Cardiac Antidysrhythmic Drugs and Action Potential

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Questions and Answers

What is the primary mechanism by which antidysrhythmic drugs work to manage cardiac rhythm disturbances?

  • Directly stimulating the autonomic nervous system to regulate heart rate.
  • Modifying ion flow across cardiac cell membranes to affect electrical impulse formation and conduction. (correct)
  • Enhancing the strength of cardiac muscle contractions to compensate for irregular rhythms.
  • Increasing myocardial excitability to ensure consistent contractions.

A medication with a positive inotropic effect would have which of the following actions on the heart?

  • Slow electrical conduction.
  • Increase the force of contraction. (correct)
  • Decrease the heart rate.
  • Shorten the refractory period.

Which of the following best describes the function of the sinoatrial (SA) node in the heart’s electrical conduction system?

  • It coordinates the contraction of the ventricles, ensuring they contract in a synchronized manner.
  • It slows down the electrical impulses from the atria before they reach the ventricles to allow for complete atrial contraction.
  • It acts as the heart’s natural pacemaker, initiating the electrical impulses that trigger each heartbeat. (correct)
  • It serves as a backup pacemaker when the SA node fails, maintaining a heart rate of 40-60 bpm.

How do Class I antidysrhythmic drugs exert their therapeutic effects on cardiac tissue?

<p>By blocking sodium channels, decreasing the rate of rise of the action potential. (C)</p> Signup and view all the answers

Which of the following electrolyte imbalances is most important to monitor in a patient taking antidysrhythmic drugs, given its significant impact on cardiac electrical stability?

<p>Potassium (B)</p> Signup and view all the answers

Why is it important to educate patients taking beta-blockers or digoxin to regularly monitor their pulse rate?

<p>To monitor for bradycardia, an expected effect that requires medication adjustment. (A)</p> Signup and view all the answers

Which action is most important when administering adenosine for paroxysmal supraventricular tachycardia (SVT)?

<p>Administering it as a rapid IV push followed by a saline flush. (D)</p> Signup and view all the answers

A patient is prescribed amiodarone for chronic atrial fibrillation. What significant adverse effect should the patient be closely monitored for?

<p>Pulmonary toxicity. (D)</p> Signup and view all the answers

In assessing the effectiveness of antidysrhythmic therapy, which outcome indicates that the treatment goals are being met?

<p>Decreased edema and fatigue. (D)</p> Signup and view all the answers

Why are older adults with hypertension, heart failure, diabetes, and thyroid disease at a higher risk of developing dysrhythmias?

<p>They often have multiple comorbidities and are on medications that can affect cardiac function. (B)</p> Signup and view all the answers

What is a crucial instruction to include when educating a patient who is starting on Class Ia antidysrhythmic medications like procainamide?

<p>Do not crush or chew the medication. (C)</p> Signup and view all the answers

A patient with ventricular dysrhythmias is prescribed lidocaine. What indicates that the lidocaine is working as intended?

<p>Decreased electrical conduction and increased rate of repolarization. (A)</p> Signup and view all the answers

For a patient taking propafenone (a Class Ic antidysrhythmic) for supraventricular tachycardia, what specific adverse effect requires immediate intervention?

<p>Heart failure or severe hypotension. (D)</p> Signup and view all the answers

Which of the following is a primary concern when administering Class II beta-blockers to a patient with asthma?

<p>They trigger acute bronchospasms. (C)</p> Signup and view all the answers

Which of the following best describes a key action to prevent adverse effects from amiodarone?

<p>Monitor for signs of pulmonary toxicity. (C)</p> Signup and view all the answers

Verapamil and diltiazem can cause which of the following?

<p>Decreased heart rate (B)</p> Signup and view all the answers

What is the primary mechanism by which digoxin slows conduction between the SA and AV nodes?

<p>Affecting sodium and potassium transport across cell membranes.. (B)</p> Signup and view all the answers

A patient taking digoxin reports seeing yellow halos around lights and experiencing cardiac arrhythmias. What immediate action should be taken?

<p>Assess the patient for signs of digoxin toxicity. (D)</p> Signup and view all the answers

What action is crucial to prevent complications when giving adenosine?

<p>Following administration with a rapid saline flush. (C)</p> Signup and view all the answers

Why is it important to avoid crushing oral sustained-release antidysrhythmic preparations?

<p>To avoid altering the drug's intended absorption rate. (A)</p> Signup and view all the answers

What nursing instruction is most important related to social determinants when providing discharge teaching for older patients on multiple medications after being prescribed antidysrhythmic drugs?

<p>Assessing the patient’s ability to afford and access their meds, and providing cost-saving strategies. (B)</p> Signup and view all the answers

What does a dromotropic medication do?

<p>Affects electrical current (D)</p> Signup and view all the answers

If a patient has a liver or renal disorder, what should be done before giving drugs affecting the cardiac action potential?

<p>Consult a physician (B)</p> Signup and view all the answers

What is the most important instruction to give patients taking beta-blockers, digoxin, or other drugs?

<p>Take their own radial pulse for 1 full minute (A)</p> Signup and view all the answers

What nursing instruction is most important when providing discharge teaching for any patient with heart problems?

<p>Notify your health care provider of any worsening dysrhythmia or toxic effects (A)</p> Signup and view all the answers

Flashcards

Dysrhythmia

Any deviation from the normal rhythm of the heart.

Antidysrhythmics

Medications used to treat and prevent disturbances in cardiac rhythm.

Action Potential

The change in distribution of ions across cardiac cell membranes that leads to cell excitability.

Cardiac Cell Charge

Inside the resting cardiac cell, there is a net negative charge.

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Sinoatrial (SA) Node

The natural pacemaker of the heart.

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Electrocardiography (ECG/EKG)

Records the electrical activity of the heart over time.

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P wave

Represents atrial depolarization.

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QRS Complex

Represents ventricular depolarization.

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T Wave

Represents ventricular repolarization.

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Supraventricular Tachycardia

Heart rate too fast and PR interval too short/unidentifiable

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Atrial Fibrillation

Absence of P waves, irregular pattern.

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Atrial Flutter

Rapid, regular atrial activity; 'sawtooth' or 'picket fence' pattern on ECG.

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Inotropic (Action)

Increase the force of heart contractions.

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Chronotropic (Action)

Affect the heart rate.

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Dromotropic (Action)

Affect the conduction speed of electrical impulses.

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Vaughan Williams Classification

Classifies antidysrhythmic drugs based on their electrophysiologic effect

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Class I Antiarrhythmics

Block sodium channels, slow impulse conduction.

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Class Ia Antiarrhythmics

Blocks sodium channels, delay repolarization. Used for Atrial fibrillation, Atrial flutter, Ventricular Tachycardia

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Class Ib Antiarrhythmics

Blocks sodium channels, has short acting, increase rate of repolarization. Used for ventricular dysrhythmias.

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Class Ic Antiarrhythmics

Blocks sodium channels, decrease electrical conduction. Used for Supraventricular Tachycardia.

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Class II Antiarrhythmics

Block beta-adrenergic receptors. Used for Atrial fibrillation, Atrial flutter

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Class III Antiarrhythmics

Block potassium channels, prolong repolarization. Used for Atrial Fibrillation

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Class IV Antiarrhythmics

Block calcium channels, slow AV node conduction. Used for Atrial Fibrillation/Aflutter, SVT.

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Digoxin

Slows conduction through the AV node and reduces ventricular rate. Used in atrial fibrillation/flutter. Very high risk of toxicity and high risk in renal impairment.

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Adenosine

Slows conduction through the AV node to convert paroxysmal SVT to sinus rhythm.

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Study Notes

  • Antidysrhythmic drugs are used for the treatment and prevention of disturbances in cardiac rhythm

Action Potential

  • Variation in distribution of ions leads to cardiac cell excitation
  • There is a spread of electrical impulse across cardiac cells due to ion movement across the cell membrane
  • The electrical impulse leads to muscle contraction

Cardiac Cell

  • Resting cardiac cells have a net negative charge relative to the outside
  • Resting Membrane Potential results from an uneven distribution of sodium, potassium and calcium ions
  • The Sodium-Potassium ATPase pump maintains this difference

Electrical Activity of the Heart

  • Sinoatrial (SA) node is the natural pacemaker
  • The SA node inherent rate is 60-100 BPM
  • AV node inherent rate is 40-60 BPM
  • The bundle of His inherent rate is 40-60 BPM
  • Left and right bundle branches inherent rate is 20-40 BPM
  • Purkinje fibers inherent rate is 20-40 BPM

Electrocardiography (ECG or EKG)

  • The P wave reflects atrial electricity
  • The PR interval reflects atrial electricity
  • The QRS complex reflects ventricular contraction and electricity
  • There is also ST segment and a T wave on an EKG

Common Atrial Dysrhythmias

  • Supraventricular Tachycardia present with a PR intervals that are too small
  • Atrial Fibrillation presents with the absence of p-waves
  • Atrial Flutter presents with a predictable pattern

Ventricular Dysrhythmias

  • Include Ventricular Tachycardia
  • Include Ventricular Fibrillation

Antidysrhythmic Drug Mechanisms of Action

  • Prolong AV node
  • Increase or decrease conduction speed
  • Alter ectopic pacemakers and SA node
  • Reduce myocardial excitability
  • Simulate autonomic nervous system
  • There are multiple different classes of medications

Inotropic, Chronotropic & Dromotropic

  • Inotropic relates to force of contraction and it can be increased or decreased
  • Chronotropic affects the rate of contractions
  • Dromotropic affects electrical current

Vaughan Williams Classification

  • It is a system for classifying antidysrhythmic drugs
  • It is based on the electrophysiologic effect of particular drugs on action potential
  • Class I drugs are: Sodium Channel Blockers, including Ia, Ib, and Ic
  • Class II drugs are Beta Blockers
  • Class III drugs are Potassium Channel Blockers
  • Class IV drugs are Calcium Channel Blockers
  • Other drugs include Digoxin and Adenosine

Class la: Sodium Channel Blocker

  • Drugs include: procainamide (Proneystl), Quinidine gluconate, disopyramide (Norpace)
  • Mechanism of Action: Blocks sodium (fast) channels, and delays repolarization
  • Used for: Atrial fibrillation, Atrial flutter, Ventricular Tachycardia, Supraventricular Tachycardia, and Wolff-Parkinson-White Syndrome
  • Adverse Effects: Systemic Lupus Syndrome, Neutropenia/Thrombocytopenia, Cardiotoxicity, and Hypotension
  • Contraindications: Pregnancy Risk Category C, Liver or renal disorders
  • Medication/Food Interactions: Interacts with other Antidysrhythmics & Antihypertensives
  • Do not crush or chew sustained-released medications during Nursing Administration

Class Ib: Sodium Channel Blocker

  • Drugs include: lidocaine(Xylocaine), mexiletine (Mexitil), tocainide (Tonocard)
  • Mechanism of Action: Decreases electrical conduction, and increases rate of repolarization
  • Used for: Ventricular Dysrhythmias
  • Adverse Effects: CNS effects like twitching, convulsions or respiratory depression
  • Contraindications: Liver and renal dysfunction
  • Medication/Food Interactions: Beta Blockers and Phenytoin increase serum levels of lidocaine
  • Nursing Administration: IV administration begins with a weight based dose that is maintained
  • Should be used for no more than 24 hours

Class Ic: Sodium Channel Blocker

  • Drugs included propafenone (Rhythmol), flecainide (Tambocor)
  • Mechanism of Action: deceases electrical conduction & excitability, and increases the rate of repolarization
  • Used for: Supraventricular Tachycardia
  • Adverse Effects: Bradycardia, Heart failure, Dizziness, and Weakness
  • Contraindications: Severe heart failure, Severe hypotension
  • Medication/Food Interactions: Digoxin, oral anticoagulants, and beta blockers
  • Nursing Administration: Monitor ECG during treatment and administer with food - do not crush tablets, and watch for bradycardia and hypotension

Class II: Beta Blocker

  • Drugs included propranolol hydrochloride (Inderal), esmolol hydrochloride (Brevibloc), and metoprolol (Lopressor)
  • Mechanism of Action: Prevents sympathetic nervous system stimulation of the heart, decreases heart rate, and slows rate of conduction through the SA node
  • Used for: Atrial fibrillation, Atrial flutter, and SVT
  • Adverse Effects: Bradycardia, hypotension, and impotence can occur
  • Contraindications: Severe heart failure and asthma
  • Medication/Food Interactions: Verapamil and Diltiazem, and it can mask the hypoglycemic effect of insulin
  • Nursing Administration: Take apical pulse daily and administer IV form slowly

Class III: Potassium Channel Blockers

  • Drugs included amiodarone (Cordarone, Pacerone), sotalol (Betapace), dofetilide (Tikosyn)
  • Mechanism of Action: Prolongs the action potential and refractory period of the cardiac cycle, decreases rate of repolarization, electrical conduction and contractility
  • Used for: Atrial Fibrillation , and recurrent ventricular fibrillation/tachycardia
  • Can cause Pulmonary fibrosis/stiffness
  • Adverse Effects: Pulmonary toxicity, sinus bradycardia and visual disturbances
  • Contraindications: AV block, bradycardia, and liver/thyroid/ respiratory dysfunction
  • Medication/Food Interactions: Diltiazem, digoxin, and warfarin may interact
  • Amiodarone is highly toxic.
  • Nursing Administration: Discontinued medications have a risk for adverse effects and patients are provided information regarding toxicities

Class IV: Calcium Channel Blockers

  • Drugs included verapamil (Calan), diltiazem (Cardizem)
  • Mechanism of Action: Depresses depolarization and decreases myocardial oxygen demand, decreases force of contraction and heart rate, and slows rate of conduction through SA and AV Node
  • Used for: Atrial Fibrillation/Aflutter or SVT
  • Adverse Effects: Bradycardia, hypotension, and constipation
  • Contraindications: SA/AV dysfunction and heart blocks
  • Medication/Food Interactions: Beta-blockers and Digoxin
  • Nursing Administration: May cause orthostatic hypotension, so change positions slowly and notify the provider for peripheral edema, or shortness of breath

Classification: Other Antidysrhythmics

  • Some medications have properties of several classes and are not placed into one particular class
  • Digoxin and Adenosine

Unclassified Antidysrhythmic Digoxin (Lanoxin)

  • Slows conduction between the SA & AV node
  • Used to slow the rate in atrial fibrillation/flutter
  • Can be administered PO or IV
  • Has a long half life and duration of action
  • High risk for toxicity that can lead to renal impairment
  • Follow Digoxin levels to determine dose
  • Adversely affects cardiac arrhythmias and Yellow halos
  • The Antidote is Digoxin Immune Fab (Digibind)
  • Inotropic effects: ↑ force of contraction
  • Chronotropic effects: ↓ rate of contractions
  • Dromotropic effects: ↓ electrical current

Unclassified Antidysrhythmic Adenosine (Adenocard)

  • Corrects only AV node problems
  • Slows conduction through the AV node
  • Used to convert paroxysmal supraventricular tachycardia to sinus rhythm
  • A very short half-life – less than 10 seconds
  • Only administered as fast IV push (6mg)
  • May cause asystole for a few seconds
  • Other adverse effects minimal

Nursing Implications

  • Thorough drug and medical history collection is important
  • Measure baseline BP/P, I & O, and cardiac rhythm
  • Measure serum potassium levels before initiating therapy
  • During therapy, monitor cardiac rhythm, heart rate, BP, general well-being, skin color, temperature, heart and lung sounds
  • Assess plasma drug levels as indicated
  • Monitor for toxic side effects
  • Instruct patients to take medications as scheduled and not to skip doses or double up for missed doses
  • Instruct patients to contact their physician for instructions if a dose is missed
  • Instruct patients not to crush or chew oral sustained-release preparations
  • Administer IV infusions with an IV pump
  • Teach patients taking beta-blockers, digoxin, and other drugs how to take their own radial pulse for 1 full minute, and to notify their physician if the pulse is less than 60 beats/minute before taking the next dose
  • Ensure that the patient knows to notify health care provider of any worsening of dysrhythmia or toxic effects
  • This is due to changes in cardiac output
  • Potential symptoms include: Shortness of breath, Edema, Dizziness, Syncope, Chest pain, Gl distress, Blurred Vision

Expected Outcomes

  • Decreased BP in hypertensive patients
  • Decreased edema
  • Decreased fatigue
  • Regular pulse rate
  • Pulse rate without major irregularities
  • Improved regularity of rhythm
  • Improved cardiac output
  • Goals should include target parameters for HR and BP

SDOH

  • Older adults with HTN, heart failure, diabetes and thyroid disease are more at risk of developing dysrhythmias
  • Lidocaine - $5 for 20 doses
  • Propranolol – 30 day supply $30-$80
  • Digoxin - $50 for 100 tablets

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