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Chapter 27 Drug Therapy for Dysrhythmias Copyright © 2021 Wolters Kluwer Health | Lippincott Williams & Wilkins Cardiac Electrophysiology #1 Dysrhythmias: abnormalities in cardiac rate or rhythm o Ventricular arrhythmias occur in the lower chambers of the heart, called the ventricles. o Suprave...
Chapter 27 Drug Therapy for Dysrhythmias Copyright © 2021 Wolters Kluwer Health | Lippincott Williams & Wilkins Cardiac Electrophysiology #1 Dysrhythmias: abnormalities in cardiac rate or rhythm o Ventricular arrhythmias occur in the lower chambers of the heart, called the ventricles. o Supraventricular arrhythmias occur in the area above the ventricles, usually in the upper chambers of the heart, called the atria Heart is an electrical pump. o Electricity resides in specialized tissues that generate and conduct electrical impulses: contractile tissue. o Activities result in effective cardiac contraction and blood distribution throughout the body. Copyright © 2021 Wolters Kluwer • All Rights Reserved Question #1 Is the following statement True or False? All cardiac tissue conducts electrical impulses. Copyright © 2021 Wolters Kluwer • All Rights Reserved Answer to Question #1 True Rationale: All cardiac tissue conducts electrical impulses. Electrical activity resides primarily in specialized tissues that can generate and conduct electrical impulses. Muscle tissue also can conduct electrical impulses but at a much slower rate. Copyright © 2021 Wolters Kluwer • All Rights Reserved Cardiac Electrophysiology #2 Heartbeats occur o Regular intervals with four events Stimulation from electrical impulse Transmission to adjacent tissue Contraction of atria, then ventricles Relaxation of atria, then ventricles Copyright © 2021 Wolters Kluwer • All Rights Reserved Cardiac Automaticity Heart’s ability to generate electrical impulse o Any part of conduction system can start an impulse. o Sinoatrial (SA) node has the fastest rate of automaticity. Serves as pacemaker site o Initiation of impulse dependent on Na and K ion movement. Copyright © 2021 Wolters Kluwer • All Rights Reserved Cardiac Excitability Heart’s ability to respond to electrical stimulus o Stimulus must reach specific threshold to cause contraction. After contraction o Period of decreased excitability where cells cannot respond to new stimulus Absolute refractory period Copyright © 2021 Wolters Kluwer • All Rights Reserved Cardiac Conductivity #1 Heart’s ability to transmit electrical impulses Typically o Impulses originate in SA node. o Transmitted through internodal pathways to atrioventricular (AV) node Impulse is delayed for a period of time. o Impulse then travels predictable route. Copyright © 2021 Wolters Kluwer • All Rights Reserved Cardiac Conductivity #2 Copyright © 2021 Wolters Kluwer • All Rights Reserved Cardiac Dysrhythmias #1 Can originate in any part of the conduction system Result from electrical impulse formation, conduction, or both Automaticity allows cells other than SA to initiate electrical impulse that culminates in contraction. o SA node failure or slow depolarization Copyright © 2021 Wolters Kluwer • All Rights Reserved Question #2 Is the following statement True or False? All electrical impulse formation originates in the SA node. Copyright © 2021 Wolters Kluwer • All Rights Reserved Answer to Question #2 False Rationale: While electrical impulses originate in the SA node of healthy cardiac tissue, cardiac dysrhythmias can originate in any part of the conduction system or from atrial or ventricular muscle. Copyright © 2021 Wolters Kluwer • All Rights Reserved Cardiac Dysrhythmias #2 Impulse origination other than in SA node o Ectopic focus Activation via Hypoxia, ischemia, hypokalemia Indicates myocardial irritability Potentially serious cardiac function impairment Copyright © 2021 Wolters Kluwer • All Rights Reserved Dysrhythmias #2 Atrial o Premature atrial complex o Atrial flutter o Atrial fibrillation Ventricular o Premature ventricular complex o Ventricular tachycardia o Ventricular fibrillation o Ventricular asystole Copyright © 2018 Wolters Kluwer · All Rights Reserved Cardiac Dysrhythmias #3 Copyright © 2021 Wolters Kluwer • All Rights Reserved ECG Graph and Commonly Measured Components- Review Copyright © 2018 Wolters Kluwer · All Rights Reserved PAC Copyright © 2018 Wolters Kluwer · All Rights Reserved 1 8 PAC Copyright © 2018 Wolters Kluwer · All Rights Reserved 1 9 PVC Copyright © 2018 Wolters Kluwer · All Rights Reserved 2 0 PVC Copyright © 2018 Wolters Kluwer · All Rights Reserved PVC Copyright © 2018 Wolters Kluwer · All Rights Reserved Sinus Tachycardia and SVT Copyright © 2018 Wolters Kluwer · All Rights Reserved 2 3 V TACH Copyright © 2018 Wolters Kluwer · All Rights Reserved 2 4 V FIB Copyright © 2018 Wolters Kluwer · All Rights Reserved 5 Antidysrhythmics Dysrhythmia o Any deviation from the normal rhythm of the heart o Associated with MI, cardiac surgery or as result of CAD (Coronary Artery Disease) Antidysrhythmics o Used for the treatment and prevention of disturbances in cardiac rhythm Copyright © 2018 Wolters Kluwer · All Rights Reserved Vaughan Williams Classification Four major classes Based on Electrophysiologic effect of particular drugs on the action potential. Class I- Sodium Channel Blockers –Class 1A-Quinidine Class 1- Sodium Channel Blockers- Class 1B - Lidocaine Class II- Beta Blockers (Propranolol) Class III- Drugs that delay Repolarization (Amiodarone) Class IV- Calcium Channel Blockers (Diltiazem) Others: Adenosine, Magnesium sulfate Copyright © 2017, Elsevier Inc. All rights reserved. Copyright © 2018 Wolters Kluwer · All Rights Reserved 26 Antidysrhythmic Drug Therapy #1 Newest goal of therapy o Prevent, relieve symptoms, or prolong survival Prior goal of pharmacotherapy: suppress dysrhythmias o Resulted in higher mortality rate among patients receiving antidysrhythmic drug therapy Copyright © 2021 Wolters Kluwer • All Rights Reserved Antidysrhythmic Drug Therapy #2- NOT RESPONSIBLE FOR COVERED IN NURSING CLASS Greater use of nonpharmacologic strategies for dysrhythmia management o Destroying dysrhythmogenic areas within the heart using ablation o Implanting devices for sensing, cardioverting, defibrillating, or pacing patient Copyright © 2021 Wolters Kluwer • All Rights Reserved Antidysrhythmic Drug Therapy #3 Indications for use o Conversion of atrial fibrillation or flutter to NSR o Maintaining NSR postconversion o Suppression of fast or irregular ventricular rate that alters cardiac output o Presence of dangerous dysrhythmias that are potentially fatal Copyright © 2021 Wolters Kluwer • All Rights Reserved Antidysrhythmic Drug Therapy #4 Mechanisms of action o Reduce automaticity o Slow conduction of impulses through the heart o Prolong refractory period Classified according to mechanism of action and conduction system effect Copyright © 2021 Wolters Kluwer • All Rights Reserved Nonpharmacologic Therapy of Dysrhythmias #1 Preferred initial treatment for several dysrhythmias o Antidysrhythmic drugs can Worsen existing dysrhythmias Cause new dysrhythmias Cause higher mortality than those not using medications Copyright © 2021 Wolters Kluwer • All Rights Reserved Question #3 Is the following statement True or False? The main goal of antidysrhythmic drugs is to suppress dysrhythmias. Copyright © 2021 Wolters Kluwer • All Rights Reserved Answer to Question #3 False Rationale: One change in the goals of drug therapy for dysrhythmias is to prevent or relieve symptoms and to prolong survival, not just suppress dysrhythmias. Copyright © 2021 Wolters Kluwer • All Rights Reserved Nonpharmacologic Therapy of Dysrhythmias #2- NOT RESPONSIBLE FOR Preferred initial treatment for several dysrhythmias (cont.) o Pacemakers o Defibrillators o Radiofrequency catheter ablation o Surgery to deactivate ectopic foci o Other strategies Copyright © 2021 Wolters Kluwer • All Rights Reserved Pharmacologic Therapy of Dysrhythmias Requires accurate ID of dysrhythmia Understanding mechanics of dysrhythmia Observing hemodynamic and ECG effects of dysrhythmia Knowledge of pharmacologic actions of specific medications Therapeutic effects outweigh potential adverse effects Copyright © 2021 Wolters Kluwer • All Rights Reserved Class I A: Sodium Channel Blockers (Quinidine) Block cardiac sodium channels, thus decrease conduction velocity in the atria, ventricles, and His-Purkinje systems. In addition, delays repolarization by blocking potassium channels. Both actions, suppress dysrhythmias. Widens the QRS complex, by slowing depolarization of the ventricles and prolongs QT interval by delaying ventricle repolarization. Oldest and most widely used class 1A drug. Uses: Supraventricular and ventricular dysrhythmias, SVT, atrial Dysrhythmias. These agents should be reserved for patients with life threatening ventricular rhythms. Black box Copyright © 2021 Wolters Kluwer • All Rights Reserved Adverse Effects: Quinidine GI: diarrhea, tinnitus, headache, nausea, vertigo, change in vision Cardiotoxicity: cardiac dysrhythmias, heart block, hypotension Copyright © 2021 Wolters Kluwer • All Rights Reserved Class 1 B Lidocaine Uses: Ventricular dysrhythmias associated with MI, cardiac catherization, cardiac surgery, and digitalis ventricular dysrhythmias. MOA: Decreases myocardial irritability in ventricles by increasing the electrical stimulation threshold of ventricular myocardial cells. Has little effect on atrial tissue Therapeutic effects 1-2 min after IV bolus Metabolized in liver Monitor serum therapeutic levels Contraindicated if allergic to local anesthetics Copyright © 2021 Wolters Kluwer • All Rights Reserved Class II Beta Blockers Four Beta Blockers are approved for treating dysrhythmias: Propranolol (Nonselective beta-adrenergic antagonist) Acebutolol Esmolol Sotalol- also blocks potassium channels Copyright © 2021 Wolters Kluwer • All Rights Reserved MOA: Beta Blockers- propranolol When block beta 1 receptors: Reduces the force on the Sympathetic stimulation of the heart. Thus,…. Decreased excitability of heart Decreased cardiac workload, and oxygen consumption Releases renin and lowers blood pressure Has a membrane-stabilizing effect contributes to its antidysrhythmic action. Copyright © 2021 Wolters Kluwer • All Rights Reserved Beta Blockers continued… Uses: Dysrhythmias caused by excessive sympathetic stimulation of the heart. Sinus tachycardia, Severe recurrent Ventricular tachycardia, Paroxysmal Atrial Tachycardia Monitor HR and BP Monitor for s/s of heart failure Use cautiously in asthma patients Contraindicated: Sinus bradycardia, high degree heart block and HF Copyright © 2021 Wolters Kluwer • All Rights Reserved . 42 Amiodarone- (Cordarone, Pacerone) Class III Blocks both the alpha- and beta-adrenergic receptors of the sympathetic nervous system Class III Drug- Block Potassium channels and thereby delay repolarization of fast potentials. As a result, they prolong action potential duration and the effective refractory period. By delaying ventricular repolarization, they prolong the QT interval. Uses: one of the most effective antidysrhythmic drugs for controlling (atrial) supraventricular and ventricular dysrhythmias Indications: management of sustained ventricular tachycardia, ventricular fibrillation, and non sustained ventricular tachycardia which are critical dysrhythmias Maintain normal sinus rhythm after used to convert atrial fibrillation and a flutter rhythm Oral or IV Copyright © 2021 Wolters Kluwer • All Rights Reserved 43 . Amiodarone (Cordarone, Pacerone) Drug interactions: Many interactions including digoxin, warfarin, diltiazem, some statins, diuretics (as they decrease k+) Contraindications: hypersensitivity, severe sinus bradycardia and heart block, hypokalemia, lactation, sensitivity to iodone Adverse effects: corneal micro deposits, which may cause visual halos, photophobia, and dry eyes; photosensitivity; pulmonary toxicity (fibrosis), paradoxical increase in dysrhythmic activity, thyroid disorders, liver toxicity, Copyright © 2021 Wolters Kluwer • All Rights Reserved 4 4 Class IV Drugs Diltiazem Calcium Channel Blocker Blocks the calcium channels in the heart. Slows AV node automaticity, Delay of AV node conduction, Reduction in myocardial contractility Controls ventricular response in atrial fib. or atrial flutter, and terminate SVT Can decrease HR by 20% Contraindicated in hypersensitivity, MI, pulmonary congestion, severe hypotension, cardiogenic shock, heart failure, and heart block. Also used to treat angina, HTN *Monitor BP, HR, and ECG. Copyright © 2021 Wolters Kluwer • All Rights Reserved Diltiazem- Continued In patients with Supraventricular Tachydysrhythmias, has 2 benefits: Suppression of excessive discharge of SA node Slowing of ventricular rate by decreasing transmission of atrial impulses through the AV node. Copyright © 2021 Wolters Kluwer • All Rights Reserved 46 . Antidysrhythmics: General Adverse Effects ALL antidysrhythmics can cause dysrhythmias! o Hypersensitivity reactions o Nausea, vomiting, and diarrhea o Dizziness o Headache, and blurred vision o Prolongation of the QT interval Copyright © 2021 Wolters Kluwer • All Rights Reserved 47 Unclassified Antidysrhythmic adenosine (Adenocard) o Slows conduction through the AV node o Used to convert PSVT to sinus rhythm o Very short half-life—less than 10 seconds o Only administered as fast intravenous (IV) push o May cause asystole (flat line) for a few seconds o Other adverse effects are minimal Copyright © 2021 Wolters Kluwer • All Rights Reserved Audience Response System Question A patient has received an IV dose of adenosine, and almost immediately the heart monitor shows asystole. What should the nurse do next? A. Check the patient’s pulse. B. Prepare to administer cardiopulmonary resuscitation. C. Set up for defibrillation. D. Continue to monitor the patient. Copyright © 2017, Elsevier Inc. All rights reserved. Copyright © 2021 Wolters Kluwer • All Rights Reserved 48 Magnesium sulfate Antidysrhythmic effects may derive from imbalances of magnesium, potassium, and calcium Hypomagnesemia increases myocardial irritability and a risk factor for atrial and ventricular dysrhythmias. Monitor magnesium levels and replacement therapy when needed. In some instances, magnesium sulfate seems to have antidysrhythmic effects even when levels are normal. Copyright © 2021 Wolters Kluwer • All Rights Reserved 50 Nursing Implications Measure baseline blood pressure (BP), pulse, input and output, and cardiac rhythm. Measure serum potassium levels before initiating therapy. Assess for conditions that may be contraindications for use of specific drugs. Assess for potential drug interactions. Instruct patients to report dosing schedules and adverse effects to physician. Instruct patients to take medications as scheduled and not to skip doses or double up for missed doses. Copyright © 2021 Wolters Kluwer • All Rights Reserved 51 . Nursing Implications (Cont.) During therapy, monitor cardiac rhythm, heart rate, BP, general well-being, skin color, temperature, and heart and lung sounds. Assess plasma drug levels as indicated. Monitor for toxic effects Teach the patient: o How to take pulse before medication administration o How to recognize symptoms of the dysrhythmia o Measures to decrease recurrence o Plan of action in case of an emergency o CPR (family) o Referral for Home Care Copyright © 2021 Wolters Kluwer • All Rights Reserved Drug Therapy in Emergency Resuscitation of Adults Oxygen Epinephrine Atropine Lidocaine Calcium chloride Copyright © 2021 Wolters Kluwer • All Rights Reserved