Chapter 40: Cardiac Glycosides, Antianginals & Antiarrhythmics
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ⓘ This audio and summary are simplified educational interpretations and are not a substitute for the original text.
Cardiac Glycosides, Antianginals & Antiarrhythmics begins by establishing the physiological principles of cardiac output, stroke volume, preload, afterload, and contractility, while highlighting the diagnostic importance of laboratory tests such as Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP), where levels greater than 100 pg/mL help differentiate heart failure from pulmonary dysfunction. A major portion of the text is dedicated to Cardiac Glycosides, particularly digoxin, detailing its mechanism of inhibiting the sodium-potassium pump to increase intracellular calcium. This results in three specific effects: positive inotropic action (increased myocardial contraction force), negative chronotropic action (decreased heart rate), and negative dromotropic action (decreased conduction speed). The summary emphasizes the critical nursing implications for digoxin, a Narrow Therapeutic Index (NTI) drug, including the risk of toxicity manifested by visual halos and bradycardia, the necessity of monitoring for hypokalemia (potassium levels lesser than 3.5 mEq/L) which potentiates toxicity, and the use of Digoxin-immune Fab as an antidote. The chapter also reviews other heart failure treatments, including phosphodiesterase (PDE) inhibitors like milrinone, and newer agents such as SGLT2 inhibitors (dapagliflozin and empagliflozin) which reduce cardiovascular mortality. Furthermore, the text categorizes antianginal agents used to treat classic (stable), unstable, and variant (vasospastic) angina: Nitrates (nitroglycerin) which reduce preload and afterload via vasodilation; Beta-blockers which lower oxygen demand by reducing heart rate and contractility; and Calcium Channel Blockers (CCBs) like verapamil, diltiazem, and nifedipine which relax coronary spasms and peripheral arterioles. Finally, the summary outlines the four classes of Antidysrhythmic drugs based on their electrophysiological effects on action potentials: Class I sodium channel blockers (IA, IB, IC) like lidocaine for ventricular dysrhythmias; Class II beta-blockers; Class III drugs that prolong repolarization such as amiodarone and adenosine; and Class IV calcium channel blockers. The content concludes with essential patient safety protocols, including pulse monitoring, managing orthostatic hypotension, and preventing drug-herb interactions.