antidysrhthmics

What two drugs may be used to treat heart block?

Atropine or isoproterenol.

What four drugs should be avoided in patients being treated with digitalis?

"Drugs that should be avoided in the digitalis-treated patient are: (1) quinidine, which increase the plasma concentration of cardiac glycosides; (2) succinylcholine, which increases the parasympathetic activity at the heart and may theoretically have an additive effect with cardiac glycosides (3) Beta-adrenergicmagonists, which may increase the likelihood of cardiac dysrhythmias; and (4) IV calcium, which may also precipitate cardiac dysrhythmias."

How is adenosine administered? Why?

Adenosine is administered (6-12 mg IV bolus for adults or 50 mcg/kg IV for children) rapidly through an intravenous (central) line or into the right atrium. Adenosine must reach the heart before it is metabolized.

Describe the metabolism and elimination of adenosine (Adenocard).

Adenosine is rapidly eliminated by enzymatic clearance (less than one minute). Specifically, adenosine is deaminated in the plasma forming inosine, or is taken up in erythrocytes (RBCs) and vascular endothelial cells where it is metabolized to inosine (by deamination) or adenosine monophosphate (by phosphorylation).

Adenosine is an effective treatment for which cardiac dysrhythmias? How does it work?

Adenosine is used to treat paroxysmal supraventricular tachycardia, including that due to conduction through accessory pathways in patients with Wolff-Parkinson-White syndrome. Adenosine blocks conduction of impulses through the AV node by hyperpolarizing AV nodal cells. Hyperpolarization occurs because adenosine binds to A1 purinergic receptors which then open potassium channels in these cells and increases the efflux of potassium from nodal cells. Hyperpolarization decreases excitability.

What are class I cardiac antidysrhythrnic drugs? Identify class IA drugs. class lB drugs. and class IC drugs. and specify how each of these groups (IA,lB, and IC) act.

Class I antidysrhythmic drugs are membrane stabilizers that work by inhibiting fast sodium ion channels. They stabilize membranes by blocking sodium channels. Class IA includes quinidine and procainamide, Class IB drugs include lidocaine, locainide and phenytoin, Class IC drugs include flecainide and propafenone.

What antidysrhythmic drugs are not local anesthetics but have local anesthetic activity?

Class I antidysrhythmic drugs produce sodium channel blockade. All class I antidysrhythmic drugs have local anesthetic activity. Only lidocaine is used both as a local anesthetic and also a class I antidysrhythmic

Class I antidysrhythmic drugs are used to treat what three conditions?

Class I drugs are used to treat acute and chronic supraventricular dysrhythmias, to slow atrial rate in atrial fibrillation, and to suppress tachydysrhythmia associated with Wolff-Parkinson-White syndrome.

"What drugs are class II cardiac antidysrhythmic drugs, and what do they do?"

Class II antidysrhythmic drugs are beta·adrenergic antagonists. Class II drugs depress automaticity (decrease heart rate by decreasing spontaneous phase 4 depolarization in nodal tissues) and decrease conduction speed of cardiac impulses

What drugs are class III cardiac antidysrhythmic drugs and what do they do?

Class III antidysrhythmic drugs prolong repolarization by blocking voltage-gated potassium channels. Amiodarone. ibutilide, dofetilide, and bretylium (no longer recommended) are class III antidysrhythmics. These drugs prolong the effective refractory period in the SA and AV nodes, atria, ventricles, and His·Purkinje fibers

"What drugs are class IV cardiac antidysrhythmic drugs, and what are they used to treat?"

Class IV antidysrhythmic drugs are the slow calcium channel blockers, including verapamil and diltiazem. These calcium entry blockers are used to treat paroxysmal supraventricular tachydysrhythmia and effectively control ventricular rate in patients who develop atrial fibrillation or flutter.

Identify 5 drugs or treatments for cardiac dysrhythmias due to digoxin toxicity.

Digoxin-induced cardiac dysrhythmias are best treated with: (1) lidocaine, (2) procainamide, (3) phenytoin, (4) propranolol, or (5) DC countershock.

On what tissue of the heart does verapamil work: atrial muscle, ventricular muscle, nodal tissue, Purkinje network?

For therapeutic effect, verapamil works on nodal tissue where it slows phase 4 depolarization. Verapamil secondarily works on phase 2 (plateau) of the ventricular muscle action potential, but this is not the best answer to the question as written

Lidocaine works on what specific tissues of the heart?

Lidocaine delays the rate of spontaneous phase 4 depolarization of ventricular cardiac cells and the His-Purkinje system by preventing or diminishing the gradual decrease in potassium ion permeability during this phase.

"What three drugs are appropriately used to treat cardiac dysrhythmias resulting from mitral valve prolapse?"

Lidocaine, esmolol, and amiodarone should be immediately available to treat cardiac dysrhythmias associated with mitral valve prolapse.

Which antidysrhythmics are appropriate for treating premature ventricular contractions? What is the drug of choice in the treatment of ventricular dysrhythmias?

Lidocaine, procainamide, tocainide, flecainide, propafenone, and quinidine are appropriate for treating premature ventricular contractions. Lidocaine is the drug of choice for treating ventricular dysrhythmias.

Would administration of adenosine via an endotracheal tube (ETT) be effective?

No. Adenosine is rapidly metabolized in the plasma by adenosine deaminase. To be effective, adenosine must be administered rapidly into a central line or the right atrium.

Should either digitalis or propranolol be discontinued in the cardiac patient prior to surgery?

No. Despite the potential for adverse drug interactions, cardiac medications being taken pre-operatively should be continued without interruption through the perioperative period "During a bilateral hernia repair under spinal anesthesia your patient develops atrial fibrillation.

A patient showing signs and symptoms of digitalis toxicity begins having premature ventricular contractions. What drugs could be given to treat this? Which of these drugs is particularly useful in suppressing cardiac ventricular dysrhythmias associated with digitalis toxicity?

Phenytoin (0.5-1.5 mg/kg IV over 5 minutes), lidocaine (1-2 mg/kg IV), or atropine (35-70 mcg/kg IV) are useful in the initial treatment of digitalis-induced ectopic dysrhythmias. Small doses of propranolol have also been effective in treating such dysrhythmias, but should not be used if conduction blockade is present. Phenytoin is particularly useful in suppressing ventricular dysrhythmias associated with digitalis toxicity.

What is your concern with giving phenytoin (Dilantin) to the hyperglycemic patient?

Phenytoin (Dilantin) partially inhibits (blunts) insulin release and may lead to increased blood glucose levels in patients who are hyperglycemic

What is the typical cause of postoperative sinus tachycardia? What is the treatment?

Postoperative ST is nearly always associated with a physiologic increase in SNS influence. Tachycardia is usually harmless, but it can precipitate acute MI in patients with coronary artery disease. Tachycardia exacerbates HTN and might indicate acidemia, hypoxemia, or malignant hyperthermia. Sinus tachycardia is treated by addressing the underlying cause. Giving analgesics for pain, IV fluids for hypovolemia, or sedatives to calm anxiety is usually sufficient. Decompressing a full bladder is helpful. Tachycardia caused by sympathomimetic drugs resolves as drug levels fall. If SNS activity is beyond control or tachycardia presents a threat, beta-blockade helps control rate.

How does procainamide (Pronestyl) work?

Procainamide, like lidocaine, slows phase 4 depolarization, which reduces automaticity.

Is treatment of atrial fibrillation during the case generally required? How can the anesthetist treat atrial fibrillation if pharmacological treatment is required?

Unless the atrial fibrillation adversely affects cardiovascular function (i.e. development of v-tach with hypotension) during anesthesia. treatment is usually not required. If treatment of supraventricular tachydysrhythmia is required. verapamil. a calcium entry blocker, is a first line drug. Verapamil slows conduction through the AV node. Esmolol could also be used to treat v-tach associated with a-fib. Other drugs mentioned for cardioversion and/or controlling ventricular rate include ibutilide and amiodarone (class III antidysrhythmics), digitalis, and propranolol.

Verapamil and diltiazem slow heart rate by working on what phase of the sinoatrial node action potential?

Verapamil and diltiazem slow heart rate by slowing phase 4 depolarization of the sinoatrial node action potential.

Calcium channel blockers such as verapamil act on what phase of the ventricular action potential?

Verapamil and other calcium channel blockers decrease myocardial (ventricular) contractility by blocking the entry of calcium during phase 2 (plateau) of the ventricular action potential. (This action of the calcium channel blockers is a side-effect, not a therapeutic effect).

His vital signs are stable. What is your treatment?"

With stable vital signs, pharmacological treatment of atrial fibrillation usually is not required.