| Digitek | |||
| Digoxin | |||
| Lanoxicaps | |||
| Lanoxin | |||
Used for digitalization and maintenance therapy.
Used IV for rapid digitalization in emergency situations.
Used principally in the prophylactic management and treatment of CHF and to control the ventricular rate in supraventricular tacchyarrhythmias (e.g., atrial fibrillation or flutter).
Digoxin is the only remaining cardiac glycoside in the US, primarily because it can be administered by various routes, it has an intermediate duration of action, and its pharmacokinetics in patients with or without renal insufficiency have been extensively studied.
Used in conjunction with ACE inhibitors, diuretics, and/or β-adrenergic blocking agents in the management of symptomatic CHF associated with left ventricular systolic dysfunction.
Therapy may be initiated in the early development of heart failure in patients who have started but not yet responded symptomatically to an ACE inhibitor or a β-adrenergic blocking agent; alternatively, digoxin may be withheld until the patient’s symptomatic response to the ACE inhibitor or β-blocker has been defined and then used only in those patients who remain symptomatic while receiving an ACE inhibitor or β-adrenergic blocking agent.
In CHF patients receiving digoxin without an ACE inhibitor or β-blocker, digoxin should not be withdrawn, but appropriate therapy with an ACE inhibitor and/or a β-blocker should be initiated.
Alleviates symptoms and improves clinical status. Beneficial effects are additive with those of ACE inhibitors and/or diuretics.
Increases cardiac output resulting in diuresis and symptomatic relief of right-sided heart failure caused by systemic venous congestion (e.g., peripheral edema) and of left-sided heart failure caused by pulmonary congestion (e.g., dyspnea, orthopnea, and paroxysmal nocturnal dyspnea).
Increases left ventricular ejection fraction and improves symptoms of heart failure (as evidenced by exercise capacity, heart failure-related hospitalizations and emergency care), while having no apparent effect on overall mortality.
Generally, most effective in the management of low-output failure secondary to hypertension, coronary artery or atherosclerotic heart disease, primary myocardial disease, nonobstructive cardiomyopathies, and valvular heart disease.
Not recommended for patients with asymptomatic left ventricular systolic dysfunction (NYHA heart failure functional class I) since only treatment to prevent progression of heart failure is indicated in these patients and digoxin has not been shown to have a demonstrable effect on such progression.
Worsens outflow obstruction as a result of its inotropic effects in patients with idiopathic hypertrophic subaortic stenosis.
Patients with certain disorders involving heart failure associated with preserved left ventricular ejection fraction (e.g., restrictive cardiomyopathy, constrictive pericarditis, amyloid heart disease, acute cor pulmonale) may be particularly susceptible to digoxin toxicity.
Management depends on the clinical situation and the patient’s condition and ventricular rate.
Although considered a drug of choice by some experts for controlling rapid ventricular rate in atrial fibrillation or flutter, digoxin is the least potent and has the slowest onset of action of all available drugs for this use.
Other antiarrhythmics (e.g., β-adrenergic blocking agents, diltiazem, IV verapamil) are first-line therapy for these supraventricular arrhythmias.
Electrical cardioversion is the treatment of choice for conversion of atrial fibrillation or flutter to normal sinus rhythm, although conversion may be attempted with a class IA antiarrhythmic agent (e.g., procainamide).
Because conversion of atrial fibrillation to normal sinus rhythm may be associated with embolism, adequate anticoagulation is recommended before administration of digoxin when atrial fibrillation is of >48 hours’ duration.
In marginal patients, in addition to adequate anticoagulation (e.g., heparin therapy), consultation with a cardiologist and diagnostic procedures to exclude atrial thrombi are indicated to assess the risks and benefits of therapeutic strategies.
Atrial arrhythmias associated with hypermetabolic states are particularly resistant to digoxin treatment, and care must to taken to avoid toxicity.
In patients with atrial arrhythmias and hypothyroidism, the requirement for digoxin is reduced.
Used to slow the heart rate when sinus tachycardia is caused by CHF.
Ventricular or atrial premature complexes caused by CHF may remit when failure is treated with digoxin, but the drug should not be used to treat premature complexes without heart failure.
Generally ineffective and not indicated for sinus tachycardia without heart failure, such as that caused by fever, anemia, blood loss, or hyperthyroidism.
Used for prevention and treatment of paroxysmal supraventricular tachycardias (PSVTs) such as paroxysmal atrial tachycardia, paroxysmal AV junctional rhythm, or paroxysmal atrial fibrillation/flutter.
A first-line therapy for paroxysmal supraventricular tachycardias in patients with impaired left ventricular function.
Not as effective in the treatment of paroxysmal atrial fibrillation as in the treatment of chronic atrial fibrillation
Treatments of choice for paroxysmal atrial tachycardia include measures to increase vagal tone (such as carotid sinus massage, Valsalva maneuver, and/or gagging) or administration of IV adenosine.
May be useful in the prophylactic management and treatment of regular supraventricular (reciprocating) tachycardia associated with Wolff-Parkinson-White (W-P-W) syndrome, but generally not alone since it may enhance conduction via the accessory pathway and, in the presence of atrial fibrillation or flutter, result in extremely rapid ventricular rates and even ventricular fibrillation.
Electrical cardioversion is the usual treatment of PSVT in W-P-W syndrome.
Do not use for the management of chaotic (multifocal) atrial tachycardia.
Generally not used in the treatment of tachyarrhythmias, especially atrial fibrillation or flutter, when anomalous AV conduction is present unless it has been shown that digoxin will not increase ventricular rate via an effect on anomalous AV pathway conduction.
Use in acute MI is controversial.
Mild left ventricular dysfunction after acute MI usually is treated with modest diuresis and afterload and preload reduction (e.g., with parenteral nitroglycerin); institution of ACE inhibitor therapy also may be appropriate.
Equivocal results with digoxin in terms of mortality, and concern about increased mortality associated with long-term milrinone therapy has prompted reexamination of digoxin use.
Can be used selectively during acute MI recovery, but generally reserved for supraventricular arrhythmias and for systolic left ventricular heart failure that is refractory to first-line agents.
Effective for persistent supraventricular tachyarrhythmias in acute MI.
Rapid digitalization can slow a rapid ventricular response and improve left ventricular function in supraventricular tachyarrhythmias, especially atrial fibrillation.
May be particularly useful for slowing a rapid ventricular response in coexisting left ventricular dysfunction.
Value in the treatment of cardiogenic shock has not been established, but occasionally used, especially when pulmonary edema is present.
Used to improve left ventricular function in cardiogenic shock and atrial fibrillation or flutter with rapid ventricular rate.
May be useful, especially in conjunction with a β-adrenergic blocking agent, in the treatment of angina pectoris when cardiomegaly and CHF are present.
Not beneficial alone in the treatment of angina pectoris without cardiomegaly and CHF.
Has been used prophylactically to prevent arrhythmias and CHF in heart disease without failure during certain stressful situations (e.g., surgery, severe illness, pregnancy).
Do not use alone or in combination with other drugs as an anorexiant for the treatment of obesity, since anorexia caused by digoxin is a symptom of toxicity, and potentially fatal arrhythmias may occur.
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