V-tach question

stable vs unstable??

There is a big difference in treatment.

stable..sorry

I would suggest a load of amiodarone to break the V-tach followed by a beta-1 blocker such as metoprolol once they were in a more life-sustaining rhythm.

Oh, forgot the why part. Most beta blockers will block circulating catecholamines such as norepinephrine, epinephrine, etc... and have a membrane stabilizing effect that decrease the chances of future tachyarrhythmias.

ok....first, treatment is patient dependent....what is the underlying disease process.

Given the little info.....lol........I'd say beta-blockers.

cardioselective beta-blockers: Primarily act (low doses only) to block stimulation of Beta-receptors in the heart, particularly in the SA and AV nodes, decreasing hr and reducing contractility----lowering CO, w/o blocking beta-2 receptors which would cause bronchoconstriction.

Examples would be: metroprolol, atenolol, esmolol, acebutelol

amiodarone....non-competitive alpha and beta-blocker....also has calcium channel blocking properties.....used as a treatment for vfib and pulseless...not stable vt that is refractory to other antiarrhythmics.

ACLS my friends calls for lidocaine or amiodarone for monomorphic VT. For polymorphic VT (torsodes)its asks one to look at the QT interval if its nomal/short the tx is the same, if long the recommendation is magnesium.

http://www.acls.net/newalgo/stach.htm

Rj

ACLS my friends calls for lidocaine or amiodarone for monomorphic VT. For polymorphic VT (torsodes)its asks one to look at the QT interval if its nomal/short the tx is the same, if long the recommendation is magnesium.

http://www.acls.net/newalgo/stach.htm

Rj

2005 ACLS algorithm (took the course yesterday) - stable vtach - amiodarone 150mg over 10 min, repeat as needed to max 2.2g/24hrs. And prepare for synchronized cardioversion.

Sotalol and Amiodarone are the main drugs to treat stable v-tach in my area.

I WOULD SUPPORT AS MY FIRST LINE OF DEFENSE ADENOSINE

STABLE SVT

UNDEFINED STABLE NARROW TACHYCARDIA AS A DIAGNOSTIC MANEUVER

NOT EFFECTIVE IN AFIB, AFLUTTER. OR VT

MECHANISM OF ACTION:

DEPRESS SA & AV NODE ACTIVITY

SLOW AV CONDUCTION

HALF LIFE= 5 SECONDS

PRECAUTIONS:

USUALLY SEE BRIEF ASYSTOLE AFTER ADM OF DRUG

DRUG INTERACTION WITH THEOPHYLLINE, DIPYRIDAMOLE,

7 CARBAMAZEPINE

PT FEEL FLUSHING, DYSPNEA, TRANSIENT CP

DOSE FOLLOWED BY IV PUSH MEDS WITH FLUID BOLUS 10-20 ML

6 MG IV OVER 1-3 SECONDS FOLLOWED BY 20 ML SALINE FLUSH THEN ELEVATE ARM (ATTACH BOTH SYRINGES TO SAME PORT) WAIT 1-2"

REPEAT 12 MG IV RAPID PUSH WAIT 1-2'

REPEAT 12 MG IV RAPID IV PUSH

AMIODARONE (CARDARONE)

WOULD BE MY SECOND LINE OF DEFENSE FOR VF/ PULSELESS VT

VENT ARRTHYTHMIAS -SYMPT PVCs

PREFERRED OVER LIDO

MECHANISM OF ACTION:

ANTI ARRTHYTHMIC POSSESSES ALFA AND BETA ANDRENERGIC BLOCKING

PROLONGS ACTION POTENTIAL DURATION

PROLONGS REFRACTORY PEROID DECREASES AV NODE CONDUCTION

DECREASES SINUS NODE FUNCTION

PRECAUTIONS

HALF LIFE IS LONG

MAY PROLONG QT

MONITOR BP, HR, QT INTERVALS

CONTRAINDICATED IN:

CARDIOGENIC SHOCK, MARKED SINUS BRADY, 2ND OR 3RD BLOCK

DOSE:

300MG IV PUSH IN CARDIAC ARREST (VT/VF)

150 MG IV PUSH FOR TACCHYS WITH PULSE (GIVE OVER 10 MINUTES)

CAN REPEAT ONE 150 MG IN 5 MINS.

DRAW 2 GLASS AMPLES THROUGH A LARGE GAUGE NEEDLE DILUTED IN 20-30 ML OF D5W

MAINTENANCE INFUSION:

1MG/MIN OVER 6 HRS. THEN

0.5 MG/MIN OVER 18 HRS.

MAX OF 2.2 G OVER 24 HRS.

lidocaine or amio gtt initially

stable vt, for how long?

You guys ROCK. I am scheduled to take ACLS in March. As of now, I know NOTHING cardiac. When Im pulled to the tele floor, I am :uhoh21: I cant read an EKG strip. I am hoping to have a good grasp after the class. We learned it in school, but if you dont use it, you lose it. And well, I lost it. lol.

I WOULD SUPPORT AS MY FIRST LINE OF DEFENSE ADENOSINE

STABLE SVT

UNDEFINED STABLE NARROW TACHYCARDIA AS A DIAGNOSTIC MANEUVER

NOT EFFECTIVE IN AFIB, AFLUTTER. OR VT

It's an old thread, but it looks like they were talking about VT, not SVT.