CHAPTER 26
DRUGS FOR DYSRHYTHMIAS
LEARNING OUTCOME 1
Explain how rhythm abnormalities can affect cardiac function.
Concepts
1. Dysrhythmias are abnormalities of electrical conduction or rhythm in the heart. Also known as arrhythmias,
they can range from harmless to life threatening.
2. The electrocardiogram may be used to record electrophysiological events in the heart and to diagnose
dysrhythmias. Proper diagnosis and pharmacotherapy can significantly affect the prognosis of a patient with
dysrhythmias.
3. The frequency of dysrhythmias in the population is difficult to predict because symptoms can range from
none to sudden death, though dysrhythmias are estimated to be quite common. Persistent or severe
dysrhythmias increase the risk of stroke and heart failure.
Table 26.1 Types of Dysrthymia
Figure 26.2 Normal ECG and Its Relationship to Impulse Conduction to the Heart
LEARNING OUTCOME 2
Illustrate the flow of electrical impulses through the normal heart.
Concepts
1. Some myocardial cells in these regions have the property of automaticity. They are able to initiate an action
potential. The electrical conduction pathway from the sinoatrial (SA) node, across both atria to the
atrioventricular (AV) node through the atrioventricular bundle (bundle of His), to the right and left bundle
branches and Purkinje fibers keeps the heart beating in a synchronized manner.
2. The purpose of the conduction system is to regulate the heart and maintain cardiac output. Trace the normal
conduction pathway in the diagram found in Figure 26.1.
Figure 26.1 Normal Conduction Pathway in the Heart
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LEARNING OUTCOME 3
Classify dysrhythmias based on their location and type of rhythm abnormality.
Concepts
1. Dysrhythmias can occur in both healthy and diseased hearts; they disrupt the regulation of the heart and may
decrease cardiac output. The exact cause of dysrhythmias is elusive, but they are closely associated with
certain conditions, such as heart disease and myocardial infarctions.
2. Dysrhythmias are classified by the location (atrial or ventricular) or type (flutter, fibrillation, or block) of
rhythm abnormality produced. Atrial fibrillation is the most common type of dysrhythmia.
3. Types of dysrhythmias include premature atrial or premature ventricular contractions (PVCs), atrial or
ventricular tachycardia, atrial or ventricular flutter and/or fibrillation, sinus bradycardia, and heart block.
LEARNING OUTCOME 4
Explain how an action potential is controlled by the flow of sodium, potassium, and calcium ions across the
myocardial membrane.
Concepts
1. Action potentials are electrical impulses that travel across the myo cardium; they are found in neural and
cardiac cells. Changes in extra- and intracellular ion polarization create the electrical impulse. A cell
membrane is said to be polarized when it is at rest. The potential across the membrane is negative inside the
cell relative to the outside, sodium and calcium are outside the cell, and potassium is inside the cell at this
time.
2. Generation of the action potential begins when sodium-ion channels open and sodium ions rush in, causing
depolarization. Then the calcium-ion channels open and calcium ions enter the cell, stimulating cardiacmuscle contraction. SA and AV cells depolarize in response to calcium-ion influx. After the brief period of
depolarization, the sodium pump removes sodium from the cell, and potassium-ion channels allow
potassium to move back into the cell. This phase is called repolarization, or a return to a polarized state.
3. Discuss the ion channels in myocardial cells as diagrammed in Figure 26.3.
4. The pharmacological strategies used to terminate dysrhythmias work in two ways: either they either block
potassium-, sodium-, or calcium-ion channels; or they prolong the refractory period, a brief period in the
conduction cycle during which myocardial cells cannot produce another action potential.
Figure 26.3 Flow of Ions During the Action Potential
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LEARNING OUTCOME 5
Identify the importance of nonpharmacologic therapies in the treatment of dysrhythmias.
Concepts
Nonpharmacological therapies for dysrhythmias include cardioversion and defibrillation for serious types of
dysrhythmias. These are both examples of an electrical shock that stops all electrical impulses in the heart and
allows the sinoatrial node to regain control. Catheter ablation identifies and destroys aberrant cardiac cells that
cause dysrhythmias. Cardiac pacemakers pace the heart at a set rate. Implantable cardioverter defibrillators
(ICD) are a combination of pacemaker and defibrillator.
LEARNING OUTCOME 6
Identify the general mechanisms of action of antidysrhythmic drugs.
Concepts
1. Antidysrhythmic drugs are categorized into four classes according to their mechanism of action. They act by
blocking conduction (flow of ions) or altering automaticity (autonomic activity). The use of antidysrhythmic
drugs is declining significantly. Although these drugs have the ability to correct dysrhythmias, they can also
worsen or even create new dysrhythmias. Nonpharmacological therapies have improved and are being used
more frequently to treat dysrhythmias.
2. Groups of antidysrhythmic drugs—see Table 26.2.
Class I: sodium-ion-channel blockers—Blocking sodium-ion channels prevents depolarization; the spread of
the action potential across the myocardium will slow, and areas of ectopic pacemaker activity will be
suppressed.
Class II: beta-adrenergic antagonists—Beta blockers slow the heart rate and decrease conduction velocity
through the AV node.
Class III: potassium-ion-channel blockers—Repolarization depends upon replacement of potassium inside
the cell. The class III medications delay repolarization of the myocardial cells and lengthen the refractory
period, which tends to stabilize dysrhythmias.
Class IV: calcium-ion-channel blockers—A blockade of calcium-ion channels reduces automaticity in the
SA node and slows impulse conduction through the AV node. This slows the heart rate and prolongs the
refractory period. Miscellaneous antidysrhythmic drugs—work by slowing conduction through the AV
node and/or decreasing automaticity of the SA node.
Table 26.2 Classification of Antidysrhythmics
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LEARNING OUTCOME 7
Describe the nurse’s role in the pharmacologic management of patients with dysrhythmias.
Concepts
1. The role of the nurse in antidysrhythmic drug therapy involves careful monitoring of a patient’s condition
and providing education as it relates to the prescribed drug treatment. Obtain a complete medical and drug
history and physical examination, including baseline ECG, vital signs, diagnostic tests, dietary habits, and
routine activity.
2. Sodium-ion-channel blockers: Monitor ECG for changes; monitor for hypotension, changes in level of
consciousness, and diarrhea. Teach the patient to not skip a dose of medication, to not take two doses at one
time, and to avoid the use of alcohol. This medication is contraindicated in those with heart failure or renal
impairment.
3. Beta-adrenergic blockers: This medication is contraindicated in patients with heart block, severe
bradycardia, AV block, and asthma. Monitor for hypotension and hypoglycemia. Elderly patients may show
signs of cognitive impairment. Teach patients to take their own pulse, how to rise slowly from sitting or
lying down, and to report signs of heart failure.
4. Potassium-ion-channel blockers: Use cautiously in patients with heart block; these medications are not
recommended for use during pregnancy (category C or D) or lactation. Teach patients to monitor for vision
changes, palpitations, jaundice, and abdominal pain and to avoid sun exposure and take with food.
5. Calcium-ion-channel blockers: Do not use for patients with sick-sinus syndrome, heart block, severe
hypotension, cardiogenic shock, and severe congestive heart failure. Monitor for hypotension, especially in
the elderly; do not use during pregnancy (category C) or lactation. Teach patients to report any palpitations,
blood pressure changes, edema, or shortness of breath and to rise slowly from a sitting or lying-down
position.
6. Miscellaneous drugs for dysrhythmias: Monitor for heart rate and blood pressure changes. Assess those
patients taking digoxin for symptoms of digoxin toxicity.
.
LEARNING OUTCOME 8
Know representative drug examples for each of the drug classes listed in Drugs at a Glance, and explain their
mechanisms of action, primary actions, and important adverse effects.
Concepts
1. Sodium-ion-channel blockers (Class I): prototype drug: procainamide (Pronestyl). The mechanism of action
of this largest group of antidysrhythmics is to block the sodium-ion channels, which slow the rate of impulse
conduction across the heart. The primary use is to correct many types of atrial and ventricular dysrhythmias.
Adverse effects include the creation of new dysrhythmias or worsening of existing ones, lupus effect,
nausea, vomiting, abdominal pain, and headache. High doses can produce CNS effects.
2. Beta-adrenergic blockers (Class II): prototype drug: propranolol (Inderal). The mechanism of action is to
block beta receptors, which reduces automaticity and slows conduction velocity across the myocardium.
The primary use is treatment of atrial dysrhythmias associated with heart failure. Adverse effects include
bradycardia, hypotension with dizziness and fainting, bronchospasms, hypoglycemia, and diminished libido.
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3. Potassium-ion-channel blockers (Class III): prototype drug: amiodarone (Cordarone). The mechanism of
action is to block potassium-ion channels in myocardial cells, which prolongs the refractory period of the
heart. The primary use is to treat resistant ventricular tachycardia and atrial dysrhythmias with heart failure.
Adverse effects include blurred vision, pneumonia-like syndrome, bradycardia, and hypotension. Potassiumion-channel blockers can create new dysrhythmias or worsen existing ones.
4. Calcium-ion-channel blockers (Class IV): prototype drug: verapamil (Calan). The mechanism of action is to
block calcium channels, which reduces automaticity and slows myocardial (AV) conduction velocity. Their
actions and effects are similar to those of beta blockers. The primary use is treatment of supraventricular
tachycardia. Adverse effects include bradycardia, hypotension, and headache.
5. Miscellaneous antidysrhythmics: Examples of miscellaneous antidysrhythmics are digoxin (Lanoxin) and
adenosine (Adenocard). The mechanism of action for both of these drugs is to decrease automaticity of the
SA node and slow conduction through the AV node but not act by blocking ion channels. The primary use
for digoxin is treatment of certain types of atrial dysrhythmias. Adenosine is used to treat serious atrial
tachycardia. Adverse effects include creating new dysrhythmias or worsening existing ones. Specific to
digoxin are nausea, vomiting, headache, and visual disturbances. Specific to adenosine are facial flushing
and dyspnea.
Prototype Drug

procainamide (Procanabid)

propranolol (Inderal, InnoPran)

amiodarone (Cordarone, Pacerone)

verapamil (Calan, Covera-HS, Isoptin SR, Verelan)
LEARNING OUTCOME 9
Use the nursing process to care for patients receiving drug therapy for dysrhythmias.
Concepts
1. Assessment: Obtain complete health history including allergies, drug history, and possible drug interactions;
do assessment of cardiac output and obtain a baseline ECG to compare throughout therapy.
2. Nursing diagnoses: Ineffective tissue perfusion, knowledge deficit, risk for injury, and decreased cardiac output.
3. Planning: Goals for the patient receiving drugs for treatment of dysrhythmia include improved cardiac
output, understanding of drug therapy, and prevention of adverse effects.
4. Implementation: Monitor cardiac rate and rhythm, monitor IV site, investigate possible causes of
dysrhythmia, and observe for correct administration of the drugs and their adverse effects.
5. Evaluation: Ideal outcomes include improved cardiac output, patient verbalization of understanding of drug
therapy, and prevention of adverse effects.
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