CARDIOVASCULAR DISORDERS

ANTI-ARRHYTHMIC DRUGS
Mr Asif Ali Lashari
Nursing lecturer
 Dysrhythmias
• Dysrythmias are abnormalities of electrical conduction that may
result in alterations in heart rate or cardiac rhythm. Sometimes
called arrhythmias.
• Dysrhythmias that originate in the atria are sometimes referred to
as supraventricular.
• Atrial fibrillation, a complete disorganization of rhythm, is the most
common type of dysrhythmia.
• Those that originate in the ventricles are generally more serious,
because they are more likely to interfere with the normal function
of the heart.
 Dysrythmias (Conti…!)
• For example, ventricular fibrillation (V-Fib) is a total
disorganization of cardiac contractions that requires immediate
reversal or the initiation of basic life support.
• Although action potentials normally begin at the SA node and
spread across the myocardium in a coordinated manner, other
regions of the heart may begin to initiate beats.
• These areas, known as ectopic foci or ectopic pacemakers,
may send impulses across the myocardium that compete with
those from the normal conduction pathway.
 Types of Dysrhythmias
Dysrythmia Type Description

Atrial or Rapid heartbeat greater than 100 beats/min in adults;

ventricular ventricular tachycardia is more serious than atrial
tachycardia tachycardia.
Atrial or Rapid, regular heartbeats; may range between 200 and
ventricular flutter 300 beats/min; atrial may require treatment but is not
usually fatal; ventricular flutter requires immediate Rx.

Atrial or Very rapid, uncoordinated contractions with complete

ventricular disorganization of rhythm; ventricular fibrillation requires
fibrillation immediate treatment.
 Types of Dysrhythmias
Dysrhythmia Type Description

Heart block Blockage in the electrical conduction system of the

heart; may be partial or complete; classified as first,
second, or third degree.

Premature atrial or An extra beat often originating from a source other than the SA
premature ventricular node; only considered serious if it occurs in high frequency;
contractions (PVCs) may be a precursor of more serious dysrhythmias.

Sinus bradycardia Slow heartbeat, less than 60 beats per minute,

originating in the sinoatrial (SA) node; may require a
pacemaker.
 Non-Pharmacologic Therapy
• The more serious types of dysrhythmias are corrected through electrical
shock of the heart, with treatments such as elective cardioversion and
defibrillation.
• The electrical shock momentarily stops all electrical impulses in the
heart, both normal and abnormal.
• The temporary cessation of electrical activity often allows the SA node
to automatically return conduction to a normal sinus rhythm.
• Cardiac pacemakers are sometimes implanted to correct the types of
dysrhythmias that cause the heart to beat too slowly.
 Phases of Myocardial Action potential
• Most anti-dysrhythmic drugs act by interfering with myocardial
action potentials.
• Action potentials occur in both neurons and cardiac muscle cells
due to differences in the concentration of certain ions found inside
and outside the cell.
• Under resting conditions, sodium ion (Na+) and calcium ion Ca2+
are found in higher concentrations outside myocardial cells, and
potassium ion (K+) is found in higher concentration inside these
cells.
• These imbalances are, in part, responsible for the slight negative
charge (80 to 90 mV) inside a myocardial cell membrane relative to
the outside of the membrane.
 Phases of Myocardial Action potential
• A cell having this negative membrane potential is called polarized.
• An action potential begins when sodium ion channels located in the
plasma membrane open and Na+ rushes into the cell, producing a
rapid depolarization, or loss of membrane potential.
• During this period, Ca2+ also enters the cell through calcium ion
channels, although the influx is slower than that of sodium.
• The entry of Ca2+ into the cells is a signal for the release of additional
intracellular calcium that is held in storage inside the sarcoplasmic
reticulum.
 Phases of Myocardial Action potential
• It is this large increase in intracellular Ca2+ that is responsible for the
contraction of cardiac muscle.
• During depolarization, the inside of the plasma membrane temporarily
reverses its charge, becoming positive. The cell returns to its polarized
state by the removal of Na+ from the cell via the sodium pump and
movement of K+ back into the cell through potassium ion channels.
• In cells located in the SA and atrioventricular (AV) nodes, it is the influx
of Ca2+, rather than Na+, that generates the rapid depolarization of
the membrane.
• Blocking potassium, sodium, or calcium ion channels is the primary
pharmacologic strategy used to prevent or terminate dysrhythmias.
 Phases of Myocardial Action potential
• The pumping action of the heart requires alternating periods
of contraction and relaxation.
• There is a brief period following depolarization, and most of
repolarization, during which the cell cannot initiate another
action potential.
• This time, known as the refractory period, ensures that the
myocardial cell finishes contracting before a second action
potential begins.
• Some antidysrhythmic drugs produce their effects by
prolonging the refractory period.
 Automaticity and Conduction of Heart
Automaticity:
• The ability to spontaneously depolarize and generate an action
potential.
Conduction:
• Movement of a cardiac action potential from one part of
the heart to another.
 Anti-Dysrhythmic Drugs

• Anti-dysrhythmic drugs act by altering specific

electrophysiological properties of the heart.
• They do this through two basic mechanisms: blocking
flow through ion channels (conduction) or altering
autonomic activity (automaticity).
Classification of Anti-dysrhythmic Drugs
 Sodium channel Blockers (CLASS I)
• Sodium channel blockers, the class I drugs, are divided into
three subgroups, IA, IB, and IC, based on subtle differences in
their mechanism of action.
• Because the action potential is dependent on the opening of
sodium ion channels, a blockade of these channels will prevent
depolarization(Contraction).
• The spread of the action potential across the myocardium will
slow, and areas of ectopic pacemaker activity will be
suppressed.
• All the sodium channel blockers have the potential to create
new dysrhythmias or worsen existing ones.
 Beta-Adrenergic Blockers (CLASS II)
• Beta-adrenergic antagonists, also called beta blockers, are widely
used for cardiovascular disorders, including HTN, MI, HF, and
dysrhythmias.
• As expected from their effects on the autonomic nervous system,
beta-adrenergic blockers slow the heart rate and decrease conduction
velocity through the AV node.
• Myocardial automaticity is reduced, and many types of dysrhythmias
are stabilized.
• These effects are primarily caused by blockade of calcium ion
channels in the SA and AV nodes, although these drugs also block
sodium ion channels in the atria and ventricles.
Beta-Adrenergic Blockers (CLASS II)
• They depress phase 4 of action potential.
 Potassium Channel Blockers (CLASS III)
• These drugs prolong the duration of the action potential and reduce
automaticity.
• After the action potential has passed and the myocardial cell is in a
depolarized state, repolarization depends on restoring potassium ions
inside the cell.
• By blocking potassium channels, the class III antidysrhythmics delay
repolarization of the myocardial cells and lengthen the refractory
period, which tends to stabilize dysrhythmias.
• The potassium channel blockers are reserved for serious
dysrhythmias. Amiodarone (Cordarone, Pacerone) is one of the more
frequently used drugs in this class and is featured as the class III
antidysrhythmic.
Potassium Channel Blockers (CLASS III)
• Within the framework of ACLS, amiodarone is used primarily to
treat ventricular fibrillation and ventricular tachycardia that occurs
during cardiac arrest and is unresponsive to shock delivery, CPR,
and vasopressors.
 Calcium Channel Blockers (CLASS IV)
• A few CCBs, such as diltiazem (Cardizem, Dilacor, others) and
verapamil (Calan Isoptin, Verelan), block calcium ion channels in both
the heart and arterioles.
• Blockade of calcium ion channels has a number of effects on the
heart that include reduced automaticity in the SA node and slowed
impulse conduction through the AV node.
• This slows the heart rate and prolongs the refractory period.
• Calcium channel blockers are only effective against supraventricular
dysrhythmias.
• As with other antidysrhythmics, bradycardia and hypotension are
frequent adverse effects.
 MISCELLANEOUS DRUGS
• Adenosine (Adenocard, Adenoscan) and digoxin (Lanoxin, Lanoxicaps),
are occasionally used to treat specific dysrhythmias.
• Adenosine is a naturally occurring nucleoside. Adenosine terminates
serious atrial tachycardia by slowing conduction through the AV node
and decreasing automaticity of the SA node.
• Its primary indication is a specific dysrhythmia known as paroxysmal
supraventricular tachycardia (PSVT), for which it is a drug of choice.
• Although digoxin is primarily used to treat HF, it is also prescribed for
certain types of atrial dysrhythmias due to its ability to decrease
automaticity of the SA node and slow conduction through the AV node
 Procainamide HCL
• Procainamide HCL: Sodium channel Blocker
• Therapeutic Effects/ Indication: To control Cardiac Dysrhythmias
PVCs, Ventricular Tachycardia.
• Mode of Action: Depression of Myocardial Excitability by slowing
conduction of cardiac tissue through atrium, bundle of His and Ventricle
to decrease cardiac dysrhythmias.
• Side effects: Anorexia, Nausea, Vomiting, Diarrhea, Headache,
Dizziness, Weakness, flushing, rash, pruritus.
• Adverse Effects: Atrioventricular block, Pleural effusion, Ventricular
tachycardia/ Fibrillation. Thrombocytopenia.
• Contraindication: Heart block, Cardiogenic shock.
 Nursing Process
Anti-Dysrrhythmic Drug
 Assessment
• Obtain health and drug history. History may include palpitations,
coughing, chest pain (type, duration and severity), previous angina or
cardiac dysrhythmias,
• Obtain baseline VS and ECG for future comparisons.
• Check early cardiac enzyme results (AST, LDH, CPK) to compare with
future laboratory results.
Nursing Diagnosis
• Decrease cardiac output.
• Anxiety related to irregular heart beat.
• High risk for activity intolerance.
 Nursing Interventions
• Monitor Vital Signs (Hypotention can occur).
• When the drug is ordered IV push or bolus, administer it over a period
of 2-3 minutes or as prescribed.
• Monitor ECG for abnormal patterns and report findings such as PVC,
increased PR and QT intervals, and/or widening of QR complex.
Increased QT interval is a risk factor for torsades de des pointes.
Client Teaching
• Instruct the client to take the prescribed drug as ordered.
• Provide specific Instructions for each drug such as photosensitivity for
amiodarone.
 Client Teaching

• Instruct the client to report side effects to the health care provider.
These can include dizziness, faintness, nausea and vomiting.
• Advise the client to avoid alcohol, caffeine and cigarettes. Alcohol
can intensify the hypotensive reaction, caffeine increases the
catecholamine level and cigarette smoking promotes
vasoconstriction.
 Chapter Summary
• Persistent or severe dysrhythmias may be lethal. Dysrhythmias are
classified by the location (atrial or ventricular) or type (flutter, fibrillation,
or block) of rhythm abnormality produced.
• Changes in sodium and potassium levels generate the action potential in
myocardial cells.
• Depolarization occurs when sodium (and calcium) rushes in;
repolarization occurs when sodium ions are removed and potassium ions
are restored inside the cell.
• Antidysrhythmic drugs are classified by their mechanism of action.
• Sodium channel blockers, the largest group of antidysrhythmics, act by
slowing the rate of impulse conduction across the heart.
 Chapter Summary
• Beta-adrenergic blockers act by reducing automaticity as well as by
slowing conduction velocity across the myocardium.
• Potassium channel blockers act by prolonging the refractory period of
the heart.
• Calcium channel blockers act by reducing automaticity and by slowing
myocardial conduction velocity. Their actions and effects are similar to
those of the beta blockers.
• Adenosine and digoxin are used for specific dysrhythmias but do not
act by blocking ion channels.