Perioperative Arrhythmias and Antiarrhythmic Drugs Quiz
40 Questions
1 Views

Choose a study mode

Play Quiz
Study Flashcards
Spaced Repetition
Chat to Lesson

Podcast

Play an AI-generated podcast conversation about this lesson

Questions and Answers

Explain the potential adverse effects of propranolol on the cardiovascular system.

Propranolol can worsen congestive heart failure by directly suppressing myocardial contractility. It may also worsen cold extremities and Raynaud's disease, and may cause drug fever, rash, nausea, and interfere with glucose metabolism leading to hypoglycemia in those being treated for diabetes mellitus.

What is the recommended approach for discontinuing beta blockers to prevent withdrawal responses?

Beta blockers should be slowly tapered to prevent withdrawal responses.

How does amiodarone affect the conduction system of the heart?

Amiodarone depresses AV node conduction and the accessory bypass tracts.

What is the recommended preoperative dose of IV amiodarone for resistant ventricular tachycardia or ventricular fibrillation?

<p>300 mg</p> Signup and view all the answers

What is the therapeutic blood concentration range for amiodarone?

<p>1-3.5 mcg/mL</p> Signup and view all the answers

What are some benign causes of perioperative cardiac arrhythmias?

<p>Transient changes in physiology such as hypovolemia (NPO) and surgical stimuli like placing central lines, retractors affecting the heart, and pneumoperitoneum reducing cardiac output.</p> Signup and view all the answers

What is the effect of anesthetic agents on cardiac arrhythmias?

<p>Anesthetic agents, including inhalation gases, can lead to hemodynamic compromise and a low oxygen delivery state.</p> Signup and view all the answers

How should pacemakers be managed in the preoperative assessment of chronic arrhythmias?

<p>Pacemakers should be assessed by identifying the underlying rhythm and pacemaker settings, and having a transcutaneous pacer ready. A magnet can be used to turn the pacemaker to asynchronous mode.</p> Signup and view all the answers

What should be considered when managing chronic pharmacological treatment for arrhythmias?

<p>The effectiveness of the drug for the individual patient should be monitored to ensure optimal treatment.</p> Signup and view all the answers

What should be looked for when dealing with AICD (automatic implantable cardioverter-defibrillator) with pharmacological treatment?

<p>New onset arrhythmias, controlled arrhythmias, and signs of hemodynamic compromise should be carefully observed.</p> Signup and view all the answers

Explain the potential side effects of lidocaine and its oral analogues, mexiletine and tocainide.

<p>The potential side effects of lidocaine include peripheral vasodilation, myocardial depression, and CNS stimulation, with potential for hypotension, bradycardia, and seizures at high doses. Mexiletine, an oral analogue of lidocaine, is used for chronic suppression of ventricular tachydysrhythmias, with epigastric burning as a side effect. Tocainide, another oral analogue of lidocaine, is no longer used.</p> Signup and view all the answers

What is the effectiveness of phenytoin in suppressing ventricular arrhythmias, and what potential side effects does it have?

<p>Phenytoin is effective in suppressing ventricular arrhythmias associated with digoxin toxicity. However, it has a potential side effect of phenytoin toxicity, which can inhibit insulin secretion and suppress the bone marrow.</p> Signup and view all the answers

Explain the effectiveness of flecainide and propafenone in suppressing different types of arrhythmias. What are their respective resemblances to other drugs?

<p>Flecainide is effective in suppressing ventricular premature beats and atrial tachyarrhythmias, but not recommended for ventricular arrhythmia after MI. It is a fluorinated local anesthetic analogue of procainamide. Propafenone suppresses ventricular and atrial tachyarrhythmias and has weak beta-blocking and calcium-blocking effects. It is an oral drug.</p> Signup and view all the answers

How do beta blockers like propranolol and esmolol control arrhythmias, and what are their common side effects?

<p>Beta blockers control the rate of ventricular response in atrial fibrillation and flutter and are effective in preventing sudden death after myocardial infarction. Their common side effects include bradycardia, hypotension, myocardial depression, and bronchospasm.</p> Signup and view all the answers

Explain the impact of weakening sympathetic nervous system activity on patients with congestive heart failure.

<p>Patients with congestive heart failure depend on increased SNS activity, so weakening their SNS activity will exacerbate CHF.</p> Signup and view all the answers

Explain the potential causes of perioperative arrhythmias.

<p>Perioperative arrhythmias can result from hypoxemia, electrolyte and acid-base disturbances, myocardial ischemia, altered sympathetic nervous system activity, bradycardia, and certain drugs.</p> Signup and view all the answers

How can hypokalemia and hypomagnesemia predispose to ventricular arrhythmias?

<p>Hypokalemia and hypomagnesemia, common in patients on diuretics, can predispose to ventricular arrhythmias by creating an imbalance in electrolytes that affects the electrical activity of the heart.</p> Signup and view all the answers

What effect does increased sympathetic nervous system activity have on the threshold for ventricular fibrillation?

<p>Increased sympathetic nervous system activity during intubation or surgical stimulation lowers the threshold for ventricular fibrillation.</p> Signup and view all the answers

How can bradycardia lead to ventricular arrhythmias?

<p>Bradycardia can lead to ventricular arrhythmias by causing temporal dispersion of refractory periods among Purkinje fibers, creating an electrical gradient between adjacent cells.</p> Signup and view all the answers

What factors can induce arrhythmias in a failing left ventricle, and how can they be controlled?

<p>Enlargement of a failing left ventricle can induce arrhythmias and is controlled by decreasing left ventricular volume with digitalis, diuretics, or vasodilators.</p> Signup and view all the answers

Explain the potential side effects and uses of lidocaine in treating arrhythmias, and compare its effectiveness and side effect profile to quinidine and procainamide.

<p>Lidocaine is primarily used for ventricular arrhythmias, with minimal effect on supraventricular tachyarrhythmias. It has a more rapid onset, greater therapeutic index, and better side effect profile than quinidine and procainamide. Its mechanism of action involves delaying the rate of spontaneous phase 4 depolarization by preventing or diminishing the gradual decrease in K+ permeability.</p> Signup and view all the answers

What are the uses and potential adverse effects of procainamide, and how does it compare to quinidine and lidocaine?

<p>Procainamide is used for ventricular tachyarrhythmias and may cause hypotension and SLE-like symptoms with chronic use. It is comparable to quinidine, which is effective for acute and chronic supraventricular arrhythmias but has a low therapeutic index and adverse effects. Lidocaine, on the other hand, is primarily used for ventricular arrhythmias and has a more rapid onset, greater therapeutic index, and better side effect profile than procainamide and quinidine.</p> Signup and view all the answers

Describe the uses and potential adverse effects of quinidine and its metabolism, and compare it to procainamide and lidocaine.

<p>Quinidine, a class 1A drug, is effective for acute and chronic supraventricular arrhythmias, but has a low therapeutic index and adverse effects. Concurrent administration of phenytoin, phenobarbital, rifampin lowers blood levels of quinidine by enhancing liver clearance. Quinidine and procainamide are both metabolized in the liver and excreted renally. Lidocaine, in contrast, is primarily used for ventricular arrhythmias with a more rapid onset, greater therapeutic index, and better side effect profile compared to quinidine and procainamide.</p> Signup and view all the answers

What are the uses and potential adverse effects of class 1C drugs, and how can wide complex ventricular rhythm be treated?

<p>Class 1C drugs such as quinidine and procainamide can lead to incessant ventricular tachycardia, especially at high doses. Wide complex ventricular rhythm can be treated with class 1C drugs and calcium channel blockers like diltiazem and verapamil.</p> Signup and view all the answers

Explain the uses and potential adverse effects of disopyramide and moricizine in treating arrhythmias.

<p>Disopyramide, comparable to quinidine, is used for atrial and ventricular tachyarrhythmias and has anticholinergic side effects. Moricizine, a phenothiazine derivative, is used for life-threatening ventricular arrhythmias and has proarrhythmic effects.</p> Signup and view all the answers

What are the mechanisms of action of Class I antiarrhythmic drugs and their clinical uses?

<p>Class I antiarrhythmic drugs work by blocking fast Na+ channels during depolarization, which decreases depolarization rate and conduction velocity. They have three subclasses (IA, IB, IC) which affect cardiac action potentials. Their clinical uses include treating acute and chronic SVT, slowing atrial rate in Afib, and suppressing tachyarrhythmias in WPW to slow everything down.</p> Signup and view all the answers

Explain the mechanisms of action and clinical uses of Class II antiarrhythmic drugs.

<p>Class II antiarrhythmic drugs, beta blockers, decrease the rate of spontaneous phase 4 depolarization, resulting in decreased SNS activity, slowing down the heart rate, and decreasing myocardial O2 demand. They do not change the duration of the action potential through the ventricular myocardium. Clinical uses include slowing down conduction through atrial tissue, prolonging the PR interval, and are good for CAD.</p> Signup and view all the answers

Describe the mechanisms of action and clinical uses of Class III antiarrhythmic drugs.

<p>Class III antiarrhythmic drugs such as amiodarone, dronedarone, and sotalol block K+ channels, prolonging depolarization, action potential, and refractory period. They decrease the proportion of the cardiac cycle where myocardial cells are excitable and susceptible to trigger. Clinical uses include treating SVT, ventricular tachyarrhythmias, Afib, and Aflutter.</p> Signup and view all the answers

What are the mechanisms of action and clinical uses of Class IV antiarrhythmic drugs?

<p>Class IV antiarrhythmic drugs, calcium channel blockers such as verapamil and diltiazem, inhibit slow calcium ion currents that may contribute to the development of tachycardias. They are good for SVTs and idiopathic VT. They block Ca channels, slow conduction in SA and AV node, and reduce contractility in the heart.</p> Signup and view all the answers

Explain the potential proarrhythmic effects of antiarrhythmic agents and their treatments.

<p>The potential proarrhythmic effects of antiarrhythmic agents include Torsades de Pointes, which can be caused by class I and class III agents. This can be potentiated by hypokalemia and hypomagnesemia. Treatments for Torsades de Pointes include magnesium sulfate, even if serum magnesium levels are normal, isoproterenol/Isuprel (chemical pacemaker drug; beta agonist), cardiac pacing, and raising serum potassium to 4.5-5.</p> Signup and view all the answers

Explain the mechanism of action of lidocaine in treating ventricular arrhythmias.

<p>Lidocaine's mechanism of action involves delaying the rate of spontaneous phase 4 depolarization by preventing or diminishing the gradual decrease in K^+ permeability.</p> Signup and view all the answers

What are the potential adverse effects of procainamide with chronic use?

<p>Procainamide with chronic use may cause hypotension and SLE-like symptoms.</p> Signup and view all the answers

What are the similarities and differences between quinidine and procainamide in terms of clinical use and metabolism?

<p>Both quinidine and procainamide are metabolized in the liver and excreted renally. Quinidine is effective for acute and chronic supraventricular arrhythmias, while procainamide is used for ventricular tachyarrhythmias.</p> Signup and view all the answers

What is the therapeutic use of disopyramide and what are its potential side effects?

<p>Disopyramide is used for atrial and ventricular tachyarrhythmias and has anticholinergic side effects.</p> Signup and view all the answers

When should moricizine be used and what proarrhythmic effects does it have?

<p>Moricizine, a phenothiazine derivative, is used for life-threatening ventricular arrhythmias and has proarrhythmic effects.</p> Signup and view all the answers

What are the mechanisms of action of Class I antiarrhythmic drugs and their clinical uses?

<p>Class I antiarrhythmic drugs work by blocking fast Na+ channels during depolarization, which decreases depolarization rate and conduction velocity. They have three subclasses (IA, IB, IC) which affect cardiac action potentials. Their clinical uses include treating acute and chronic SVT, slowing atrial rate in Afib, and suppressing tachyarrhythmias in WPW to slow everything down.</p> Signup and view all the answers

Explain the mechanisms of action and clinical uses of Class II antiarrhythmic drugs.

<p>Class II antiarrhythmic drugs, beta blockers, decrease the rate of spontaneous phase 4 depolarization, resulting in decreased SNS activity, slowing down the heart rate, and decreasing myocardial O2 demand. They do not change the duration of the action potential through the ventricular myocardium. Clinical uses include slowing down conduction through atrial tissue, prolonging the PR interval, and are good for CAD.</p> Signup and view all the answers

Describe the mechanisms of action and clinical uses of Class III antiarrhythmic drugs.

<p>Class III antiarrhythmic drugs such as amiodarone, dronedarone, and sotalol block K+ channels, prolonging depolarization, action potential, and refractory period. They decrease the proportion of the cardiac cycle where myocardial cells are excitable and susceptible to trigger. Clinical uses include treating SVT, ventricular tachyarrhythmias, Afib, and Aflutter.</p> Signup and view all the answers

What are the mechanisms of action and clinical uses of Class IV antiarrhythmic drugs?

<p>Class IV antiarrhythmic drugs, calcium channel blockers such as verapamil and diltiazem, inhibit slow calcium ion currents that may contribute to the development of tachycardias. They are good for SVTs and idiopathic VT. They block Ca channels, slow conduction in SA and AV node, and reduce contractility in the heart.</p> Signup and view all the answers

Explain the potential proarrhythmic effects of antiarrhythmic agents and their treatments.

<p>The potential proarrhythmic effects of antiarrhythmic agents include Torsades de Pointes, which can be caused by class I and class III agents. This can be potentiated by hypokalemia and hypomagnesemia. Treatments for Torsades de Pointes include magnesium sulfate, even if serum magnesium levels are normal, isoproterenol/Isuprel (chemical pacemaker drug; beta agonist), cardiac pacing, and raising serum potassium to 4.5-5.</p> Signup and view all the answers

Study Notes

Cardiac Antiarrhythmic Drugs Overview

  • Class 1A and 1C drugs such as quinidine and procainamide can lead to incessant ventricular tachycardia, especially at high doses
  • Wide complex ventricular rhythm can be treated with class 1C drugs and calcium channel blockers like diltiazem and verapamil
  • Quinidine, a class 1A drug, is effective for acute and chronic supraventricular arrhythmias, but has a low therapeutic index and adverse effects
  • Procainamide, another class 1A drug, is used for ventricular tachyarrhythmias and may cause hypotension and SLE-like symptoms with chronic use
  • Disopyramide, comparable to quinidine, is used for atrial and ventricular tachyarrhythmias and has anticholinergic side effects
  • Moricizine, a phenothiazine derivative, is used for life-threatening ventricular arrhythmias and has proarrhythmic effects
  • Lidocaine, primarily used for ventricular arrhythmias, has minimal effect on supraventricular tachyarrhythmias and is effective in suppressing re-entry arrhythmias
  • Lidocaine’s mechanism of action involves delaying the rate of spontaneous phase 4 depolarization by preventing or diminishing the gradual decrease in K+ permeability
  • Concurrent administration of phenytoin, phenobarbital, rifampin lowers blood levels of quinidine by enhancing liver clearance
  • Quinidine and procainamide are both metabolized in the liver and excreted renally
  • Lidocaine has a more rapid onset, greater therapeutic index, and better side effect profile than procainamide and quinidine
  • Lidocaine's IV form has no preservative, while IM lidocaine has nearly complete absorption and a specific dosing regimen.

Studying That Suits You

Use AI to generate personalized quizzes and flashcards to suit your learning preferences.

Quiz Team

Related Documents

Ch. 21 Antiarrhythmic Drugs & Lecture PDF

Description

Test your knowledge of perioperative arrhythmias and antiarrhythmic drugs with this quiz. Explore the causes and treatment of arrhythmias, the classification of antiarrhythmic agents based on their mechanisms of action, and the potential proarrhythmic effects of these medications. Gain a deeper understanding of how these drugs target ion channels and physiological processes in the heart.

More Like This

Use Quizgecko on...
Browser
Open
Browser
Browser