Ppt chapter 45

Copyright © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins
Antiarrhythmic Agents
Chapter 45

The Conducting System of the Heart

Five Phases of the Action Potential of the
Cardiac Muscle Cell
• Phase 0: Occurs when the cell reaches a point of
stimulation
• Phase 1: Short period during which the sodium ion
concentration equalizes inside and outside of the cell
• Phase 2 (Plateau Stage): Occurs as the cell membrane
becomes less permeable to sodium, calcium slowly enters
the cell, and potassium begins to leave the cell

Five Phases of the Action Potential
of the Cardiac Muscle Cell (cont.)
• Phase 3: A time of rapid repolarization as the sodium
gates are closed and potassium flows out of the cell
• Phase 4: The cell comes to rest; the sodium–potassium
pump returns the membrane to its resting membrane
potential, and spontaneous depolarization begins again

Types of Cardiac Arrhythmias
• Tachycardia (faster-than-normal heart rate)
• Bradycardia (slower-than-normal heart rate)
• Premature atrial contractions (PACs) or premature
ventricular contractions (PVCs)
• Atrial flutter
• Atrial fibrillation or ventricular fibrillation
• Alterations in conduction through the muscle (heart
blocks and bundle branch blocks)

Causes of Cardiac Arrhythmias
• Electrolyte disturbances that alter the action potential
• Decreases in oxygen delivered to the cells
• Structural damage changing the conduction pathway
through the heart
• Acidosis or accumulation of waste products altering the
action potential
• Drugs that alter the action potential or cardiac conduction

Classifications of Antiarrhythmics
• Class I: Block the sodium channels in the cell membrane
during an action potential
• Class II: Block beta-receptors, causing a depression of
phase 4 of the action potential
• Class III: Block potassium channels, prolong phase 3 of
the action potential
• Class IV: Block calcium channels in the cell membrane

Cardiac Action Potentials

Question
Please answer the following statement as true or false.
One cause of cardiac arrhythmias is a decrease in oxygen
delivered to the cells.

Answer
True
Rationale: Causes of cardiac arrhythmias include:
electrolyte disturbances that alter the action potential;
decreases in oxygen delivered to the cells; structural
damage changing the conduction pathway through the
heart; acidosis or accumulation of waste products
altering the action potential and drugs that alter the
action potential or cardiac conduction

Sub-Classes of Class I Antiarrhythmic
Drugs
• Class Ia: Depress phase 0 of the action potential and
prolong the action potential duration
• Class Ib: Depress phase 0 somewhat and actually
shorten the duration of the action potential
• Class Ic: Markedly depress phase 0, with a resultant
extreme slowing of conduction

Class I Antiarrhythmic
• Actions
– Decreases depolarization, decreasing automaticity of the
ventricular cells; increases ventricular fibrillation threshold
• Indications
– Management of acute ventricular arrhythmias during
cardiac surgery or MI
• Pharmacokinetics
– Widely distributed after injection or after rapid absorption
through GI tract
– Hepatic metabolism and excreted in the urine

Class I Antiarrhythmic (cont.)
• Contraindications
– Allergy, bradycardia or heart block, CHF, hypotension
or shock, electrolyte disturbances
• Caution
– Renal or hepatic dysfunction or pregnancy
• Adverse Effects
– CNS effects: Dizziness, fatigue, slurred speech
– GI – Nausea and vomiting
– CV – Arrhythmias

Class I Antiarrhythmic (cont.)
• Adverse Effects (cont.)
– Respiratory depression
– Misc. – Rash, loss of hair, and potential bone marrow
suppression
• Drug-to-Drug Interactions

Class II Antiarrhythmic
• Actions
– Competitively block beta receptor sites in the heart
and kidneys
– Decrease heart rate, cardiac excitability, and cardiac
output
– Slow conduction though the AV node
• Indications
– Treatment of supraventricular tachycardia and PVCs

Class II Antiarrhythmic (cont.)
– Absorbed from GI tract and undergo hepatic
metabolism, excreted in the urine
– Sinus bradycardia, AV block, cardiogenic shock, CHF,
asthma, or respiratory depression, pregnancy, and
lactation
• Caution
– Diabetes, thyroid dysfunction, renal or hepatic
dysfunction

Class II Antiarrhythmic (cont.)
• Adverse Effects
– Related to the effects of blocking beta receptors in the
sympathetic nervous system
– CNS – Dizziness, insomnia, dreams, and fatigue
– CV – Hypotension, bradycardia, AV block, arrhythmias
– Respiratory – Bronchospasm and dyspnea
– GI – Nausea, vomiting, anorexia
– Misc. – Loss of libido, decreased exercise tolerance,
alterations in blood glucose levels
– Verapamil

Class III Antiarrhythmic
• Actions
– Block potassium channels and slow the outward movement of potassium
during phase 3 of the action potential
– This action prolongs the action potential
• Indications
– Life-threatening ventricular arrhythmias
– Maintenance of sinus rhythm after conversion of atrial arrhythmias
– Absorbed and widely distributed, metabolized in the liver and excreted in
the kidneys
– When used for life-threatening arrhythmias there is no contraindication

Class III Antiarrhythmic (cont.)
• Caution
– Shock, hypotension, respiratory depression,
prolonged QT interval, renal or hepatic disease
• Adverse Effects
– Nausea, vomiting, weakness, dizziness, arrhythmia
– Digoxin or Quinidine
– Other specific drug interactions vary with individual
drugs

Class IV Antiarrhythmic
• Actions
– Block the movement of calcium ions across the cell
membrane
– Depressing the generation of action potential
– Delaying phases 1 and 2 of repolarization
– Slow conduction through the AV node
• Indications
– Supraventricular tachycardia
– Control the ventricular response to rapid atrial rates

Class IV Antiarrhythmic (cont.)
– Well absorbed, protein bound, metabolized in the
liver, and excreted in urine
– Allergy, sick sinus syndrome or heart block,
pregnancy, lactation, CHF, hypotension
• Caution
– Idiopathic hypertrophic subaortic stenosis

Class IV Antiarrhythmic (cont.)
• Adverse Effects
– Dizziness, weakness, fatigue, depression, GI upset,
hypotension, CHF, and shock
– Many drug-to-drug interactions

Question
Which of the following is an adverse effect of the class II
antiarrhythmics?
A. Bronchospasm
B. Flatus
C. Colitis
D. Centralized edema

Answer
A. Bronchospasm
Rationale: Adverse effects that involve the respiratory
system include bronchospasm and dyspnea

Other Drugs Used to Treat Arrhythmias
• Adenosine (Adenocard)
– Used to convert supraventricular tachycardia to sinus
rhythm when vagal maneuvers have been ineffective
• Digoxin
– Slows calcium from leaving the cell, prolonging the
action potential and slowing conduction and heart
rate

Use of Antiarrhythmic Across
the Lifespan

Prototype Class I Antiarrhythmic

Prototype Class II Antiarrhythmic

Prototype Class II Antiarrhythmic
(Continued)

Prototype Class III Antiarrhythmic

Prototype Class III Antiarrhythmic
(Continued)

Prototype Class IV Antiarrhythmic

Prototype Class IV Antiarrhythmic
(Continued)

Nursing Considerations for Antiarrhythmic
Therapy
• Assessment: History and Physical Exam
• Nursing Diagnosis
• Implementation
• Evaluation

Ppt chapter 45

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