Antiarrhythmic Drugs

UPDATED ON MAY 4, 2024

BY IRIS DAWN TABANGCORA, RN

Antiarrhythmics address arrhythmia by altering cells’ automaticity

and conductivity.

 All cells in the heart are capable of undergoing spontaneous

contractions (automaticity). Therefore, these cells are capable of
generating excitatory impulses.
 Disruptions in the conduction of these impulses affect
contractility of the heart as well as the volume of blood pumped
by the heart each minute (cardiac output).
  Arrhythmia is the term applied for disruptions that interfere with
generation of impulses and conduction of these impulses to
the myocardium.
Table of Contents
 Antiarrhythmic: Generic and Brand Names
 Disease Spotlight: Arrhythmias
 Class I antiarrhythmics
 Therapeutic Action
 Indications
 Pharmacokinetics
 Contraindications and Cautions
 Adverse Effects
 Interactions
 Class II antiarrhythmics
 Therapeutic Action
 Indications
 Pharmacokinetics
 Contraindications and Cautions
 Adverse Effects
 Interactions
 Class III antiarrhythmics
 Therapeutic Action
 Indications
 Pharmacokinetics
 Contraindications and Cautions
 Adverse Effects
 Interactions
 Class IV antiarrhythmics
 Therapeutic Action
 Indications
 Pharmacokinetics
 Contraindications and Cautions
 Adverse Effects
 Interactions
 Nursing Considerations for Antiarrhythmics
 Nursing Assessment
 Nursing Diagnoses
 Implementation with Rationale
 Evaluation
 Recommended Resources
 See Also
  We have a pill for that…
 References and Sources
Antiarrhythmic: Generic and Brand Names
Here is a table of commonly encountered antiarrhythmic drugs, their
generic names, and brand names:

 Class I Antiarrhythmics
 Class IA
 disopyramide (Norpace)
 procainamide (Pronestyl)
 quinidine (Quinaglute, Quinidex)
 Class IB
 lidocaine (Xylocaine)
 mexiletine (Mexilitil)
 Class IC
 flecainide (Tambocor)
 propafenone (Rythmol)
 Class II Antiarrhtyhmics
 acebutolol (Sectral)
 esmolol (Brevibloc)
 propranolol (inderal)
 Class III Antiarrhythmics
 ibutilide (Corvert)
 sotalol (Betapace)
 Class IV Antiarrhythmics
 verapamil (Calan, Covera-HS)
 Other antiarrhthmics
 adenosine (Adenocard)
 digoxin (Lanoxin)
 dronedarone (Multaq)
Disease Spotlight: Arrhythmias
Arrhythmias (also called dysrhythmias) involve changes in the
automaticity and conductivity of the heart cells.

To better understand this condition, there are two concepts vital to be

mastered: conductivity and automaticity.

Conductivity: is the property of the heart cells to transmit

spontaneous impulses starting from the sinoatrial (SA) node, activating
all parts of the heart muscle almost spontaneously. Conductivity is the
basis of cardiac contraction and relaxation, allowing the heart to beat.
Different areas of the specialized conductive system include:

 SA node – impulse generation of 60-100 impulses per minute

 AV node – 40-50 impulses per minute
 Ventricular muscle cells – 10-20 impulses per minute
Automaticity: is the property of the heart cells to undergo
spontaneous depolarization during relaxation. This is because at this
point, potassium flows out of the cell while sodium moves inside: the
condition necessary to produce an action potential. Here are the five
phases of action potential:

 Phase 0 – depolarization phase; stage in which cell reaches

point of stimulation. This phase is characterized by
open sodium gates and sodium ions rushing towards the cell
leading to action potential. There is absence of charge difference
between the outside and the inside of the membrane.
 Phase 1 – a very short period wherein concentration of sodium
equalizes inside and outside of the cell
 Phase 2 – plateau phase; stage in which cell is trying to go
back to its resting stage (repolarization). The cell becomes less
permeable to sodium, potassium begins to leave the cell,
and calcium starts to enter the cell.
 Phase 3 – rapid repolarization phase; stage in which the
sodium gates are closed and potassium flows out of the cell.
 Phase 4 – resting phase; stage in which sodium-potassium
pump restores the cell’s resting membrane potential in
preparation for the next action potential.
Types of arrhythmias

Depending on factors causing them, here are different types of

arrhythmias:

 Changes in rate: tachycardia, bradycardia

 Stimulation from ectopic focus: premature atrial contractions
(PACs), premature ventricular contractions (PVCs), atrial
flutter and/or fibrillation (AF), ventricular fibrillation
 Alterations in conduction through the muscle: heart blocks,
bundle branch block
 It can be triggered by the following: electrolyte disturbances,
decreased oxygen supply to the cells, structural damage of the
 conduction system, drug effects, acidosis, and lactic acid
accumulation.
Class I antiarrhythmics
 This class blocks sodium channels in the cell membrane during
action potential. Subgroup under this class is based on their
mechanism in blocking sodium channels.
 These class are local anesthetics and membrane-stabilizing
agents because of their ability to bind more quickly to sodium
channels.
Therapeutic Action

 Class I antiarrhythmics stabilize cell membrane by depressing

phase 0 of action potential. They bind to sodium channels and
change the duration of action potential of the cells.
 Class Ia drugs depress phase 0 and prolong duration of action
potential.
 Class Ib drugs somewhat depress phase 0 and shorten duration
of action potential.
 Class Ic drugs markedly depress phase 0 and extremely slows
conduction but has little effect on the duration of action potential.
Indications

 Primarily indicated for decreasing workload of the heart and

relieving HF
 Digoxin is especially indicated for atrial flutter, atrial fibrillation,
and paroxysmal atrial tachycardia.
Children

 Antiarrhythmics are not often used for this age group

Adults

Usually indicated for emergency cases.

 Evaluation of drug regimen should be done carefully and
regularly to ensure effectiveness and patient safety.
 Drug safety for pregnant women not established.
 This drug can enter breast milk and has been associated with
various side-effects.
 Antiarrhythmics I, III, and IV are strictly prohibited to lactating
women.
Older adults
  They are more susceptible to drug toxicity because of underlying
conditions that would interfere with metabolism and excretion of
drug.
 Renal and hepatic function should always be monitored.
Pharmacokinetics

Route Onset Peak Duration

IM 5-10 min 5-15 min 2h

IV Immediate Immediate 10-20 min

Half-life (T1/2) Metabolism Excretion

10 min, then 1.5-3 h liver urine

Contraindications and Cautions

 Allergy to Class I antiarrhythmics. Prevent severe

hypersensitivity reactions.
 Bradycardia, heart block. Unless an artificial pacemaker is in
place, the conduction-altering effect of drug can lead to total
heart block.
 HF, hypotension, shock. Exacerbated by effects of drug on
action potential.
 Electrolyte imbalance. Can alter drug effectiveness
 Renal, hepatic dysfunction. Interfere with drug bioavailability
and excretion
 Pregnancy and lactation. Can cause potential adverse effects
to the fetus or neonate.
Adverse Effects

 CNS: dizziness, drowsiness, fatigue, twitching, mouth numbness,

slurred speech, vision changes, tremors
 CV: arrhythmias, hypotension, vasodilation, potential for cardiac
arrest
 Respiratory: respiratory depression
  Hema: bone marrow depression
 EENT: rash, hypersensitivity reactions, hair loss
Interactions

 Digoxin, beta-blockers: increased risk for developing arrhythmias

 Quinidine with digoxin: quinidine competes with digoxin at renal
transport sites so it can increase chances of developing digoxin
toxicity
 Cimetidine: increased Class Ia toxicity
 Anticoagulants: increased risk of bleeding
Class II antiarrhythmics
 This class interferes with action potential by blocking beta
receptors in the heart and kidneys. This, in turn, blocks phase 4
of action potential.
 Class II antiarrhythmics are beta-adrenergic blockers.
Therapeutic Action

 Class II antiarrhythmics engage in competitive inhibition of beta

receptors specifically found in the heart and kidneys. For this
reason, there is decreased in heart rate, excitability, and cardiac
output. Conduction through AV node also slows down. In the
kidneys, release of renin is decreased.
 These effects decrease blood pressure and the stabilize the
highly-excitable heart. As a result, workload of the heart is
lessened.
Indications

 This class is specifically indicated for treatment of

supraventricular tachycardia and premature ventricular
contractions (PVCs).
 Children: antiarrhythmics are not often used for this age group
 Adults: usually indicated for emergency cases. Evaluation of
drug regimen should be done carefully and regularly to ensure
effectiveness and patient safety. Drug safety for pregnant women
not established. This drug can enter breast milk and has been
associated with various side-effects. Antiarrhythmics I, III, and IV
are strictly prohibited to lactating women.
 Older adults: are more susceptible to drug toxicity because of
underlying conditions that would interfere with metabolism and
excretion of drug. Renal and hepatic function should always be
monitored.
Pharmacokinetics

Route Onset Peak Duration

Oral 20-30 min 60-90 min 6-12 h

IV Immediate 1 min 4-6 h

Half-life (T1/2) Metabolism Excretion

3-5 h liver urine

Contraindications and Cautions

 Sinus bradycardia (<45 beats per minute), heart block.

Exacerbated by the therapeutic effects of the drug.
 HF, cardiogenic shock, asthma, respiratory
depression. Exacerbated by blocking beta receptors.
 Pregnancy and lactation. Can cause potential adverse effects
to the fetus or neonate.
 Diabetes, thyroid dysfunction. Altered by blockade of beta-
receptors
 Renal, hepatic dysfunction. Interfere with bioavailability and
excretion of drugs.
Adverse Effects

 CNS: dizziness, fatigue, dreams, insomnia

 CV: arrhythmias, hypotension, bradycardia, AV blocks, alteration
in peripheral perfusion
 Respiratory: bronchospasm, dyspnea
 GI: anorexia, diarrhea, constipation, nausea, vomiting
 Other: loss of libido, decreased tolerance to exercise, alterations
in blood glucose level
Interactions

 Verapamil: increased adverse drug effects

 Insulin: increased hypoglycemia
Class III antiarrhythmics
 This class prolongs and slows down the outward movement of
potassium during phase 3 of action potential. These drugs act
directly on the heart muscles to prolong repolarization and
refractory period.
 All of these drugs are proarrhythmic and have the possibility of
inducing arrhythmias.
Therapeutic Action

 Class III antiarrhythmics’ ability to prolong refractory period

and repolarization increases the threshold for ventricular
fibrillation.
 These are used to treat life-threatening arrhythmias for which no
other drugs have been effective.
 This class can also act on peripheral tissues to decrease
peripheral resistance.
Indications

 Amiodarone is the drug of choice for ventricular fibrillation and

pulseless ventricular tachycardia.
 Children: antiarrhythmics are not often used for this age group
 Adults: usually indicated for emergency cases. Evaluation of
drug regimen should be done carefully and regularly to ensure
effectiveness and patient safety. Drug safety for pregnant women
not established. This drug can enter breast milk and has been
associated with various side-effects. Antiarrhythmics I, III, and IV
are strictly prohibited to lactating women.
 Older adults: are more susceptible to drug toxicity because of
underlying conditions that would interfere with metabolism and
excretion of drug. Renal and hepatic function should always be
monitored.
Pharmacokinetics

Route Onset Peak Duration

Oral 2-3 d 3-7 h 6-8 h

IV Immediate 20 min Infusion

 Route Onset Peak Duration

Half-life (T1/2) Metabolism Excretion

10 d liver urine

Contraindications and Cautions

 AV Block. Ibutilide and dofetilide exacerbate this health

condition.
 Renal, hepatic dysfunction. Interfere with bioavailability and
excretion of drugs.
 Shock, hypotension, respiratory depression, prolonged QT
interval. Depressed action potentials can worsen these health
problems.
Adverse Effects

 CNS: weakness, dizziness

 CV: arrhythmias, HF
 GI: nausea, vomiting, GI distress
 Amiodarone is associated with liver toxicity, ocular abnormalities,
and very serious cardiac arrhythmias.
Interactions

 Digoxin, quinidine: increased toxic drug effects

 Antihistamines, phenothiazines, tricyclic antidepressants:
increased risk of proarrhythmias
 Dofetilide combined with ketoconazole, verapamil, cimetidine:
increased risk for adverse drug effects
 Sotalol combined with antacids, NSAIDs, and aspirin: loss of
effectiveness of sotalol
Class IV antiarrhythmics
 Include two calcium-channel blockers, namely: diltiazem and
verapamil.
  This class blocks the movement of calcium towards the cell
membrane.
Therapeutic Action

 Class IV antiarrhythmics depress action potential generation

and slows down phases 1 and 2 of action potential. This action
slows down both conduction and automaticity.
Indications

 Other uses of diltiazem and verapamil include treatment

for hypertension and angina.
 Children: antiarrhythmics are not often used for this age group
 Adults: usually indicated for emergency cases. Evaluation of
drug regimen should be done carefully and regularly to ensure
effectiveness and patient safety. Drug safety for pregnant women
not established. This drug can enter breast milk and has been
associated with various side-effects. Antiarrhythmics I, III, and IV
are strictly prohibited to lactating women.
 Older adults: are more susceptible to drug toxicity because of
underlying conditions that would interfere with metabolism and
excretion of drug. Renal and hepatic function should always be
monitored.
Pharmacokinetics

Route Onset Peak Duration

Oral 30-60 min 2-3 h 6-8 h

IV Immediate 2-3 min Unknown

Half-life (T1/2) Metabolism Excretion

3.5-6 h liver urine

Contraindications and Cautions

  Allergy to calcium-channel blockers. Prevent hypersensitivity
reactions.
 Heart block (sick sinus syndrome). Unless an artificial
pacemaker is in place, heart blocks can be exacerbated by the
effects of the drug.
 HF, hypotension. Exacerbated by hypotensive effect of the
drug.
 Pregnancy, lactation. Potential adverse effects to neonate or
fetus.
 Renal, hepatic dysfunction. Interfere with bioavailability and
excretion of drugs.
Adverse Effects

 CNS: weakness, dizziness, fatigue, depression, headache

 CV: hypotension, shock, edema, HF, arrhythmia
 GI: nausea, vomiting, GI distress
Interactions

 Verapamil with beta-blockers: increased risk of cardiac

depression
 Digoxin: additive slowing of AV node conduction
 Atracurium, pancuronium, vecuronium: increased respiratory
depression
 Increased risk of cardiac depression if IV preparation of these
drugs were given 48 hours within administration of IV beta-
adrenergic blockers.
 Diltiazem can increase serum level of cyclosporine.
Nursing Considerations for Antiarrhythmics
Here are important nursing considerations when administering
antiarrhythmics.

Nursing Assessment

These are the important things the nurse should include in

conducting assessment, history taking, and examination:

 Assess for the mentioned contraindications to this drug (e.g.

renal dysfunction, heart blocks, hypersensitivity, etc.) to prevent
potential adverse effects.
  Conduct thorough physical assessment before beginning drug
therapy to establish baseline status, determine effectivity of
therapy, and evaluate potential adverse effects.
 Assess patient’s neurological status to determine potential CNS
drug effects.
 Assess cardiac status closely (e.g. blood pressure, heart rate and
rhythm, heart sounds, ec.) to determine whether change in drug
dose is imperative.
 Monitor respiratory rate, rhythm, and depth to assess for
respiratory depression and detect changes associated with
development of HF.
 Monitor laboratory test results including complete blood count,
renal and liver function tests to determine the need for possible
change in dose and identify toxic effects.
Nursing Diagnoses

Here are some of the nursing diagnoses that can be formulated in the
use of this drug for therapy:

 Decreased cardiac output related to cardiac effects of the drug

 Ineffective tissue perfusion related to decreased blood flow to
different parts of the body
 Altered sensory perception related to CNS drug effects
 Risk for injury related to weakness and dizziness
Implementation with Rationale

These are vital nursing interventions done in patients who are taking
antiarrhythmics:

 Titrate the dose to the smallest amount enough to manage

arrhythmia to decrease the risk of drug toxicity.
 Monitor cardiac rhythm closely to detect potentially serious
adverse effects and to evaluate drug effectiveness.
 Provide comfort and safety measures (e.g. raising side rails,
adequate room lighting, noise control) to help patient tolerate
drug effects.
 Ensure maintenance of emergency drugs and equipment at
bedside to promote prompt treatment in cases of severe toxicity.
 Educate patient on drug therapy including drug name, its
indication, and adverse effects to watch out for to enhance
patient understanding on drug therapy and thereby promote
adherence to drug regimen.
Evaluation

Here are aspects of care that should be evaluated to determine

effectiveness of drug therapy:

 Monitor patient response to therapy through assessment of

cardiac output and rhythm.
 Monitor for adverse effects (e.g. sedation, respiratory depression,
CNS effects).
 Evaluate patient understanding on drug therapy by asking
patient to name the drug, its indication, and adverse effects to
watch for.
 Monitor patient compliance to drug therapy.