CONTENTS

therapeutic use of digoxin

• Indications
• Dosing
• Digoxin levels

digoxin & cardiac glycoside poisoning

• Physiology of cardiac glycosides
• Epidemiology
• Clinical manifestations
• ECG features ➡️
• Differential diagnosis
• Digoxin levels
• Treatment
  • Decontamination
  • Digoxin-specific antibody fragments
  • Hemodynamic stabilization
  • Electrolyte management

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therapeutic use of digoxin

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contraindications, drug interactions, side effects 👎

contraindications

• [1] Bradycardia risk factors:
  • Advanced or complete heart block.
  • Pre-existing sinus node disease.
• [2] Severe tachycardia (digoxin is unlikely to be effective).
• [3] Ventricular tachycardia (digoxin may increase cardiac excitability).
• [4] Desire to pursue rhythm control strategy (digoxin will make it harder to convert AF to sinus rhythm).
  • Potential need for DC cardioversion in the near term (digoxin may complicate this; ideally, stop digoxin for >24 hours before cardioversion). (Paw & Shulman 2025)
• [5] Renal failure (relative contraindication; makes dosing more challenging).
• [6] Electrolyte abnormalities:
  • Hypokalemia and/or hypomagnesemia (severe hypokalemia is an absolute contraindication). These may sensitize the myocardium to digoxin, potentially causing digoxin toxicity even at levels <2 ng/mL. (Wellington 3e)
  • Hypercalcemia (calcium overload increases the risk of digoxin-induced arrhythmia).
  • Hypocalcemia (there is no risk of toxicity, but digoxin may be ineffective). (Wellington 3e)
• [7] Thyrotoxicosis (relative contraindication). Digoxin is often ineffective for two reasons. First, patients with thyrotoxicosis have increased renal clearance and an increased volume of distribution, which can make it challenging to achieve adequate digoxin levels. Secondly, the higher sympathetic tone of these patients may render digoxin relatively less effective. (28822529) 

drug-drug interactions

• P-glycoprotein inhibitors & inducers: 📖
• Drugs that interfere with GI absorption:
  • Antacids.
  • Cholestyramine.
  • Metoclopramide.
  • Phenytoin.
  • Sucralfate.
• Reduced digoxin degradation by gut microflora increases drug absorption (e.g., macrolides, tetracycline). (39089856)
• AV nodal blocking agents (pharmacodynamic risk of bradyarrhythmias):
  • Beta-blockers.
  • Nondihydropyridine calcium channel blockers (diltiazem, verapamil).
• QT prolonging medications:
  • Digoxin increases early afterdepolarizations, which can promote torsade de pointes.
• IV calcium:
  • Rapid administration of IV calcium may promote digoxin toxicity.

side effects

• Clinical manifestations of digoxin toxicity are discussed below.

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indications, advantages 👍

overview: role of digoxin for AF in the ICU

• Digoxin may have a role in rate control for selected patients (as described below).
• (Digoxin may actually tend to reduce the likelihood of conversion into sinus rhythm, so it doesn't have any role in a rhythm-control strategy.)

optimal candidates for digoxin have:

• (1) Chronic AF:
  • Digoxin tends to perpetuate AF, rather than favoring cardioversion back to normal sinus rhythm.
  • Digoxin may be less effective in rate control of paroxysmal AF, so it shouldn't be used as a sole therapy for paroxysmal AF. (Griffin 2022)
• (2) Heart failure with reduced ejection fraction:
  • Digoxin is the only agent that reduces heart rate while simultaneously functioning as a positive inotrope.
  • Digoxin may be uniquely beneficial for patients with heart failure whose hemodynamics are very tenuous, who may have difficulty tolerating a negative inotrope.
• (3) Mild or moderate tachycardia for which immediate control isn't necessary:
  • Digoxin takes several hours to work, and it's not tremendously potent.
  • Digoxin is less effective in hyperadrenergic states, since it functions primarily as a vagotonic agent.
• (4) Adequate renal function:
  • The presence of preserved renal function makes dosing of digoxin easier and a bit safer.
  • This isn't an absolute requirement, because careful dosing and monitoring within the ICU allow digoxin to be given safely even in the presence of renal dysfunction.

if digoxin fails

• Digoxin is not a highly potent agent, so it may not achieve optimal heart rate control.
• If digoxin does fail, it may be combined with a beta-blocker. The presence of digoxin may reduce the required dose of beta-blocker, thereby improving hemodynamic stability. (31700500) Thus, the combination of digoxin plus a beta-blocker may be effective for some patients with systolic heart failure.

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dosing

IV digoxin loading (digitalization)

• Digoxin requires some time to take effect. When administered intravenously, digoxin may take effect within ~1.5-4 hours. (39089856) When initiated in the ICU, digoxin will nearly always be started with intravenous loading doses.
• Total IV loading dose: (package insert, 23616674)
  • Normal renal function: 8-12 mcg/kg ideal body weight (usually ~600-1,000 mcg).
  • Renal insufficiency: 6-10 mcg/kg ideal body weight.
  • Err on the lower end in patients with renal dysfunction, hypothyroidism, and/or reduced muscle mass.
• Typically, 50% of the total loading dose is given initially, followed by 25% given twice, every 4-6 hours. Monitor for effect:
  • ⚠️ If an adequate heart rate is achieved, subsequent doses may be omitted.
  • ⚠️ If bradycardia occurs, further administration should be held.

maintenance doses

• Typical maintenance dose:
  • Patients <70 years old with normal renal function: 250 mcg daily.
  • Patients over 70 years old, or with renal dysfunction: 125 mcg daily.
  • Patients who are both >70 YO and have renal dysfunction: 62.5 mcg daily.
• The table below provides typical maintenance doses, based on the patient's renal function and lean body weight. (Package insert)
  • Note that distribution correlates with lean body weight (due to minimal distribution into adipose tissue).
• Digoxin has a long half-life (~36-48 hours, or longer in renal insufficiency). Therefore, steady state may not be reached until about a week after a dose adjustment.

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monitoring

• Digoxin levels are discussed further below.

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pharmacology

• Chemical properties:
  • Molecular weight: 781 g/mol.
  • LogP: ~1.3-1.8 (moderate lipophilicity).
• Absorption:
  • The oral bioavailability of digoxin tablets is ~70% (but may range from ~40-90%). Oral elixir may have slightly higher bioavailability (~80%).
  • A rough conversion from oral to IV is 0.67 (i.e., 150 ug PO = 80 ug IV). (Paw and Shulman 2025; Welington 3e)
  • Roughly ~10% of patients have gut bacteria capable of degrading digoxin into less active compounds (causing an oral bioavailability of ~40%). In such patients, antibiotic administration may cause an increase in digoxin exposure.
  • The onset of action occurs 2-6 hours after ingestion.
    • Onset of action is ~2 hours.
    • The peak effect occurs ~6 hours after administration. (39089856)
  • Factors that could slow the absorption of oral digoxin include:
    • Gastroparesis (including acutely slowed transit due to opioids or anticholinergics).
    • P-glycoprotein inducers (this may cause drug secretion back into the gut lumen).
    • Malabsorption syndromes.
• Distribution:
  • Protein binding is 25% (mostly to albumin).
  • The volume of distribution is ~6 liters/kg (high tissue binding to Na/K ATPase pumps, especially in the heart, kidneys, and skeletal muscle).  Vd may be decreased in the elderly, lower muscle mass, renal failure, and hypothyroidism.  Vd is increased in hyperthyroidism.
  • Digoxin does cross the blood-brain barrier.
  • Digoxin is dosed based on lean body weight (since it doesn't distribute substantially into adipose tissue).
• Metabolism:
  • Only ~15% is metabolized.
  • CYP450 enzymes are not involved.
  • Hepatic impairment has minimal effect on digoxin pharmacokinetics.
• Elimination:
  • 60-80% is excreted unchanged in the urine.
    • Renal clearance involves glomerular filtration, tubular secretion, and tubular reabsorption.
    • P-glycoprotein mediates tubular secretion (P-glycoprotein inhibitors will increase digoxin levels, whereas P-glycoprotein inducers will decrease digoxin levels.)
    • Digoxin isn't efficiently removed by dialysis due to extensive tissue binding.
  • ~30% of clearance is nonrenal (including biliary excretion).
• Half-life & duration of action:
  • The half-life is ~36-48 hours in patients with normal renal function.
  • In anuria, the half-life may extend to ~3.5-5 days.

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physiology of cardiac glycosides

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mechanism of action of digoxin

• (1) Digoxin inhibits the cardiac Na/K antiporter. This causes an increase in intracellular sodium and a decrease in intracellular potassium.
  • The decrease in intracellular potassium is what causes hyperkalemia in patients with digoxin overdose.
• (2) The increase in intracellular sodium causes an increase in sodium excretion through the Na/Ca exchanger, which increases intracellular calcium levels.
• (3) Increased intracellular calcium increases inotropy.
• (4) Increased inotropy often causes a reflexive increase in vagal tone. For patients in atrial fibrillation, increased vagal tone will decrease the conduction rate through the atrioventricular node, thereby slowing the ventricular rate.

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epidemiology

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factors causing chronic digoxin intoxication

• Most cases of digoxin intoxication are chronic and unintentional due to the gradual accumulation of digoxin over time. Precipitating factors for chronic intoxication may include the following:
• [1] Digoxin is renally cleared, so any cause of kidney injury may cause accumulation.
• [2] Drug interactions can reduce digoxin metabolism (see above).
• [3] Tissue sensitivity to digoxin may be increased by:
  • Hypokalemia.
  • Hypomagnesmia.
  • Hypercalcemia.
  • Myocardial ischemia.
  • Hypoxemia.
• [4] Digoxin may interact with other AV-nodal blockers to promote synergistic bradycardia.

other cardiac glycosides

• Various cardiac glycosides are found in plants (e.g., oleander, henbane, foxglove, milkweed, lily of the valley). Ingestion of these plants is not uncommon in some locales.
• Bufadienolide is a cardioactive steroid found in the skin of Bufo toads, which is utilized as an aphrodisiac.

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clinical manifestations

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acute vs. chronic toxicity

• Acute toxicity:
  • Generally starts with gastrointestinal symptoms.
  • Neurological symptoms develop later (as the drug subsequently distributes to the brain).
• Chronic toxicity: Insidious onset of neurologic symptoms, with fewer gastrointestinal symptoms.

cardiac manifestations may include arrhythmias, shock

• Sinus bradycardia or high-degree AV block.
• Supraventricular tachycardias with atrioventricular block are classic for digoxin toxicity:
  • Atrial fibrillation with slow ventricular rate.
  • Atrial fibrillation with junctional escape rhythm.
  • Focal atrial tachycardia with AV block.
• Junctional tachycardia.
• Ventricular arrhythmias are more often seen in chronic toxicity:
  • Ventricular bigeminy.
  • Ventricular tachycardia, ventricular fibrillation.
  • Bidirectional ventricular tachycardia strongly suggests the presence of digoxin.
• Hypotension and cardiogenic shock may occur. (37650725)

GI

• Anorexia, nausea/vomiting.
• Abdominal pain.
• Diarrhea.
• Mesenteric ischemia (rare).

neurologic

• Delirium.
• Fatigue.
• Visual disturbances, which may include:
  • Altered color perception.
  • Blurred vision.
  • Halos.
  • Photophobia.
  • Diplopia, blindness.
• Seizures rarely may occur.

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differential diagnosis

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common differential diagnostic considerations:

• Calcium channel blocker intoxication or beta-blocker intoxication.
• Alpha-agonist intoxication (e.g., clonidine) – may cause greater somnolence and miosis than digoxin.
• Hypothyroidism.
• Hypothermia.
• Myocardial infarction.
• Hyperkalemia of any etiology.
  • BRASH syndrome.
• Chronic cardiac conduction system disease.

related differential diagnoses

• Differential diagnosis of bradycardia.
• Differential diagnosis of delirium.

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digoxin levels

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timing of the digoxin level

• Monitoring the therapeutic use of digoxin:
  • The drug level must be checked several hours after the last digoxin dose to allow for distribution (e.g., >8 hours after an oral dose). Ideally, this should be a trough level.
  • The safest approach to digoxin dosing in the ICU among tenuous or dynamic patients is to monitor the digoxin level closely:
    • Check the trough level daily with AM labs.
    • Adjust the daily dose as needed, depending on the trough level.
    • As the patient stabilizes, digoxin levels may be spaced out.
• After acute intoxication:
  • Check a baseline digoxin level and repeat another level six hours after ingestion.
  • Digoxin levels usually peak around ~3 hours post-ingestion. Early digoxin levels (<6 hours) may be very high and overestimate the total body load since full tissue distribution hasn't occurred. (37861975) 
  • Digoxin requires ~6 hours to distribute into the tissues following oral intake.  The post-distribution level most accurately reflects the severity of intoxication and helps calculate the dose of DSFab. (27041802)
• For chronic intoxication, a single digoxin level is adequate (provided that it is obtained >6 hours after the last dose).

interpretation of the digoxin level in digoxin intoxication

• Therapeutic level:
  • 0.5-2 ng/mL is regarded broadly as a therapeutic range.
  • 0.5-1 ng/mL might be ideal for the treatment of refractory HFrEF.
  • 0.5-1.2 ng/mL might be ideal for the treatment of AF. (39089856)
  • 1-2 ng/mL levels may improve contractility, so these aren't unreasonable levels for closely monitored ICU patients.
  • Chronic levels close to 2 ng/mL may occasionally cause symptoms of toxicity.
• Potentially scary:
  • Acute intoxication: >10 ng/ml (>12.8 nM/L).
  • Chronic intoxication: >4 ng/ml (>5.1 nM/L).
  • However, serum digoxin levels don't always correlate well with tissue levels and clinical toxicity. Patients can have elevated digoxin levels without clinical toxicity.
• After receiving antibody fragments, levels are meaningless (the lab will measure free and also bound digoxin).
  • Total serum digoxin will often increase rapidly (8-20 fold with normal kidney function, or up to 33-fold with impaired kidney function). (37861975)
  • At this point, total digoxin levels can't be used to guide the dosing strategy for DSFab. (37861975)

interpretation of the “digoxin level” in intoxication with other cardiac glycosides

• For patients with non-digoxin glycosides, digoxin level may be used as a qualitative assay.
• A positive “digoxin level” may suggest the presence of a cardiac glycoside, but the exact level lacks clinical significance.
• The performance characteristics with different glycosides is largely unknown, but in the appropriate context this could help support the diagnosis of a non-digoxin cardiac glycoside intoxication.

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decontamination

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• Activated charcoal may be given if a patient presents within roughly an hour of an acute digoxin ingestion.
• By the time patients develop symptoms of digoxin toxicity, they will be outside the window of time when decontamination is beneficial.

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digoxin-specific antibody fragments (DSFab)

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💡Assess the need for DSFab early and order promptly because the delay from ordering to clinical benefit is generally at least ~2 hours.

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indications for DSFab

stronger indications

• Significant dysrhythmia or hemodynamic instability.
• Potassium ≧6.5 mEq/L (if hyperkalemia appears to be caused by an acute digoxin intoxication). (37650725)

weaker indications

• Acute ingestion of >10 mg (although a lower treatment threshold is recommended in patients >60, as they are at higher risk).
• Digoxin level:
  • >13 nM (10 ng/ml) soon after ingestion in acute poisoning.
  • >10 nM (7.8 ng/ml) six hours post-ingestion.
  • >7.7 nM (6 ng/ml) in chronic poisoning. (37861975)  
• Renal failure.
• Altered mental status.
• Moderate to severe GI symptoms.

severe hypokalemia may be a relative contraindication to immediate DSFab administration

• DSFab may need to be temporarily withheld initially (to prevent the development of worsening hypokalemia).
• DSFab may cause potassium to enter the cells, thereby exacerbating hypokalemia.
• This is similar to how an insulin infusion may need to be delayed while treating hypokalemia.

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potential complications from DSFab

• Hypokalemia (due to potassium shifting into cells).
• Exacerbation of heart failure or atrial fibrillation (due to sudden withdrawal of digoxin therapy).
• Serum sickness.
• Anaphylaxis.

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dosing of DSFab

general aspects & dose units

• 1 Vial = 40 mg antibody fragments = neutralizes 0.5 mg digoxin. Two brands are available (Digibind and DigiFab), which seem interchangeable.
• Timing of response to DSFab:
  • Some clinical response should be seen within ~20 minutes.
  • Arrhythmias often improve within 30-45 minutes. (37861975)
  • Complete response occurring within ~1.5-3 hours.
• Assessment of response to DSFab:
  • ECG findings.
  • Hemodynamics (e.g., blood pressure).
  • ⚠️ Potassium level (this may fall, so potassium should be followed carefully). (37861975)

traditional vs. newer approaches to dosing DSFab

• DSFab is very expensive and often in limited supply.
• Traditional dosing used relatively liberal amounts with a goal of complete, immediate neutralization of all digoxin. This is probably a misguided approach for the following reasons:
  • [1] Providing an excessive dose upfront may cause DSFab to be excreted by the kidneys before digoxin has time to be absorbed out of the tissues. (37861975)
  • [2] Complete neutralization is unnecessary to clinically resolve the toxicity. Among patients with atrial fibrillation or heart failure on chronic digoxin treatment, complete neutralization could cause aggregation of AF and/or CHF symptoms.
• A narrative review and expert consensus recommended giving half of the dose required to achieve full neutralization (i.e., half of the traditional dose). (37650725)
• Dutch guidelines recommend a relatively restrictive strategy with dosing titrated to clinical effect. (37861975)

acute poisoning

• Traditional dosing:
  • Known digoxin ingestion: The number of vials is estimated as 1.6(mg of digoxin ingested).
  • Empiric administration if levels are unknown: Give 5 vials (if hemodynamically stable) or 10 vials (if unstable), reevaluate clinically in 30 minutes.
• Dutch guidelines:
  • If cardiac arrest is imminent: Starting dose 10-20 vials (400-800 mg), repeat dose PRN 10 vials (400 mg).
  • If the patient is more stable, the starting dose is 2 vials (80 mg), and the repeat dose is PRN 2 vials (80 mg).

chronic poisoning

• Traditional dosing:
  • Number of vials is estimated as (digoxin level in ng/ml)(wt in kg)/100.  However, lower doses may be considered initially for patients with chronic digoxin toxicity who are clinically stable (e.g., initiate therapy with three vials and follow clinically to determine whether additional treatment is warranted). (33476509)
  • Empiric administration if levels are unknown: start with 3-6 vials, reevaluate clinically.
• Dutch guidelines:
  • If cardiac arrest imminent: Start dose is 6 vials (240 mg), repeat dose PRN 6 vials (240 mg).
  • If patient is more stable: Start dose is 1 vial (40 mg), repeat dose PRN 1 vial (40 mg).

non-digoxin cardiac glycosides

• DSFab may be effective in non-digoxin cardiac glycoside intoxication (e.g., plant or animal toxins). Digoxin levels in these situations are not quantitatively meaningful, so DSFab must be dosed empirically based on clinical severity.
• For patients with critical cardiac dysfunction, 10-20 vials may be utilized.(26505271) Larger doses may be needed than for digoxin intoxication, since DSFab may have lower affinity for non-digoxin cardiac glycosides.

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rebound

• DSFab is generally excreted in the kidneys with a half-life of ~15-20 hours. Digoxin has a longer half-life (~40 hours). Therefore, it is possible that DSFab could be renally excreted, and subsequently, free digoxin levels could begin to rise again, leading to rebound toxicity.
• Timing of rebound:
  • With normal renal function: may occur ~12-24 hours after DSFab given.
  • Renal dysfunction: may occur up to 10 days after DSFab given. (37861975)  
• The treatment of rebound is readministration of DSFab. The decision to treat must be based on symptoms and EKG findings, rather than digoxin levels (since digoxin levels will be unreliable after administration of DSFab).

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hemodynamic stabilization

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volume resuscitation

• Fluid should often be used carefully because many patients on digoxin have severe underlying heart disease.
• Bedside echocardiography may help assess the potential benefit of fluid resuscitation.

bradycardia

• ⚠️ The best treatment is generally DSFab.
• Atropine is a good temporizing measure (since patients with digoxin toxicity have excess vagal tone). A reasonable dosing scheme might be to start with 1 mg and repeat as needed, to a maximum total cumulative dose of 3 mg.(26505271)
• 🛑 Avoid pacing or beta-agonists if possible, as these may provoke ventricular tachycardia.

tachycardia

• ⚠️ The best treatment is generally DSFab.
• Avoid cardioversion if possible for supraventricular tachycardias, given concern for inducing ventricular tachycardia.
• For ventricular tachycardia:
  • Lidocaine may be the first-line agent.
  • Magnesium sulfate may be useful. (37650725)
  • Amiodarone or procainamide may be less useful due to a risk of exacerbating poor AV conduction.
• If hypomagnesemia is present, this should be corrected.

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electrolyte management

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Hypokalemia, hypercalcemia, and hypomagnesemia can exacerbate the effects of digoxin toxicity. Alternatively, hyperkalemia itself may be dangerous and require treatment. 

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hypomagnesemia

• Hypomagnesemia may exacerbate digoxin toxicity (since magnesium is a cofactor in the Na/K exchange channel).
• Treat hypomagnesemia aggressively, particularly in patients who are having arrhythmias (more on hypomagnesemia therapy here).

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hypokalemia

• Hypokalemia is a favorable prognostic sign, but it doesn't guarantee a good outcome (for example, the patient may have an independent disease process causing hypokalemia).
• Hypokalemia may exacerbate digoxin toxicity, so it must be treated (more on treating hypokalemia here).
• If the patient is early in the course of their intoxication, there may be a risk that the potassium levels will increase as the digoxin intoxication worsens (rebound hyperkalemia).
• If DSFab is administered, it may cause potassium to enter the cells, exacerbating hypokalemia. In severe hypokalemia, DSFab may be withheld initially to prevent the development of severe hypokalemia (similar to the way an insulin infusion is initially withheld in a patient with diabetic ketoacidosis who is hypokalemia).

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hyperkalemia

signifcance and general approach

• Hyperkalemia is a poor prognostic sign, especially in the context of acute digoxin intoxication. Among one series of patients with acute digoxin intoxication before the availability of DSFab, all patients with potassium levels above 5.5 mM died. (4715199)
• Severe hyperkalemia (K>6.5 mM) is a sign of life-threatening digoxin toxicity. (37650725)

treatment: role of DSFab

• DSFab is the preferred treatment for severe hyperkalemia.
• The precise potassium level that should be a trigger to administer DSFab is unclear, with a recent consensus guideline suggesting K ≧6.5 mM. (39265879)
• Further discussion of DSFab is above: ⚡️

treatment: conventional therapies for hyperkalemia

• ⚠️ Avoid treating hyperkalemia too aggressively. In the context of digoxin intoxication, hypokalemia is more dangerous than mild hyperkalemia. Mild hyperkalemia could theoretically help drive potassium into cardiomyocytes via Na/K-ATPase, which could theoretically be beneficial. DSFab will cause a potassium shift into cells, so aggressive treatment of hyperkalemia plus DSFab could cause an overshoot hypokalemia.
• Indications for conventional therapies for hyperkalemia might include the following:
  • [i] Marked hyperkalemia, especially if hyperkalemia seems to be contributing to instability (e.g., contributing to AV block and bradycardia). (33476509) Alternatively, one consensus review article suggested that if DSFab is being given, DSFab alone should be sufficient to treat a potassium level of 5.5-6.5 mM. (37650725) 
  • [ii] In chronic digoxin intoxication, hyperkalemia may be multifactorial and only partially due to digoxin (especially in the context of renal dysfunction). In this context, conventional therapies for hyperkalemia may be required. (37861975)
• Conventional therapies could involve some combination of the following, depending on clinical context:
  • IV insulin and glucose.
  • Isotonic bicarbonate fluid resuscitation.
  • Potassium-wasting diuretics plus crystalloid (to facilitate renal potassium excretion).
  • Oral potassium binder (sodium zirconium cyclosilicate).
  • (More on the management of hyperkalemia here.)
• ⚠️ Calcium is contraindicated for the management of hyperkalemia due to severe digoxin intoxication. It's debated whether calcium is safe in this context, but there is no compelling evidence of benefit here, so calcium is probably best avoided. A consensus guideline strongly endorsed that IV calcium is unhelpful. (39265879)

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hypercalcemia

• Hypercalcemia is less common encountered, but if seen this may promote digoxin toxicity.
• The management of hypercalcemia is discussed here.

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questions & discussion

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