Ask the Clinical Instructor: A Q&A Column for Those New to the Cath Lab
Todd is the Cardiology Manager for Memorial Hermann Southeast in Houston, Texas. He also teaches an online RCIS Review course for Spokane Community College, in Spokane, Washington, and regularly presents with RCIS Review Courses.
I don’t understand why there is a difference in dosages of Cordarone for different situations. Isn’t it a case of “more is better”? — Online submission
Cordarone, generically called amiodarone, does have specific doses for specific situations. We often describe the differences in dosages as a “dead” dose and a “live” dose. To answer this question, there needs to be a short review of amiodarone.
Amiodarone (Figure 1) is indicated for persistent or recurrent ventricular fibrillation (VF)/pulseless ventricular tachycardia (VT), VT with a pulse (stable) and uncertain wide complex tachycardias. Amiodarone is the preferred treatment for shock- refractory VF/pulseless VT (Figure 2) when an antiarrythmic agent is thought to be indicated.1
The American Heart Association has assigned amiodarone as a Class IIb (acceptable, safe and useful) intervention in these cases. Amiodarone is indicated after defibrillations and administration of a vasopressor (epinephrine or vasopressin). The dosage of amiodarone is simple in these cases, with a “dead dose” of 300 mg IV push. If needed, a repeat dose can be administered ONCE at a dose of 150mg IV push.
As a side note, lidocaine can be administered in place of amiodarone if it is not available. Evidence-based medicine has not shown lidocaine to be superior nor inferior to amiodarone for discharge from hospital survival rates. However, amiodarone has shown a benefit for higher rate of survival to hospital admission.
Amiodarone does also have medication incompatibilities. In our setting, the biggest potential is the incompatibility of amiodarone when mixed with either heparin or sodium bicarbonate. In these cases, precipitation would be expected.
A tachycardia rhythm (with pulse, of course) (Figure 3) is considered unstable in the presence of altered mental status, ongoing chest pain or hypotension. A patient who is considered ‘unstable’ based upon those standards would proceed to immediate synchronized cardioversion.
In the case of the patient in VT with a pulse, who is not considered unstable, the dosage of amiodarone changes slightly. The dosage of amiodarone in this “live dose” case would be 150mg over 10 minutes. Many providers will dilute this amount in a 50 or 100 cc IV bag so that it can be infused via a pump, instead of manually by a syringe. Amiodarone can be repeated like this, as needed, up to a total of 2.2 grams over 24 hours.
In either case, some form of IV drip may be considered after resolution of the dysrhythmia. This can often be at a rate of 1mg/min over 6 hours, then 0.5 mg/min for 18 hours, or as the physician prescribes, based upon the patient’s clinical condition. CAUTION: Amiodarone drips MUST be mixed and administered from a glass container, as the medication will be absorbed into the plastic. You may ask, “What about the tubing?” According to the manufacturer guidelines, the small amount of leeching that will occur in the tubing is compensated for in the dosage rate.
To answer the original question as to why the dosages are different, extensive research on my part has not been able to find a solid scientific reason behind the difference. However, understanding the actions of the medication, and the clinical reason it is being given can allow for an ‘educated guess’. Amiodarone has numerous potential side effects. The one that we would be most concerned about in the cath lab is hypotension.
When we give medications, we want to try and use the lowest possible dose to achieve the desired therapeutic outcome. In the case of VF, we have nothing to lose, so we can use the highest dose recommended by the manufacturer (300mg-‘dead dose’). Any side effects that might arise can be managed as encountered…should the patient live to see them.
In the case of someone with a pulse, and with some form of cardiac output (which we would expect to be poor), we would want to use a lower dose (150mg-‘live dose’) over 10 minutes. The combination of the lower dose and slower administration rate would likely reduce the chance of the severe hypotension that can be seen after amiodarone administration. Amiodarone also has beta blocker-like actions on the sinoatrial (SA) and atrioventricular (AV) nodes and slows intra-cardiac conduction via sodium channel effects. These actions also could cause a decrease in cardiac output.
Todd Ginapp can be contacted at firstname.lastname@example.org.
1. Field JM, ed. ACLS Resource Text. Dallas, TX: American Heart Association; January 2008.
2. Opie LH, Gersh BJ. Drugs for the Heart. 6th edition. Philadelphia, PA: Elsevier Health Sciences (Saunders); October 2004.
3. Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med 1999; 341(12):871–878.