Digoxin: A cardiotonic glycoside obtained mainly from Digitalis lanata; it consists of three sugars and the aglycone DIGOXIGENIN. Digoxin has positive inotropic and negative chronotropic activity. It is used to control ventricular rate in ATRIAL FIBRILLATION and in the management of congestive heart failure with atrial fibrillation. Its use in congestive heart failure and sinus rhythm is less certain. The margin between toxic and therapeutic doses is small. (From Martindale, The Extra Pharmacopoeia, 30th ed, p666)Digitoxin: A cardiac glycoside sometimes used in place of DIGOXIN. It has a longer half-life than digoxin; toxic effects, which are similar to those of digoxin, are longer lasting. (From Martindale, The Extra Pharmacopoeia, 30th ed, p665)Cardenolides: C(23)-steroids with methyl groups at C-10 and C-13 and a five-membered lactone at C-17. They are aglycone constituents of CARDIAC GLYCOSIDES and must have at least one double bond in the molecule. The class includes cardadienolides and cardatrienolides. Members include DIGITOXIN and DIGOXIN and their derivatives and the STROPHANTHINS.Cardiotonic Agents: Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE).Cardiac Glycosides: Cyclopentanophenanthrenes with a 5- or 6-membered lactone ring attached at the 17-position and SUGARS attached at the 3-position. Plants they come from have long been used in congestive heart failure. They increase the force of cardiac contraction without significantly affecting other parameters, but are very toxic at larger doses. Their mechanism of action usually involves inhibition of the NA(+)-K(+)-EXCHANGING ATPASE and they are often used in cell biological studies for that purpose.Medigoxin: A semisynthetic digitalis glycoside with the general properties of DIGOXIN but more rapid onset of action. Its cardiotonic action is prolonged by its demethylation to DIGOXIN in the liver. It has been used in the treatment of congestive heart failure (HEART FAILURE).Eleutherococcus: A plant genus in the family ARALIACEAE, order Apiales, subclass Rosidae. It is best known as an adaptogen and a substitute for PANAX GINSENG.Nerium: A plant genus of the family APOCYNACEAE. It is a very poisonous plant that contains cardioactive agents.Digitalis Glycosides: Glycosides from plants of the genus DIGITALIS. Some of these are useful as cardiotonic and anti-arrhythmia agents. Included also are semi-synthetic derivatives of the naturally occurring glycosides. The term has sometimes been used more broadly to include all CARDIAC GLYCOSIDES, but here is restricted to those related to Digitalis.Anti-Arrhythmia Agents: Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade.Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug.Ouabain: A cardioactive glycoside consisting of rhamnose and ouabagenin, obtained from the seeds of Strophanthus gratus and other plants of the Apocynaceae; used like DIGITALIS. It is commonly used in cell biological studies as an inhibitor of the NA(+)-K(+)-EXCHANGING ATPASE.Radioimmunoassay: Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation.P-Glycoprotein: A 170-kDa transmembrane glycoprotein from the superfamily of ATP-BINDING CASSETTE TRANSPORTERS. It serves as an ATP-dependent efflux pump for a variety of chemicals, including many ANTINEOPLASTIC AGENTS. Overexpression of this glycoprotein is associated with multidrug resistance (see DRUG RESISTANCE, MULTIPLE).Magnesium Sulfate: A small colorless crystal used as an anticonvulsant, a cathartic, and an electrolyte replenisher in the treatment of pre-eclampsia and eclampsia. It causes direct inhibition of action potentials in myometrial muscle cells. Excitation and contraction are uncoupled, which decreases the frequency and force of contractions. (From AMA Drug Evaluations Annual, 1992, p1083)Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Digitalis: A genus of toxic herbaceous Eurasian plants of the Plantaginaceae which yield cardiotonic DIGITALIS GLYCOSIDES. The most useful species are Digitalis lanata and D. purpurea.Poisoning: A condition or physical state produced by the ingestion, injection, inhalation of or exposure to a deleterious agent.Charcoal: An amorphous form of carbon prepared from the incomplete combustion of animal or vegetable matter, e.g., wood. The activated form of charcoal is used in the treatment of poisoning. (Grant & Hackh's Chemical Dictionary, 5th ed)Magnesium Deficiency: A nutritional condition produced by a deficiency of magnesium in the diet, characterized by anorexia, nausea, vomiting, lethargy, and weakness. Symptoms are paresthesias, muscle cramps, irritability, decreased attention span, and mental confusion, possibly requiring months to appear. Deficiency of body magnesium can exist even when serum values are normal. In addition, magnesium deficiency may be organ-selective, since certain tissues become deficient before others. (Harrison's Principles of Internal Medicine, 12th ed, p1936)Heart Failure: A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.Heart: The hollow, muscular organ that maintains the circulation of the blood.Heart Rate: The number of times the HEART VENTRICLES contract per unit of time, usually per minute.Internet: A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.Developing Countries: Countries in the process of change with economic growth, that is, an increase in production, per capita consumption, and income. The process of economic growth involves better utilization of natural and human resources, which results in a change in the social, political, and economic structures.Software: Sequential operating programs and data which instruct the functioning of a digital computer.Medication Errors: Errors in prescribing, dispensing, or administering medication with the result that the patient fails to receive the correct drug or the indicated proper drug dosage.Waiting Lists: Prospective patient listings for appointments or treatments.Medication Adherence: Voluntary cooperation of the patient in taking drugs or medicine as prescribed. This includes timing, dosage, and frequency.Developed Countries: Countries that have reached a level of economic achievement through an increase of production, per capita income and consumption, and utilization of natural and human resources.Glycosides: Any compound that contains a constituent sugar, in which the hydroxyl group attached to the first carbon is substituted by an alcoholic, phenolic, or other group. They are named specifically for the sugar contained, such as glucoside (glucose), pentoside (pentose), fructoside (fructose), etc. Upon hydrolysis, a sugar and nonsugar component (aglycone) are formed. (From Dorland, 28th ed; From Miall's Dictionary of Chemistry, 5th ed)Tablets: Solid dosage forms, of varying weight, size, and shape, which may be molded or compressed, and which contain a medicinal substance in pure or diluted form. (Dorland, 28th ed)Half-Life: The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity.Metabolic Clearance Rate: Volume of biological fluid completely cleared of drug metabolites as measured in unit time. Elimination occurs as a result of metabolic processes in the kidney, liver, saliva, sweat, intestine, heart, brain, or other site.Drugs, Generic: Drugs whose drug name is not protected by a trademark. They may be manufactured by several companies.Atrial Fibrillation: Abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.Administration, Oral: The giving of drugs, chemicals, or other substances by mouth.Pharmacists: Those persons legally qualified by education and training to engage in the practice of pharmacy.Solutions: The homogeneous mixtures formed by the mixing of a solid, liquid, or gaseous substance (solute) with a liquid (the solvent), from which the dissolved substances can be recovered by physical processes. (From Grant & Hackh's Chemical Dictionary, 5th ed)Injections: Introduction of substances into the body using a needle and syringe.Neomycin: Antibiotic complex produced by Streptomyces fradiae. It is composed of neomycins A, B, and C. It acts by inhibiting translation during protein synthesis.Paromomycin: An oligosaccharide antibiotic produced by various STREPTOMYCES.Propafenone: An antiarrhythmia agent that is particularly effective in ventricular arrhythmias. It also has weak beta-blocking activity.Framycetin: A component of NEOMYCIN that is produced by Streptomyces fradiae. On hydrolysis it yields neamine and neobiosamine B. (From Merck Index, 11th ed)Amiodarone: An antianginal and class III antiarrhythmic drug. It increases the duration of ventricular and atrial muscle action by inhibiting POTASSIUM CHANNELS and VOLTAGE-GATED SODIUM CHANNELS. There is a resulting decrease in heart rate and in vascular resistance.Emergencies: Situations or conditions requiring immediate intervention to avoid serious adverse results.Emergency Treatment: First aid or other immediate intervention for accidents or medical conditions requiring immediate care and treatment before definitive medical and surgical management can be procured.Emergency Medicine: The branch of medicine concerned with the evaluation and initial treatment of urgent and emergent medical problems, such as those caused by accidents, trauma, sudden illness, poisoning, or disasters. Emergency medical care can be provided at the hospital or at sites outside the medical facility.Emergency Service, Hospital: Hospital department responsible for the administration and provision of immediate medical or surgical care to the emergency patient.Emergency Medical Services: Services specifically designed, staffed, and equipped for the emergency care of patients.Hospital Rapid Response Team: Multidisciplinary team most frequently consisting of INTENSIVE CARE UNIT trained personnel who are available 24 hours per day, 7 days per week for evaluation of patients who develop signs or symptoms of severe clinical deterioration.

Myocardial uptake of digoxin in chronically digitalized dogs. (1/952)

1 The time course of myocardial uptake of digoxin, increase in contractility and changes in myocardial potassium concentration was studied for 90 min following an intravenous digoxin dose to long-term digitalized dogs. 2 Nineteen dogs were investigated by the use of a biopsy technique which allowed sampling before and after administration of digoxin. 3 Ten minutes after administration of digoxin the myocardial concentration increased from 60 to 306 nmol/kg tissue, the myocardial concentration of digoxin was significantly lower (250 nmol/kg tissue) after 30 min and then increased again. 4 The transmural myocardial distribution of digoxin was uniform before and 90 min after administration of digoxin in long-term digitalized dogs but at 10 min after administration, both the subepicardial and the subendocardial concentration of digoxin were significantly lower than that of the mesocardial layer. 5 During the first 10 min the dp/dtmax increased to 135% of the control level. The increase remained unchanged during the rest of the study. 6 Myocardial potassium decreased throughout the study. 7 The M-configuration of the myocardial uptake curve and the non-uniformity of myocardial distribution of digoxin observed at 10 min after administrating digoxin to long-term digitalized dogs indicate that the distribution of myocardial blood flow may be changed during chronic digitalization.  (+info)

Fetal tachycardias: management and outcome of 127 consecutive cases. (2/952)

OBJECTIVE: To review the management and outcome of fetal tachycardia, and to determine the problems encountered with various treatment protocols. STUDY DESIGN: Retrospective analysis. SUBJECTS: 127 consecutive fetuses with a tachycardia presenting between 1980 and 1996 to a single tertiary centre for fetal cardiology. The median gestational age at presentation was 32 weeks (range 18 to 42). RESULTS: 105 fetuses had a supraventricular tachycardia and 22 had atrial flutter. Overall, 52 fetuses were hydropic and 75 non-hydropic. Prenatal control of the tachycardia was achieved in 83% of treated non-hydropic fetuses compared with 66% of the treated hydropic fetuses. Digoxin monotherapy converted most (62%) of the treated non-hydropic fetuses, and 96% survived through the neonatal period. First line drug treatment for hydropic fetuses was more diverse, including digoxin (n = 5), digoxin plus verapamil (n = 14), and flecainide (n = 27). The response rates to these drugs were 20%, 57%, and 59%, respectively, confirming that digoxin monotherapy is a poor choice for the hydropic fetus. Response to flecainide was faster than to the other drugs. Direct fetal treatment was used in four fetuses, of whom two survived. Overall, 73% (n = 38) of the hydropic fetuses survived. Postnatally, 4% of the non-hydropic group had ECG evidence of pre-excitation, compared with 16% of the hydropic group; 57% of non-hydropic fetuses were treated with long term anti-arrhythmics compared with 79% of hydropic fetuses. CONCLUSIONS: Non-hydropic fetuses with tachycardias have a very good prognosis with transplacental treatment. Most arrhythmias associated with fetal hydrops can be controlled with transplacental treatment, but the mortality in this group is 27%. At present, there is no ideal treatment protocol for these fetuses and a large prospective multicentre trial is required to optimise treatment of both hydropic and non-hydropic fetuses.  (+info)

Ventriculo-atrial time interval measured on M mode echocardiography: a determining element in diagnosis, treatment, and prognosis of fetal supraventricular tachycardia. (3/952)

OBJECTIVE: To determine whether M mode echocardiography can differentiate fetal supraventricular tachycardia according to the ventriculo-atrial (VA) time interval, and if the resulting division into short and long VA intervals holds any relation with clinical presentation, management, and fetal outcome. DESIGN: Retrospective case series. SUBJECTS: 23 fetuses with supraventricular tachycardia. MAIN OUTCOME MEASURES: A systematic review of the M mode echocardiograms (for VA and atrioventricular (AV) interval measurements), clinical profile, and final outcome. RESULTS: 19 fetuses (82.6%) had supraventricular tachycardia of the short VA type (mean (SD) VA/AV ratio 0.34 (0.16); heart rate 231 (29) beats/min). Tachycardia was sustained in six and intermittent in 13. Hydrops was present in three (15.7%). Digoxin, the first drug given in 14, failed to control tachycardia in five. Three of these then received sotalol and converted to sinus rhythm. All fetuses of this group survived. Postnatally, supraventricular tachycardia recurred in three, two having Wolff-Parkinson-White syndrome. Four fetuses (17.4%) had long VA tachycardia (VA/AV ratio 3.89 (0.82); heart rate 226 (10) beats/min). Initial treatment with digoxin was ineffective in all, but sotalol was effective in two. Heart failure caused fetal death in one and premature delivery in one. All three surviving fetuses had recurrences of supraventricular tachycardia after birth: two had the permanent form of junctional reciprocating tachycardia and one had atrial ectopic tachycardia. CONCLUSIONS: Careful measurement of ventriculo-atrial intervals on fetal M mode echocardiography can be used to distinguish short from long VA supraventricular tachycardia and may be helpful in optimising management. Digoxin, when indicated, may remain the drug of choice in the short VA type but appears ineffective in the long VA type.  (+info)

Common variant in AMPD1 gene predicts improved clinical outcome in patients with heart failure. (4/952)

BACKGROUND: This study was undertaken to identify gene(s) that may be associated with improved clinical outcome in patients with congestive heart failure (CHF). The adenosine monophosphate deaminase locus (AMPD1) was selected for study. We hypothesized that inheritance of the mutant AMPD1 allele is associated with increased probability of survival without cardiac transplantation in patients with CHF. METHODS AND RESULTS: AMPD1 genotype was determined in 132 patients with advanced CHF and 91 control reference subjects by use of a polymerase chain reaction-based, allele-specific oligonucleotide detection assay. In patients with CHF, those heterozygous (n=20) or homozygous (n=1) for the mutant AMPD1 allele (AMPD1 +/- or -/-, respectively) experienced a significantly longer duration of heart failure symptoms before referral for transplantation evaluation than CHF patients homozygous for the wild-type allele (AMPD1 +/+; n=111; 7.6+/-6.5 versus 3.2+/-3.6 years; P<0.001). The OR of surviving without cardiac transplantation >/=5 years after initial hospitalization for CHF symptoms was 8.6 times greater (95% CI: 3.05, 23.87) in those patients carrying >/=1 mutant AMPD1 allele than in those carrying 2 wild-type AMPD1 +/+ alleles. CONCLUSIONS: After the onset of CHF symptoms, the mutant AMPD1 allele is associated with prolonged probability of survival without cardiac transplantation. The mechanism by which the presence of the mutant AMPD1 allele may modify the clinical phenotype of heart failure remains to be determined.  (+info)

Penetration of digoxin into cerebrospinal fluid. (5/952)

The concentration of digoxin in the cerebrospinal fluid (CSF) of ten patients receiving conventional oral doses of this cardiac glycoside has been measured by a radioimmunoassay technique. Digoxin was undetected in eight patients and barely detectable in two, suggesting the presence of a significant blood-CSF barrier for digoxin. The implication of these findings is discussed.  (+info)

Clinical practice guidelines for heart failure. (6/952)

Development of guidelines can be a difficult process; each organization or institution must establish the rules and criteria for including specific therapies and the level of complexity needed. Specific outcomes must be incorporated, including maintenance of comfort and functionality, freedom from hospitalization, and survival. In existing guidelines for the management of heart failure, angiotensin-converting enzyme (ACE) inhibitor therapy is clearly the gold standard. However, there is still a high mortality with ACE inhibitor therapy; the key may be choosing the right patients. Current guidelines reflect the uncertainty regarding digoxin before the Digitalis Investigation Group (DIG) trial; obviously, these guidelines should be revisited. Clinical practice guidelines for the management of heart failure need to be revised to include a better consensus on beta-blockade, the new data on digoxin, emerging data on angiotensin II receptor antagonists, and current thinking on anticoagulant therapy.  (+info)

Cost of heart failure to the healthcare system. (7/952)

From an economic, mortality, and functional standpoint, heart failure is clearly a disease that needs to be targeted. We can develop a model for heart failure to determine the impact that specific management strategies will have on the overall cost to the system, which by itself can tell us some interesting things because we're currently spending twice as much on transplantation as on digoxin therapy. We can then use this model to assess the impact of different strategies, such as greater use of angiotensin-converting enzyme (ACE) inhibitors or digoxin therapy.  (+info)

The effect of steady-state ropinirole on plasma concentrations of digoxin in patients with Parkinson's disease. (8/952)

AIMS: The aim of this single-blind study was to assess the effect of ropinirole, a novel treatment for Parkinson's disease, on the steady-state pharmacokinetics and safety of digoxin in 10 patients with Parkinson's disease. METHODS: There were three parts to the study: digoxin once daily plus placebo three times daily for 1 week; digoxin once daily plus ropinirole three times daily for 6 weeks; and digoxin once daily plus placebo three times daily for 1 week. Serial blood samples were collected over 24 h at the end of each part of the study for pharmacokinetic assessment. Pre-dose blood samples were collected on specific days throughout the study to assess the attainment of steady-state plasma levels of digoxin. The primary endpoints were AUC(0, tau) and Cmax for digoxin. RESULTS: There was a mean decrease of 10% in digoxin AUC (0, tau) (90% CI: 0.79, 1.01) and a 25% decrease in digoxin Cmax (90% CI: 0.58, 0.97) when ropinirole was co-administered, compared with digoxin alone Cmin plasma values for digoxin, however, were fairly constant throughout the study (point estimates 0.99, 95% CI: 0.85, 1.15). Changes in trough levels of digoxin are believed to be the most reliable way of assessing steady-state concentrations of digoxin, and therefore the clinical significance of an interaction. Changes in Cmax are too readily influenced by other factors. CONCLUSIONS: These results therefore indicate that on pharmacokinetic grounds no dose adjustment is necessary for digoxin co-administered with ropinirole.  (+info)

  • Digoxin inhibits sodium-potassium ATPase, an enzyme that regulates the quantity of sodium and potassium inside cells. (nih.gov)
  • High amounts of the electrolyte potassium (K+) in the blood (hyperkalemia) is characteristic of digoxin toxicity. (wikipedia.org)
  • Digoxin inhibits the membrane Na-K-ATPase pump, this results in an increase in intracellular sodium which in turn cause an increase in intracellular calcium (via the sodium and calcium exchanger) and an increase in extracellular potassium. (litfl.com)
  • The beneficial effects of digoxin result from direct actions on cardiac muscle, as well as indirect actions on the cardiovascular system mediated by effects on the autonomic nervous system. (nih.gov)
  • The effects of digoxin in heart failure are mediated by its positive inotropic and neurohormonal deactivating effects, whereas the effects of the drug in atrial arrhythmias are related to its vagomimetic actions. (nih.gov)
  • We report a case of IIH that demonstrates the effects of digoxin, a medication that may benefit patients for whom other treatments have failed or who are unable or unwilling to undergo surgical procedures. (jaoa.org)
  • Our objective was to examine the influence of ritonavir on P-glycoprotein (P-gp) activity in humans by characterizing the effect of ritonavir on the pharmacokinetics of the P-gp substrate digoxin in individuals with known MDR1 genotypes. (unthsc.edu)
  • although data are limited, the effect of ritonavir on digoxin pharmacokinetics appears to occur across all tested MDR1 genotypes. (unthsc.edu)
  • Otherwise, based on pharmacokinetic modelling and case series, it is recommended to give 80 mg bolus of digoxin immune Fab, repeated as required according to clinical parameters (ECG & HR) because the onset of clinical response is usually rapid. (litfl.com)
  • Digoxin pharmacokinetic parameters were determined on day 1 (digoxin administration alone) and on day 9 (coadministration of lapatinib and digoxin), and parameters were compared to determine the effects of lapatinib on digoxin absorption. (elsevier.com)
  • Digoxin pharmacokinetic parameter values were determined using noncompartmental methods. (unthsc.edu)
  • Calcium-blocking blood pressure medicines like nifedipine ( Procardia ), diltiazem ( Cardizem CD ) or verapamil ( Calan SR ) may also increase digoxin levels. (peoplespharmacy.com)
  • Following oral administration, peak serum concentrations of digoxin occur at 1 to 3 hours. (nih.gov)
  • Overall, 75% (9/12) of subjects had higher concentrations of digoxin after ritonavir administration. (unthsc.edu)
  • Impact of neonatal treatment with cardioactive glycosides (digoxin, ouabain) on receptor binding capacity, blood level and cardiac function in the adult rat. (elsevier.com)
  • Background: Transabdominal injection of digoxin into the amniotic fluid or fetus to induce fetal demise before dilation and evacuation (D&E) abortion has become common practice since the passage of the Partial-Birth Abortion Ban Act in 2007. (elsevier.com)
  • The classic teaching is that if you give calcium to a patient with digoxin toxicity (because of the hyperkalaemia), you will kill them. (litfl.com)
  • there are five human case reports showing a temporal relationship between calcium administration and death in digoxin toxicity. (litfl.com)
  • But its okay, there were several animal models that also seemed to show an increase in mortality and morbidity after administration of calcium in digoxin toxicity. (litfl.com)
  • In the undifferentiated hyperkalaemic patient giving calcium is required (you are not going to wait 1 hour to get the digoxin level back). (litfl.com)
  • For example, one kind of positive inotrope called digoxin strengthens the force of the heartbeat by increasing the amount of calcium in the heart's cells. (answersdrive.com)
  • There is little evidence on acute digoxin toxic patients. (litfl.com)
  • 4 The possible application of the measurement of the binding of 12‐alpha‐[3H]‐digoxin to the study of biochemical pharmacological events occurring during digoxin therapy is discussed. (ox.ac.uk)
  • The researchers warned that digoxin should be used with great caution and that patients' plasma levels should be monitored until randomised controlled trials are carried out. (meducation.net)
  • The drop seems steepest in patients seen as susceptible to digoxin toxicity, say researchers, and there's evidence that it's used more 'in patient populations that may potentially benefit the most. (meducation.net)
  • Well, not really, the animals were made severely hypercalcemic before they received digoxin (not what we see in digoxin toxic patients). (litfl.com)
  • Patients with digoxin toxicity will often be hyperkalemic. (litfl.com)
  • This study compared the effects of beta blocker and digoxin on mortality in patients with both AF and HF. (answersdrive.com)
  • At hospital discharge, digoxin was prescribed in 36% (n = 709) of the patients, whereas HF was present in 27% (n = 528) of the cohort. (elsevier.com)
  • A digoxin test is used to monitor the concentration of the drug in the blood. (labtestsonline.org)
  • As demonstrated by RIA, re-exposure to digoxin at 2 months of age was followed within 30 min by a more than twofold increase in serum digoxin over the not pretreated control and, although a steady concentration decrease followed, the experimental rats still had a higher serum digoxin level than the controls at 4 h. 3. (elsevier.com)
  • In high doses, digoxin increases sympathetic outflow from the central nervous system (CNS). (nih.gov)
  • Other ECG changes that suggest digoxin toxicity include bigeminal and trigeminal rhythms, venticular bigeminy, and bidirectional ventricular tachycardia. (wikipedia.org)
  • Digoxin is supplied as 125 mcg (0.125 mg) or 250 mcg (0.25 mg) tablets for oral administration. (nih.gov)
  • Magnesium suppresses digoxin-induced ventricular arrhythmias while phenytoin and lidocaine suppresses digoxin-induced ventricular automaticity and delay afterdepolarizations without depressing AV conduction. (wikipedia.org)
  • Digoxin can cause any number of arrhythmias either tachy or brady-arrhythmias, although the classic description is of automaticity. (litfl.com)