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Lehne’s Pharmacology 9th Edition – Chapter 49: Antidysrhythmic Drugs | NCLEX-Style Questions with Answers & Rationales | A-Graded Nursing Exam Resource
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Calcium channel blockade has the same impact on cardiac action potentials as does beta blockade, so these agents have nearly identical effects on cardiac function; that is, they reduce automaticity in the SA node, delay conduction through the AV node, and reduce myocardial contractility. Potassium channel blockers act by delaying repolarization of fast potentials. Sodium channel blockers block sodium channels to slow impulse conduction in the atria, ventricles, and His-Purkinje system.
"When ventricular contraction slows, atrial contraction is also slowed."
Dysrhythmic activity in the atria does not significantly reduce cardiac output but can be dangerous when dysrhythmic impulses cross the AV node, causing ventricular dysrhythmias, which can be life threatening. Treating ventricular dysrhythmia helps improve ventricular pumping. These drugs do not restore normal sinus rhythm. To prevent stroke, an anticoagulant, such as warfarin, is used. Slowing ventricular contraction does not affect the rate of atrial contraction. Restoring normal sinus rhythm requires cardioversion, short-term treatment with amiodarone or sotalol, or RF ablation of the dysrhythmia source.
After cardioversion for atrial flutter, patients may continue to need long-term therapy with either a class IC agent or a class III agent to prevent recurrence. Patients undergoing DC cardioversion need to take warfarin 3 to 4 weeks before the procedure and for several weeks afterward. Beta blockers are not indicated for postprocedural prophylaxis. Class IC and class III agents are antidysrhythmic drugs.
"I should report pain and swelling in my joints when taking this drug." d. "I will need to have blood tests at regular intervals while taking this drug."
Blood dyscrasias are a rare but potentially fatal side effect of procainamide and are an indication for withdrawing the drug. Procainamide should be taken around the clock at evenly spaced intervals. Lupus-like symptoms may occur; inflammation of the joints is one manifestation and should be reported so that antinuclear antibody (ANA) titers can be monitored. Because of the risk of lupus-like symptoms and blood dyscrasias, blood tests need to be done weekly at first and then periodically thereafter.
This patient is showing signs that are common with high therapeutic levels of lidocaine. Because lidocaine is rapidly degraded, slowing the rate of infusion can help remove excess drug from the circulation. Seizures are possible with toxic doses; diazepam should be used to control seizures. It is not necessary to discontinue the infusion, because this patient is showing signs common to high therapeutic doses. Respiratory arrest is possible with toxic doses; mechanical ventilation may be needed.
c. Notify the provider to request that another drug be used for peripheral neuropathy pain. d.
Mexiletine is an antidysrhythmic medication that can also cause dysrhythmias. It is used to treat the pain associated with peripheral neuropathy in diabetic patients, but it is contraindicated in diabetic patients with heart disease, and so it should be stopped now that this patient has developed a heart disorder. Because it is contraindicated, the nurse will not teach the patient about side effects with other agents. It can exacerbate cardiac symptoms, so it should not be used to treat dysrhythmias in diabetic patients. There is no indication for tests of renal and hepatic function.
Propranolol is contraindicated in patients with asthma, because it is a nonselective beta-adrenergic antagonist and can cause bronchoconstriction and exacerbate asthma. It is used to treat tachyarrhythmias and paroxysmal atrial tachycardia evoked by emotion, so it is not contraindicated for patients with these conditions. It lowers blood pressure, so it would be helpful in patients with hypertension.
Rationale: The goal is to suppress abnormal electrical activity and restore normal rhythm and rate.
A. Respiratory rate B. Serum calcium C. Apical pulse D. Pupillary response
Rationale: Apical pulse must be assessed; hold the dose if HR is <60 bpm to prevent bradycardia or toxicity.
Rationale: Beta-blockers decrease sympathetic stimulation, which slows conduction and reduces ectopic beats.
Rationale: Pulmonary toxicity is a life-threatening complication associated with long-term amiodarone use.
9. The nurse is reviewing a patient’s medications. Which drug interaction increases the risk of digoxin toxicity when used with antidysrhythmics? A. Amiodarone B. Atorvastatin C. Acetaminophen D. Amlodipine
Rationale: Amiodarone increases digoxin levels and toxicity risk. Monitor closely when used together.
A. “Skip doses if you feel well.” B. “Take the medication with high - fat meals only.” C. “Check your pulse daily and report rates under 60 bpm.” D. “You may stop the medication once your ECG normalizes.”
Rationale: Patients must monitor their heart rate and report bradycardia, especially with digoxin, beta-blockers, or CCBs.
Amiodarone has many toxic effects. Liver toxicity is rare but serious and should be reported and the drug discontinued. Dermatologic toxicity can occur, and sunblock helps protect the skin, which, with prolonged exposure to the sun, can turn bluish gray. Drinking grapefruit juice can increase amiodarone levels. Pulmonary toxicity is the greatest concern, and patients with pulmonary symptoms should report these to the provider.
a. "Adenosine acts by suppressing action potentials in the SA and AV nodes." b. "Adenosine can be used to prevent paroxysmal supraventricular tachycardia and Wolff-Parkinson- White syndrome." c. "Adenosine has a half-life that lasts only a few seconds and must be given intravenously." d. "Adenosine is not effective for treating atrial fibrillation, atrial flutter, or ventricular dysrhythmias."
Adenosine is used to terminate paroxysmal supraventricular tachycardia (SVT) and Wolff-Parkinson- White (WPW) syndrome, not to prevent symptoms. Adenosine suppresses action potentials in the SA and AV nodes. Because it has a very short half-life of 1.5 to 10 seconds, it must be given IV bolus, as close to the heart as possible. Adenosine is not active against atrial fibrillation, atrial flutter, or ventricular dysrhythmias.
Digoxin increases automaticity in the Purkinje fibers, which contributes to dysrhythmias caused by digoxin. Decreased automaticity in the AV node is a desired effect of digoxin. Digoxin does not increase automaticity in the SA node. It does not increase AV node conduction.
atrial flutter; lidocaine b. tachycardia; atropine c. first-degree heart block; verapamil [Calan] d.
With ventricular fibrillation there is no cardiac output, because the pumping action of the heart stops. Treatment with electrical countershock is indicated to restore cardiac function. Atrial flutter, tachycardia, and first-degree heart block do not result in the lowest cardiac output.
In the CAST, class IC dysrhythmic drugs were used to prevent dysrhythmias after MI. These drugs were found to actually double the rate of mortality. The antidysrhythmic drugs did not reduce mortality or the risk of a second MI. They should not be used for any MI patients with associated dysrhythmias unless the dysrhythmias are life threatening.
d. Renal function tests e.
Amiodarone has many potential toxic side effects, including pulmonary toxicity, ophthalmic effects, and thyroid toxicity, so these systems should be evaluated at baseline and periodically while the patient is taking the drug. A complete blood count is not indicated. Renal function tests are not indicated.