Pharmacotherapy of Dysrhythmias 39 Pharmacotherapy of Dysrhythmias

Adams Chapter 39 Question 2 A client who is receiving intravenous lidocaine (Xylocaine) for ventricular dysrhythmias exhibits confusion and anxiety. The appropriate response by the nurse would be to:

Question 2 Choices Withhold the drug and notify the health care provider immediately. Increase the infusion rate and calm the client. Discontinue the infusion and administer the antidote. Decrease the infusion rate and monitor for confusion.

Question 2 Answer Withhold the drug and notify the health care provider immediately. Increase the infusion rate and calm the client. Discontinue the infusion and administer the antidote. Decrease the infusion rate and monitor for confusion.

Question 2 Rationale The first sign of lidocaine toxicity involves confusion, anxiety, tremors, and paresthesia. If these symptoms are manifested in a client receiving lidocaine, the nurse should withhold the medication and immediately notify the prescriber. Option 2 is incorrect because increasing the infusion rate would increase the serum level of the drug and consequently make the client even more toxic.

Question 2 Rationale Calming the client will probably be ineffective, since the anxiety is due to a toxic level of the drug. Option 3 is incorrect because the only way to reduce a toxic serum level of lidocaine is to discontinue the medication and allow the drug to be excreted through physiological mechanisms. There is no antidote.

Question 2 Rationale Option 4 is incorrect because simply reducing the infusion rate will be a dangerous action when the client is suffering from toxic drug levels.

Question 3 The client is prescribed a beta-adrenergic antagonist for the treatment of atrial dysrhythmias associated with heart failure. The nurse knows that this drug will have what physiologic effect?

Question 3 Choices Increased heart rate and reduced respiratory status Decreased heart rate and conduction velocity Elimination of phase 4 of the action potential Flattened T wave on the ECG pattern

Question 3 Answer Increased heart rate and reduced respiratory status Decreased heart rate and conduction velocity Elimination of phase 4 of the action potential Flattened T wave on the ECG pattern

Question 3 Rationale Beta blockers reduce heart rate and reduce the rate of cardiac conduction. This action decreases the incidence of cardiac dysrhythmias by blocking calcium ion channels in the SA and AV nodes. Option 1 is incorrect because beta-adrenergic antagonist (aka beta-blockers) slow the heart and do not reduce respiratory status.

Question 3 Rationale Option 3 is incorrect because phase 4 of the action potential is when the myocardial cell is resting and the exchange of ions (sodium, calcium, and potassium) has not yet started. To eliminate this phase would reduce the resting phase of the heart.

Question 3 Rationale Option 4 is incorrect because the assessment findings of a flattened T wave on the ECG complex usually represents ischemia (inadequate blood flow) to the myocardium and is always bad.

Question 4 A client is being discharged with a diagnosis of dysrhythmias. The nurse is teaching the client about amiodarone (Cordarone). What client teaching is needed related to this medication?

Question 4 Choices Avoid crowds while taking this medication. Avoid birth control pills and use an alternate form of birth control. Wear protective clothing and a barrier-type sunscreen. Use an electric razor to shave.

Question 4 Answer Avoid crowds while taking this medication. Avoid birth control pills and use an alternate form of birth control. Wear protective clothing and a barrier-type sunscreen. Use an electric razor to shave.

Question 4 Rationale One problem associated with this drug is photosensitivity. The patient should be instructed to avoid direct sunlight and wear protective clothing and barrier type sunscreen lotions. Option 1 is incorrect. Avoiding crowds is an instruction given to a client who is immune suppressed. Amiodarone is not known to cause this problem.

Question 4 Rationale Option 2 is incorrect because amiodarone does not seem to interact with oral contraceptives. Option 4 is incorrect. This is an instruction that a nurse should give the patient when the drug causes bleeding tendencies. This is not a typical adverse effect with amiodarone.

Learning Outcomes Identify disorders associated with an increased risk of dysrhythmias. Explain how rhythm abnormalities can affect cardiac function. Diagram a typical cardiac action potential and label the flow of potassium, sodium, and calcium ions during each phase.

Learning Outcomes Design a table that indicates the classification of dysrhythmias and the types of drugs used to treat them. Describe general principles in the management of dysrhythmias. Identify the primary mechanisms of action of antidysrhythmic drugs.

Learning Outcomes For each of the classes shown in the chapter outline, identify the prototype and representative drugs and explain the mechanism(s) of drug action, primary indications, contraindications, significant drug interactions, pregnancy category, and important adverse effects.

Learning Outcomes Use the nursing process to care for patients receiving drug therapy for dysrhythmias.

PharmFACT

Etiology of Dysrhythmias 39.1 Some dysrhythmias produce no patient symptoms, while others may be life threatening.

Dysrhythmias Some are asymptomatic Others require immediate treatment

Typical Symptoms Dizziness Weakness Fatigue Decreased exercise tolerance Palpitations Dyspnea Syncope

Diseases Associated with Dysrhythmias HTN Cardiac valve disease CAD Hyper/hypokalemia MI CVA Diabetes mellitus CHF

Phases and Measurement of the Cardiac Action Potential 39.2 The phases of cardiac action potential include rapid depolarization, a long plateau, and repolarization.

Phases of Myocardial Action Potential

Myocardial Action Potential Phase 4 Cell is resting Membrane potential slowly increasing toward threshold potential Phase 0 Action potential begins when threshold potential is reached Sodium rushes in producing rapid depolarization Calcium enters at a slower rate

Myocardial Action Potential Phase 1 Brief transient phase Inside of plasma membrane reverses charge becoming positive Phase 2 Plateau reached in which depolarization is maintained Additional calcium enters Contraction of cardiac muscle Efflux of potassium from cells

Myocardial Action Potential Phase 3 Calcium channels close Additional potassium channels open Repolarization returns negative resting membrane potential Refractory period Brief period where depolarization cannot occur Ensures myocardial cell finishes contracting before another action potential begins

Connection Checkpoint 39.1 From what you learned in Chapter 33, what are the three types of calcium channels? Which type is blocked by calcium channel blocker medications?

Phases and Measurement of the Cardiac Action Potential 39.3 The electrocardiogram is used to measure electrical conduction across the myocardium.

ECG and Electrical Conduction

Classification of Dysrhythmias 39.4 Dysrhythmias are classified by the impulse origin and type of rhythm abnormality produced.

Types of Dysrhythmias Bradydysrhythmias Tachydysrhythmias HR < 60 bpm Common in older adults Major indication for pacemakers Tachydysrhythmias HR > 100 bpm Incidence increases in older adults and those with preexisting cardiac disease

Common Bradydysrhythmias Sinus bradycardia Sick sinus syndrome AV conduction block

Common Tachydysrhythmias Atrial tachycardia Atrial flutter Atrial fibrillation Ventricular tachycardia Ventricular fibrillation

General Principles of Dysrhythmia Management 39.5 Antidysrhythmic drugs are only used when there is a clear benefit to the patient.

General Management Principles Asymptomatic dysrhythmias Little or no benefit to treatment with medications Acute dysrhythmias In life-threatening cases medications warranted Prophylaxis of dysrhythmias Initiated for high risk patients Avoid drug combinations that increase QT interval

General Management Principles Nonpharmacologic treatment Cardioversion Defibrillation Identification and destruction of myocardial cells responsible for abnormal conduction Cardiac pacemakers ICDs

Drugs for Dysrhythmias 39.6 Antidysrhythmic drugs are classified by their mechanism of action.

Antidysrhythmic Drugs Therapeutic goals Terminate existing dysrhythmia Prevent abnormal rhythms Classification is based on the stage they affect action potential Use has declined in recent years

Sodium Channel Blockers: Class I 39.7 Class I antidysrhythmics act by blocking ion channels in myocardial cells.

Sodium Channel Blockers Largest group of antidysrhythmics Similar in structure and function to local anesthetics

Ion Channels in Myocardial Cells

Class IA Block sodium channels during phase 0 of action potential

Prototype Drug: Procainamide (Procan SR, Pronestyl) Therapeutic Classification Antidysrhythmic, Class IA Pharmacologic Classification Sodium channel blocker Pregnancy Category C

Prototype Drug: Procainamide (Procan SR, Pronestyl) Mechanism of Action Blocks sodium ion channels in myocardial cells Reduces automaticity and slows velocity of action potential

Prototype Drug: Procainamide (Procan SR, Pronestyl) Indications Ventricular tachycardia during CPR Refractory ventricular fibrillation during CPR Pulseless ventricular tachycardia during CPR PAT, Aflutter, Afibrillation Prophylaxis of PSVT Drug of last choice for ACLS Contraindications 2nd or 3rd degree AV heart block Severe HF Peripheral neuropathy Myasthenia gravis Shock Severe hypotension Precautions Lupus Renal impairment Bone marrow suppression

Prototype Drug: Procainamide (Procan SR, Pronestyl) Drug Interactions Additive cardiac depressant with other antidysrhythmics Additive anticholinergic adverse effects with anticholinergics May increase levels of amiodarone or quinidine Hypotension with antihypertensives

Prototype Drug: Procainamide (Procan SR, Pronestyl) Adverse Effects Nausea Vomiting Abdominal pain Headache Fever Anorexia Weakness At high doses Confusion Psychosis

Prototype Drug: Procainamide (Procan SR, Pronestyl) Nursing Responsibilities Check apical and radial pulses before dose Continuous ECG and BP monitoring during IV administration Assess for adverse effects Monitor therapeutic blood level

Prototype Drug: Procainamide (Procan SR, Pronestyl) Patient/Family Teaching Immediately report adverse effects Check weight Monitor pulse rates Avoid alcohol Report decreased effectiveness Do not take other medications or supplements Medic alert identification

Similar Drugs to Procainamide Quinidine Disopyramide (Norpace)

Class IB Drugs Lidocaine, mexiletine, phenytoin Shorten refractory period Little effect on conduction velocity Primary indications are ventricular dysrhythmias

Class IC Drugs Flecainide, propafenone Profoundly decrease conduction velocity PR, QRS, and QT intervals are often prolonged Life-threatening atrial dysrhythmias Pronounced prodysrhythmic effect

Other Class I Agents Moricizine (ethmozine) Unique properties attributed to all Class I subclasses Discontinued in 2007 due to lack of demand

Beta-Adrenergic Antagonists: Class II 39.8 Beta-adrenergic antagonists reduce automaticity as well as slow conduction velocity in the heart.

Beta-Adrenergic Antagonists Treat HTN, MI, HF, and dysrhythmias Block calcium channels in SA and AV nodes Slow HR Decrease conduction velocity Include acebutolol (Sectral), esmolol (Brevibloc), propranolol (Inderal)

Connection Checkpoint 39.2 Both alpha1 blockers and beta1 blockers are used to treat HTN but only the beta1 blockers are antidysrhythmics. From what you learned in Chapter 20, explain why the selective alpha blockers are not used to treat dysrhythmias.

Potassium Channel Blockers: Class III 39.7 Class I antidysrhythmics act by blocking ion channels in myocardial cells.

Potassium Channel Blockers Block potassium ion channels in myocardial cells Delay repolarization Prolong refractory period Limited use due to serious adverse effects

Prototype Drug: Amiodarone (Cordarone, Pacerone) Therapeutic Classification Antidysrhythmic, Class III Pharmacologic Classification Potassium channel blocker Pregnancy Category D

Prototype Drug: Amiodarone (Cordarone, Pacerone) Mechanism of Action Exact mechanism unknown Blocks potassium channels but also blocks sodium ion channels and inhibits sympathetic activity

Mechanism of Action of Amiodarone Click here to view an animation on the mechanism of action of amiodarone.

Prototype Drug: Amiodarone (Cordarone, Pacerone) Indications Atrial and ventricular dysrhythmias Resistant Vtach Recurrent fibrillation Contraindications Severe bradycardia Cardiogenic shock Sick sinus syndrome Severe sinus node dysfunction 3rd degree AV block Hypersensitivity to iodine Lactation COPD Precautions Electrolyte imbalances

Prototype Drug: Amiodarone (Cordarone, Pacerone) Drug Interactions Metabolized by cytochrome P450 enzymes Markedly inhibits metabolism of many drugs Enhances actions of anticoagulants Potentiate dysrhythmias with other antidysrhythmic agents May increase phenytoin levels

Prototype Drug: Amiodarone (Cordarone, Pacerone) Adverse Effects Nausea Vomiting Anorexia Fatigue Dizziness Hypotension Visual disturbances Rashes Photosensitivity Serious Adverse Effects Pneumonia-like syndrome Prodysrhythmic action

Prototype Drug: Amiodarone (Cordarone, Pacerone) Nursing Responsibilities Monitor BP during IV infusion Assess for adverse effects Baseline lab tests Assess respiratory status Supervise ambulation Baseline ophthalmic exam

Prototype Drug: Amiodarone (Cordarone, Pacerone) Patient/Family Teaching Immediately report respiratory difficulty Do not take with grapefruit juice Check pulse daily Take oral drug consistently at same time of day Wear dark glasses/eye exams Do not take with other drugs or supplements Notify if suspected pregnancy

Similar Drugs to Amiodarone Dofetilide (Tikosyn) Ibutilide (Corvert) Sotalol (Betapace, betapace AF, Sorine)

Calcium Channel Blockers: Class IV 39.10 Calcium channel blockers are used to treat atrial dysrhythmias.

Calcium Channel Blockers Limited number approved as antidysrhythmics Diltiazem (Cardizem, Dilacor, others) Verapamil (Calan, Isoptin, others) Effects similar to beta-adrenergic antagonists Safe and well-tolerated by most patients Monitor for bradycardia and hypotension

Connection Checkpoint 39.3 Nifedipine (Procardia) is a prototype CCB discussed in Chapter 33. From what you learned in Chapter 33, why is this drug (and other dihydropyridines) not effective in treating dysrhythmias?

Miscellaneous Antidysrhythmics 39.11 Adenosine and digoxin used for specific dysrhythmias.

Adenosine (Adenocard, Adenoscan) Naturally occurring nucleoside Activates potassium channels in SA and AV nodes Terminates tachycardia Primary indication is PSVT 10 second half life so adverse effects are self-limiting

Digoxin (Lanoxin) Primarily used for HF Can be prescribed for atrial flutter, fibrillation, or PSVT Not effective against ventricular dysrhythmias Patients must be carefully monitored for toxicity, drug interactions, and adverse effects