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Recognition and Treatment Sinus node dysfunction Recognition and treatment 12 The Nurse Practitioner • Vol. 38,37, No. 112 www.tnpj.com Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Sinus node dysfunction: Recognition and treatment 2.8 CONTACT HOURS Abstract: Sinus node dysfunction (SND) refers to a wide range of abnormalities involving sinus node and atrial impulse generation and propagation. SND occurs at any age and is commonly encountered in clinical practice. Clinicians must be able to accurately diagnose this syndrome, which can present from asymptomatic bradycardia to atrial standstill. By Karla Rusk, MS, RN, CCRN, ANP-BC, ACNP-BC, and Kristine Scordo, PhD, RN, ACNP-BC, FAANP r. S is a 78-year-old male (previously an avid to a wide range of abnormalities involving sinus node and walker) with a history of hypertension and osteo- atrial impulse generation/propagation.2,3 Although SND M arthritis. His medications include losartan (50 mg occurs at any age, the incidence increases exponentially daily) and arthritis strength acetaminophen p.r.n. He pre- with advanced age,3 the mean age for diagnosis is 68 years, sented to the clinic for evaluation at his daughter’s insis- and both genders are equally affected.4,5 The incidence of tence with a 6-month history of fatigue, some dyspnea on this disorder is diffi cult to establish since it may be intermit- exertion (DOE), and dizziness. According to his daughter’s tent, and patients may be free from symptoms for many report, he is also experiencing periods of confusion, and years. Furthermore, when the patient is symptomatic, the she expressed concern about possible dementia. He denied symptoms may be attributed to some other cause. Available chest pain or pressure, palpitations, syncope, or near syn- estimates are that SND occurs in 1 of every 600 cardiac cope. His resting ECG (see 12-Lead ECG: Sinus bradycardia) patients over age 65 and accounts for approximately half of indicates sinus bradycardia with a ventricular rate of 51 the pacemaker implants in the United States.5 Therefore, beats/minute (bpm). There is no evidence of ST or T wave SND can be commonly encountered in clinical practice. As changes, left ventricular (LV) hypertrophy, or conduction such, clinicians must be able to accurately diagnose this abnormalities. Physical exam is essentially unremarkable syndrome, which can present from asymptomatic bradycar- with a resting heart rate (HR) of 56 and BP of 128/78. Blood dia to atrial standstill. was drawn for a thyroid-stimulating hormone, complete blood count, basic metabolic profi le, and a nuclear stress ■ Etiology test was performed to rule out myocardial ischemia as a Most cases of SND are idiopathic, and the cause may be possible cause for fatigue and DOE. Nuclear stress test re- multifactorial.5 The causes of SND may be classifi ed as in- sults revealed a peak HR of 107 bpm, only 75% of his age- trinsic (related to pathologic changes in the sinus node and/ predicted maximal HR. Nuclear imaging demonstrated or atrial tissue), or extrinsic (disturbance of sinus node normal LV function with an ejection fraction (EF) of 60% function caused by the infl uences of other factors in absence and no inducible ischemia or prior myocardial injury. Stress of structural abnormalities).4,6 (See Etiology of SND.) test results were consistent with chronotropic incompetence and suggested sinus node dysfunction (SND) as a source ■ Intrinsic factors of Mr. S’s symptoms. Degenerative and/or fi brotic changes in the sinoatrial (SA) node region are the predominant cause of intrinsic chang- ■ Introduction es that lead to SND.5,7,8 These changes may result from isch- SND, previously known as sick sinus syndrome, was fi rst emia, infl ammation, surgical trauma, or as part of the aging 1 6 Illustration by Jana Blašková/istockphoto © described as a clinical entity in the late 1960s. SND refers process. With age, the intrinsic HR (defi ned as the HR in Key words: cardiac pacemaker therapy, sick sinus syndrome, sinus node dysfunction www.tnpj.com The Nurse Practitioner • December 2012 13 Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Sinus node dysfunction: Recognition and treatment the absence of autonomic nerve activity) declines, and SA Congenital heart disease and familial disorders of conduction time (SACT) increases;9 age-related changes in sinus node function can occur in younger individuals ion channels have been suggested as a possible cause.3 including the newborn.3 Typically, corrective surgical However, these pathologic changes may also result from procedures, such as the Mustard procedure performed for concomitant conditions such as hypertension, atheroscle- transposition of the great vessels and closure of atrial rotic cardiovascular disease, cardiomyopathy, infi ltrative septal defects, contribute to SND.7,8 A genetic component disease, myocarditis, and collagen vascular diseases.2,8,10,11 also appears to play a role in the development of SND in Since SND is typically diagnosed in individuals in their 70s children and young adults3,12 as does an autoimmune or 80s, coexisting cardiovascular disorders are likely.2 mechanism.13 12-Lead ECG: Sinus bradycardia ■ Extrinsic factors Numerous factors can affect sinus node function without causing structural dis- turbances including medications, auto- nomic nervous system influences, and metabolic disturbances. Cardioactive drugs may initiate/aggravate sinus brady- cardia or chronotropic incompetence.4 The medications most likely to affect sinus node function are beta-adrenergic block- ers, calcium channel blockers, antiar- rhythmic drugs (specifi cally Class IA, IC, and III), and cardiac glycosides.8,11 (See Classification of antiarrhythmic drugs.) Psychotropic medications may also con- tribute to sinus node depression.4,14 Infl uences from the autonomic ner- vous system can affect normal sinus node Etiology of SND function. Parasympathetic stimulation slows the sinus discharge rate and increas- Intrinsic Extrinsic • Idiopathic/degenerative • Pharmacologic agents es the intranodal conduction time, result- 4 • Ischemic heart disease – Class IA, IC, III antiarrhythmic agents ing in sinus node exit block at times. • Hypertensive heart disease – Beta adrenergic blockers Individuals with conditions such as va- • Cardiomyopathy – Calcium channel blockers sovagal syncope and carotid sinus hyper- – Infi ltrative diseases – Cardiac glycosides sensitivity frequently have associated ü Sarcoidosis, amyloidosis – Antihypertensives (such as clonidine, bradycardia.4,8 Heightened vagal tone • Surgical trauma methyldopa) from excessive physical training may re- – Congenital heart disease – Antipsychotics (such as lithium, sult in syncope related to bradycardia or phenothiazine derivatives) ü Mustard procedure atrioventricular (AV) conduction abnor- – Antidepressants (such as ü ASD closure 7 amitriptyline) malities in otherwise healthy individuals. – Cardiac transplant • Autonomic Hyperthyroidism and hypothyroidism • Infl ammation – Vasovagal syncope (cardioinhibitory) produce changes in the cardiovascular sys- – Collagen vascular disease – Carotid sinus hypersensitivity tem. Thyroid hormone affects the action – Rheumatic fever • Metabolic potential duration and repolarization cur- • Infection – Hypothyroidism rents in the cardiac myocytes, resulting in – Viral myocarditis – Hyperkalemia changes in HR and development of dys- – Lyme disease – Hypoxia rhythmias;15 in hypothyroidism, this pro- • Neuromuscular disorders – Intracranial hypertension duces bradycardia. Electrolyte imbalances • Familial (particularly hyperkalemia) can result in Adapted from Vijayaraman P, Ellenbogen K. Bradyarrhythmias and pacemakers. In: Fuster V, Walsh R, bradycardia, sinus arrest, and SA exit block Harrington R, eds. Hurst’s the Heart. 13th ed. New York, NY: McGraw-Hill; 2011. as well as AV block.5 14 The Nurse Practitioner • Vol. 37, No. 12 www.tnpj.com Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Sinus node dysfunction: Recognition and treatment Classifi cation of antiarrhythmic drugs Class Action Medication Examples IA Inhibits fast sodium channel, decreases automaticity, depresses • Disopyramide phase 0, and prolongs the action potential duration. • Procainamide • Quinidine IB Inhibits fast sodium channel, depresses phase 0 slightly, and • Lidocaine shortens action potential duration. • Mexiletine IC Inhibits fast sodium channel, depresses phase 0 markedly, slows • Flecainide His-Purkinje conduction profoundly leading to a prolonged QRS • Propafenone duration. II Depresses phase 4 depolarization, blocks sympathetic stimulation • Acebutolol of the conduction system. • Esmolol • Propranolol III Blocks potassium channel, prolongs phase 3 repolarization, • Amiodarone prolongs action potential duration. • Dofetilide • Dronedarone • Ibutilide • Sotalol (also has class II effects) IV Inhibits inward calcium channel, depresses phase 4 depolarization, • Diltiazem Lengthens repolarization in phases 1 and 2. • Verapamil Source: Adapted from Morton PG, Fontaine DK. Critical Care Nursing A Holistic Approach. 9th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins. 2009:333. ■ Pathophysiology termination of a tachydysrhythmia, resulting in inadequate The pathophysiologic mechanisms for SND include failure cerebral blood fl ow.2,8 Sinus bradycardia, even if severe, is of impulse generation and failure of the impulse to spread rarely
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