D5W

[Ace844]

For Amiodarone specifically, because of it's actions as a sodium channel blocker, you wouldn't really want to use NS to mix it. The bigger issue is the container. Amiodarone will leach some of the material out of a standard IV bag/tubing.

None of the solutions are absolutely recommended over any other one. You would probably need to find out from your medical control why one and not the other.

"AZCEP,"

I thought Amiodarone is a Vaughn-Williams class 3 anti-arrythmic is it not? If so, wouldn't that make it a potassium channel blocker, and if so how then would it relate to the mechanisim you mentioned? I know it has class 1-1a-2 properties, but how great is the class 1 effects versus the class 3? Just curious,

ACE844

[AZCEP]

Amiodarone got placed in class III due to it's major effect, which is K+ channel blockade.

It also has class I-Na+ channel blocking, class II-beta blocking, and class IV-Ca++ channel blocking properties. Because it does all of these things, in varying degrees depending on the patient, they had to put it somewhere.

From http://www.rxlist.com/cgi/generic4/cordarone_iv_cp.htm :

Amiodarone is generally considered a class III antiarrhythmic drug, but it possesses electrophysiologic characteristics of all four Vaughan Williams classes. Like class I drugs, amiodarone blocks sodium channels at rapid pacing frequencies, and like class II drugs, it exerts a noncompetitive antisympathetic action. One of its main effects, with prolonged administration, is to lengthen the cardiac action potential, a class III effect. The negative chronotropic effect of amiodarone in nodal tissues is similar to the effect of class IV drugs. In addition to blocking sodium channels, amiodarone blocks myocardial potassium channels, which contributes to slowing of conduction and prolongation of refractoriness. The antisympathetic action and the block of calcium and potassium channels are responsible for the negative dromotropic effects on the sinus node and for the slowing of conduction and prolongation of refractoriness in the atrioventricular (AV) node. Its vasodilatory action can decrease cardiac workload and consequently myocardial oxygen consumption.

Also on the administration side:

Admixture Incompatibility

Cordarone I.V. in D5W is incompatible with the drugs shown below.

Y-SITE INJECTION INCOMPATIBILITY

Drug Vehicle Amiodarone Concentration Comments

Aminophylline D5W 4 mg/mL Precipitate

Cefamandole Nafate D5W 4 mg/mL Precipitate

Cefazolin Sodium D5W 4 mg/mL Precipitate

Mezlocillin Sodium D5W 4 mg/mL Precipitate

Heparin Sodium D5W Precipitate

Sodium Bicarbonate D5W 3 mg/mL Precipitate

So because it will precipitate with the sodium containing solutions, perhaps that is why it is recommended to use D5W to mix instead of NS.

[Ace844]

"AZCEP,"

Thanks for the info., I asked because I have been unable to find any source which quantifies the class 1 properties versus the others in any of the usual places. So I was curious if you had any info. in that realm of it's mechanisim. Thanks for the help, and additional info above., and the explanation on preciptiatory effects.

ACE844

[FL_Medic]

wow, I'm glad you asked that class 1 question, I have just learned alot about amiodorone.

[Ace844]

For those who are interested, this is the closest I could to the info. I posted earlier.

HTH,

ACE844

"Mosby's Drug Consult

Copyright © 2006 Mosby, Inc”

CLINICAL PHARMACOLOGY:

Mechanism of Action

Amiodarone is generally considered a Class III antiarrhythmic drug, but it possesses electrophysiologic characteristics of all four Vaughan Williams classes. Like Class I drugs, amiodarone blocks sodium channels at rapid pacing frequencies, and like Class II drugs, it exerts a noncompetitive antisympathetic action. One of its main effects, with prolonged administration, is to lengthen the cardiac action potential, a Class III effect. The negative chronotropic effect of amiodarone in nodal tissues is similar to the effect of Class IV drugs. In addition to blocking sodium channels, amiodarone blocks myocardial potassium channels, which contributes to slowing of conduction and prolongation of refractoriness. The antisympathetic action and the block of calcium and potassium channels are responsible for the negative dromotropic effects on the sinus node and for the slowing of conduction and prolongation of refractoriness in the atrioventricular (AV) node. Its vasodilatory action can decrease cardiac workload and consequently myocardial oxygen consumption.

Amiodarone HCl IV administration prolongs intranodal conduction (Atrial-His, AH) and refractoriness of the atrioventricular node (ERP AVN), but has little or no effect on sinus cycle length (SCL), refractoriness of the right atrium and right ventricle (ERP RA and ERP RV), repolarization (QTc), intraventricular conduction (QRS), and infranodal conduction (His-ventricular, HV). A comparison of the electrophysiologic effects of amiodarone HCl IV and oral amiodarone HCl is shown in TABLE 1.

TABLE 1 Effects of IV and Oral Amiodarone HCl on Electrophysiologic Parameters

Formulation SCL QRS QTc AH HV ERP RA ERP RV ERP AVN

IV NC NC NC Inc NC NC NC Inc

Oral Inc NC Inc Inc NC Inc Inc Inc

Inc Increases.

NC No Change.

At higher doses (>10 mg/kg) of amiodarone HCl IV, prolongation of the ERP RV and modest prolongation of the QRS have been seen. These differences between oral and IV administration suggest that the initial acute effects of amiodarone HCl IV may be predominantly focused on the AV node, causing an intranodal conduction delay and increased nodal refractoriness due to slow channel blockade (Class IV activity) and noncompetitive adrenergic antagonism (Class II activity).

CLINICAL PHARMACOLOGY:

Electrophysiology/Mechanism of Action

In animals, amiodarone HCl is effective in the prevention or suppression of experimentally induced arrhythmias. The antiarrhythmic effect of amiodarone HCl may be due to at least two major properties: (1) a prolongation of the myocardial cell-action potential duration and refractory period and (2) noncompetitive α- and β-adrenergic inhibition.

Amiodarone HCl prolongs the duration of the action potential of all cardiac fibers while causing minimal reduction of dV/dt (maximal upstroke velocity of the action potential). The refractory period is prolonged in all cardiac tissues. Amiodarone HCl increases the cardiac refractory period without influencing resting membrane potential, except in automatic cells where the slope of the prepotential is reduced, generally reducing automaticity. These electrophysiologic effects are reflected in a decreased sinus rate of 15-20%, increased PR and QT intervals of about 10%, the development of U-waves, and changes in T-wave contour. These changes should not require discontinuation of amiodarone HCl as they are evidence of its pharmacological action, although amiodarone HCl can cause marked sinus bradycardia or sinus arrest and heart block. On rare occasions, QT prolongation has been associated with worsening of arrhythmia.

[AZCEP]

Now, let's take a step sideways and think about how Amiodarone will do what it says it does.

amiodarone blocks sodium channels at rapid pacing frequencies

As the rate of electrolyte movement increases the degree of block of the sodium channels increases.

it exerts a noncompetitive antisympathetic action

This is the beta-blocking effect, which will work on the stimulus formation in the SA node, and the conduction through the AV node

lengthen the cardiac action potential, a Class III effect

This is the part of the program where the potassium is trying to move back into the cells, because of the prolonged phase 3 of the action potential, the potassium can take longer to move in, although it is not directly blocked from doing so. At the same time, the sodium is trying to move out of the cell. Because of the sodium channel blockade mentioned, the sodium will try to find other ways out. The potassium channel fills this need nicely, and the action becomes a physiologic block.

The negative chronotropic effect of amiodarone in nodal tissues is similar to the effect of Class IV drugs

This is caused by the increased use of the calcium channel by the smaller potassium ion. Because the potassium channel is blocked by the outward movement of the sodium, the potassium tries to find another route into the cell. Since the calcium channel is much larger than the potassium, the potassium ion will try to move in through it. With the changes in the pathways for the electrolytes to enter/exit the cell, the conduction of the impulses is also slowed down.

The vasodilatory effects are really hit and miss. Some patients are very sensitive to them, and some don't respond at all to this effect. This property is related to the Class II anti-dysrhythmic properties noted above.

[Ridryder 911]

Don't forget Amiodarone, will increase Dig effects by 70% and if they are on Coumadin, can increase their INR (clotting time) by 100%.. so it does have some potential nasty side effects....

Yes, Johnny & Roy were taught, like I was..." D[sub:3b34d4a7f2]5[/sub:3b34d4a7f2]W TKO".... on most medical calls, because as stated isotonic then changes over to carry into the cell wall... this was also when we used strictly microdrips on medical to prevent fluid overload and give a precise amount of fluid in...

R/r 911

[EMS49393]

This is so exciting! This is by far the most educational post I've read on here in a long time. 20 to everyone involved. Thanks, I learned something new, and I appreciate that so much.

[AZCEP]

We do aim to please!

Some simple pathophysiology, sprinkled with a bit of pharmacology, stir in some critical thinking.

Bippity, Bobbity, Boo! You know how something works.

[Ace844]

We do aim to please!

Some simple pathophysiology, sprinkled with a bit of pharmacology, stir in some critical thinking.

Bippity, Bobbity, Boo! You know how something works.

Alittle bitty PSA message as to why EDUCATION IS SO IMPORTANT IN THIS CAREER! Also, a bit of quick insight as to why we all say it's so important.

Strong work and succinctly put "AZCEP,"

Out Here,

ACE844