augments perfusion during CPR

v-fib

pulseless v-tach

asystole

pulseless electrical activity

cardiac arrest indications:  v. fib and pulseless v. tach unresponsive to defib

non-cardiac arrest indications:  a. fib and stable v. tach

1. AE amiodarone

acute:  hypotension and bradycardia

chronic:  N/V, anorexia, liver dysfunction, pulmonary fibrosis

...also:

hypo/hyperthyroidsim, cyanotic skin color, photosensitivity, peripheral neuropathies

similar to amiodarone, but NOT used for a. fib

cardiac arrest:  v. fib and pulseless v. tach unresponsive to defib

non-cardiac arrest:  stable v. tach

-dizziness, paresthesia, agitation, disorientation, hallucinations

carefule dosing if pt has CHF, liver dz, shock, or >70

-torsades de pointes

-suspected hypomagnesemic state

-ibutilide incuded v-tach

-refractory v. arrhythmias

-digoxin toxicity

non cardiac arrest situation:  giving too fast may cause hypotension, flushing, bradycardia

toxicity occurs rarely at very high levels and is usu in conjunction with renal fail

anticholinergic- increases SA firing and AV conduction

cardiac arrest:  asystole and pulseless electrical activity

non cardiac arrest:  symptomatic bradycardia, AV block (primary, or secondary type 2)

cardiac arrest situations we discussed

usu this drug is always administered during cardiac arrest

-v. fib

-pulseless v. tach

-asystole

-PEA

epinephrine or vasopressin for improved perfusion to brain and heart

med to "fix" rhythm in:

v. fib and pulseless v. tach

-amiodarone

-lidocaine

unstable:  synchronized cardioversion

stable:  amiodarone, lidocaine

1.  slow rate w/:

diltiazem

bb

digoxin

amiodarone

1.  control rate

2.  prevent VTE

3.  convert to NSR and maintain NSR

preferred classes of drugs to tx supraventricular arrhythmia

and alternative choices

1.  BB

2.  non-dihydropyridine CCBs

alt:

digoxin and amiodarone

non-dihydropyridine class!  (dihydropyridine class for HTN only)

-diltiazem

-verapamil

directly slows conduction velocity at AV node

-both are vasodilators so watch for hypotension

-signs of CHF, if pt has decent ejection fraction- OK to use

esmolol and metoprolol

blocks B1 receptors in heart = decreased conduction to AV and increased refractory at AV 

esmolol has half life of 9 minutes

-bradycardia, hypotension, decreased CO

-CNS adverse effects:  fatigue, lethargy, depression, sexual dysfunction

contraindicated in asthmatics

tricks baroreceptors into thinking pressure is higher than what is (increased vagal tone) so they stimulate decreased conduction

does not have any effect on BP and it improves contractility of heart

*worry less about hypotension and will not exacerbate CHF

they both decrease the number of impulses going through the AV by:

decreasing conduction velocity to AV node

and increasing refractory period of AV node

toxicity:  N/V, hallucinations, AV block, sinus pauses, arrhythmias, vision changes

therapeutic level = 1-2.4 ng/ml

another alt choice to tx a. fib/flutter

-antagonist to both beta and calcium channel receptors, so slows rate down

-may convert to NSR

-OK to  use in pt with left ventricular dysfunction

serious long term risks:

-pulmonary fibrosis

-hypo/hyperthyroidsim

-hepatic dysfunction

-skin discoloration

-ocular toxicities

short term risks:  bradycardia, heart block, N/V, hypotension (IV), drug intrxns (w/ warfarin, digoxin, statins)

drug of choice for tx of:

paroxysmal supraventricular tachycardia (PSVT) or AV nodal reentry

adenosine

(verapamil, diltiazem, bb also effective)

adenosine interrupts conduction at AV node to break reentry

5 sec half life!

89-98% conversion success

peripheral vasodilation- hypotension, flushing, SOB, chest tightness, apprehension (all short duration)

caffeine antagonizes

caution in pt with obstructive lung dz

contraindicated in heart transplant pt

3wk warfarin (INR 2-3) prior to elective conversion

after, 4wks warfarin

IV heparin via continuous drip

attempt conversion

after, 4 wks warfarin

rate control

-well tolerated and can then focus on controlling HR, symptoms, and preventing VTE

rhythm control not recommended

-pt often revert back to a. fib and require long-term anti-arrhythmic tx to maintain NSR

-efficacy unreliable, studies have show does not improve mortatliy

-for pts with persistent sxs

-pt unable to control rate

-CHF sxs

-not an anti-coag candidate

-younger pt or lone a. fib

amiodarone

-provides rate control, may convert to NSR, may maintain NSR

serious long term effects:  pulm fibrosis, hypo/hyperthyroidism, hepatic dysfunction

short term effects:  bradycardia, heart block, N/V, hypotension, drug intrxns (warfarin, digoxin, statins)