Digitalis glycosides cardiac arrhythmias

Parenteral therapy The dangers of parenteral use of quinidine are increased in the presence of AV block or absence of atrial activity. Administration is more hazardous in patients with extensive myocardial damage. Use of quinidine in digitalis-induced cardiac arrhythmia is extremely dangerous because the cardiac glycoside may already have caused serious impairment of intracardiac conduction system. Too rapid IV administration of as little as 200 mg may precipitate a fall of 40 to 50 mm Hg in arterial pressure. 

The effects of digitalis glycosides might be increased by rises in blood calcium levels, and the use of intravenous calcium may result in the development of potentially life-threatening digitalis-induced cardiac arrhythmias. Teriparatide appears not to affect the calcium-mediated pharmacodynamics of digoxin. 

The most common imbalances are a loss of potassium and water. Other electrolytes, namely magnesium, sodium, and chlorides, are also lost. When too much potassium is lost, hypokalemia (low blood potassium) occurs (see Home Care Checklist Preventing Potassium Imbalances). In certain patients, such as those also receiving a digitalis glycoside or those who currently have a cardiac arrhythmia, hypokalemia has the potential to create a mo re serious arrhythmia Hypokalemia is... 

CARD IAC ARRHYTH MI AS AN D DIZZIN ESS. Patients receiving a diuretic (particularly a loop or thiazide diuretic) and a digitalis glycoside concurrently require frequent monitoring of the pulse rate and rhythm because of the possibility of cardiac arrhythmias. Any significant changes in the pulse rate and rhythm are immediately reported to the primary health care provider. 

Alterations in the serum potassium level are hazardous because they can result in cardiac arrhythmias. Drugs that may cause hyperkalemia despite normal renal function include potassium itself, 13 blockers, digitalis glycosides, potassiumsparing diuretics, and fluoride. Drugs associated with hypokalemia include barium, 13 agonists, caffeine, theophylline, and thiazide and loop diuretics. 

Potassium and digitalis interact in two ways. First, they inhibit each other s binding to Na+/K+ ATPase therefore, hyperkalemia reduces the enzyme-inhibiting actions of cardiac glycosides, whereas hypokalemia facilitates these actions. Second, abnormal cardiac automaticity is inhibited by hyperkalemia (see Chapter 14 Agents Used in Cardiac Arrhythmias). Moderately increased extracellular K+ therefore reduces the effects of digitalis, especially the toxic effects. 

Adverse effects Thiazide diuretics induce hypokalemia and hyperuricemia in 70% of patients, and hyperglycemia in 10% of patients. Serum potassium levels should be monitored closely in patients who are predisposed to cardiac arrhythmias (particularly individuals with left ventricular hypertrophy, ischemic heart disease, or chronic congestive heart failure) and who are concurrently being treated with both thiazide diuretics and digitalis glycosides (see p. 160). Diuretics should be avoided in the treatment of hypertensive diabetics or patients with hyperlipidemia. 

Myocardial infarction predisposes to cardiac arrhythmia with digitalis glycosides or sympathomimetics. 

Cardiovascular, e.g. from foxglove (Digitalis), mistletoe (Viscum album)) and lily-of-the-valley (Convallaria) which contain cardiac glycosides that cause vomiting, diarrhoea and cardiac arrhythmia. 

Phenytoin has a stabilising effect on the myocardial cells so that the toxic threshold of digoxin at which arrhythmias occur is raised. However, the bradycardic effects of the digitalis glycoside are not opposed and the lethal dose is unaltered, so that the cardiac arrest reported would appear to be the result of excessive bradycardia. It seems possible that the fall in plasma digitoxin levels may be due to a phenytoin-induced increase in the metabolism of the digitoxin by the liver. ... 

Serious cardiac arrhythmias can develop in patients receiving digitalis glycosides who are given suxamethonium (succinylcho-line) or pancuronium. 

Established interactions. The CSM in the UK advises that, as potentially serious hypokalaemia may result from beta2 agonist therapy, particular caution is required in severe asthma, as this effect may be potentiated by theophylline and its derivatives, corticosteroids, diuretics, and by hypoxia. Hypokalaemia with concurrent use of thiazide and loop diuretics may be reduced or even abolished by the addition of spironolactone or high-dose triamterene. Plasma potassium levels should therefore be monitored in patients with severe asthma. Hypokalaemia may result in cardiac arrhythmias in patients with ischaemic heart disease and may also affect the response of patients to drugs such as the digitalis glycosides and an-tiarrhythmics. 

Calcium ion facilitates the toxic actions of cardiac glycosides by accelerating the overloading of intracellular calcium stores that appears to be responsible for digitalis-induced abnormal automaticity. Hypercalcemia therefore increases the risk of a digitalis-induced arrhythmia. The effects of magnesium ion appear to be opposite to those of calcium. These interactions mandate careful evaluation of serum electrolytes in patients with digitalis-induced arrhythmias. 

The most common cardiac manifestations of glycoside toxicity include atrioventricular junctional rhythm, premature ventricular depolarizations, bigeminal rhythm, and second-degree atrioventricular blockade. However, it is claimed that digitalis can cause virtually every variety of arrhythmia. 

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