Progress in Cardiovascular Nursing® (ISSN 0889-7204) is published Quarterly (March, June, Sept., Dec.

) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT 06484. Copyright ©2007
by Le Jacq. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system,
without permission in writing from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for
commercial purposes, please contact Karen Hurwitch at KHurwitch@bos.blackwellpublishing.com or 781-388-8470.

www.lejacq.com ID: 7398

Considerations in Drug Therapy

Steven R. Kayser, PharmD; Michael L. Hess, MD; Maureen P. Flattery, RN, MS, ANP, Section Editors

Amiodarone: Development, Clinical Indications,

and Safety
William Cahoon Jr, PharmD; Maureen P. Flattery, RN, MS, ANP; Michael L. Hess, MD

A miodarone, a benzofuran deriva-

tive with complex antiarrhythmic
activity, was originally conceptualized
as a potent coronary vasodilator and
antianginal agent.1 Amiodarone was
developed in Belgium in 1962, but the
recognition of its efficacy and safety as
an antiarrhythmic was slow to develop.
Initial investigations of the antianginal
effects of amiodarone were reported in
1967, followed by recognition of its
antiarrhythmic properties in rabbits
in 1969.1,2 Interest in its potential
use as an antiarrhythmic grew follow-
ing the publication of human clinical
efficacy data in 1976. Rosenbaum and
colleagues3 reported that amiodarone
was remarkably effective in both the
treatment and suppression of multiple
atrial and ventricular arrhythmias.
Following further investigations
and clinical experience in multiple
European countries, use of amio-
darone for refractory arrhythmias in
the United States became more com-
mon. By the early 1980s, American
physicians began acquiring the drug
from Europe and Canada for patients
with difficult-to-treat arrhythmias.
Amiodarone did not have US Food
and Drug Administration (FDA)
approval in the United States, but the
FDA sanctioned the drug’s acquisition
and use on a limited basis. Amiodarone
became one of the first Treatment
Investigational New Drugs (Treatment
INDs), which are medications with
preliminary evidence of efficacy in a
life-threatening disorder for which no
effective alternative treatment exists.4
More than 600 American cardiologists
treated approximately 20,000 patients
From the Virginia Commonwealth University Health System, Richmond, VA
Address for correspondence:
William Cahoon, PharmD, Virginia Commonwealth University Health System,
PO Box 980042, Richmond, VA 23298
E-mail: wcahoon@mcvh-vcu.edu
with amiodarone under its status as a
Treatment IND.5,6
Demand for this agent grew with
positive clinical experience to the
point that amiodarone finally gained
FDA approval in 1985.6 Although
FDA-approved solely for recurrent,
life-threatening ventricular arrhyth-
mias, the expansive use of amiodarone
has come to include both ventricular
and supraventricular arrhythmias.7
Amiodarone is now consistently one of
the top 200 generic drugs (measured
by retail dollars) with estimated total
sales of approximately $87 million in
20068; however, amiodarone is not
a benign drug, with several reported
interactions and adverse effects.
Pharmacology
Amiodarone is a benzofuran derivative
not chemically related to any other
antiarrhythmic agent. Although its
precise mechanism of action has not
been delineated, the antiarrhythmic
effect is related to at least 2 properties: a-
adrenergic and b-adrenergic inhibition
and prolongation of myocardial cell
action potential and cardiac refractory
period. A Vaughan-Williams class III
agent, amiodarone blocks potassium
channels (IKr ) and delays repolarization
of myocardial tissue. This effect increases
the duration of the action potential and
the refractoriness of cardiac tissue to
depolarization, thereby prolonging the
QT interval. These electrophysiologic
actions lead to a decrease in heart rate
by 15% to 20% and an increase in the
QT interval by about 10%.9 In addition
to class III antiarrhythmic properties,
amiodarone also exhibits properties
of other classes, including blockade
of sodium and calcium channels and
noncompetitive b-receptor blockade.10
In addition to electrophysiologic
properties, intravenous amiodarone
also has effects on hemodynamics.1,11–
13
Initially conceptualized as a potent
coronary vasodilator, intravenous ami-
odarone acts to relax vascular smooth
muscle and reduce peripheral vascular
resistance.12 Despite negative inotro-
pic effects on the left ventricle, the
decrease in systemic vascular resis-
tance and myocardial oxygen demand
results in a slightly increased cardiac
output.9 Decrease in systemic vascu-
lar resistance results in hypotension
in 16% of individuals; this is the
most common adverse effect seen with
intravenous administration.14 In con-
trast with intravenous amiodarone,
oral administration results in no sig-
nificant change in left ventricular ejec-
tion fraction and a dramatically lower
incidence of hypotension.9,15,16
Amiodarone undergoes extensive
hepatic metabolism, specifically cyto-
chrome P (CYP) 450 3A–mediat-
ed N-deethylation to N-desethyla-
miodarone.10 The primary metabolite

Summer 2007 Progress in Cardiovascular Nursing 173

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Progress in Cardiovascular Nursing® (ISSN 0889-7204) is published Quarterly (March, June, Sept., Dec.) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT 06484. Copyright ©2007
by Le Jacq. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system,
without permission in writing from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for
commercial purposes, please contact Karen Hurwitch at KHurwitch@bos.blackwellpublishing.com or 781-388-8470.

Table. Cardiovascular Drug Interactions With Amiodarone

Concomitant Agent Amiodarone Effect Management
Digoxin Increases digoxin concentration by 50%
Discontinue digoxin or decrease
dose by 50%
Warfarin Prolongs prothrombin time and increases INR Decrease warfarin dose by 33%–
50%; monitor INR
Simvastatin Increases risk of rhabdomyolysis and myopathy Simvastatin ≤20 mg/d
Antiarrhythmic agents Increases antiarrhythmic agent concentration; Decrease dose of concomitant agent
may prolong QT by 50%
Abbreviation: INR, international normalized ratio.

achieves concentrations similar to the
parent compound and, according to
canine studies, may be responsible for
70% of the antiarrhythmic efficacy of
amiodarone.17 The drug is primarily
eliminated in the bile, with less than
1% of the drug excreted unchanged in
the urine. As a result, dosage adjust-
ment is not necessary in patients with
renal impairment.9 Specific recom-
mendations for dosage adjustment are
not available for patients with hepatic
impairment, although consideration
should be given to appropriate dos-
ing in patients with advanced hepatic
disease because the drug is extensively
metabolized in the liver.14 The elimi-
nation of amiodarone is widely vari-
able (half-life range, 15 to 142 days)
with a mean half-life of 58 days.9
Amiodarone is lipophilic and highly
protein-bound, resulting in a large
volume of distribution that ranges
from 1.3 to 65.8 L/kg.14 Because
amiodarone is lipophilic, common
clinical practice is to decrease the
dose in the elderly and those with low
body fat.7
Clinical Indications
Amiodarone is currently FDA-
approved solely for prevention of life-
threatening ventricular arrhythmias,
although it is used clinically for a variety
of ventricular and supraventricular
arrhythmias.9 Indications include
perioperative prophylaxis of atrial
fibrillation with cardiac surgery,
conversion and maintenance of sinus
rhythm in atrial fibrillation, and use
in acute cardiac life support (shock-
refractory ventricular fibrillation or
pulseless ventricular tachycardia).14
A double-blind, randomized pla-
cebo-controlled trial performed by
Daoud and associates18 evaluated the
use of oral amiodarone before cardiac
surgery. Postoperative atrial fibrilla-
tion occurs in 10% to 40% of patients
undergoing cardiac surgery; therefore,
the purpose of this trial was to assess
the efficacy of amiodarone in the pre-
vention of atrial fibrillation. Patients
were randomized to either amiodarone
200 mg 3 times daily or matching pla-
cebo for a minimum of 7 days before
surgery, followed by amiodarone 200
mg daily or placebo until discharge.
Amiodarone led to a statistically signif-
icant reduction in postoperative atrial
fibrillation compared with placebo
(25% vs 53%, respectively; p=.003).
Although effective, perioperative ami-
odarone has not been widely used in
the prevention of postoperative atrial
fibrillation. The efficacy and safety of
perioperative b-blockade has relegated
amiodarone to use as an alternative
agent in patients with contraindica-
tions to b-blockers.19
Amiodarone demonstrated efficacy
in restoration of sinus rhythm in a
randomized placebo-controlled trial
by Vardas and colleagues.20 Patients
with atrial fibrillation of varying dura-
tion were randomized to intravenous
amiodarone (300 mg for 1 hour, fol-
lowed by 20 mg/kg for 24 hours) fol-
lowed by oral amiodarone for 1 month
(600 mg/d for 3 weeks, followed by
400 mg/d for 1 week) or matching
placebo. At 1 month, restoration of
sinus rhythm was demonstrated to
be more common with amiodarone
than with placebo (80% vs 40%; odds
ratio 6.21; 95% confidence interval
3.33–11.57; p<.0001). Conversion
to sinus rhythm was influenced by
patient-specific factors such as dura-
tion of atrial fibrillation and size of
the left atrium. Current American
College of Cardiology/American
Heart Association (ACC/AHA)
guidelines state that “administration
of amiodarone is a reasonable option
for pharmacological cardioversion of
atrial fibrillation” (class IIa, level A
recommendation).21
Amiodarone has also demonstrated
efficacy in maintaining sinus rhythm.
Roy and coworkers22 performed a
prospective, randomized trial to com-
pare the ability of amiodarone to
prevent recurrence of atrial fibrillation
with that of sotalol and propafenone.
Patients with at least 1 episode of atrial
fibrillation in the previous 6 months
were randomly assigned to amiodarone,
sotalol, or propafenone. Following an
average of 16 months of follow-up,
amiodarone-treated patients were less
likely to have a recurrence of atrial
fibrillation than were those treated
with sotalol or propafenone (35% vs
63%; p<.001). Although amiodarone
is not considered first-line therapy for
maintenance of sinus rhythm in those
with no (or minimal) heart disease,
current ACC/AHA guidelines recom-
mend the drug for patients with sub-
stantial left ventricular hypertrophy or
heart failure.21
Use of amiodarone in patients
with cardiac arrest secondary to
shock-refractory ventricular fibrilla-
tion or tachycardia was evaluated by
Kudenchuk and associates.23 In this
randomized, double-blind placebo-
controlled trial, patients with out-of-

174 Progress in Cardiovascular Nursing Summer 2007

®
Progress in Cardiovascular Nursing® (ISSN 0889-7204) is published Quarterly (March, June, Sept., Dec.) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT 06484. Copyright ©2007
by Le Jacq. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system,
without permission in writing from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for
commercial purposes, please contact Karen Hurwitch at KHurwitch@bos.blackwellpublishing.com or 781-388-8470.
hospital cardiac arrest from ventricu-
lar fibrillation were randomized to
intravenous amiodarone 300 mg or
placebo. Patients treated with amio-
darone were significantly more likely
to survive to hospital admission than
were those given placebo (44% vs
34%; p=.03; odds ratio, 1.6; 95%
confidence interval, 1.1–2.4; p=.02).
Based on these data, amiodarone has
become the first-line antiarrhythmic
agent for managing pulseless ventricu-
lar tachyarrhythmias.24,25
In spite of its original indication for
suppressing life-threatening ventricu-
lar dysrhythmias and the beneficial
effect that has been demonstrated with
pulseless cardiac arrest, amiodarone
does not increase survival in patients
at risk for sudden cardiac death.
The Sudden Cardiac Death in Heart
Failure Trial (SCD-HeFT) was a mul-
ticenter trial to determine the value of
amiodarone to prevent sudden death
in patients with congestive heart fail-
ure (CHF).26 Patients with New York
Heart Association class II or III CHF
symptoms and a left ventricular ejec-
tion fraction ≤35% were randomized
to receive amiodarone (n=845), place-
bo (n=847), or a single-lead implant-
able defibrillator (n=829) in addition
to conventional CHF therapy. There
were 244 deaths (29%) in the placebo
group, 240 deaths (28%) in the amio-
darone group, and 182 deaths (22%)
in the defibrillator group. Amiodarone
was found to be similar to placebo
in preventing sudden death in this
patient population.
Adverse Effects
and Safety
In part because of its prolonged half-
life and accumulation with extended
exposure, amiodarone is associated with
multiple adverse effects.27 In clinical trials,
adverse effects occurred in three-fourths
of all patients and led to permanent
discontinuation in 7% to 18%.9 These
effects involve several organ systems and
require close monitoring and follow-up.
Ocular, skin, thyroid, gastrointestinal,
and pulmonary effects are associated
with amiodarone therapy.
Summer 2007
®
The majority of patients on amio-
darone therapy develop corneal microde-
posits, which lead to visual halos or
blurred vision in as many as 10% of
patients. For patients who experience
vision changes, corneal microdeposits
are reversible with dose reduction or
discontinuation of amiodarone.9
Amiodarone induces photosensitivi-
ty in 10% of those on therapy.9 Perhaps
more concerning is a blue-gray discol-
oration of sun-exposed skin following
long-term amiodarone use. Skin discol-
oration is reversible, although several
months may pass before resolution.28
Patients should be counseled to use
sun barrier creams and minimize sun
exposure to reduce this risk.29
Amiodarone is an iodine-contain-
ing compound, and thyroid abnor-
malities are associated with its use.
In iodine-sufficient areas, such as the
United States, hypothyroidism is more
common; hyperthyroidism occurs
more frequently in countries with low
iodine intake.30 Hypothyroidism has
been reported to affect up to 10%
of patients in case series, with hyper-
thyroidism present in 2%.9 Thyroid
function tests should be performed
at amiodarone initiation and every 6
months thereafter.29
Gastrointestinal intolerance has been
reported in 10% to 33% of patients
on amiodarone therapy, especially in
patients who are receiving an oral load-
ing dose of 400 mg twice daily.9 Effects
may subside with a decrease in dose.
Elevations in liver function test values
to >2 times normal occur in 15% to
50% of patients, although hepatitis
and cirrhosis affect <3%.29 As with
thyroid function tests, liver function
tests should be performed at amio-
darone initiation and every 6 months
thereafter.29 If liver function test values
increase to >3 times baseline, consider-
ation should be given to amiodarone
dose reduction or discontinuation.9
The most serious adverse effect asso-
ciated with amiodarone is pulmonary
toxicity. The true incidence is difficult
to establish because patients on amio-
darone therapy may have co-existing
heart failure or underlying pulmonary
disorders. Early case series estimated
an incidence of up to 10%. Reported
pulmonary toxicities may result from
alveolar edema, interstitial pneumoni-
tis, or interstitial fibrosis.9 Pulmonary
function testing should be performed
at amiodarone initiation and to eval-
uate unexplained dyspnea while on
therapy. Amiodarone should be discon-
tinued or the dose reduced in patients
with suspected or confirmed pulmo-
nary toxicity or a decrease in diffus-
ing capacity.9,28,29 Chest radiography
should be performed before initiation
of therapy and yearly thereafter.29
Cardiovascular Drug
Interactions
Metabolism of CYP by amiodarone
results in the potential for multiple drug
interactions. Amiodarone inhibits p-
glycoprotein and CYP1A2, CYP2C9,
CYP2D6, and CYP3A4 enzymes,
resulting in increased concentrations of
other medications metabolized via these
pathways.9 For example, amiodarone
administration results in 70% higher
digoxin concentrations after 1 day
of concomitant administration.9
If a patient stabilized on digoxin is
prescribed amiodarone, the digoxin
should be discontinued or the dose
decreased by 50%.9,28 Amiodarone
also results in increased warfarin
concentrations, which lead to elevated
prothrombin time and international
normalized ratio.9,28 Patients receiving
concomitant amiodarone and warfarin
therapy should be monitored closely
via anticoagulation laboratory tests.
In patients taking warfarin before
amiodarone initiation, the warfarin dose
should be decreased by 33% to 50%.9
The metabolism of another commonly
used cardiovascular medication,
simvastatin, is also decreased with
amiodarone therapy.9 This results in an
increased risk of rhabdomyolysis and
myopathy. The simvastatin dose should
not exceed 20 mg/d while patients are
on amiodarone therapy.9,28
Other antiarrhythmic agents are
occasionally used in combination with
amiodarone. Amiodarone may increase
concentrations of these concomitantly
Progress in Cardiovascular Nursing 175
Progress in Cardiovascular Nursing® (ISSN 0889-7204) is published Quarterly (March, June, Sept., Dec.) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT 06484. Copyright ©2007
by Le Jacq. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system,
without permission in writing from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for
commercial purposes, please contact Karen Hurwitch at KHurwitch@bos.blackwellpublishing.com or 781-388-8470.
used agents, leading to the possibil-
ity of prolonged QT intervals and
increased proarrhythmic effects. The
combination of amiodarone with other
antiarrhythmics should be reserved for
patients with life-threatening ventricu-
lar arrhythmias that are not suppressed
with single-agent therapy. The dose
of these agents used concomitantly
with amiodarone should be decreased
by 50%.9 These drug interactions are
summarized in the Table.
Clinical Considerations
Initiation of amiodarone therapy
is usually begun in a monitored
hospital environment. The usual
recommendation is to begin with 400
mg 3 times daily for 3 days, decrease
to 400 mg twice daily for 2 weeks,
and then decrease to 400 mg daily
for 2 weeks. Maintenance dosage is
usually 200 mg/d. Nausea, vomiting,
and abdominal pain may require an
adjustment in the loading dose.
References
1 Singh BN. Amiodarone: historical develop-
ment and pharmacologic profile. Am Heart J.
1983;106:788–796.
2 Canada AT, Lawrence LJ, Haffajee CI, et al.
Amiodarone for tachyarrhythmias: pharmacolo-
gy, kinetics, and efficacy. Drug Intell Clin Pharm.
1983;17:100–104.
3 Rosenbaum MB, Chiale PA, Halpern MS, et al.
Clinical efficacy of amiodarone as an antiarrhyth-
mic agent. Am J Cardiol. 1976;38:934–944.
4 Investigational new drug, antibiotic, and
biological drug product regulations; treat-
ment use and sale; final rule. Fed Regist.
1987;52(99):19466–19467.
5 Flieger K. FDA finds new ways to speed treatments
to patients. FDA Consum. 1993;27(8):14–18.
6 Work of cardiology community results in approv-
al of amiodarone. FDA Drug Bull. 1986;16:4–5.
7 Zimetbaum P. Amiodarone for atrial fibrillation.
N Engl J Med. 2007;356:935–941.
8 Top 200 generic drugs by retail dollars in 2006.
http://www.drugtopics.com/drugtopics/data/
articlestandard/drugtopics/072007/405102/
article.pdf. Accessed June 15, 2007.
9 Amiodarone HCl (Pacerone) [package insert].
Minneapolis, MN: Upsher-Smith; 2006.
10 Chow MS. Intravenous amiodarone: pharmacol-
ogy, pharmacokinetics, and clinical use. Ann
Pharmacother. 1996;30:637–643.
11 Naccarelli GV, Rinkenberger RL, Dougherty
AH, et al. Amiodarone: pharmacology and anti-
arrhythmic and adverse effects. Pharmacotherapy.
1985;5:298–313.
12 Remme WJ, Van Hoogenhuyze DC, Krauss
XH, et al. Acute hemodynamic and antiischemic
effects of intravenous amiodarone. Am J Cardiol.
176 Progress in Cardiovascular Nursing
Conclusions
Today, amiodorone is the most
widely prescribed antiarrhythmic
drug. This is especially true for
heart failure patients for whom it is
the antiarrhythmic drug of choice.
Younger patients who require
antiarrhythmic therapy should
perhaps be given a trial of sotalol
or propafenone before starting
amiodarone because of the potential
for the development of irreversible
pulmonary fibrosis. Initiation
of amiodarone should occur in a
monitored environment with oral
loading preferred to intravenous
loading. The pharmacokinetics of
the drug are such that there is little
difference in effectiveness between
oral and intravenous loading, and the
intravenous load may be associated
with hypotension. Up to 33% of
patients may develop nausea and
abdominal pain during the initiation
of therapy necessitating a decrease in
1985;55:639–644.
13 Remme WJ, Van Hoogenhuyze DC, Kruyssen
DA, et al. Amiodarone. Haemodynamic profile
during intravenous administration and effect
on pacing-induced ischaemia in man. Drugs.
1985;29(suppl 3):11–22.
14 Micromedex Healthcare Series. https://www.
thomsonhc.com. Accessed June 15, 2007.
15 Ellenbogen KA, O’Callahan WG, Colavita PG, et
al. Cardiac function in patients on chronic amio-
darone therapy. Am Heart J. 1985;110:376–381.
16 Sheldon RS, Mitchell LB, Duff HJ, et al. Right
and left ventricular function during chronic amio-
darone therapy. Am J Cardiol. 1988;62:736–740.
17 Nattel S, Davies M, Quantz M. The antiarrhythmic
efficacy of amiodarone and desethylamiodarone,
alone and in combination, in dogs with acute myo-
cardial infarction. Circulation. 1988;77:200–208.
18 Daoud EG, Strickberger SA, Man KC, et al.
Preoperative amiodarone as prophylaxis against
atrial fibrillation after heart surgery. N Engl J
Med. 1997;337:1785–1791.
19 Bradley D, Creswell LL, Hogue CW, et al.
Pharmacologic prophylaxis. American College of
Chest Physicians guidelines for the prevention and
management of postoperative atrial fibrillation after
cardiac surgery. Chest. 2005;128(2 suppl):39S–47S.
20 Vardas PE, Kochiadakis GE, Igoumenidis NE, et
al. Amiodarone as a first-choice drug for restoring
sinus rhythm in patients with atrial fibrillation.
Chest. 2000;117:1538–1545.
21 Fuster V, Rydén LE, Cannom DS, et al. ACC/
AHA/ESC 2006 guidelines for the management
of patients with atrial fibrillation—executive
summary: a report of the American College of
Cardiology/American Heart Association Task
dosing.9 Maintenance dosing should
be titrated to the lowest effective
dose, usually 100 to 200 mg/d.
Fortunately, malignant ventricular
arrhythmias during loading are rare
in spite of widening of the QRS
complex and prolongation of the
QT interval. Either hypothyroidism
or hyperthyroidism is a common
side effect of the drug, and thyroid-
stimulating hormone levels should
be carefully monitored. Yearly chest
radiography is a must. Amiodarone
therapy should not extend beyond 5
years. In spite of the initial indication
for malignant ventricular arrhythmias,
long-term amiodarone therapy does
not prevent sudden death. The
use of amiodarone for control of
supraventricular dysrhythmias is much
more common. Thus, amiodarone is
truly a double-edged sword. It is a
highly effective but potentially toxic
drug that requires careful monitoring
throughout its use.
Force on Practice Guidelines and the European
Society of Cardiology Committee for Practice
Guidelines. J Am Coll Cardiol. 2006;48:854–906.
22 Roy D, Talajic M, Dorian P, et al. Amiodarone to
prevent recurrence of atrial fibrillation. N Engl J
Med. 2000;342:913–920.
23 Kudenchuk PJ, Cobb LA, Copass MK, et al.
Amiodarone for resuscitation after out-of-hospi-
tal cardiac arrest due to ventricular fibrillation. N
Engl J Med. 1999;341:871–878.
24 Dager WE, Sanoski CA, Wiggins BS, et al.
Pharmacotherapy considerations in advanced cardiac
life support. Pharmacotherapy. 2006;26:1703–1729.
25 Emergency Cardiovascular Care Committee,
Subcomittees, and Task Forces of the American
Heart Association. 2005 American Heart
Association guidelines for cardiopulmonary
resuscitation and emergency cardiovascular care.
Circulation. 2005;112(suppl):IV1–IV203.
26 Bardy GH, Lee KL, Mark DB, et al. Amiodorone
or an implantable cardioverter-defibrillator
for congestive heart failure. N Engl J Med.
2005;352:225–237.
27 Raeder EA, Podrid PJ, Lown B. Side effects and
complications of amiodarone therapy. Am Heart
J. 1985;109:975–983.
28 Siddoway LA. Amiodarone: guidelines
for use and monitoring. Am Fam Physician.
2003;68:2189–2196.
29 Goldschlager N, Epstein AE, Naccarelli G, et
al. Practical guidelines for clinicians who treat
patients with amiodarone. Arch Intern Med.
2000;160:1741–1748.
30 Martino E, Bartalena L, Bogazzi F, et al. The
effects of amiodarone on the thyroid. Endocr Rev.
2001;22:240–254.
Summer 2007