have i been lucky?

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Gas you down

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in prep for oral boards, heard that lido can precipitate RVR in a pt w/ afib or flutter. is this common knowledge or what? i never knew this, and bet i've done this before. i mean c'mon, who doesn't have afib these days!!!:idea:
 
in prep for oral boards, heard that lido can precipitate RVR in a pt w/ afib or flutter. is this common knowledge or what? i never knew this, and bet i've done this before. i mean c'mon, who doesn't have afib these days!!!:idea:

Did not know that. Found an old reference about this:

http://www.ncbi.nlm.nih.gov/pubmed/636985

"Lidocaine-induced ventricular rate increases are common in atrial flutter and fibrillation, particularly in patients who are also receiving quinidine."
 
semi common knowledge
 
in prep for oral boards, heard that lido can precipitate RVR in a pt w/ afib or flutter. is this common knowledge or what? i never knew this, and bet i've done this before. i mean c'mon, who doesn't have afib these days!!!:idea:

1. Dose related (at least 1-1.5 mg/kg)
2. Associated with Quinidine use (not common these days)
 
Indirect vagal effects

The direct effect of Class IA antiarrhythmic drugs on action potentials is significantly modified by their anticholinergic actions. Inhibiting vagal activity can lead to both an increase in sinoatrial rate and atrioventricular conduction, which can offset the direct effects of the drugs on these tissues. Although a IA drug may effectively depress atrial rate during flutter, it can lead to an increase in ventricular rate because of an increase in the number of impulses conducted through the atrioventricular node (anticholinergic effect), thereby requiring concomitant treatment with a beta-blocker or calcium-channel blocker to slow AV nodal conduction. These anticholinergic actions are most prominent at the sinoatrial and atrioventricular nodes because they are extensively innervated by vagal efferent nerves. Different drugs within the IA subclass differ in their anticholinergic actions (see table below).
 
characteristics. More detailed information on specific drugs can be found at www.rxlist.com. Class IA: atrial fibrillation, flutter; supraventricular & ventricular tachyarrhythmias quinidine* anticholinergic (moderate) cinchonism (blurred vision, tinnitus, headache, psychosis); cramping and nausea; enhances digitalis toxicity procainamide anticholinergic (weak); relatively short half-life lupus-like syndrome in 25-30% of patients disopryamide anticholinergic (strong) negative inotropic effect Class IB: ventricular tachyarrhythmias (VT) lidocaine* IV only; VT and PVCs good efficacy in ischemic myocardium tocainide orally active lidocaine analog can cause pulmonary fibrosis mexiletine orally active lidocaine analog good efficacy in ischemic myocardium phenytoin digitalis-induced arrhythmias Class IC: life-threatening supraventricular tachyarrhythmias (SVT) and ventricular tachyarrhythmias (VT) flecainide* SVT can induce life-threatening VT propafenone SVT & VT; β-blocking and Ca++-channel blocking activity can worsen heart failure moricizine VT; IB activity



http://www.cvpharmacology.com/antiarrhy/sodium-blockers.htm
 
Because of its vagolytic effect and resultant rapid ventricular response, quinidine should not be given without prior administration of agents that slow AV nodal conduction. Many antiarrhythmic agents, especially flecainide and propafenone, may slow the atrial rate, allowing more atrial impulses to be conducted through the AV node, which results in a faster ventricular rate.74 In fact, many episodes of wide QRS tachycardia in patients with AF treated with flecainide or propafenone appear to be secondary to atrial flutter with 1:1 AV node conduction associated with QRS widening.82 83 The resultant arrhythmia is often misdiagnosed as ventricular tachycardia. This situation can be prevented or treated by the addition of agents that slow AV node conduction, for example, digitalis, ß-adrenergic blockers, or calcium channel blockers. Occasionally, treatment of patients with tachycardia-bradycardia syndrome worsens sinus node function, resulting in symptomatic bradyarrhythmias that require pacemaker support.
 
in prep for oral boards, heard that lido can precipitate RVR in a pt w/ afib or flutter. is this common knowledge or what? i never knew this, and bet i've done this before. i mean c'mon, who doesn't have afib these days!!!:idea:

Now that I have provided references to the Oral Board question of I.V. Lidocaine and possible RVR let's cut to the real world.

In most patients these days with chronic A.fib/A. flutter the chance of inducing Rapid Ventricular rate with 100mg of lidocaine is pretty small. I give 100mg I.V. routinely with my inductions and haven't seen one CLINICAL case. It could be because of concomitant use of B Blockers or Calcium Channel Blockers or it could also be due to the fact that Lidocaine is pretty safe in this group (well-controlled) provided the Class 1A or Class 1C agents are NOT Also on board.

However, new onset A.Fib/A. Flutter is a different story altogether and I would be wary of giving I.V. Lidocaine to that subgroup.
 
in prep for oral boards, heard that lido can precipitate RVR in a pt w/ afib or flutter. is this common knowledge or what? i never knew this, and bet i've done this before. i mean c'mon, who doesn't have afib these days!!!:idea:

Didn't know. Thanks. Figured Lido was a vitamin.
 
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