Digoxin: Difference between revisions
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==Mechanism of Action== | ==Mechanism of Action== | ||
All of digoxin’s actions are mediated through its effects on Na-K ATPase. This enzyme, the “sodium pump,” is responsible for maintaining the intracellular milieu throughout the body by moving sodium ions out of and potassium ions into cells. By inhibiting Na-K ATPase, digoxin | |||
*causes increased availability of intracellular calcium in the myocardium and conduction system, with consequent increased inotropy, increased automaticity, and reduced conduction velocity | |||
*indirectly causes parasympathetic stimulation of the autonomic nervous system, with consequent effects on the [[sinoatrial node|sino-atrial]] (SA) and [[atrioventricular nodes|atrioventricular (AV) nodes]] | |||
*reduces [[catecholamine ]]reuptake at nerve terminals, rendering blood vessels more sensitive to endogenous or exogenous catecholamines | |||
*increases [[baroreceptor ]]sensitization, with consequent increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increment in mean arterial pressure | |||
*increases (at higher concentrations) [[sympathetic ]]outflow from the central nervous system (CNS) to both cardiac and peripheral sympathetic nerves | |||
allows (at higher concentrations) progressive efflux of intracellular [[potassium]], with consequent increase in serum potassium levels. | |||
The cardiologic consequences of these direct and indirect effects are an increase in the force and velocity of myocardial systolic contraction (positive inotropic action), a slowing of the heart rate (negative chronotropic effect), decreased conduction velocity through the AV node, and a decrease in the degree of activation of the sympathetic nervous system and renin-angiotensin system (neurohormonal deactivating effect). | |||
==References== | ==References== | ||
Revision as of 16:01, 28 February 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Abdurahman Khalil, M.D. [2]
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Overview
Digoxin INN is a purified cardiac glycoside similar to Digitoxin extracted from the foxglove plant, Digitalis lanata,[1] which was discovered by William Withering. Its corresponding aglycone is digoxigenin, and its acetyl derivative is acetyldigoxin. Digoxin is widely used in the treatment of various heart conditions, namely atrial fibrillation, atrial flutter and sometimes heart failure that cannot be controlled by other medication.
Category
Cardiac glycosides.
US Brand Names
LANOXIN®, DIGOXIN®, DIGOX®.
FDA Package Insert
DIGOXIN injection®
| Indications and Usage | Dosage and Administration | Dosage Forms and Strengths | Contraindications | Warnings and Precautions | Adverse Reactions | Drug Interactions | Use in Specific Populations | Overdosage | Description | Clinical Pharmacology | Nonclinical Toxicology | Clinical Studies | How Supplied/Storage and Handling | Patient Counseling Information | Labels and Packages
DIGOXIN tablet®
| Indications and Usage | Dosage and Administration | Dosage Forms and Strengths | Contraindications | Warnings and Precautions | Adverse Reactions | Drug Interactions | Use in Specific Populations | Overdosage | Description | Clinical Pharmacology | Nonclinical Toxicology | Clinical Studies | How Supplied/Storage and Handling | Patient Counseling Information | Labels and Packages
Mechanism of Action
All of digoxin’s actions are mediated through its effects on Na-K ATPase. This enzyme, the “sodium pump,” is responsible for maintaining the intracellular milieu throughout the body by moving sodium ions out of and potassium ions into cells. By inhibiting Na-K ATPase, digoxin
- causes increased availability of intracellular calcium in the myocardium and conduction system, with consequent increased inotropy, increased automaticity, and reduced conduction velocity
- indirectly causes parasympathetic stimulation of the autonomic nervous system, with consequent effects on the sino-atrial (SA) and atrioventricular (AV) nodes
- reduces catecholamine reuptake at nerve terminals, rendering blood vessels more sensitive to endogenous or exogenous catecholamines
- increases baroreceptor sensitization, with consequent increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increment in mean arterial pressure
- increases (at higher concentrations) sympathetic outflow from the central nervous system (CNS) to both cardiac and peripheral sympathetic nerves
allows (at higher concentrations) progressive efflux of intracellular potassium, with consequent increase in serum potassium levels.
The cardiologic consequences of these direct and indirect effects are an increase in the force and velocity of myocardial systolic contraction (positive inotropic action), a slowing of the heart rate (negative chronotropic effect), decreased conduction velocity through the AV node, and a decrease in the degree of activation of the sympathetic nervous system and renin-angiotensin system (neurohormonal deactivating effect).
References
- ↑ Hollman A (1996). "Digoxin comes from Digitalis lanata". British Medical Journal. 312 (7035): 912.
http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=58f45aba-ff6f-43cc-bb88-be40a9f7beda
http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=41c16cff-b03e-405e-a617-d6f45d3ce2bd