Perioperative Arrhythmias and Antiarrhythmic Drugs Quiz

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.

Beta blockers should be slowly tapered to prevent withdrawal responses.

Amiodarone depresses AV node conduction and the accessory bypass tracts.

300 mg

1-3.5 mcg/mL

Transient changes in physiology such as hypovolemia (NPO) and surgical stimuli like placing central lines, retractors affecting the heart, and pneumoperitoneum reducing cardiac output.

Anesthetic agents, including inhalation gases, can lead to hemodynamic compromise and a low oxygen delivery state.

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.

The effectiveness of the drug for the individual patient should be monitored to ensure optimal treatment.

New onset arrhythmias, controlled arrhythmias, and signs of hemodynamic compromise should be carefully observed.

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.

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.

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.

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.

Patients with congestive heart failure depend on increased SNS activity, so weakening their SNS activity will exacerbate CHF.

Perioperative arrhythmias can result from hypoxemia, electrolyte and acid-base disturbances, myocardial ischemia, altered sympathetic nervous system activity, bradycardia, and certain drugs.

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.

Increased sympathetic nervous system activity during intubation or surgical stimulation lowers the threshold for ventricular fibrillation.

Bradycardia can lead to ventricular arrhythmias by causing temporal dispersion of refractory periods among Purkinje fibers, creating an electrical gradient between adjacent cells.

Enlargement of a failing left ventricle can induce arrhythmias and is controlled by decreasing left ventricular volume with digitalis, diuretics, or vasodilators.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Lidocaine's mechanism of action involves delaying the rate of spontaneous phase 4 depolarization by preventing or diminishing the gradual decrease in K^+ permeability.

Procainamide with chronic use may cause hypotension and SLE-like symptoms.

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.

Disopyramide 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.

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.

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.

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.

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.

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.