The monitoring described above may suggest increases or decreases in digoxin doses.Additional monitoring, and in some cases anticipatory dose adjustment, may be indicated around the time of various changes in the patient’s internal milieu, includingnormal development through childhood; concomitant drug use should be considered when adjusting the estimated digoxin dose (see PRECAUTIONS: Drug Interactions);new co-administration of an antibiotic, especially if the patient had required high doses of digoxin in order to achieve modest serum concentrations, raising the suspicion that a substantial fraction of administered digoxin was being destroyed by colonic bacteria; andchanges in renal function (see Table 3 above).
Digoxin Oral Solution, USP is indicated for the treatment of mild to moderate heart failure.
Digoxin increases left ventricular ejection fraction and improves heart failure symptoms as evidenced by exercise capacity and heart failure-related hospitalizations and emergency care, while having no effect on mortality.Where possible, digoxin should be used with a diuretic and an angiotensin-converting enzyme inhibitor, but an optimal order for starting these three drugs cannot be specified.Digoxin increases myocardial contractility in children with congestive heart failure.
Allergy to digoxin is rare.
In such patients (who may or may not have similar reactions to other forms of digitalis), the use of digoxin is contraindicated.Digitalis glycosides are contraindicated in ventricular fibrillation.
Patients with Wolff-Parkinson-White syndrome who develop atrial fibrillation are at high risk of ventricular fibrillation.
Treatment of these patients with digoxin leads to greater slowing of conduction in the atrioventricular node than in accessory pathways, and the risks of rapid ventricular response leading to ventricular fibrillation are thereby increased.By slowing conduction in nodal tissue, digoxin administration can exacerbate Sick Sinus Syndrome and can cause a greater degree of atrioventricular block.
Some signs and symptoms (anorexia, nausea, vomiting, and certain arrhythmias) can equally result from digoxin toxicity as from congestive heart failure.
Misidentification of their etiology might lead the clinician to continue or increase digoxin dosing, when dosing should actually be suspended.
When the etiology of these signs and symptoms is not obvious, measurement of serum digoxin levels may be helpful.In patients with hypertrophic cardiomyopathy (formerly called idiopathic hypertrophic subaortic stenosis), the positive inotropic effect of digoxin leads to an increased subvalvular outflow gradient.
Digoxin is rarely beneficial in patients with this condition.Chronic constrictive pericarditis is not generally associated with any inotropic defect, so heart failure of this etiology is unlikely to respond to treatment with digoxin.
By slowing the resting heart rate, digoxin may actually decrease cardiac output in these patients.Patients with amyloid heart disease may be more susceptible to toxicity from digoxin.Digoxin is of limited value in patients with restrictive cardiomyopathies, although it has been used for rate control in the subgroup of patients with atrial fibrillation.