DIGOXIN

Therapeutic Class: Drug for heart failure

Pharmacologic Class: Cardiac glycoside

ACTIONS AND USES: The primary benefit of digoxin is its ability to increase the contractility or strength of myocardial contraction, a positive inotropic action. Digoxin accomplishes this by inhibiting Na⁺-K⁺ ATPase, the critical enzyme responsible for pumping sodium ions out of the myocardial cell in exchange for potassium ions. As sodium accumulates, calcium ions are released from their storage areas in the cell. The release of calcium ions produces a more forceful contraction of the myocardial fibers. By increasing myocardial contractility, digoxin directly increases cardiac output, thus alleviating symptoms of HF and improving exercise tolerance.

The improved cardiac output results in increased urine production and a desirable reduction in blood volume, relieving distressing symptoms of pulmonary congestion and peripheral edema. In addition to its positive inotropic effect, digoxin affects impulse conduction in the heart. Digoxin has the ability to suppress the sinoatrial (SA) node and slow electrical conduction through the atrioventricular (AV) node. Because of these actions, digoxin is sometimes used to treat dysrhythmias.

ADMINISTRATION ALERTS: Take the apical pulse for 1 full minute, noting rate, rhythm, and quality before administering. If the pulse is below the parameter established by the health care provider (usually 60 beats per minute), withhold the dose and notify the provider. Check for recent serum digoxin level results before administering. If the level is higher than the parameter established by the health care provider (usually 1.8 ng/mL), withhold the dose and notify the provider. Use with caution in geriatric and pediatric patients because these populations may have inadequate renal and hepatic metabolic enzymes. Pregnancy category A.

ADVERSE EFFECTS: The most dangerous adverse effect of digoxin is its ability to create dysrhythmias, particularly in patients who have hypokalemia or impaired renal function. Because diuretics can cause hypokalemia and are often used to treat HF, concurrent use of digoxin and diuretics must be carefully monitored. Other adverse effects of digoxin therapy include nausea, vomiting, fatigue, anorexia, and visual disturbances such as seeing halos, a yellow-green tinge, or blurring. Periodic serum drug levels should be obtained to determine whether the digoxin concentration is within the therapeutic range.

CONTRAINDICATIONS: Patients with AV block or ventricular dysrhythmias unrelated to HF should not receive digoxin because the drug may worsen these conditions. Digoxin should be administered with caution to older adults because these patients experience a higher incidence of adverse effects. Patients with renal impairment should receive lower doses of digoxin, because the drug is excreted by this route. The drug should be used with caution in patients with MI, cor pulmonale, or hypothyroidism. 

INTERACTIONS: Drug–Drug: Digoxin interacts with many drugs. Concurrent use of digoxin with diuretics can cause hypokalemia and increase the risk of dysrhythmias. Use with ACE inhibitors, spironolactone, or potassium supplements can lead to hyperkalemia and reduce the therapeutic action of digoxin. Administration of digoxin with other positive inotropic drugs can cause additive effects on heart contractility. Concurrent use with beta blockers may result in additive bradycardia. Antacids and cholesterol-lowering drugs can decrease the absorption of digoxin. If calcium is administered IV together with digoxin, it can increase the risk of dysrhythmias. Quinidine, verapamil, amiodarone, and alprazolam will decrease the distribution and excretion of digoxin, thus increasing the risk of digoxin toxicity. 

RELATED;

1.  CONGESTIVE CARDIAC FAILURE

2.  HYPERTENTION

3.  PHARMACOLOGY AND THERAPEUTICS

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