Arrhythmias



Arrhythmias


Cynthia A. Sanoski

Andrew M. Peterson



Cardiac arrhythmias are abnormal cardiac rhythms, including tachyarrhythmias (an increase in heart rate) and bradyarrhythmias (a decrease in heart rate). Arrhythmias may be asymptomatic or symptomatic, causing palpitations, weakness, loss of consciousness, heart failure (HF), and sudden death. Searching for a reversible cause of the arrhythmia is the first step in patient care. However, in many cases, antiarrhythmic drugs (AADs) are necessary to permit stabilization until the underlying condition is normalized. Many patients require chronic drug therapy for an arrhythmia due to an underlying disease condition that makes them chronically susceptible to cardiac arrhythmias that are associated with high morbidity and mortality rates.


CAUSES

Arrhythmias may result from structural or electrical/conduction system changes in the heart that may compromise cardiac function and cardiac output. Conditions that give rise to arrhythmias include myocardial ischemia, chronic HF, hypertension, valvular heart disease, hypoxemia, thyroid abnormalities, electrolyte disturbances, drug toxicity, excessive caffeine or ethanol ingestion, anxiety, and exercise. Some of these conditions are reversible, and some cause structural changes that are not reversible.




DIAGNOSTIC CRITERIA

The practitioner must first assess the patient via a thorough and sometimes urgent history and physical examination. There may be no symptoms, or the patient may present with symptoms such as chest pain, shortness of breath, decreased level of consciousness, syncope, confusion, diaphoresis, weakness, and palpitations. The practitioner should ask when the symptoms started, how long they have lasted, their frequency, and how the patient tolerated the symptoms.

It also is important to assess the patient’s risk factors for development of arrhythmias, such as previous coronary artery disease (CAD), myocardial infarction (MI), dilated or hypertrophic cardiomyopathy, hypertension, valvular heart disease, alcohol or drug abuse, or prescription drug use (e.g., digoxin, AADs). The practitioner should focus the physical examination on heart rate and blood pressure; presence of extra, irregular, or skipped beats; rate, rhythm, amplitude, and symmetry of peripheral pulses; and response to exercise.

Laboratory and diagnostic studies also are vital in diagnosing arrhythmias. The practitioner should examine the 12-lead electrocardiogram (ECG) for evidence of myocardial ischemia; calculation of the PR interval, QRS interval, and QT interval; presence of premature atrial or ventricular contractions;
characteristics of Wolff-Parkinson-White (WPW) syndrome; presence or absence of P waves; and relationship between P waves and QRS complexes. Continuous cardiac monitoring is needed for patients who have episodes of life-threatening arrhythmias so that electrical cardioversion and/or AADs can be administered as immediate interventions.


A complete blood count, basic metabolic profile (to assess electrolyte concentrations), thyroid function tests, and a digoxin level should be performed as necessary to determine any underlying causes of the arrhythmia. In addition, an echocardiogram should be performed to assess left ventricular (LV) function. If myocardial ischemia is suspected as a cause of the arrhythmia, the patient should undergo further evaluation with measurement of cardiac enzymes, performance of cardiac stress testing, and, possibly, cardiac catheterization.


INITIATING DRUG THERAPY

During the past several decades, the treatment approach for both atrial and ventricular arrhythmias has been gradually shifting away from the use of AADs toward the use of various nonpharmacological therapies. Several factors have likely contributed to the decline in AAD use over the years. The negative results of the Cardiac Arrhythmia Suppression Trial (CAST) likely had a significant influence on the downward prescribing patterns of class I AADs. In addition, increasing clinical evidence to support the use of nonpharmacological strategies for the treatment of both supraventricular and ventricular arrhythmias has likely contributed to the decline in the use of AADs as a whole. Numerous studies establishing that a rhythm-control regimen does not confer any benefit over a rate-control regimen in patients with persistent atrial fibrillation (AF) may have also contributed to this decline in AAD use.

Treatable conditions may cause the arrhythmia. Identification of treatable causes before administering an AAD is a priority. Conditions that may cause arrhythmias are electrolyte imbalances (e.g., hypokalemia, hypomagnesemia), drug overdose, drug interactions with other medications or herbal supplements, renal failure, thyroid disorders, metabolic acidosis, hypovolemia, MI, pulmonary embolism, cardiac tamponade, tension pneumothorax, dissecting aortic aneurysm, hypoxemia, and valvular or congenital defects in the heart.

Nonpharmacological therapies, such as radiofrequency catheter ablation and implantable cardioverter-defibrillators (ICDs), are also available to treat various arrhythmias. ICDs are used in the management of ventricular arrhythmias, and their benefits have been demonstrated in several clinical trials (Antiarrhythmics Versus Implantable Defibrillators [AVID] Investigators, 1997; Bardy et al., 2005; Buxton et al., 1999; Connolly et al., 2000; Kuck et al., 2000; Moss et al., 1996, 2002). Radiofrequency catheter ablation permanently terminates the arrhythmia by ablating the focal area where the arrhythmia occurs. This procedure can be used for AF, atrial flutter (AFl), and symptomatic drug-refractory ventricular tachycardia (VT).


Goals of AAD Therapy

The overall goals of AAD therapy are to relieve the acute episode of irregular rhythm, establish sinus rhythm (SR), and prevent further episodes of the arrhythmia. Typical agents used to treat arrhythmias include AADs (classes I through IV), digoxin, adenosine, and atropine (Table 23.1).


Drug Classification

AADs are organized into four classes, I (Ia, Ib, Ic), II, III, and IV (Vaughan Williams, 1984). Although the Vaughan Williams classification system is the most widely used method for grouping AADs based on their electrophysiologic actions, using this classification system requires some points of exception to be made. This system is somewhat incomplete, and it excludes certain drugs including digoxin, adenosine, and




atropine. In addition, the classification is not pure, and there is some overlapping of drugs into more than one category. For instance, amiodarone and dronedarone have electrophysiologic properties of all four Vaughan Williams classes. Furthermore, this system does not take into account that the active metabolites of AADs may have different electrophysiologic effects than their parent drugs. For example, N-acetyl procainamide (NAPA), the major active metabolite of procainamide, blocks outward potassium channels and therefore can be considered a class III AAD. Although procainamide blocks outward potassium channels, it also primarily blocks inward sodium currents, thereby making it a class Ia AAD. Therefore, the overall electrophysiologic effect produced by procainamide depends upon the relative concentrations of procainamide and NAPA that are present in the body, which can vary based on several clinical factors. The Vaughan Williams classification scheme (Box 23.3) identifies drugs that block sodium channels (class Ia, Ib, and Ic), those that are β-blockers (class II), those that block potassium channels (class III), and those that are nondihydropyridine calcium channel blockers (CCBs) (class IV).








TABLE 23.1 Overview of Selected Antiarrhythmic Agents

































































































































































































Generic (Trade) Name and Dosage


Selected Adverse Effects


Contraindications


Special Considerations


adenosine (Adenocard)


Headache, chest pain, lightheadedness, dizziness, nausea, flushing, dyspnea, blurred vision


2nd-/3rd-degree heart block or sick sinus syndrome in the absence of a pacemaker


Monitor ECG during administration.


Use cautiously in patients with asthma (bronchoconstriction may occur).


Each dose should be immediately followed with a 10-mL saline flush.



Adult: 6 mg IV push over 1-2 s; repeat with 12 mg IV push if sinus rhythm not obtained within 1-2 min after first dose; may repeat 12-mg dose a second time if no response in 1-2 min


amiodarone (Cordarone, Nexterone, Pacerone)


AF


IV: hypotension, bradycardia, heart block, phlebitis


2nd-/3rd-degree heart block or sick sinus syndrome in the absence of a pacemaker


Advise patient to apply sunscreen and to minimize areas of exposure to sun.



Adult IV: 5 mg/kg over 30 min, then continuous infusion of 1 mg/min for 6 h, then 0.5 mg/min; convert to PO when hemodynamically stable and able to take PO medications


Adult PO: 400 mg bid-tid for 1 wk, until patient receives ˜10 g total, then 200 mg PO daily


PO: corneal microdeposits, optic neuritis, nausea, vomiting, anorexia, pulmonary fibrosis, bradycardia, tremor, ataxia, paresthesias, insomnia, constipation, abnormal liver function tests, hypothyroidism, hyperthyroidism, blue-gray discoloration of skin, photosensitivity



Patients should have chest x-ray performed annually. Liver function and thyroid function tests should be performed every 6 mo. Pulmonary function tests and ophthalmologic exam should be performed if patient becomes symptomatic. A chest x-ray, pulmonary function tests, liver function tests, and thyroid function tests should also be performed at baseline. An ophthalmologic exam should be performed at baseline if the patient has significant visual abnormalities.


Monitor for drug interactions (CYP3A4 substrate; CYP3A4, 2C9, 2D6, and P-gp inhibitor).


Pulseless VT/VF



Adult IV: 300 mg IV push/IO; can give additional 150 mg IV push/IO if persistent VT/VF; if stable rhythm achieved, initiate continuous infusion at 1 mg/min for 6 h, then 0.5 mg/min; convert to PO when hemodynamically stable and able to take PO medications (see PO dose under stable VT)


Stable VT (with a pulse)



Adult IV: 150 mg (diluted in 100 mL of D5W or saline) over 10 min; may repeat dose every 10 min, if necessary for breakthrough VT; if stable rhythm achieved, initiate continuous infusion at 1 mg/min for 6 h, then 0.5 mg/min; convert to PO when hemodynamically stable and able to take PO medications


Adult PO: 1,200-1,600 mg/d in 2 or 3 divided doses for 1 wk, until patient receives ˜15 g total, then 300-400 mg PO daily


atropine


Palpitations, tachycardia, dry mouth, dizziness


Acute angle-closure glaucoma, obstructive uropathy, tachycardia, obstructive disease of GI tract


Administer IV over 1 min.


Monitor ECG during administration.



Adult: 0.5 mg IV every 3-5 min; not to exceed 3 mg total dose


digoxin (Lanoxin)


Anorexia, nausea, vomiting, diarrhea, headache, dizziness, vertigo, visual disturbances (yellow-green halos), confusion, hallucinations, arrhythmias, AV conduction disturbances (heart block, AV junctional rhythm, bradycardia)


2nd-/3rd-degree heart block or sick sinus syndrome in the absence of a pacemaker


Teach patient how to take pulse.


Dose adjustment required in renal impairment.


Monitor for drug interactions (P-gp substrate).



Adult LD (IV or PO): 0.25-0.5 mg over 2 min; may give 0.125-0.25 mg q6h for 2 more doses for a total dose of 1 mg or 10-15 mcg/kg


Adult MD: 0.125-0.25 mg IV or PO daily in normal renal function


diltiazem (Cardizem)


Dizziness, headache, edema, heart block, bradycardia, HF exacerbation, hypotension


2nd-/3rd-degree heart block or sick sinus syndrome in the absence of a pacemaker, LVSD


Teach patient how to take pulse and blood pressure.


Monitor for drug interactions (CYP3A4 substrate and inhibitor).



Adult IV: 0.25 mg/kg over 2 min; if ventricular rate remains uncontrolled after 15 min, can repeat with 0.35 mg/kg over 2 min; then initiate continuous infusion of 5-15 mg/h


Adult PO: Start with 30 mg four times daily and ↑ to 180-480 mg/d in divided doses (SR can be given once daily)


disopyramide (Norpace)


Hypotension, HF exacerbation, nausea, anorexia, dry mouth, urinary retention, blurred vision, constipation, TdP


2nd-/3rd-degree heart block or sick sinus syndrome in the absence of a pacemaker, LVSD


Dose adjustment required in renal impairment (CrCl ≤ 40 mL/min; SR form not recommended when CrCl ≤40 mL/min).


Monitor for drug interactions (CYP3A4 substrate).



Adult (<50 kg): IR: 100 mg PO q6h; SR: 200 mg PO q12h


Adult (>50 kg): IR: 150 mg PO q6h; SR: 300 mg PO q12h; may ↑ up to 800 mg/d


dofetilide (Tikosyn)


Chest pain, headache, dizziness, insomnia, nausea, diarrhea, dyspnea, TdP


CrCl < 20 mL/min, QT interval >440 msec, concomitant use of cimetidine, dolute-gravir, hydrochlorothiazide, ketoconazole, megestrol, prochlorperazine, QTc-prolonging drugs, trimethoprim/sulfamethoxazole, or verapamil


Patients must be hospitalized for ≥3 days for therapy initiation.


Dose adjustment required in renal impairment (CrCl ≤60 mL/min).


Dose must also be adjusted based on QT interval.


Monitor for drug interactions.



Adult: 125-500 mcg PO bid


dronedarone (Multaq)


Nausea, vomiting, diarrhea, HF exacerbation, hepatic impairment, pulmonary toxicity, renal impairment/failure


Permanent AF, NYHA class IV HF, NYHA class II-III HF with recent hospitalization for decompensated HF, 2nd-/3rd-degree heart block or sick sinus syndrome in the absence of a pacemaker, heart rate <50 beats/min, concurrent use of potent CYP3A4 inhibitors or QTc-prolonging drugs, QT interval ≥500 msec, PR interval >280 msec, severe hepatic impairment, history of amiodarone-induced hepatic or pulmonary toxicity


Instruct patient to report adverse reactions or any signs/symptoms of HF immediately.


Monitor for drug interactions (CYP3A4 substrate; CYP2D6, CYP3A4, and P-gp inhibitor).



Adult: 400 mg PO bid (with meals)


esmolol (Brevibloc)


Hypotension, wheezing, bronchospasm, heart block, bradycardia, HF exacerbation


2nd-/3rd-degree heart block in the absence of a pacemaker, decompensated HF, sinus bradycardia


Use with caution in patients with LVSD.



Adult: 500 mcg/kg/min IV for 1 min, then maintenance infusion of 50 mcg/kg/min; if inadequate response, rebolus with 500 mcg/kg/min for 1 min and ↑ infusion rate by 50 mcg/kg/min; repeat this process until desired response achieved or maximum infusion rate of 300 mcg/kg/min is reached


flecainide


Dizziness, headache, lightheadedness, syncope, blurred vision or other visual disturbances, dyspnea, HF exacerbation, arrhythmias


2nd-/3rd-degree heart block in the absence of a pacemaker, recent MI, ischemic heart disease, cardiogenic shock, HF


Dose adjustment required in renal impairment (CrCl ≤ 50 mL/min).


Monitor for drug interactions (CYP2D6 substrate).



Adult: 50 mg PO q12h up to a maximum of 300 mg/d


ibutilide (Corvert)


TdP, hypotension, heart block, headache, nausea


Preexisting hypokalemia or hypomagnesemia, QT interval >440 msec


Monitor ECG during administration.


Stop infusion if QT interval prolongation or ventricular arrhythmias occur.


Correct electrolyte abnormalities before administering.



Adult (<60 kg): 0.01 mg/kg IV over 10 min; can repeat with another dose if AF/AFl does not terminate within 10 min after end of initial dose


Adult (≥60 kg): 1 mg IV over 10 min; can repeat with another dose if AF/AFl does not terminate within 10 min after end of initial dose


lidocaine (Xylocaine)


Pulseless VT/VF


Seizures, confusion, stupor, dizziness, bradycardia, respiratory depression, slurred speech, blurred vision, muscle twitching, tinnitus


Hypersensitivity to amide local anesthetics, 2nd-/3rd-degree heart block in the absence of a pacemaker


A lower infusion rate (1-2 mg/min) should be used in older adults or patients with HF or hepatic disease.


Monitor for drug interactions (CYP1A2 and CYP3A4 substrate)



Adult: 1-1.5 mg/kg IV push/IO; may give additional 0.5-0.75 mg/kg IV push/IO every 5-10 min, if persistent VT/VF (maximum cumulative dose = 3 mg/kg); if stable rhythm achieved, initiate continuous infusion of 1-4 mg/min


Stable VT (with a pulse)



Adult: 1-1.5 mg/kg IV push; may give additional 0.5-0.75 mg/kg IV push every 5-10 min, if persistent VT (maximum cumulative dose = 3 mg/kg); if stable rhythm achieved, initiate continuous infusion of 1-4 mg/min


metoprolol (Lopressor)


Bradycardia, HF exacerbation, heart block, bronchospasm, fatigue, ↓ exercise tolerance, dizziness, hypotension


2nd-/3rd-degree heart block in the absence of a pacemaker, decompensated HF, heart rate <45 beats/min


Use IV with caution in patients with LVSD.


Teach patient how to take pulse and blood pressure.


Instruct patient to not discontinue drug abruptly (may lead to hypertensive crises, angina, or MI).


Use metoprolol succinate (SR) when initiating PO therapy in patients with LVSD.



Adult IV: 2.5-5 mg over 2 min; can repeat every 5 min (maximum cumulative dose = 15 mg over 10- to 15-min period)


Adult PO: IR: 25 mg bid; SR: 50 mg daily; may ↑ up to 400 mg/d


mexiletine


Dizziness, drowsiness, paresthesias, blurred vision, tremor, seizures, confusion, arrhythmias, nausea, vomiting


2nd-/3rd-degree heart block in the absence of a pacemaker, cardiogenic shock


Monitor for drug interactions (CYP1A2 and CYP2D6 substrate).



Adult: 200 mg PO q8h; may ↑ up to 400 mg PO q8h


procainamide


Bradycardia, heart block, hypotension, HF exacerbation, TdP


Hypersensitivity to procaine, 2nd-/3rd-degree heart block in the absence of a pacemaker


Monitor ECG during administration.


Stop infusion if QT interval prolongation or ventricular arrhythmias occur.


Use with caution, if at all, in renal impairment.



Adult: 15-18 mg/kg IV over 60 min, then continuous infusion of 1-4 mg/min


propafenone (Rythmol)


Dizziness, drowsiness, HF exacerbation, blurred vision, arrhythmias, heart block, bradycardia, taste disturbances, bronchospasm


2nd-/3rd-degree heart block in the absence of a pacemaker, bradycardia, cardiogenic shock, HF, bronchospastic disorders


Teach patient how to take pulse and blood pressure.


Instruct patient to not discontinue drug abruptly (may lead to hypertensive crises, angina, or MI).



Adult: IR: 150 mg PO q8h (up to a maximum of 300 mg PO q8h); SR: 225 mg PO q12h (up to a maximum of 425 mg PO q12h)


propranolol


Bradycardia, HF exacerbation, heart block, bronchospasm, fatigue, ↓ exercise tolerance, dizziness, hypotension


2nd-/3rd-degree heart block or sick sinus syndrome in the absence of a pacemaker, LVSD


Relatively contraindicated in asthma


Teach patient how to take pulse and blood pressure.


Instruct patient to not discontinue drug abruptly (may lead to hypertensive crises, angina, or MI).



Adult IV: 1 mg over 1 min; may repeat every 5 min up to a total dose of 5 mg


Adult PO: 10-20 mg q6-8h; can ↑ to 80-240 mg/d in 2-4 divided doses


quinidine


TdP, heart block, hypotension, tinnitus, diarrhea, nausea, vomiting, fever, HF exacerbation, thrombocytopenia


Allergy or sensitivity to quinidine or cinchona derivatives, long QT syndrome (may predispose to TdP)


Instruct patient to take drug with food if GI distress occurs.


Monitor for drug interactions (CYP3A4 substrate; CYP2D6 inhibitor).



Adult: Sulfate: 200-400 mg PO q6h, up to a maximum of 600 mg PO q6h


Gluconate: 324 mg PO q8-12h, up to a maximum of 972 mg PO q8-12h


sotalol (Betapace, Betapace AF) AF (Betapace AF)


Bradycardia, heart block, HF exacerbation, TdP, bronchospasm


2nd-/3rd-degree heart block in the absence of a pacemaker, bradycardia, HF, asthma, long QT syndrome (may predispose to TdP)


Patients must be hospitalized for ≥3 days for therapy initiation.


Teach patient how to take pulse and blood pressure.


Dose adjustment required in renal impairment (CrCl ≤ 60 mL/min)


Instruct patient to not discontinue drug abruptly (may lead to hypertensive crises, angina, or MI).



Adult: 80 mg PO bid, up to a maximum of 160 mg PO bid


Ventricular Arrhythmias (Betapace)



Adult: 80 mg PO bid, up to a maximum of 320 mg PO bid


verapamil (Calan)


Constipation, bradycardia, heart block, HF exacerbation, hypotension, dizziness, peripheral edema


2nd-/3rd-degree heart block or sick sinus syndrome in the absence of a pacemaker, LVSD


Encourage patient to ↑ fluid and fiber intake to combat constipation.


Teach patient how to take pulse and blood pressure.


Monitor for drug interactions (CYP3A4 substrate and inhibitor).



Adult IV: 2.5-5 mg over 2 min; if ventricular rate remains uncontrolled after 15-30 min, can double initial dose and administer over 2 min; then initiate continuous infusion of 5-10 mg/h


Adult PO: 240-360 mg/d in 3 divided doses (SR can be given once daily)


AF, atrial fibrillation; AFl, atrial flutter; AV, atrioventricular; bid, twice daily; CrCl; creatinine clearance; CYP, cytochrome P-450, D5W, 5% dextrose in water; ECG, electrocardiogram; GI, gastrointestinal; HF, heart failure; IO, intraosseous; IR, immediate-release; IV, intravenous; LD, loading dose; LVSD, left ventricular systolic dysfunction; MD, maintenance dose; MI, myocardial infarction; NYHA, New York Heart Association; P-gp, P-glycoprotein; PO, oral; SR, sustained release; TdP, torsades de pointes; tid, 3 times daily; VF, ventricular fibrillation; VT, ventricular tachycardia.



Class I AADs

This class of drugs, known as the sodium channel blockers, may be subdivided into classes Ia, Ib, and Ic according to the rate of sodium channel dissociation. These agents vary in the rate at which they bind and then dissociate from the sodium channel receptor. Class Ib AADs bind to and dissociate from the sodium channel receptor quickly (“fast on-off”), while class Ic AADs slowly bind to and dissociate from this receptor (“slow on-off”). The binding kinetics of the class Ia AADs are intermediate between those of the class Ib and Ic agents. In addition, class I AADs possess rate dependence, whereby sodium channel blockade is greatest at fast heart rates (i.e., tachycardia) and least during slower heart rates (i.e., bradycardia) (see Table 23.1).





Class II AADs

β-Blockers are useful in suppressing ventricular arrhythmias. They also are used for treating many supraventricular arrhythmias because of their ability to block receptor sites in the conduction system and subsequently slow AV nodal conduction and the SA nodal rate, which in turn slows the ventricular rate. Furthermore, β-blockers are helpful when used in combination with other AADs or in treating the underlying cause of some arrhythmias (ischemia, catecholamine excess) (see Table 23.1).

β-Blockers decrease automaticity (decrease the slope of phase 4 depolarization in the sinus node and in the Purkinje fibers) and conduction velocity (phase 0) and prolong refractoriness (phase 3). Changes in the ECG caused by β-blockers are a sinus bradycardia, consisting of a normal or slightly prolonged PR interval and occasional shortening of the QT interval. In addition to being negative chronotropic drugs (decrease AV nodal conduction), β-blockers are also negative inotropic agents (decrease cardiac contractility). Both of these properties enable β-blockers to decrease myocardial oxygen consumption, which is useful especially in patients with underlying CAD. Patients with sinus node dysfunction or AV conduction system defects may have significant sinus bradycardia when a β-blocker is initiated.

In general, β-blockers lower the heart rate and blood pressure, decrease myocardial contractility, decrease oxygen consumption in the myocardium, and lower cardiac output. β-Blockers have a diverse range of uses, including paroxysmal supraventricular tachycardia (PSVT), AF, AFl, and arrhythmias caused by catecholamine excess, ischemia, mitral valve prolapse, hypertrophic cardiomyopathy, and MI. β-Blockers also reduce complex ventricular arrhythmias, including VT. The VF threshold is increased with the use of β-blockers in animal models, and β-blockers have been found to decrease VF in patients with acute MI. β-Blockers reduce myocardial ischemia, which may reduce the likelihood of VF. All β-blockers (without intrinsic sympathomimetic activity) are relatively similar in efficacy for the treatment of supraventricular and ventricular arrhythmias. Selection of a particular β-blocker is usually based on the safety profile of the individual agent.

The adverse effects associated with β-blockers depend on their selectivity for β1 or β2 receptors. Bronchospasm may be seen in patients with asthma and chronic obstructive pulmonary disease; this adverse effect is not eliminated by the use of selective β1-blockers since these agents gradually become nonselective as the dose is increased. HF, hypotension, bradycardia, and depression also are common adverse effects of β-blockers. In addition, patients receiving β-blockers often report fatigue and impotence.


Class III AADs

Class III AADs include amiodarone, dofetilide, dronedarone, ibutilide, and sotalol. Ibutilide and dofetilide are used to treat AF and AFl. Amiodarone and sotalol can be used to treat both supraventricular and ventricular arrhythmias. Dronedarone is FDA approved to reduce the risk of hospitalization from cardiovascular (CV) causes in patients in SR with a history of paroxysmal or persistent AF.

Patients receiving class III AADs should be monitored closely for ECG changes such as increased ventricular ectopy and changes in PR interval, QRS duration, and QT interval. Practitioners should avoid using class III AADs concomitantly with other drugs that can prolong the QT interval to minimize the risk of TdP (see Table 23.1).


Amiodarone

Amiodarone is a unique drug in that it possesses electrophysiologic characteristics of all four Vaughan Williams classes of AADs. While amiodarone is primarily a potassium channel blocker (blocks the rapid and slow components of the delayed rectifier potassium current), it also blocks sodium channels, has nonselective β-blocking activity, and has weak calcium channel blocking properties. As a result, amiodarone reduces automaticity (phase 4) and conduction velocity (phase 0) and prolongs refractoriness (phase 3). When administered intravenously, amiodarone’s β-blocking and calcium channel blocking activities are more predominant. Amiodarone has minimal to no negative inotropic effects, which makes it one of the few AADs that can be safely used in patients with HFrEF.

Amiodarone is approved by the FDA for the management of life-threatening recurrent ventricular arrhythmias. However, its off-label use for AF has increased over the past decade not only because of its increased efficacy in maintaining
SR as compared to other AADs but also because of it is one of the few AADs proven to be safe in patients with concomitant SHD. Amiodarone is often given IV for the acute treatment of life-threatening ventricular arrhythmias, such as VT or VF. IV amiodarone can also be used to terminate AF acutely. Even though ICDs now play a primary role in the chronic management of ventricular arrhythmias, amiodarone is still used in patients who refuse or are not candidates for these devices. Also, amiodarone (with a β-blocker) can also be used as adjunctive therapy in these patients if frequent ICD discharges occur (Connolly et al., 2006).

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Nov 11, 2018 | Posted by in PHARMACY | Comments Off on Arrhythmias
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