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31 Cards in this Set
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DigoxinIs the drug of choice for rate control in paroxysmal AFHas a proven mortality benefit in cardiac failurePlasma concentrations correlate well with toxicityHypokalemia predisposes to the pt to digitalis toxicityRapid IV infusion can cause hypotension |
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Digoxin |
Adjust maintenance dose by estimating CrCl and measuring serum levels In heart failure, higher dosages have no additional benefit and may increase toxicity; decreased renal clearance may lead to increased toxicity In geriatric patients, use lean body weight to calculate dose |
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What are the severe drug interactions |
aluminum hydroxideamiodaroneamphotericin b deoxycholateatenololazithromycinbetaxololbisoprololcalcium carbonateclarithromycincolchicinecyclosporinedexlansoprazoledofetilidedronedaroneeluxadolineerythromycin baseerythromycin ethylsuccinateerythromycin lactobionateerythromycin stearateesmololesomeprazolefamotidineflecainidehuman parathyroid hormone, recombinanthydroxychloroquine sulfateibuprofen/famotidinelansoprazolelevobunolollily of the valleymetoprololnadololnebivololnizatidineomeprazolepantoprazoleprocainamidepropafenonepropranololquinidinerabeprazolerevefenacinroxithromycinsodium bicarbonatesodium citrate/citric acidsotalolsucralfatetelaprevirtimololvandetanibvenetoclaxverapamil |
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Warnings |
Warnings Contraindications Hypersensitivity Ventricular fibrillation Cautions Use caution in chronic constrictive pericarditis, electrical cardioversion, severe bradycardia, severe heart failure, severe pulmonary disease, sick sinus syndrome, ventricular tachycardia, ventricular premature contractions, Wolff-Parkinson-White syndrome, electrolyte imbalance, hypothyroidism or hyperthyroidism, hypoxia, idiopathic hypertrophic subaortic stenosis, renal disease, concomitant diuretics Not recommended in patients with acute myocardial infarctionAvoid in patients with myocarditisRisk of advanced or complete heart block in patients with sinus node disease and AV block Very narrow margin between effective therapeutic and toxic dosages: Therapeutic range, 0.5-2 ng/mL (target 0.5-1 ng/mL); toxic range, >2.5 ng/mL Generally avoid if left ventricular systolic function preserved, although may be used for ventricular rate control in subgroup with chronic atrial fibrillation Less effective in presence of hypokalemia or hypocalcemia; avoid hypercalcemia or hypomagnesemia, which may predispose to serious arrhythmias Heart failure patients with preserved ventricular function, including acute cor pulmonale, amyloid heart disease, and constrictive pericarditis may be susceptible to digoxin toxicity May cause false-positive ST-T changes during exercise testing Do not switch between different PO forms or between brand and generic forms of digoxin; bioavailability variesSerum levels drawn within 6-8 hours of dose will be falsely high because of prolonged distribution phaseIncreased risk of estrogen-like effects in geriatric patientsBeriberi heart disease may not respond adequately if underlying thiamine deficiency not correctedAtrial arrhythmias are difficult to treat if associated with hypermetabolic (hyperthyroidism) or hyperdynamic (hypoxia) states; treat underlying condition before initiating therapyAvoid extravasation; ensure proper needle or catheter placement prior to and during administrationMonitor for proarrhythmic effects, especially with digoxin toxicityUse caution in patients with acute myocardial infarction; may increase myocardial oxygen demand; during acute coronary syndrome, digoxin administered IV may be used to slow a rapid ventricular response and improve left ventricular function in the acute treatment of atrial fibrillation associated with severe LV function and heart failure or hemodynamic instabilityMonitor serum concentration closely when used for rate control in patients with atrial fibrillation; serum concentration that is not properly controlled are associated with increased risk of mortalityConsider use of digoxin only in heart failure with reduced ejection fraction when symptoms remain despite guideline-directed medical therapy; withdrawal of digoxin in clinically stable patients with heart failure may lead to recurrence of heart failure symptomsIn hypertrophic cardiomyopathy, outflow obstruction may worsen due to positive inotropic effects of digoxin; avoid use unless used to control ventricular response with atrial fibrillation; in the absence of atrial fibrillation, digoxin is potentially harmful in the treatment of dyspnea in patients with hypertrophic cardiomyopathyAvoid rapid IV administration in digitalized patients; may produce serious arrhythmias Not necessary to routinely reduce or hold digoxin therapy prior to elective electrical cardioversion for atrial fibrillation; however, exclusion of digoxin toxicity is necessary prior to cardioversion; whithold digoxin and delay cardioversion until toxicity subsides if signs of digoxin excess exist |
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Mechanism of action |
Digoxin inhibits Na-K ATPase, which in turn causes increased availability of intracellular calcium in the myocardium and conduction system. Inotropy and automaticity are subsequently increased while conduction velocity is reduced. Therapy indirectly causes parasympathetic stimulation of autonomic nervous system, with consequent effects on the sino-atrial (SA) and atrioventricular (AV) nodes. Digoxin 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. At higher concentration, increases sympathetic outflow from the central nervous system (CNS) to both cardiac and peripheral sympathetic nerves. It also allows progressive efflux of intracellular potassium, with consequent increase in serum potassium levels
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What |
digoxin is a cardiac glycoside that was historically used for "dropsy" (edema) and is currently used as an inotrope to improve systolic dysfunction in patients with congestive heart failure (CHF) and as an atrioventricular nodal blocking agent for managing atrial tachydysrhythmias. Digoxin may improve the quality of life in CHF patients, but it does not provide a mortality benefit.
. Potassium greater than five meq/L in acute overdoseAcute ingestions greater than 10 mg in an adult or greater than 4 mg in a childDigoxin Concentration greater than 15 ng/mL measured at any timeDigoxin Concentration greater than 10 ng/mL measured 6 hours post ingestion.Empiric dosing of DSFab can be given at a dose of ten to 20 vials for critically ill patients after acute overdose, three to six vials for chronic toxicity in adults, or one to two vials for chronic toxicity in children. DSFab also can be dosed as follows:(0.8 times the ingested dose)/0.5 = Number of vials of DSFab for acute overdose(Digoxin level (steady state) x Weight (kg))/100 = Number vials of DSFab for acute or chronic overdoseDSFab fragments also can be given for poisoning with natural toxins, but the dosing is unclear.The typical DSFab infusion is over 30 minutes, but it may be given as a bolus for critical patients. The onset of effect is approximately 20 minutes, with complete effect usually seen within 90 minutes. Care should be taken to completely reverse digoxin in patients who are chronically taking digoxin, as reversal may exacerbate their underlying disease. These patients should be closely monitored afterward for the same reasons. If DSFab is not available, then treatments such multidose-activated charcoal, atropine, and antidysrhythmics such as phenytoin or lidocaine may be employed. Cardioversion and pacing may induce dysrhythmias and are typically not used, but they may be needed in patients without other therapeutic options.Dialysis also may be indicated in the patient with acute renal failure or refractory hyperkalemia; however, it is not useful as a treatment for digoxin toxicity itself.Disposition depends on the patient's symptoms and stability as well as their potassium and digoxin levels.Pearls and Other IssuesMany analyzers cannot measure free digoxin concentrations, and in this setting, digoxin levels should not be followed after administration of DSFab.In patients with the end-stage renal disease, dissociation of the DSFab-digoxin complex may occur and cause recurrent toxicity.Calcium is traditionally considered contraindicated in hyperkalemic patients with digoxin toxicity for fear of 'stone heart syndrome,' an irreversible state of global myocardial contraction. This is based on animal evidence and case report, but more recent literature found no evidence of increased mortality with calcium administration. In general, hyperkalemia in the setting of digoxin toxicity should be treated primarily with DSFab fragments if available.A classic but uncommon side effect of digoxin is the appearance of yellow halos around lights, called xanthopsia, and altered color vision, called chromatopsia. This may have influenced the work of Dutch impressionist painter Vincent Van Gogh in paintings such as "The Starry Night" as he reportedly used foxglove for the treatment of his 'dropsy' which is an old term for edema due to CHF. |
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What are the types of digoxin toxicity |
Digoxin toxicity can present acutely, by an intentional or accidental overdose, or chronically, such as when patients on digoxin develop worsening renal function. Similar toxicity can occur after exposure to cardioactive steroids in plants such as oleander, red squill, or dogbane or from animals such as Bufo toads |
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What brings about the toxicity |
Digoxin exhibits its therapeutic and toxic effects by poisoning the sodium-potassium ATPase. The subsequent increase in intracellular sodium leads to increased intracellular calcium by decreasing calcium expulsion through the sodium-calcium, cation exchanger. Higher intracellular calcium increases inotropy which can be of symptomatic benefit in CHF. At toxic levels, automaticity can be increased as well. Digoxin also increases vagal tone by decreasing dromotropy at the AV node. This can be used to control atrial tachydysrhythmias. |
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What is the epidemiology |
EtiologyEpidemiology Approximately 1% of CHF patients treated with digoxin develop toxicity. Additionally, 1% of adverse drug effects in patients greater than age 40 are due to digoxin toxicity; the incidence rises to greater than 3% in patients over age 85. Plant ingestions account for 80% of pediatric exposure; the remaining 20% of pediatric ingestions arise from medications. In general, ventricular dysrhythmias are more common in the elderly whereas supraventricular dysrhythmias are more common in children. |
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What are the primary causes of digoxin toxicity |
PathophysiologyIncreased intracellular calcium from the poisoning of the Na-K transporter and AV nodal blockade from increased vagal tone are the primary causes of digoxin toxicity. The former leads to increased automaticity and inotropy; the latter leads to decreased dromotropy. |
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What is the place of high K in acute and chronic poisoning of digoxin |
Hyperkalemia can be a marker of severe toxicity in acute poisoning. The role of potassium is less clear in chronic toxicity, although it has been linked to higher mortality despite traditional teaching that hypokalemia worsens the dysfunction at the Na-K transporter. |
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What are the toxokinetics |
Digoxin's therapeutic half-life is between 30 to 40 hours, but this may change in overdose. Digoxin excretion is primarily renal, and for this reason, patients with poor or worsening renal function, such as patients who are elderly or have CKD, are more likely to develop toxicity. Digoxin levels start to plateau at 6 hours, which is after tissue redistribution has occurred; earlier levels may thus be misleadingly high. Cardiovascular toxicity may have delayed manifestation of up to 8 to 12 hours post ingestion |
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What are the systems affected in digoxin toxicity |
Heart GI _ |
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What are the common symptoms |
Gastrointestinal upset is the most common symptom of digoxin toxicity. Patients also may report visual symptoms, which classically present as a yellow-green discoloration, and cardiovascular symptoms, such as palpitations, dyspnea, and syncope. Elderly patients frequently will present with vague symptoms, such as dizziness and fatigue. |
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What is the most historical symptom |
The most important historical detail in evaluating a random digoxin level is the time of the last dose |
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How do you evaluate acute digoxin toxicity |
For patients with acute digoxin toxicity, it is critical to obtain an ECG, a basic metabolic panel, and digoxin levels on arrival. These tests should be repeated at 6 hours post ingestion. |
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What are the ECG findings in digoxin toxicity |
Digoxin effect on the ECG is characterized by diffuse scooping of the ST segments which can be seen with therapeutic levels and is not associated with toxicity. The most common ECG abnormality is frequent PVCs, although the "pathognomonic" ECG finding is bidirectional ventricular tachycardia. However, this has been reported in aconitine poisoning. In the setting of acute overdose, acetaminophen and aspirin levels can help screen for occult overdose. |
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How should we evaluate chronic digoxin toxicity |
In chronic toxicity, the cause of toxicity should be sought. Common causes include infection, renal failure, and accidental overdose.
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What is the place of serum digoxin levels in toxicity |
Serum digoxin levels do not always correlate with toxicity given variable tissue levels and other factors affecting digoxin's toxicodynamic effects. |
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Treatment |
Digoxin-specific antibody antigen-binding fragments (DSFab), brand name Digibind or Digifab, are an effective antidote that directly binds digoxin. DSFab is indicated for life-threatening toxicity including: Ventricular arrhythmias High-grade heart blocks Hypotension Symptomatic bradycardia |
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