McKenna's Pharmacology for Nursing, 2e

711

C H A P T E R 4 5 Antiarrhythmic agents

CHAPTER SUMMARY ■■ Disruptions in the normal rate or rhythm of the heart are called arrhythmias (also known as dysrhythmias). ■■ Electrolyte disturbances, decreases in the oxygen delivered to the cells leading to hypoxia or anoxia, structural damage that changes the conduction pathway, acidosis or the accumulation of waste products or drug effects can lead to disruptions in the automaticity of the cells or in the conduction of the impulse that result in arrhythmias. The result can be changes in heart rate (tachycardias or bradycardias); stimulation from ectopic foci in the atria or ventricles that cause an uncoordinated muscle contraction; or blocks in the conduction system (e.g. AV heart block, bundle-branch blocks) that alter the normal movement of the impulse through the system. ■■ Arrhythmias cause problems because they alter the haemodynamics of the cardiovascular system. They can cause a decrease in cardiac output related to the uncoordinated pumping action of the irregular rhythm, leading to lack of filling time for the ventricles. Any of these effects can interfere with the delivery of blood to the brain, to other tissues or to the heart muscle. ■■ Antiarrhythmics are drugs that alter the action potential of the heart cells and interrupt arrhythmias. The CAST study found that the long-term treatment of arrhythmias may actually cause cardiac death, so these drugs are now indicated only for the short-term treatment of potentially life-threatening ventricular arrhythmias. ■■ Class I antiarrhythmics block sodium channels, depress phase 0 of the action potential and generally prolong the action potential, leading to a slowing of conduction and automaticity. ■■ Class II antiarrhythmics are beta-adrenergic receptor blockers that prevent sympathetic stimulation. ■■ Class III antiarrhythmics block potassium channels and prolong phase 3 of the action potential. ■■ Class IV antiarrhythmics are calcium channel blockers that shorten the action potential, disrupting ineffective rhythms and rates. ■■ A person receiving an antiarrhythmic drug needs to be constantly monitored while being stabilised and throughout the course of therapy to detect the • Report any of the following to your healthcare provider: chest pain, difficulty breathing, palpitations, numbness or tingling . • Tell any doctor, nurse or other health provider involved in your care that you are taking this drug. • Keep this drug, and all medications, out of the reach of children.

• Schedule regular medical appointments while you are on this drug to evaluate your heart rhythm and your response to the drug and to monitor your blood levels of important electrolytes that affect heart function. • Do not stop taking this medication. If you have to stop the medication, contact your healthcare provider immediately.

development of arrhythmias or other adverse effects associated with alteration of the action potentials of other muscles or nerves.

Knowing your strengths and weaknesses helps you to study more effectively. Take a PrepU Practice Quiz to find out how you measure up!

ONLINE RESOURCES

An extensive range of additional resources to enhance teaching and learning and to facilitate understanding of this chapter may be found online at the text’s accompanying website, located on thePoint at http://thepoint.lww.com. These include Watch and Learn videos, Concepts in Action animations, journal articles, review questions, case studies, discussion topics and quizzes. BIBLIOGRAPHY Braunwald, E. & Bonow, R. O., MD Consult LLC (2012). Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine (9th edn). Philadelphia: Elsevier Saunders. Epstein, A. E., Hallstrom, A. P., Rogers, W. J., Liebson, P. R., Seals, A. A., Anderson, J. L., et al. (1993). Mortality following ventricular arrhythmia suppression by encainide, flecainide, and moricizine after myocardial infarction. The original design concept of the Cardiac Arrhythmia Suppression Trial (CAST). JAMA, 270, 2451–2455. Farrell, M. & Dempsey, J. (2014). Smeltzer & Bare’s Textbook of Medical-Surgical Nursing (3rd edn). Sydney: Lippincott Williams & Wilkins. Goodman, L. S., Brunton, L. L., Chabner, B. & Knollmann, B. C. (2011). Goodman and Gilman’s Pharmacological Basis of Therapeutics (12th edn). New York: McGraw-Hill. Greener, M. (2010). The nurse’s role in the management of atrial fibrillation. Nurse Prescribing, 8(11) , 532, 534–537. Hurst, J. W., Fuster, V., Walsh, R. A. & Harrington, R. A. (Eds.). (2011). Hurst’s the Heart (13th edn). New York: McGraw-Hill. McKenna, L. (2012). Pharmacology Made Incredibly Easy (1st Australian and New Zealand edn). Sydney: Lippincott Williams & Wilkins. McKenna, L. & Mirkov, S. (2014). McKenna’s Drug Handbook for Nursing and Midwifery (7th edn). Sydney: Lippincott Williams & Wilkins. Mosher, M. C. (2011). Amiodarone-induced hypothyroidism and other adverse effects. Dimensions of Critical Care Nursing, 30(2) , 87–93. Naganathan, V. (2013). Cardiovascular drugs in older people. Australian Prescriber, 36(6) , 190–194.