse check can occur, but once you have an advanced airway, then EtCO2 is placed and pulse checks no longer occur unless you have a spike in EtCO2, which can also aid in decreasing peri-shock pause with no time dedicated to the insensitive pulse check. Pulse checks would then only occur at the end of a 200 cycle.
Hands-on defibrillation is cool, but I don't think particularly advantageous. I worry that this would empower the compressor to continue too long and introduce fatigue and poor quality CPR. Having a very specific timing sequence to change the compressor and deliver a very rapid shock, if needed, has more utility. With a bi-phasic defibrillator the chance of injury is almost zero, unless you also fall down. Mono-phasic is a different story - ouch!
Team focused or high-performance CPR is great, but in NC we like to draw on our NASCAR roots and use the term pitcrew CPR. Having specific assignments is only the first step, each assignment must also have very specific, timed tasks to complete. This will likely become even more important as EMS continues to embrace termination on scene and the ED sees less cardiac resuscitations - we will get rusty. We already see the impact on our residents as they do not have the opportunity to run a great deal of codes because our surrounding EMS agencies only transport with ROSC. Team training and specific assignments with specific assignment tasks will become even more necessary for the ED.
This technique really keeps you on track with near continous compressions with minimal interruptions. In the ED and hospital it seems we look for any and every excuse to stop compressions. Happy to share our EMS Pitcrew CPR Protocols to anyone interested - easily adopted to ED use. robnelso@wakehealth.edu
Thanks,
Darrell