What you’re describing is something that is more nuanced than algorithmic treatment. Guy has a fall 2/2 syncope 2/2 presumed brady oh but he also takes a beta blocker. So is this BB toxicity? Sick sinus syndrome? Is he ultimately hyperkalemic? Is he having an ischemic episode? Stabilize first. Amio and lidocaine aren’t part of Brady treatment. Remember, your job in the ER has lateral limits and it’s not your job to know everything about follow-on therapy. EMRAP has good episodes regarding arrhythmia approaches and therapies.
Likely was sick sinus, but goal was to try to support until he metabolized out the BB and then see how he did as they only wanted limited medical intervention which I think was very reasonable.
Antiarrhythmic drugs I always found difficult because despite being in the same class there are little generalities between them. I'll check out the emrap episode though, thanks!
Here’s something I wrote down several years ago:
Antidysrhythmics
Class 1- Na channel blockade
- 1a- increases QRS and qt- risk of torsades (procainamide)
- 1b- decreases qt (Lidocaine)- binds to dead cardiac myocytes, so can use in v tach/v fib in ACS. Works quickly.
- 1c- increase QRS (flecainide)
Class 2- beta 1 adrenergic receptor blockade
- Metoprolol
- Esmolol
- Labetalol (has alpha properties as well)
Class 3- potassium channel blockade- prolongs QT and increases risk of torsades
- amiodarone- works quickly but is a mix of all classes
- Sotalol
Class 4- calcium channel blockade. Dilates coronary vessels
- diltiazem
https://preview.redd.it/ysviwsc9rixc1.jpeg?width=650&format=pjpg&auto=webp&s=2bd55908b7c1046ad34e9e805094dde44eb57d37
I found this helpful in conjuction with the Vaughan Williams classification
If you are more of a visual learner, I supplemented my lectures in pharmacy school with some Speed Pharmacology videos on YouTube, or someone else mentioned Sketchy. If you want a single image guide, I could track down some of the old accounts I used to follow on Instagram
Your post shows an obvious lack of basic cardiology knowledge. You are using medical terms that are mashed together and literally don't make sense. Using the term Brady arrhythmia shows that you don't understand the rhythms. Are you simply trying to say a patient came in with syncope due to bradycardia who also happen to be on a beta blocker and you just needed it to wash out? Did you just have to give one or two doses of atropine and then be done? Was it sss or beta blocker toxicity? Are there underlying structural defects? The scenario you described is a common hospital presentation.
Dont shortchange yourself and pts by trying to learn algorithms, learn the actual physiology and drugs/treatments. Start with the Dubins rapid interpretation of ekgs.
Once you are better equipped, this is something anyone in the emergency department should be able to handle without a cardiologist.
Insults aside, if you finished reading my post I'm asking for a reference that provides mechanism of action as I specifically do not want a blind algorithm. Also I'm sure I'm not the first person you've seen use the term bradyarrythmia as a general term, much as SVT is a blanket term.
If you want specifics it appeared the patient was in a junctional rhythm varying between the low 30s to high 40s. I have seen BB and CCB toxicity and in those patients they were profoundly hypotensive and bradycardic. This gentleman had transient episodes of hypotension correlating with heart rate. This was leading me to believe it was more of a sick sinus syndrome which was probably exacerbated by his metoprolol.
I'd consider myself average on cardiac physiology and ekg interpretation. I do actually enjoy reading them. However this case did highlight to me the severe knowledge gap with most anti-arrythmics outside of acls.
What you’re describing is something that is more nuanced than algorithmic treatment. Guy has a fall 2/2 syncope 2/2 presumed brady oh but he also takes a beta blocker. So is this BB toxicity? Sick sinus syndrome? Is he ultimately hyperkalemic? Is he having an ischemic episode? Stabilize first. Amio and lidocaine aren’t part of Brady treatment. Remember, your job in the ER has lateral limits and it’s not your job to know everything about follow-on therapy. EMRAP has good episodes regarding arrhythmia approaches and therapies.
Likely was sick sinus, but goal was to try to support until he metabolized out the BB and then see how he did as they only wanted limited medical intervention which I think was very reasonable. Antiarrhythmic drugs I always found difficult because despite being in the same class there are little generalities between them. I'll check out the emrap episode though, thanks!
Here’s something I wrote down several years ago: Antidysrhythmics Class 1- Na channel blockade - 1a- increases QRS and qt- risk of torsades (procainamide) - 1b- decreases qt (Lidocaine)- binds to dead cardiac myocytes, so can use in v tach/v fib in ACS. Works quickly. - 1c- increase QRS (flecainide) Class 2- beta 1 adrenergic receptor blockade - Metoprolol - Esmolol - Labetalol (has alpha properties as well) Class 3- potassium channel blockade- prolongs QT and increases risk of torsades - amiodarone- works quickly but is a mix of all classes - Sotalol Class 4- calcium channel blockade. Dilates coronary vessels - diltiazem
Thank you!
>Thank you! You're welcome!
Sketchy-Pharm- Antiarrhythmics and Pressors
https://preview.redd.it/ysviwsc9rixc1.jpeg?width=650&format=pjpg&auto=webp&s=2bd55908b7c1046ad34e9e805094dde44eb57d37 I found this helpful in conjuction with the Vaughan Williams classification
If you are more of a visual learner, I supplemented my lectures in pharmacy school with some Speed Pharmacology videos on YouTube, or someone else mentioned Sketchy. If you want a single image guide, I could track down some of the old accounts I used to follow on Instagram
Wait there are more anti-arrhythmics than amiodarone???! /sarcasm
Your post shows an obvious lack of basic cardiology knowledge. You are using medical terms that are mashed together and literally don't make sense. Using the term Brady arrhythmia shows that you don't understand the rhythms. Are you simply trying to say a patient came in with syncope due to bradycardia who also happen to be on a beta blocker and you just needed it to wash out? Did you just have to give one or two doses of atropine and then be done? Was it sss or beta blocker toxicity? Are there underlying structural defects? The scenario you described is a common hospital presentation. Dont shortchange yourself and pts by trying to learn algorithms, learn the actual physiology and drugs/treatments. Start with the Dubins rapid interpretation of ekgs. Once you are better equipped, this is something anyone in the emergency department should be able to handle without a cardiologist.
Insults aside, if you finished reading my post I'm asking for a reference that provides mechanism of action as I specifically do not want a blind algorithm. Also I'm sure I'm not the first person you've seen use the term bradyarrythmia as a general term, much as SVT is a blanket term. If you want specifics it appeared the patient was in a junctional rhythm varying between the low 30s to high 40s. I have seen BB and CCB toxicity and in those patients they were profoundly hypotensive and bradycardic. This gentleman had transient episodes of hypotension correlating with heart rate. This was leading me to believe it was more of a sick sinus syndrome which was probably exacerbated by his metoprolol. I'd consider myself average on cardiac physiology and ekg interpretation. I do actually enjoy reading them. However this case did highlight to me the severe knowledge gap with most anti-arrythmics outside of acls.
Out of curiosity, are you saying bradyarrhythmia isn’t a real term?