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AACN Advanced Critical Care


Volume 21, Number 4, pp.333338
2010, AACN

Drug
Update

Earnest Alexander, PharmD, and


Gregory M. Susla, PharmD
Department Editors

Clinical Utility and Adverse Effects


of Amiodarone Therapy
Melissa Roberts, PharmD

raditional Vaughan Williams classes I and III antiarrhythmic medications are


T
associated with a high incidence of proarrhythmias. In 1985, amiodarone
(Pacerone, Cordarone) was introduced to the market as a novel new drug to
treat ventricular arrhythmias. Its unique mechanism of action produced desirable arrhythmia suppression with a significantly lower incidence of torsades de
pointes than agents that were currently on the market.1 Amiodarone is known
to block 4 major contributors to myocardial conduction. Unlike other agents,
amiodarone interferes with multiple ion channels, which makes it a hybrid of all
of the Vaughan Williams class antiarrhythmics; more specifically, it blocks potassium, sodium, and calcium channels. It also possesses qualities of a -adrenergic
blocker. -Blockade decreases the myocardium excitability by prolonging the
action potential and increasing the refractory period. A 15% to 20% decrease
in heart rate as well as a 10% increase in the PR-QT interval is expected with
amiodarone use.2
Amiodarone has an extensive side effect profile and requires close monitoring. An approved Medication Guide2 was mandated by the Food and Drug
Administration (FDA) in 2005 to be dispensed to all patients starting amiodarone therapy. A few reasons for this new requirement included the high volume of amiodarone prescriptions dispensed in 2004, the off-label use in atrial
fibrillation, and the potential for the serious risks associated with amiodarone
therapy to be overlooked.3 This educational handout alerts patients to the most
common side effects associated with therapy, describes symptoms that should
be immediately brought to a physicians attention, and explains when and how
amiodarone should be taken.2 Although the FDA only requires outpatient pharmacies to dispense the medication guide with new prescriptions, it is imperative
for patients (even when hospitalized) to have all the necessary information to
make an informed decision before starting therapy.
Labeled Indications
Amiodarone is approved by the FDA to treat recurrent ventricular fibrillation as
well as recurrent ventricular tachycardia, which results in hemodynamic instability. The package insert states that amiodarone should be used only to treat
life-threatening recurrent ventricular arrhythmias when other medical management has failed or is intolerable; however, current clinical practice uses amiodarone frequently for both FDA-approved indications and off-label uses. It is
strongly recommended, but not required, to initiate therapy in a hospital setting

Melissa Roberts (formerly Pierce) is Pharmacy Practice Resident, Memorial Medical Center, 1086
Franklin St, Johnstown, PA 15905 (mpierce@conemaugh.org).
DOI: 10.1097/NCI.0b013e3181ef86fe

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secondary to its multiple drug interactions,


side effect profile, and potential to exacerbate
arrhythmias.2
Pharmacokinetics
Amiodarone exhibits slow sporadic oral absorption, and only approximately 50% of the dose
reaches systemic circulation. Although peak
plasma concentrations are reached within 3 to 7
hours, full effects are not usually seen for 1 to 3
weeks.2,4 When the drug is taken with food, especially high-fat meals, the rate and extent of oral
absorption increases. Not only can amiodarone
reach up to 4 times higher concentrations in the
blood, it also reaches peak concentrations
approximately 40% faster in the presence of
food.2 Amiodarone has an extremely long halflife of 20 to 47 days2,5 when administered intravenously and 15 to 142 days2 when given orally,
and it has a strong affinity to accumulate in adipose tissue as well as organs with a high blood
supply (eg, spleen, liver, lung).2,4 For this reason,
patients on long-term therapy who stop taking
the drug but require reinitiation may see full
effects much sooner than would a treatmentnaive patient. The same is true for drug interactions. Despite cessation of therapy, drug
interactions can persist far beyond discontinuation.2 Caution should be exercised when using
amiodarone with other medications that can
displace it from protein binding because it is
highly protein bound (96%).2,5
Amiodarone is metabolized by the liver
(predominantly cytochrome P 450 3A4), with
subsequent secretion into the bile.2,5 Less than
1% of amiodarone and its metabolites are
eliminated through the kidneys. Currently, no
dosage adjustments are recommended for
either renal or hepatic dysfunction; however,
amiodarones major involvement in the liver
lends itself to multiple drug interactions
(Table 1).1 One major metabolite results from
hepatic metabolism called desethylamiodarone.2,5 It is unknown whether desethylamiodarone demonstrates any antiarrhythmic
benefits in humans, but it has been shown to
do so in animal models.2 Caution should be
exercised for use with elderly patients, because
clearance may be decreased in this population as well as in people with severe leftventricular dysfunction.2
Place in Therapy
Supraventricular tachycardia following open
heart surgery can occur in more than 60% of

patients, depending on the type of procedure


performed.7 Prophylactic treatments with medications such as -blockers and antiarrhythmics
have been shown to decrease the incidence of
atrial fibrillation and atrial flutter by nearly
half.8 A double-blind, randomized, placebo-controlled trial titled PAPABEAR published in
2005 evaluated the effectiveness and safety of
amiodarone therapy compared with placebo following elective coronary artery bypass-grafting surgery with or without valve repair.9 Overall,
amiodarone reduced the rate of supraventricular
tachycardia by approximately 50% (16.1% in
the amiodarone group vs 29.5% in the placebo
group, P .001); however, amiodarone therapy
was associated with a statistically significant
number of cardiac side effects including bradycardia requiring temporary pacing (5.7% vs
2.0%) and QTc prolongation (1.3% vs 0%).
Given the increased cost and deleterious outcomes associated with postoperative atrial fibrillation, careful consideration regarding risk and
benefit should be made when using amiodarone
for cardiac surgery prophylaxis.9
No FDA-approved indication is available
to use amiodarone for pharmacologic cardioversion of atrial fibrillation to normal
sinus rhythm; however, the most recent American College of Cardiology/American Heart
Association/European Society of Cardiology
practice guidelines recommend both oral and
intravenous regimens when medical cardioversion is indicated.10 Regardless of the duration
of atrial fibrillation (the guidelines use 7 days
as the point of reference for changes in therapy
choice), amiodarone is regarded as a class IIa
recommendation for cardioversion. If a patient
has been in atrial fibrillation for more than
48 hours, anticoagulation is necessary. Clinicians
are highly encouraged to initiate therapy in a
hospital setting secondary to the adverse
effects associated with both the medication
itself and the conversion to sinus rhythm. The
most common adverse effects associated with
intravenous administration include hypotension (seen in 16% of patients),5,11 bradycardia,
and QTc prolongation.10 Amiodarone has a
44% success rate in acute cardioversion and
65% efficacy in maintaining sinus rhythm12;
however, as is the case with other antiarrhythmics, the longer a patient is in atrial fibrillation, the more difficult it is to convert to sinus
rhythm, regardless of the agent used.
Traditional management of atrial fibrillation had been primarily treatment with

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Drug Update

VO L U M E 2 1 N U M B E R 4 O C TO B E R D E C E M B E R 2 010

Table 1: Clinically Significant Drug Interactions With Amiodaronea


Medication

Risk of
Interactionb

Clinical Intervention

Category X

Use is contraindicated

QTc prolongation
Artemether
Dronedarone
Lumefantrine
Nilotinib
Pimozide
Quinine
Tetrabenazine
Thioridazine
Ziprasidone
Azithromycin

Category D

Amiodarone decreases the


metabolism of:
Everolimus

Category X

Use is contraindicated

Tolvaptan
Colchicine

Category D

Cyclosporine
Eplerenone
Fentanyl
Flecainide
Tamoxifen
HMG-CoA reductase
inhibitors

No interaction with pravastin and fluvastatin


Maximum dose simvastatin 20 mg daily
Maximum dose Lovastain 40 mg daily

Starting digoxin: 0.125 mg daily in normal


renal function, 0.125 mg every other day in
kidney dysfunction

Digoxin

Already on digoxin: Decrease digoxin dose by 50%


Warfarin

Starting warfarin: 2.5 mg daily


Decrease warfarin dose by 25%40% depending
on amiodarone dose

Other interaction
Silodosin

Category X

Use is contraindicated

Topotecan
Grapefruit juice
Protease inhibitors
a

These data are from amiodarone [package insert]2 and Sanoski.6 Amiodarone is a CYP 3A4 substrate, strong inhibitor of
CYP 1A2, 2C9, 2D6, and 3A4, and P-Glycoprotein inhibitor.
b

Drug interaction categories: Dconsider therapy modification, Xcontraindicated.

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antiarrhythmic medications until 5 major studies were published comparing rate with rhythm
control.1317 All these trials found similar end
points that showed that rate control was
equally as effective as rhythm control when
assessing all-cause mortality and was also associated with fewer side effects. The Atrial Fibrillation Follow-up Investigation of Rhythm
Management trial was the largest of these studies, including 4060 patients with atrial fibrillation.17 The hard end point of all-cause mortality
was assessed in each group. At the end of the
5-year follow-up, death in the rhythm-control
group was 23.8% compared with 21.3% in the
rate-controlled group. In addition, this study
found that 80% of patients in the rhythmcontrol group versus 73% in the rate-control
group required hospitalization. The above findings have changed clinical practice, and now
both methods of treatment are considered
acceptable and should be individualized on the
basis of patient-specific characteristics.17 Amiodarone is considered first-line therapy in the
American College of Cardiology/American
Heart Association/European Society of Cardiology practice guidelines for patients with atrial
fibrillation and concomitant heart failure when
rhythm control is chosen.10
Warnings and Precautions
Although amiodarone is a highly used and effective medication, it also possesses many serious
adverse effects that often limit its use (Table 2).
This article individually reviews 6 predominant complications of amiodarone therapy
that should be monitored on a regular basis.
These complications are most commonly associated with long-term oral therapy secondary
to the drugs long half-life and potential to
accumulate over time.2
Pulmonary Toxicity

Two major types of pulmonary toxicity are


associated with amiodarone therapy: hypersensitivity pneumonitis and interstitial/alveolar
pneumonitis. Hypersensitivity pneumonitis is a
T-cellmediated response that typically occurs
early in therapy.2,19 Once this condition develops, amiodarone should be immediately discontinued and steroid therapy initiated. Furthermore,
these patients should not receive amiodarone
again, because it can result in a more fulminate
reaction upon secondary exposure.2 Interstitial/alveolar pneumonitis is distinguishable
from the hypersensitivity reaction because it is

not T-cell mediated and typically occurs after


months to years of long-term therapy; moreover,
the proposed mechanism of lung damage is
thought to result from oxygen radical release
and/or phospholipidosis.2,19,20 Although completely removing amiodarone therapy is desirable in interstitial pneumonitis, a dose
reduction may also prove beneficial in
patients who have no alternative. Adding
steroids can also help improve symptoms. In
most cases, this toxicity is reversible over 2 to
3 weeks. Patients may be rechallenged at a
lower dose if the benefits of amiodarone therapy are found to outweigh the risks.2 It is of
paramount importance to identify and evaluate
any signs or symptoms of pulmonary compromise (eg, new onset shortness of breath, chest
pain, nonproductive cough) immediately.19
Arrhythmias

One of the major concerns regarding antiarrhythmics is their potential to act as proarrhythmics and cause torsades de pointes; this is
particularly true with Vaughan Williams classes Ia,
Ic, and III.12 Amiodarone has the unique benefit
of rarely being associated with torsades de
pointes,5 and when it does occur, it is usually in
the presence of predisposing factors such as
electrolyte abnormalities. The unique multimodal mechanism of action does lend itself to
the development of symptomatic bradycardia,
atrioventricular nodal block, and QTc prolongation. For these reasons, amiodarone is contraindicated in sinus node dysfunction, which
causes sinus bradycardia, second- and thirddegree atrioventricular heart block, and bradycardia, resulting in syncope.2
Liver Injury

Acute liver injury is common among patients


receiving amiodarone therapy. It is usually
benign and evidenced only through an increase
in liver function tests (alanine transaminase,
aspartate aminotransferase, and -glutamyl
transpeptidase). Amiodarone therapy does not
require adjustment until liver function tests
reach 3 times the upper limit of normal or if
liver function tests double in a patient who had
an elevated baseline before initiating amiodarone. In rare instances, fatal liver disease
has occurred.2,11
Visual Impairments

Amiodarone has been implicated in patients


who develop visual impairments, which range

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Drug Update

VO L U M E 2 1 N U M B E R 4 O C TO B E R D E C E M B E R 2 010

Table 2: Adverse Effects of Amiodarone Therapya


Adverse Effect
Pulmonary toxicity

Monitoring Parameter

Signs/Symptoms

Clinical Intervention

Pulmonary function
tests

Shortness of breath,
wheezing, decreased
breath sounds

Hypersensitivity pneumonitis:
Discontinue amiodarone and
start corticosteroidsCannot
be rechallenged

Chest radiography

Bradycardia/
Arrhythmiasb

Electrocardiography

Hepatotoxicityb

Liver function tests

Vision Impairment

Slit-lamp examination

Interstitial/alveolar pneumonitis:
Discontinue amiodarone or
decrease the dose and start
corticosteroidsCan be
rechallenged at a lower dose
Chest pain and dizziness

Decrease the dose or


discontinue amiodarone
Decrease the dose or
discontinue amiodarone if
liver function tests 3 times
the upper limit of normal or
double from baseline

Blurred vision, halos,


decreased peripheral
vision

Symptomatic corneal
microdeposits
Decrease the dose or
discontinue therapy
Optic neuritis
Discontinue therapy immediately

Thyroid dysfunction Thyroid function tests

Dermatologic

Physical examination

Thyrotoxicosis
New onset arrhythmias,
tachycardia

Hyperthyroidism
Discontinue or reduce dose of
amiodarone, give antithyroid
medication

Hypothyroid
Weight gain, fatigue,
constipation,
depression

Hypothyroid
Give thyroid supplement

Light sensitivity
Slate-blue discoloration
of the skin

Patient education: advise the


use of sunblock, limit sun
exposure, wear protective
clothing while in the sun

These data are from amiodarone [package insert], Sanoski, and Newman et al.

18

Black box warning.

from blurred vision to permanent blindness. The


vast majority of patients will develop corneal
microdeposits but, in most cases, will be asymptomatic; however, as many as 10% of patients
will experience blurred vision or see halos.2,21,22
In this population, reducing the dose or discontinuing therapy can reverse these effects.2 In contrast, a noncausal relationship has been
identified between amiodarone therapy and
optic neuritis and/or neuropathy. Peripheral
vision deficits and clouded vision should prompt
immediate ophthalmic examination.2,22

Thyroid Function

Amiodarone plays a significant role in thyroid


function and has the ability to cause both
hypothyroidism and hyperthyroidism. This drug
is an iodine-containing compound (approximately
37% iodine by weight), which can result in lifethreatening arrhythmias.2,23 Signs of thyrotoxicosis
are not always evident; however, new onset
and/or recurrent arrhythmias should prompt
evaluation of thyroid function.2,18,23 Dose reduction and/or amiodarone discontinuation is
necessary in these patients. Rapid reversal of

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amiodarone-induced hyperthyroidism is unlikely


secondary to a stored surplus of active thyroid
hormones.2 In contrast, hypothyroidism may
result from amiodarones ability to decrease T3
levels and increase T4 levels through direct inhibition of peripheral conversion.2,18 Hypothyroidism occurs more frequently (in up to 10% of
patients) but is less likely to result in fatal
arrhythmias; thus, it is regarded as the less dangerous of the 2 disorders.2,23
Dermatologic Conditions

Long-term amiodarone therapy, especially at


doses greater than 400 mg/d, is associated
with 2 common dermatologic conditions.2
Approximately 10% of patients are reported
to experience light sensitivity.2,19 Proper patient
education can help prevent photosensitivity.
Patients should be counseled on using proper
precautions while in the sun, such as using
protective sunblock, wearing light-colored
clothing that covers the skin, and limiting the
amount of UV-A/UV-B exposure. Less commonly, a phenomenon referred to as blueman syndrome can occur from melatonin
and lipofuscin deposits in the skin, creating the
appearance of a slate-blue discoloration on the
skin that is reversible upon discontinuation of
therapy or dose reduction. Reversal is slow
and can take years to completely resolve.19,24
Conclusion
The multimodal mechanism of action of amiodarone has enabled its use for the treatment and
recurrence of both ventricular and atrial arrhythmias despite its limited original FDA-approved
indications. Proven efficacy through welldesigned clinical trials has helped amiodarone
find its place in therapy; however, the benefit
of long-term therapy must be weighed against
the toxic side effect profile. Careful consideration should be given regarding patients quality
of life, adverse effects, and long-term outcomes.
REFERENCES
1. Babatin M, Lee SS, Pollak PT. Amiodarone hepatotoxicity. Curr Vasc Pharmacol. 2008;6(3):228236.
2. Amiodarone [package insert]. Princeton, NJ: Zydus
Pharmaceuticals USA Inc; 2009.
3. Neff M. Practice guideline briefs. Am Fam Physician.
2005;71(7):14331434.
4. Haffagee CI. Clinical pharmacokinetics of amiodarone.
Clin Cardiol. 1987;10(7) (suppl 1):I6I9.

5. Chow MS. Intravenous amiodarone: pharmacology,


pharmacokinetics, and clinical use. Ann Pharmacother.
1996;30(6):637643.
6. Sanoski CA. Atrial and ventricular arrhythmias: evolving
practices. In: Richardson M, Chant C, Cheng JWM, Chessman KH, Hume AL, Hutchison LC, eds. Pharmacotherapy
Self-Assessment Program: Book 1: Cardiology. 7th ed.
Lenexa, KS: American College of Clinical Pharmacy; 2010:
125152.
7. Creswell LL, Schuessler RB, Rosenbloom M, Cox JL.
Hazards of postoperative atrial arrhythmias. Ann Thorac
Surg. 1993;56(3):539549.
8. Crystal E, Garfinkle MS, Connolly SS, Ginger TT, Sleik K,
Yusuf SS. Interventions for preventing post-operative
atrial fibrillation in patients undergoing heart surgery.
Cochrane Database Syst Rev. 2004;(4):CD003611.
9. Mitchell LB, Exner DV, Wyse DG, et al. Prophylactic oral
amiodarone for the prevention of arrhythmias that begin
early after revascularization, valve replacement, or repair:
PAPABEAR: a randomized controlled trial. JAMA. 2005;
294(24):30933100.
10. Fuster V, Rydn LE, Asinger RW, et al. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation:
executive summary. J Am Coll Cardiol. 2001;38(4):12311266.
11. Cahoon W, Flattery MP, Hess ML. Amiodarone: development, clinical indications, and safety. Prog Cardiovasc
Nurs. 2007;22(3):173176.
12. Medscape. http://img.medscape.com/fullsize/migrated
/577/475/euro577475.tab1.gif. Accessed March 26, 2010.
13. Carlsson J, Miketic S, Windeler J, et al. Randomized trial
of rate-control versus rhythm-control in persistent atrial
fibrillation: the strategies of treatment of atrial fibrillation
(STAF) study. J Am Coll Cardiol. 2003;41:16901696.
14. Hagens VE, Ranchor AV, Van Sonderen E, et al. Effect of rate
or rhythm control on quality of life in persistent atrial fibrillation. Results from the rate control versus electrical cardioversion (RACE) study. J Am Coll Cardiol. 2004;43:241247.
15. Hohnloser SH, Kuck KH, Lilienthal J. Rhythm or rate control in atrial fibrillationPharmacological Intervention
in Atrial Fibrillation (PIAF): a randomised trial. Lancet.
2000;356:17891794.
16. Opolski G,Torbicki A, Kosior DA, et al. Rate control vs rhythm
control in patients with nonvalvular persistent atrial fibrillation: the results of the Polish how to treat chronic atrial
fibrillation (HOT CAFE) study. Chest. 2004;126:476486.
17. Wyse DG, Waldo AL, DiMarco JP, et al. A comparison of
rate control and rhythm control in patients with atrial
fibrillation. N Engl J Med. 2002;347(23):18251833.
18. Newman CM, Price A, Davies DW, Gray TA, Weetman AP.
Amiodarone and the thyroid: a practical guide to the
management of thyroid dysfunction induced by amiodarone therapy. Heart. 1998;79:121127.
19. Gonzalez P, Otero MJ, Barrueco M, Dominguez-Gil A.
Amiodarone-induced skin pigmentation and pulmonary
fibrosis. Hosp Pharm. 2002;37(6):615618.
20. Martin WJ, Rosenow EC. Amiodarone pulmonary toxicity.
Recognition and pathogenesis (part 2). Chest. 1988;93(6):
12421248.
21. Burns KE, Piliotis E, Garcia BM, Ferguson KA. Amiodarone
pulmonary, neuromuscular, and ophthalmological toxicity. Can Respir J. 2000;7(2):193197.
22. Santaella RM, Fraunfelder FW. Ocular adverse effects associated with systemic medications. Drugs. 2007;67(1):8485.
23. Martino E, Bartalena L, Bogazzi F, Braverman LE. The
effects of amiodarone on the thyroid. Endocr Rev. 2001;
22(2):240254.
24. Delage C, Lagac R, Huard J. Pseudocyanotic pigmentation of the skin induced by amiodarone: a light and electron microscopic study. Can Med Assoc J. 1975;112(10):
12051208.

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AACN

Advanced
Critical Care
Test writer: Jane Baron, RN, CS, ACNP
Contact hour: 1.0
Synergy CERP: Category A
Passing score: 8 correct (73%)

CE Test Instructions
To receive CE credit for this test (ID# ACC2141), mark your answers on the form below, complete the enrollment information and submit it with the $10.00 processing fee (nonmembers only; payable in US funds) to the
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Test ID#: ACC2141
FORM EXPIRES
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Fee: $10 (no fee for
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Clinical Utility and Adverse Effects of


Amiodarone Therapy
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answer per question. You may photocopy this form.
A

1.

4.

6.

8.

10.

2.

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7.

9.

11.

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CE Test Questions

Clinical Utility and Adverse Effects of Amiodarone Therapy


Objectives:
Upon completion of this article, the reader will be able to:
1. Identify FDA-approved indications and current off-label uses of amiodarone.
2. Examine the pharmacokinetics of amiodarone.
3. Review warnings and precautions of amiodarone.

1. Which statement is true?


a. Amiodarone blocks only potassium channels.
b. Amiodarone possesses qualities of a -adrenergic
blocker.
c. Amiodarone blocks only calcium channels.
d. Amiodarone is available only in intravenous form.

7. What percent reduction of supraventricular


tachycardia occurred with the use of amiodarone
during the PAPABEAR trial?
a. 10%
b. 20%
c. 35%
d. 50%

2. What percent decrease in heart rate can be expected


with amiodarone?
a. 5%10%
b. 10%15%
c. 15%20%
d. 25%

8. What are the most common adverse effects of


intravenous administration of amiodarone?
a. Hypotension, bradycardia, and QTc prolongation
b. Respiratory distress, tachycardia, and PR prolongation
c. Bundle branch block, hypotension, and blue skin
discoloration
d. Hypertension, ST depression, and tachycardia

3. Which arrhythmia treatment is FDA approved for


amiodarone?
a. Atrial fibrillation
b. Sinus node dysfunction
c. Recurrent ventricular fibrillation
d. Atrioventricular node dysfunction

9. What are two major types of pulmonary toxicity


associated with amiodarone?
a. Respiratory failure and adult respiratory distress syndrome
b. Hypersensitivity pneumonitis and interstitial pneumonitis
c. Pulmonary edema and pneumonia
d. Pulmonary embolism and alveolitis

4. What type of meal increases oral absorption of


amiodarone?
a. High protein
b. High starch
c. High sugar
d. High fat

10. Amiodarone therapy is contraindicated for use with


which rhythm?
a. Atrial fibrillation
b. Sinus node dysfunction
c. Recurrent ventricular fibrillation
d. Recurrent ventricular tachycardia

5. What is the half-life of oral amiodarone?


a. 510 days
b. 2047 days
c. 15142 days
d. 50174 days

11. Which statement is true?


a. Fatal liver disease is a common adverse effect of
amiodarone therapy.
b. Hypothyroidism is more dangerous than hyperthyroidism
when associated with amiodarone therapy.
c. Two dermatologic conditions associated with long-term
amiodarone therapy are photosensitivity and blue man
syndrome.
d. Reversal of dermatologic symptoms is immediate with
discontinuation of amiodarone therapy.

6. Which statement is true?


a. Amiodarone is highly protein bound.
b. Amiodarone is eliminated via the kidneys.
c. One major metabolite from lung metabolism is
desethylamiodarone.
d. Caution should be exercised in elderly patients because of
increased clearance of the drug.

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