Ventricular rate

The risk of atrial flutter is a 2 1 transmission to the ventricles generating a high ventricular rate. The therapeutic goal is to reduce transmission to 3 1 or 4 1 by administration of either (3-adrenoceptor antagonists, Ca2+ channel blockers or amiodarone. Quinidine must not be used in this arrhythmia, since it accelerates AV-conduction due to its vagolytic effect. 

The cardiotonics are used to treat HF and atrial fibrillation. Atrial fibrillation is a cardiac arrhythmia characterized by rapid contractions of the atrial myocardium, resulting in an irregular and often rapid ventricular rate. See Chapter 40 for more information on various arrhythmias and treatment. 

If ventricular rate is more than 150 bpm, prepare for immediate cardioversion... 

Immediate cardioversion is generally not needed if ventricular rate is <150 bpm... 

Current recommendations are for the addition of digoxin for patients who remain symptomatic despite an optimal HF regimen consisting of an ACE inhibitor or ARB, (3 -blocker, and diuretic. In patients with concomitant atrial fibrillation, digoxin may be added to slow ventricular rate regardless of HF symptomology. 

Compare and contrast the mechanisms of action of drugs used for ventricular rate control, conversion to sinus rhythm and maintenance of sinus rhythm in patients with AF, and explain the importance of anticoagulation for patients with AF. 

The goals of treatment of AF are (1) ventricular rate control with drugs that inhibit AV nodal conduction (2) restoration... 

Antiarrhythmic drug therapy for maintenance of sinus rhythm/reduction in frequency of episodes of AF should be initiated only in patients in whom symptoms persist despite maximal doses of drugs for ventricular rate control. 

The AV node is incapable of conducting 350 to 600 impulses per minute however, it may conduct 100 to 200 impulses per minute, resulting in ventricular rates ranging from 100 to 200 bpm. 

Ventricular Rate Control is achieved by inhibiting the proportion of electrical impulses conducted from the atria to the ventricles through the AV node. Therefore, drugs that are effective for ventricular rate control are those that inhibit AV nodal impulse conduction P-blockers, diltiazem, verapamil, and digoxin (Tables 6-5 and 6-6). Amiodarone also inhibits AV nodal conduction, but is not a preferred drug for ventricular rate control in AF due to its unfavorable adverse-effect profile (Table 6-6). 

A decision strategy for long-term rate control in patients with paroxysmal or permanent AF is presented in Fig. 6-6. In general, while digoxin is effective for ventricular rate control in... 

TABLE 6-5. Drugs for Ventricular Rate Control in Atrial Fibrillation... 

FIGURE 6-5. Decision algorithm for ventricular rate control using intravenous drug therapy for patients presenting with the first detected episode or an episode of persistent atrial fibrillation that is hemody-namically stable. 

FIGURE 6-6. Decision algorithm for long-term ventricular rate control with oral drug therapy for patients with paroxysmal or permanent atrial fibrillation, bpm, beats per minute CCB, calcium channel blocker (diltiazem or verapamil) HF, heart failure LV, left ventricular function LVEF, left ventricular ejection fraction. (Algorithm adapted with permission from Tisdale JE, Moser LR. Tachyarrhythmias. In Mueller BA, Bertch KE, Dunsworth TS, et al. (eds.) Pharmacotherapy Self-Assessment Program, 4th ed. Kansas City American College of Clinical Pharmacy 2001 ... 

In recent years, numerous studies have been performed to determine whether drug therapy for maintenance of sinus rhythm is preferred to drug therapy for ventricular rate control.28-31 In these studies, patients have been assigned randomly to receive therapy either with drugs for rate control or with drugs for rhythm control (Table 6-8). These studies have found... 

Monitor the patient to determine whether the goal of ventricular rate control is met heart rate less than 100 bpm or decrease in heart rate of 20% from the pretreatment value. 

Furthermore, pH determination has been used in other clinical research, both alone and in combination with other measurements. This research includes studies into the relationship between extracellular and intracellular pH in an ischemic heart [6, 7], the pH of airway lining fluid in respiratory disease [8], the study of pH as a marker for pyloric stenosis [9], malnutrition in alkalotic peritoneal dialysis patients [10], pH modulation of heterosexual HIV transmission [11, 12], and wound prevention and treatment [13], In addition, pH changes due to blood acidosis have been used to trigger and pace the ventricular rate of an implanted cardiac pacemaker [14], Research using pH measurements... 

If patients are hemodynamicaUy stable, the focus should be directed toward control of ventricular rate. Drugs that slow conduction and increase refractoriness in the AV node should be used as initial therapy. In patients with normal LV function (left ventricular ejection fraction >40%), IV j3-blockers (propranolol, metoprolol, esmolol), diltiazem, or verapamil is recommended. If a high adrenergic state is the precipitating factor, IV /J-blockers can be highly effective and should be considered first. In patients with left ventricular ejection fraction <40%, IV diltiazem and verapamil... 

Indications. Verapamil is used as an antiarrhythmic drug in supraventricular tachyarrhythmias. In atrial flutter or fibrillation, it is effective in reducing ventricular rate by virtue of inhibiting AV-conduction. Verapamil is also employed in the prophylaxis of angina pectoris attacks (p. 308) and the treatment of hypertension (p. 312). Adverse effects Because of verapamil s effects on the sinus node, a drop in blood pressure fails to evoke a reflex tachycardia Heart rate hardly changes bradycardia may even develop. AV-block and myocardial insufficiency can occur. Patients frequently complain of constipation. 

Atrial flutter or fibrillation. An excessive ventricular rate can be decreased by verapamil (p. 122) or cardiac glycosides (p. 130). These drugs inhibit impulse propagation through the AV node, so that fewer impulses reach the ventricles. 

Atrial flutter Digitalis slows the heart normal sinus rhythm may appear. Often, flutter is converted to atrial fibrillation with a slow ventricular rate. 

Atrial fibrillation Peak digoxin body stores larger than the 8 to 12 mcg/kg required for most patients with heart failure and normal sinus rhythm have been used for control of ventricular rate in patients with atrial fibrillation. Titrate doses of digoxin used for the treatment of chronic atrial fibrillation to the minimum dose that achieves the desired ventricular rate control without causing undesirable side effects. Data are not available to establish the appropriate resting or exercise target rates that should be achieved. 

Atrial flutter or fibrillation Reversion to sinus rhythm may be preceded by a progressive reduction in degree of AV block to a 1 1 ratio, which results in an extremely rapid ventricular rate. Prior to use in atrial flutter, pretreat with digitalis preparation. 

Atrial tachyarrhythmias Digitalize patients with atrial flutter or fibrillation prior to administration to ensure that enhancement of AV conduction does not increase ventricular rate beyond acceptable limits. 

Heart block If first-degree heart block develops, reduce dosage. If the block persists, drug continuation must depend upon the benefit compared with the risk of higher degrees of heart block. Development of second- or third-degree AV block or unifascicular, bifascicular, or trifascicular block requires discontinuation of therapy, unless ventricular rate is controlled by a ventricular pacemaker. 

Acceleration of ventricular rate - Acceleration of ventricular rate may occur when administered to patients with atrial flutter or fibrillation. 

As with other Class I agents, patients treated with flecainide for atrial flutter have been reported with 1 1 atrioventricular conduction due to slowing the atrial rate. A paradoxical increase in the ventricular rate also may occur in patients with atrial fibrillation who receive flecainide. Concomitant negative chronotropic therapy such as digoxin or beta-blockers may lower the risk of this complication. 

If second-or third-degree AV block, or right bundle branch block associated with a left hemiblock occurs, discontinue therapy unless a ventricular pacemaker is in place to ensure an adequate ventricular rate. 

Premature ventricular contractions (PVCs) During conversion or marked reduction in ventricular rate, benign complexes of unusual appearance (sometimes resembling PVCs) may occur after IV verapamil. 

Atrial fibrillation is commonly associated with heart failure, and the prevalence of atrial fibrillation is related to the severity of heart failure, with less than 5% affected with very mild heart failure to nearly 50% affected with advanced heart failure [66]. Heart failure and atrial fibrillation are both common cardiovascular disorders and share the same demographic risk factors, including age, history of hypertension, prior myocardial infarction, and valvular heart disease [67, 68]. Further, the incidence of heart failure increases dramatically after the diagnosis of atrial fibrillation [69]. Progression of LV dysfunction can clearly be associated with rapid ventricular rates [70-76]. Conversely, conversion to normal sinus rhythm or control of ventricular response in atrial fibrillation can improve LV function [71-74, 77]. Accordingly, rate control becomes very important in patients with heart failure and dilated cardiomyopathy, and likely even more so when ischemia from rapid rates complicate the patient s course. 

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