Causes and mechanisms of development
Cardiac glycoside overdose occurs due to their ability to undergo material accumulation in the body, as well as their extremely narrow therapeutic index. The disorders are divided into cardiac and extracardiac manifestations. Concomitant hypokalemia and hypomagnesemia, which frequently develop if the patient is taking loop or thiazide diuretics, play a special role in triggering arrhythmias.
Cardiac disorders and arrhythmias
Cardiovascular system involvement in intoxication is life-threatening:
- Ventricular extrasystoles: occur due to increased automaticity resulting from intracellular ion imbalance (hypokaligistia and hypercalcigistia). The rhythm frequently takes the form of bigeminy (an extrasystole following every normal contraction) or trigeminy (following every two).
- Atrioventricular block: develops due to a negative dromotropic effect caused by enhanced vagal influences on the heart.
- Ventricular fibrillation: chaotic contractions of fibers at a rate of 450–600 per minute, rapidly progressing to asystole and cardiac arrest. This is the most common cause of mortality.
Principles of treatment and antidote therapy
Management of overdose requires a comprehensive approach:
- Specific therapy: the most effective agents are digoxin antibody fragments.
- Correction of AV block: atropine is used, which blocks cardiac $M_2$ muscarinic receptors, eliminates the inhibitory effect of the vagus nerve (n. vagus) on the atrioventricular node, and improves conduction.
- Electrolyte balance correction: potassium chloride and combined agents (Panangin, Asparkam) are used. Magnesium ions act as activators of $Na^+,K^+$-ATPase, ensuring potassium transport into cardiomyocytes.
- Calcium chelation: disodium edetate (Trilon B) is administered intravenously to chelate excess $Ca^{2+}$ ions in the blood.
- Antidote therapy: unithiol, as a thiol (-SH) group donor, forms disulfide bridges with the glycoside, releasing the intrinsic thiol groups of $Na^+,K^+$-ATPase and restoring its transport function.
Treatment of extrasystoles
When ventricular extrasystoles develop, class IB sodium channel blockers are prescribed, specifically phenytoin and lidocaine. The choice of these medications is justified by the fact that they act primarily on ventricular tissue, effectively stabilizing the heart rhythm.
Briefly: answers to topical questions
What extracardiac manifestations occur in digitalis toxicity?
Digitalis toxicity causes systemic extracardiac adverse effects affecting the digestive, visual, and nervous systems. These manifestations include:
- Dyspeptic disorders — nausea, vomiting, diarrhea.
- Visual disturbances — xanthopsia as a specific symptom (a color vision abnormality where perceived objects appear tinged in yellow and green).
- Neurological and psychiatric disorders — headaches, sleep disturbances, psychomotor agitation, hallucinations.
What ECG changes, aside from arrhythmias, are characteristic of cardiac glycoside action and overdose?
In addition to the arrhythmogenic effect, the medicinal action of cardiac glycosides is characterized by the following ECG changes:
- ST-segment shift — characteristic "scooped-out" depression.
- T-wave alteration — decrease in its amplitude.
- Q-T interval alteration — shortening.
Antidote chain: "Antibodies remove digoxin, Atropine relieves vagal nerve block, Unithiol rescues enzymes via thiol groups, and Trilon B chelates calcium."
Class and exam questions
Which arrhythmia is the most frequent cause of death in digitalis toxicity?
Ventricular fibrillation with a fiber contraction rate of 450–600 per minute, rapidly progressing to asystole.
What is the mechanism of action of unithiol in this intoxication?
Unithiol serves as a sulfhydryl group donor, forms disulfide bridges with the glycoside, and releases the intrinsic thiol groups of $Na^+,K^+$-ATPase, restoring its activity.
Which diuretics contribute to provoking arrhythmias during glycoside administration?
Loop and thiazide diuretics, as they induce hypokalemia and hypomagnesemia.
Which drug is the agent of choice for treating AV block?
Atropine, which blocks $M_2$ muscarinic receptors and eliminates the inhibitory effect of the vagus nerve on the atrioventricular node.
What else to study on this topic
- Material accumulation of cardiac glycosides and its pharmacokinetic aspects
- The role of ion imbalance (hypokaligistia and hypercalcigistia) in increasing automaticity
- Pharmacological properties of class IB sodium channel blockers (phenytoin, lidocaine) in arrhythmias
- Chelating agents and features of calcium ion binding in systemic circulation
- Influence of the vagus nerve (n. vagus) and the negative dromotropic effect on conduction
Master the entire topic in the «Pharmacology» course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Digitalis toxicity" and 5,304 more subject pages
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 116 video lessons on the subject
Other topics in the section "Cardiovascular Drugs"
Free video lessons: pharmacologyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.