Podcast
Questions and Answers
Digoxin, derived from the foxglove plant, is primarily used in the management of which conditions?
Digoxin, derived from the foxglove plant, is primarily used in the management of which conditions?
- Hypertension and bradycardia
- Asthma and chronic obstructive pulmonary disease (COPD)
- Heart failure with reduced ejection fraction (HFREF) and atrial fibrillation/flutter (correct)
- Hyperlipidemia and peripheral artery disease
The therapeutic range for Digoxin is wide, making it safe to administer without regular monitoring.
The therapeutic range for Digoxin is wide, making it safe to administer without regular monitoring.
False (B)
What electrolyte imbalance is commonly observed in digoxin toxicity, often leading to increased mortality risk?
What electrolyte imbalance is commonly observed in digoxin toxicity, often leading to increased mortality risk?
Hyperkalemia
Digoxin inhibits the ______ enzyme in cardiac myocytes.
Digoxin inhibits the ______ enzyme in cardiac myocytes.
Match the following PGP inhibitors with their respective drug class or action:
Match the following PGP inhibitors with their respective drug class or action:
Which of the following best describes the mechanism by which digoxin increases myocardial contractility?
Which of the following best describes the mechanism by which digoxin increases myocardial contractility?
Digoxin is primarily excreted via the hepatic route; therefore, liver function is more critical to monitor than renal function.
Digoxin is primarily excreted via the hepatic route; therefore, liver function is more critical to monitor than renal function.
Name one ocular symptom commonly associated with digoxin toxicity.
Name one ocular symptom commonly associated with digoxin toxicity.
In suspected acute digoxin toxicity, ______ can be administered within 2 hours of ingestion to reduce absorption.
In suspected acute digoxin toxicity, ______ can be administered within 2 hours of ingestion to reduce absorption.
Match the following electrolyte imbalances with their effects on digoxin toxicity:
Match the following electrolyte imbalances with their effects on digoxin toxicity:
What is the primary indication for using digoxin-specific antibody (Fab) fragments in digoxin toxicity?
What is the primary indication for using digoxin-specific antibody (Fab) fragments in digoxin toxicity?
Following administration of digoxin-specific antibody (Fab) fragments, serum digoxin levels accurately reflect the clinical status of the patient.
Following administration of digoxin-specific antibody (Fab) fragments, serum digoxin levels accurately reflect the clinical status of the patient.
What is the term for the characteristic ECG changes seen with therapeutic digoxin use, including ST depression and T-wave changes?
What is the term for the characteristic ECG changes seen with therapeutic digoxin use, including ST depression and T-wave changes?
Drugs that induce PGP function may result in ______ digoxin levels.
Drugs that induce PGP function may result in ______ digoxin levels.
Match each risk factor with its potential mechanism for increasing digoxin toxicity:
Match each risk factor with its potential mechanism for increasing digoxin toxicity:
A patient on digoxin presents with nausea, vomiting, and confusion. Which initial investigation is most important to perform?
A patient on digoxin presents with nausea, vomiting, and confusion. Which initial investigation is most important to perform?
Hyperkalemia potentiates the effects of digoxin, increasing the risk of toxicity.
Hyperkalemia potentiates the effects of digoxin, increasing the risk of toxicity.
Name one common cardiac manifestation of digoxin toxicity seen on ECG.
Name one common cardiac manifestation of digoxin toxicity seen on ECG.
Digoxin exerts a negative chronotropic effect by increasing ______ tone.
Digoxin exerts a negative chronotropic effect by increasing ______ tone.
Match each ECG finding with its corresponding association in digoxin toxicity:
Match each ECG finding with its corresponding association in digoxin toxicity:
Which of the following best explains how hypomagnesemia potentiates digoxin toxicity?
Which of the following best explains how hypomagnesemia potentiates digoxin toxicity?
Digoxin toxicity typically presents with atrial tachyarrhythmias with a rapid ventricular response.
Digoxin toxicity typically presents with atrial tachyarrhythmias with a rapid ventricular response.
What is the common gastrointestinal symptom that patients with both acute and chronic digoxin toxicity may experience?
What is the common gastrointestinal symptom that patients with both acute and chronic digoxin toxicity may experience?
In patients with pacemakers, the effects of digoxin toxicity may be ______ by the paced rhythm.
In patients with pacemakers, the effects of digoxin toxicity may be ______ by the paced rhythm.
Match the following clinical features with whether they are more commonly associated with acute or chronic digoxin toxicity:
Match the following clinical features with whether they are more commonly associated with acute or chronic digoxin toxicity:
Which of the following best describes the rationale for monitoring electrolytes in patients taking digoxin?
Which of the following best describes the rationale for monitoring electrolytes in patients taking digoxin?
Volume depletion decreases the risk of digoxin toxicity because it concentrates the drug in the bloodstream.
Volume depletion decreases the risk of digoxin toxicity because it concentrates the drug in the bloodstream.
Other than digoxin, name one medication that should be withheld in the initial management of digoxin toxicity.
Other than digoxin, name one medication that should be withheld in the initial management of digoxin toxicity.
Following Fab fragment administration, a return to normal Na+/K+/ATPase function can result in profound ______.
Following Fab fragment administration, a return to normal Na+/K+/ATPase function can result in profound ______.
Match each investigation with its primary utility in assessing digoxin toxicity:
Match each investigation with its primary utility in assessing digoxin toxicity:
Why is psychological support considered in the ongoing management of digoxin toxicity?
Why is psychological support considered in the ongoing management of digoxin toxicity?
Patients who experience rebound toxicity after Fab fragment administration typically show immediate improvement and do not require further monitoring.
Patients who experience rebound toxicity after Fab fragment administration typically show immediate improvement and do not require further monitoring.
Other than arrhythmias, what is a significant cardiovascular complication that can result from digoxin toxicity, potentially leading to cardiac arrest?
Other than arrhythmias, what is a significant cardiovascular complication that can result from digoxin toxicity, potentially leading to cardiac arrest?
Xanthopsia is a side effect of digoxin toxicity characterized by ______ discolouration in vision.
Xanthopsia is a side effect of digoxin toxicity characterized by ______ discolouration in vision.
Match the following drugs with their potential interaction with digoxin:
Match the following drugs with their potential interaction with digoxin:
In the context of digoxin toxicity, what is the 'stone heart theory,' and why is it controversial?
In the context of digoxin toxicity, what is the 'stone heart theory,' and why is it controversial?
The presence of 'digitalis effect' on an ECG always indicates digoxin toxicity and requires immediate intervention.
The presence of 'digitalis effect' on an ECG always indicates digoxin toxicity and requires immediate intervention.
List one differential diagnosis to consider in cases of suspected digoxin toxicity.
List one differential diagnosis to consider in cases of suspected digoxin toxicity.
Patients with acute digoxin toxicity are likely to remain asymptomatic for ______ hours after ingestion.
Patients with acute digoxin toxicity are likely to remain asymptomatic for ______ hours after ingestion.
Match each clinical scenario with the most appropriate initial management strategy in suspected digoxin toxicity:
Match each clinical scenario with the most appropriate initial management strategy in suspected digoxin toxicity:
Flashcards
Digoxin
Digoxin
Cardiac glycoside used in HFREF and AF/flutter, with a narrow therapeutic range (0.5-0.9 µg/L).
Digoxin Mechanism
Digoxin Mechanism
Inhibits Na+/K+/ATPase, increasing intracellular calcium and vagal tone, affecting contractility and AV node conduction.
Digoxin Toxicity
Digoxin Toxicity
Occurs at >1.5 µg/L; caused by overdose, CKD, drug interactions, or electrolyte imbalance.
Digoxin Toxicity Risk Factors
Digoxin Toxicity Risk Factors
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Digoxin Toxicity Features
Digoxin Toxicity Features
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Digoxin Toxicity Investigations
Digoxin Toxicity Investigations
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Digoxin Toxicity Management
Digoxin Toxicity Management
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Digoxin Toxicity Complications
Digoxin Toxicity Complications
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Digoxin Indications
Digoxin Indications
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Digoxin: Positive Inotropic Action
Digoxin: Positive Inotropic Action
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Digoxin: Negative Chronotropic Action
Digoxin: Negative Chronotropic Action
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Digoxin: Monitoring
Digoxin: Monitoring
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PGP Inhibitors and Digoxin
PGP Inhibitors and Digoxin
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Digoxin and Hyperkalemia
Digoxin and Hyperkalemia
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Digoxin and Hypokalemia
Digoxin and Hypokalemia
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Xanthopsia
Xanthopsia
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ECG Findings in Digoxin Toxicity
ECG Findings in Digoxin Toxicity
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Digitalis Effect on ECG
Digitalis Effect on ECG
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Diagnosing Digoxin Toxicity
Diagnosing Digoxin Toxicity
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Initial Digoxin Toxicity Management
Initial Digoxin Toxicity Management
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Indications for Digoxin Fab Fragments
Indications for Digoxin Fab Fragments
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Study Notes
- Digoxin is a cardiac glycoside derived from the foxglove plant, used to treat HFREF and AF/flutter.
- It has a narrow therapeutic range of 0.5-0.9 µg/L.
Mechanism of Action
- Digoxin inhibits Na+/K+/ATPase, which increases intracellular calcium, leading to increased contractility.
- It also enhances vagal tone, decreasing AV node conduction.
Toxicity
- Toxicity occurs at levels >1.5 µg/L.
- Common causes include overdose, CKD, drug interactions (e.g., amiodarone, verapamil), and electrolyte imbalances.
Risk Factors
- Being over 55
- CKD
- Use of PGP inhibitors
- Electrolyte imbalances (hypokalemia, hypomagnesemia, hypercalcemia)
- Hypothyroidism
- Intercurrent illness
Clinical Features
- Cardiac symptoms: arrhythmias, bradycardia
- Gastrointestinal symptoms: nausea, vomiting
- Neurological symptoms: confusion, weakness
- Ocular symptoms: xanthopsia, blurred vision
Investigations
- ECG: to monitor for bradyarrhythmias, PVCs
- Serum digoxin levels
- U&Es
- Magnesium
- Calcium levels
- Serial ECG monitoring
Management
- Withhold the digoxin, correct any electrolyte imbalances, and monitor cardiac activity.
- Administer Fab fragments for life-threatening arrhythmias, cardiac arrest, or hyperkalemia >5.5 mmol/L.
Complications
- Life-threatening arrhythmias
- Cardiac arrest
- Rebound toxicity post-Fab fragments
- Hypokalemia
Aetiology
- Digoxin is used in heart failure with reduced ejection fraction (HFREF) and for rate control in supraventricular tachyarrhythmias like atrial fibrillation (AF) and atrial flutter.
- Elderly patients and those with renal impairment require dose reductions.
- It has positive inotropic and negative chronotropic effects.
Pharmacodynamics
- It increases myocardial contractility by inhibiting the Na+/K+/ATPase enzyme, increasing intracellular sodium, and ultimately enhancing calcium availability.
- At lower doses, digoxin stimulates the vagus nerve, reducing the automaticity of the sinoatrial node and slowing AV node conduction.
Monitoring
- Regular monitoring of serum digoxin during maintenance treatment is not required unless clinically indicated such as suspected toxicity.
- Renal function and electrolytes need to be routinely monitored.
Digoxin Toxicity: Details
- The safe therapeutic range is 0.5-0.9 micrograms/L
- Toxicity may develop when serum digoxin levels reach 1.5-3.0 micrograms/L and becomes highly likely over this range.
- Acute toxicity involves a rapid rise in serum digoxin levels, commonly from overdose.
- Chronic toxicity develops over time due to overmedication, kidney disease, electrolyte imbalances, or drug interactions.
P-Glycoprotein (PGP) Inhibition
- PGPs are efflux transporters affecting digoxin absorption and clearance.
- Inhibitors like verapamil, amiodarone, and erythromycin can increase digoxin levels.
- Inducers like rifampicin and St John’s wort may decrease digoxin levels.
Electrolyte Derangement and Digoxin Toxicity
- Hyperkalemia is common in digoxin toxicity and a predictor of mortality.
- Hypokalemia and hypercalcemia potentiate digoxin's effects.
- Hypomagnesemia may also exacerbate toxicity, often alongside hypokalemia.
Clinical Features of Toxicity
- Symptoms can be nonspecific and include fatigue, headache, and weakness.
- Cardiac issues are the most concerning, potentially leading to fatal arrhythmias.
- Xanthopsia (yellow vision) is a known side effect indicating toxicity.
Acute vs. Chronic Toxicity
- Acute toxicity typically presents with GI symptoms early on, followed by neurological and cardiac issues.
- Chronic toxicity, more common in the elderly, develops insidiously with more prominent neurological features.
Differential Diagnoses
- Beta-blocker toxicity
- Calcium channel blocker toxicity
- Ischemic heart disease
- Hypothyroidism
Investigations: ECG Findings
- ECG can show various arrhythmias, with PVCs being the most common.
- Acute toxicity often causes bradycardia with PR and QRS prolongation.
- The digitalis effect includes ST depression and T-wave changes, which are normal with digoxin use, not toxicity.
Lab Investigations
- Electrolyte levels, renal function, and magnesium levels should be checked.
- Serum digoxin levels should be measured immediately in chronic toxicity or 6 hours post-acute overdose.
Diagnosis
- The digoxin toxicity diagnosis is primarily clinical, based on exposure and symptoms.
- Elevated serum digoxin levels are supportive but not definitive.
Management: Initial Steps
- If acute ingestion is recent, administer activated charcoal.
- Withhold digoxin and any potentiating medications.
- Provide supportive care like antiemetics and IV fluids.
- Correct any electrolyte imbalances.
Digoxin Binding Therapy: Fab Fragments
- Use Fab fragments for life-threatening cases.
- Improvement is usually seen quickly, but monitor for rebound toxicity and hypokalemia.
- Following administration of fab fragments, serum digoxin levels become unreliable.
Ongoing Management
- Address underlying causes like kidney injury or sepsis.
- Provide psychological support for overdose cases.
Cardiotoxicity
- Manage acute cardiac manifestations per ALS guidelines.
Complications of Digoxin Toxicity
- Life-threatening arrhythmias
- Cardiac arrest
- CNS depression
- GI disturbance
- Treatment complications may include anaphylaxis, hypokalemia, and recurrence of previous arrhythmias.
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