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(36:05) Continuing on learning the language of the heart Kelly & Ron discuss Battlestar Galactica (the original series) as well as places further down the heart. Ventricular rhythms, the pulseless part of the algorithm (PEA), why to give drugs or epi first, when to use Edison therapy, or when it is time to all in to end efforts. Also, Kelly discusses how things one learns in school, and the algorithms for giving drugs, can be very very different than what may happen in the field.
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Guys here is the agility test for one of the agencies I have applied for:
Performing eight minutes of cardiopulmonary resuscitation (CPR) on a
manikin. With another applicant, carrying 200-lbs. (which is secured onto an
auxiliary stretcher) down a flight of stairs, load the weight onto an
ambulance stretcher, and load the stretcher into an ambulance. Then the applicant and partner must unload the stretcher, take the weight
off of the ambulance stretcher, and carry the 200-lbs. back up the stairs. After they have the weight back up the stairs, they must lift one end of
the auxiliary stretcher up to their shoulders.
Talk about a workout .
Hey guys, love the show and been listening since day one, but for the first time I truly disagree with something that Kelly has said. During the podcast, while rightfully expressing a skeptical view of the various antiarrhythmics in cardiac arrest, regarding Torsades de Pointes (TdP) youstated, “the drug for it is only magnesium if the cause is low magnesium levels.” I too disagree with a lot of the pharmacotherapy we provide, but have always taken for granted that mag sulfate did more than just correct hypomagnesemia since I know it’s a fairly useful for controlling rapid a-fib, which is usually not due to hypoMg+ . So I went looking for an answer…
The first problem is that I can’t find any convincing evidence that hypomagnesemia actually causes a prolonged-QT, necessary for the diagnosis of TdP (otherwise it’s just polymorphic v-tach). There’s numerous articles that state it can be a finding, but the one paper referenced on the topic is from 1982 and I can’t even find an abstract. On the other hand, in Chou’s “Electrocardiography in Clinical Practice,” one of the masters of electrocardiography states, “Hypomagnesemia and hypermagnesemia do not produce specific ECG patterns in animals and humans. Personal experience suggests that neither hyper- nor hypomagnesemia has a detectable effect on the QT interval in humans.” So while the condition may indeed predispose someone to arrhythmias and is often present along with other electrolyte imbalances that may prolong the QTi, we shouldn’t be attributing their TdP to hypoMg+.
Since we’re not even worried about low mag at this point, the big causes of a prolonged QT we’d see are drugs and medications, electrolyte imbalances (hypoK+ and hypoCa++), and congenital Long-QT Syndrome. There’s others of course, but I don’t have time to go through them all. After consulting Dr. Google and skimming through a bunch of papers of limited applicability along with the AHA’s most recent guidelines on the matter, there’s a common theme. The consensus seems to be that we barely understand all of the effects magnesium has an the heart’s conduction system, and although there is limited data available on it’s actual use for TdP in cardiac arrest, it seems to have a a definite antiarrhythmic effect in all of the above causes of QT prolongation and TdP. The efficacy of it’s use in ACLS scenarios is far from proven and I agree with the IIb level of evidence recommendation from the AHA, but there’s definitely far more to it’s action than just correcting magnesium levels.
Sorry for the long, drawn-out post, but I figured if I had to disagree with someone I look up to in EMS, I’d better back up what I have to say, even if it is a quibble on a fairly minor point. Now I’m just a newbie at this and it’s very likely you know something (or a lot of things…) I don’t, but if you’d like to know where I got these crazy notions, shoot me an email (I’m assuming you can see it when I post) and I’ll respond once I stop giggling from the excitement of being judged worthy of your time. Thanks,
– VinceD
Thanks for the information, Vince.
I’ve long said that many other things besides hypomagnesemia can precipitate TDP, chief among them antiarrhythmic toxicity and bradycardias. I don’t think I mentioned congenital long QT syndrome in the podcast, but I should have.
I’ve often said that we should leave the selective cardiotoxins in the box in favor of Edison medicine, particularly in ventricular arrhythmias. The points you cite demonstrate the shallowness of our understanding of antiarrhythmics in general and mag in particular.
Looks like I’ve got some research to do!
If you really want to throw people for a loop, call vasopressin by one of it’s other common names. Anti-diuretic hormone. 😀
Us Kelly’s “selective cardiotoxins” opinion in an assignment – referenced 🙂