Digoxin toxicity

Question 1

Cardiotoxic drugs are

Answer 1

• Digitalis.
• BB.
• CCB

Question 2

Digitalis is used in the management of

Answer 2

congestive heart failure and atrial fibrillation.

Question 3

Mode of Digitalis toxicity

Answer 3

1-Accidental in children.
2-Intentional.
3-Chronic digoxin poisoning

Question 4

Chronic digoxin poisoning is caused by

Answer 4

long standing treatment in elderly patients with pre existing renal and cardiac disease. It results from large doses of digoxin relative to age, changing renal function, concurrent diuretic administration which may produce hypokalemia and hypomagnesaemia.

Question 5

Mechanism of Digitalis toxicity

Answer 5

1-Cardiac glycosides produce reversible inhibition of sodium-potassium-activated adenosine triphosphatase (Na+/K+-ATPase) pump, which causes increased intracellular sodium and decreased intracellular potassium.
2-Inhibition of Na+/K+-ATPase in skeletal muscle results in increased extracellular potassium and contributes to hyperkalemia.
3-Accumulation of intracellular calcium leads to increased excitability. Leading to various types of dysrhythmias whether atrial or ventricular.
4-Vagotonic effects, resulting in bradycardia and AV block with toxic doses.

Question 6

Clinical presentation of Digitalis Acute overdose:

Answer 6

• Vomiting,
• Hyperkalemia,
• Sinus bradycardia, sinoatrial arrest,
• AV block.
• Ventricular tachycardia or fibrillation .
• Hypotension
• cardiac arrest.

Question 7

Clinical presentation of Chronic Digitalis intoxication:

Answer 7

• visual disturbances (blurred vision, abnormal color perceptions of yellow or yellow-green halos may occur),
• weakness,
• sinus bradycardia,
• ventricular arrhythmias (ventricular tachycardia, and ventricular fibrillation)
• Hypokalemia and hypomagnesemia (from chronic diuretic use and it worsen the tachy-arrhythmias).

Question 8

Investigations

Answer 8

1. Electrolytes
   -Hyperkalemia is an early predictor of need for antidotal therapy.
   -Hypokalemia exacerbates chronic toxicity.
   -Hypercalcemia and hypomagnesemia exacerbate cardiac glycoside toxicity.
   2- Serum digoxin concentration (SDC)
   -Therapeutic SDC is 0.6 – 2.1 ng/ml.
   -In acute toxicity, it should be measured 6 h post-ingestion.
2. Renal functions
   Renal impairment weakens elimination of glycosides.
3. ECG and continuous cardiac monitor
   -Bradycardia,
   -AV block.
   -atrial or ventricular dysrhythmias
   -Nonspecific ST segment sagging and T wave abnormalities are consistent with digitalis treatment.
   -Peaked T waves may occur in hyperkalemia.

Question 9

Treatment of Digitalis toxicity

Answer 9

• Emergency measures (ABCD)
• Elimination
• GL is of limited value. GL increases vagal tone and may precipitate or worsen bradycardia. Consider pre-treatment with atropine.
• MDAC is beneficial because digoxin has an enterohepatic circulation.
• Cholestyramine will interrupt the enterohepatic circulation.
• Because of the large Vd, hemodialysis and hemoperfusion do not increase clearance.

Question 10

Antidote of Digitalis

Answer 10

• (Digibind) Digoxin specific monoclonal antibodies (Fab fragments) are effective for digoxin toxicity.
• The Fab fragment binds free digoxin. Once the digoxin-Fab complex is formed, the digoxin molecule is no longer pharmacologically active.
• Dose depends on SDC or amount ingested and body weight.
• Reversal of signs of digitalis intoxication usually occurs within 30–60 minutes of administration.
• Monitor potassium level as hypokalemia may occur due to reactivation of Na+/K+-ATPase.

Question 11

INDICATIONS of using antidote

Answer 11

-hyperkalemia (> 5 mEq/L)
-presence of life-threatening arrhythmias (eg, ventricular arrhythmias)
-Hemodynamically significant bradycardia unresponsive to atropine.
-Laboratory
1-SDC 6 h post-ingestion > 10 ng/ml in adults, or > 5 ng/ml in children
2-SDC > 15 ng/ml at anytime
-Ingestion of ≥ 10 mg in adults, or ≥ 4 mg in children
-Chronic toxicity with significant GI symptoms, mental deterioration, renal impairment, or dysrhythmias of acute onset.
-Suspected toxicity with unavailable SDC

Question 12

Treatment of complications

Answer 12

• Atropine for sinus bradycardia.
• Ventricular dysrhythmias: if Fab is unavailable:
  1. Phenytoin
  2. Lidocaine
  3. Magnesium sulfate .
• Cardiac pacing (temporary pacemaker) in serious AV block if Fab fragments are not immediately available.
• Hyperkalemia > 5.5 mEq/L: if Fab is unavailable:
  1. Glucose/insulin
  2. NaHCO3
• These methods facilitate the redistribution of potassium intracellularly

Question 13

AVOID THE FOLLOWING in Digitalis toxicity:

Answer 13

• Calcium preparations
• Quinidine and procainamide
• Calcium channel blockers,
• Beta-blockers