Long Qt and Torsade

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urge

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Can someone explain to me the following?

If you have a pt with long qt syndrome the treatment to prevent torsade is beta blockers. However, if someone is in torsade the treatment is isuprel, a beta agonist (plus mag and some other stuff). That's a bit hard for me to understand. Anyone care to shine some light into the subject?
 
Can someone explain to me the following?

If you have a pt with long qt syndrome the treatment to prevent torsade is beta blockers. However, if someone is in torsade the treatment is isuprel, a beta agonist (plus mag and some other stuff). That's a bit hard for me to understand. Anyone care to shine some light into the subject?
The theory is:
In people with inherited long QT syndrome it is believed that surges of sympathetic activity could trigger the episodes of torsade and that's why beta blockers are used to prevent them.
That's also why sympathetic nerve blocks have been used successfully in some cases to prevent torsade in these patients.
This theory is not well supported and many people argue that anything that causes bradycardia could worsen long QT.
The treatment for an episode of torsade is usually magnesium or pacing as long as the patient is not pulseless, If pacing is not available Isuprel could be attempted (chemical pacing) but it wouldn't be my first choice.
 
The theory is:
In people with inherited long QT syndrome it is believed that surges of sympathetic activity could trigger the episodes of torsade and that's why beta blockers are used to prevent them.
That's also why sympathetic nerve blocks have been used successfully in some cases to prevent torsade in these patients.
This theory is not well supported and many people argue that anything that causes bradycardia could worsen long QT.
The treatment for an episode of torsade is usually magnesium or pacing as long as the patient is not pulseless, If pacing is not available Isuprel could be attempted (chemical pacing) but it wouldn't be my first choice.

Choice or not, isuprel is well documented as treatment for torsade.
Why do you want to slow the HR to prevent torsade, but if torsade happens then you should increase the HR? One thing is against the other. Can you imagine yourself setting up an esmolol drip and an isuprel drip to do the case? The whole thing does not make sense.
 
Choice or not, isuprel is well documented as treatment for torsade.
Why do you want to slow the HR to prevent torsade, but if torsade happens then you should increase the HR? One thing is against the other. Can you imagine yourself setting up an esmolol drip and an isuprel drip to do the case? The whole thing does not make sense.
Isuprel is a treatment for torsade in some books but in my opinion pacing is your treatment of choice for a torsade that doesn't respond well to Magnesium.
Adrenergic blockade on the other hand is effective in decreasing the frequency of the torsade episodes in patients with hereditary long QT syndrome who don't qualify for an AICD.
I have done Stellate ganglion blocks a couple of times on these patients to determine their response to surgical sympathectomy and I know it works.
The theory as I said is preventing sympathetic surges that are thought to trigger the torsade episodes.
 
Feel free to flame away, but i think it has something with to do with keeping the QRS from landing on the T wave. When that happens your heart goes all haywire and ur in Vtach or torsades. If you keep the HR from speeding up with B-blockers the ventricular depolarization(qrs) cannot be triggered while the ventricle is reporlarization(t wave). I believe you can iatrogenically do this if you do a syncronized cardioversion on the T wave(ie the Sync is wrong on the cardioverter). Isoprotenerol i believe then increases SA node discharge and the theory is to overdrive suppress the torsades? I absolutely did not look this up so please feel free to flame away and correct me, sad thing is im doing med/cards this month👎
 
I think the issue is torsades that is refractory to mag, i.e. goes in and out of NSR and into TDP. Since these cases are usually preceded by a 'pause', it makes sense to try and eliminate that pause with a chronotropic agonist.

For someone in frank torsdades, id put the pads on and dose the mag twice and try and beta-BLOCK down to NSR and then shock them.
 
I think the issue is torsades that is refractory to mag, i.e. goes in and out of NSR and into TDP. Since these cases are usually preceded by a 'pause', it makes sense to try and eliminate that pause with a chronotropic agonist.

For someone in frank torsdades, id put the pads on and dose the mag twice and try and beta-BLOCK down to NSR and then shock them.
No, If they are in Torsades Don't try to beta block them, beta blockers are meant as prophylaxis not treatment of acute episodes.
Torsades= Magnesium, if no response then pacing if no pacer available try Isuprel until you get a pacer.
If they become pulseless treat it like you treat Vfib.
 
The mainstay of treatment of TdP in pts with congenital long QT syndrome (LQT) is beta blockade. I can say treatment because TdP is typically a paroxysmal phenomenon which often spontaneously resolves (But not always). This is because for most pt's with LQT TdB are brought on by high catecholamine states such as exercise/ excitement etc. The inciting event is often a VPC occuring during the prolonged repol period. There is good evidence for BB use. In a series of around 900 pts thre was a decrease in SCD/syncope events from about 1/yr to less than 0.3/yr when maximally beta blocked. Interestingly there is a subset of pts (LQT3 mutation) in which TdP is brought on not by high catecholamine states but by states which cause slowing of the heart rate such as sleep and rest. These pts respond less well to BB. The recommendation for pt's with LQT is to add dual chamber pacing in addition to the BB to pts who are maximally beta blocked and still symptomatic. This has been shown to reduce the incidence of these events. As far as acute treatment the guidelines are clear at least as far as the AHA and ACC are concerned. As above if there is hemodynamic compromise then defibrillation is warranted. Short of that there are two strong recommendations that are supported by good evidence: 1. Correct lyte abnormalities and d/c offending medications. 2. TC pacing for pts with TdP who have bradycardia and heart block. There are further recommendations which do have some supporting evidence: 1. IV Mag sulfate. 2. Pacing in combination with BB for pts with sinus bradycardia and TdP (this can be used in the acute setting). 3. Pacing for pt's with pause dependant TdP. 4. Isopreteronol in pts who do not have congenital LQT and have pause dependant TdP.

I hope this was helpful

But don't take my word for it I'm just a dumb ol Fam 🙂 Med resident.
 
you are right plankton, im not sure why i put beta blockade in there, i think i got the isuprel and esmolol circuits switched 😉
 
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