Cardiac glycoside poisoning (including digoxin) - EMCrit Project
2021年5月13日 · mechanism of action of digoxin (1) Digoxin inhibits the cardiac Na/K antiporter (orange oval, above). 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.
Pharmacological treatment of cardiac glycoside poisoning
Therapeutic options to treat cardiac glycoside toxicity include pharmacological antagonists of bradycardia, reversal of Na + ‐K + ‐ATPase inhibition or enhanced elimination of the cardiac glycoside.
Cardiac glycoside - Wikipedia
In terms of inotropic activity, excessive cardiac glycoside dosage results in cardiac contractions with greater force, as further calcium is released from the SR of cardiac muscle cells. Toxicity also results in changes to heart chronotropic activity, resulting in multiple kinds of dysrhythmia and potentially fatal ventricular tachycardia .
Role of Mitochondrial Dysfunction in Cardiac Glycoside Toxicity
The findings reveal the mechanism behind cardiac glycoside toxicity and show that improving mitochondrial Ca 2+ retention by mNCE inhibition can mitigate these effects, particularly with respect to the suppression of Ca 2+-triggered arrhythmias, while enhancing positive inotropic actions. These results suggest a novel strategy for the treatment ...
A review of cardiac glycosides: Structure, toxicokinetics, clinical ...
2019年2月1日 · Most case reports of poisoning caused by CGs are associated with cardiovascular toxicity, causing a variety of arrhythmias and lesions in the heart tissue. Experimental studies also describe important similarities among different CGs, especially regarding species sensitivity.
The 3 most common scenarios resulting in cardiac glycoside toxicity are as follows: (1) intentional or accidental acute ingestion leading to acute toxicity, (2) systemic accumulation secondary to hepatic or renal dysfunction, and (3) systemic accumula-
Inflammasome inhibition blocks cardiac glycoside cell toxicity
2019年8月8日 · Cardiac glycoside toxicity is evident in human but not murine immune cells. We next sought to examine the response to cardiac glycosides using knockout mice deficient in factors key to inflammasome activation of pyroptosis/IL-1β, such as caspase-1, apoptosis-associated specklike protein containing a CARD, the NOD-like receptor, and gasdermin D.
Mechanism of cardiac glycoside-induced toxicity: physiology ...
1983年5月15日 · Results obtained indicate that ouabain-induced toxicity may in part result from an increase in coronary resistance producing myocardial hypoxia, cell damage, and arrhythmias. Preliminary studies suggest that the membrane-stabilizing action of propranolol appears to be the basis of its protective effect.
Acute toxicity may include nausea, vomiting, abdominal pain, lethargy, bradycardia, dysrhythmias, and hyperkalemia. Chronic toxicity may include bradycardia with or without heart block, other dysrhythmias, nausea, delirium, and vision changes. For early acute ingestion, we recommend GI decontamination.
Cardiovascular Drug Toxicity - Critical Care Clinics
Two different approaches are suggested for management of cardiac glycoside toxicity depending on whether the patient presents with an acute overdose or chronic toxicity. A treatment approach is proposed for sodium channel blocker poisoning, although supportive evidence is sparse.