Quinidine cardiovascular effects

The place of the dmg in dentistry [153 4] and in electro-convulsive therapy [ 154] (with a description of a technique to surmount difficulties arising from the concurrent use ot suxamethonium) has been evaluated. A refined radio telemetric technique has enabled a detailed study [155] of the cardiovascular effects of propanidid to be made, resulting in strong evidence for a transient procainamide- or quinidine-like depression of myocardial conductive tissue. The above publications [150-5] quote a large number of relevant references. 

Adverse effects include insomnia, sedation, and cardiovascular abnormalities due to anticholinergic activity and a direct quinidine-like effect on the heart. 

The cardiovascular adverse effects associated with quinidine therapy are hypotension and tachycardia, both of which are related to its a-adrenoceptor blocking actions. The tachycardia may be a reflex adjustment to the fall in blood pressure or may also be a direct action of the dmg on sympathetic nerve terminals leading to an increased release of NE. Quinidine also produces ringing in the ears (cinchonism) (1,2). 

Preliminary studies [241, 249, 250] of the cardiovascular and sympatholytic properties of prenylamine demonstrated that coronary blood flow and oxygenation could be increased under experimental conditions (in dogs) and that the drug interacted in complex fashion with sympathetically innervated organs, but the picture presented was someudiat confused because of the many uncontrolled variables and limitations of the actual techniques used. Anti-arrhythmic activity of potency comparable with that of quinidine, plus local anaesthetic properties, were also demonstrated [251] but the same worker was notable to reproduce these effects in intact live animals with any consistency. Large doses of the drug actually provoked cardiac fibrillation in some cases. 

The hemodynamic alterations produced by procainamide are similar to those of quinidine but are not as intense. Alterations in circulatory dynamics vary according to the cardiovascular state of the individual. The hypotensive effects of procainamide are less pronounced after intramuscular administration and seldom occur after oral administration. 

A large number of prescription and nonprescription drugs, as well as a variety of plants and mushrooms, can inhibit the effects of acetylcholine at muscarinic receptors. Some drugs used for other purposes (eg, antihistamines) also have anticholinergic effects. Many of them have other potentially toxic actions. For example, antihistamines such as diphenhydramine can cause seizures tricyclic antidepressants, which have anticholinergic, quinidine-like, and a-blocking effects, can cause severe cardiovascular toxicity. 

The adverse effects of most serious concern relate to the cardiovascular system and seizure threshold. Actions on the adrenergic and cholinergic systems probably contribute to both hypotensive and direct cardiac effects, including alterations in heart rate, quinidine-like delays in conduction, and reduced myocardial contractility. The seizure threshold is lowered, increasing the frequency of epileptic seizures. All of these adverse effects can occur at therapeutic dosages in susceptible populations, such as elderly people, children, and people with cardiac problems or epilepsy, but are also a major cause of morbidity and mortality in accidental or intentional overdosage. Doses in excess of 500 mg can be seriously toxic, and death is fairly common when doses of 2 g or more are taken. 

Muir W W 1995 The haemodynamic effects of milrinone HCI In halothane anaesthetized horses. Equine Veterinary Journal Supplement 19 108-113 Muir W W, Mcguirk S M 1985 Pheirmacology and pharmacokinetics of drugs used to treat cardiac disease in horses. Veterinary Clinics of North America Equine Practice 1 335-352 Muir W W D, Mcguirk S 1987 Cardiovascular drugs. Their pharmacology and use In horses. Veterinary Clinics of North America Equine Practice 3 37-57 Muir W W D, Reed S M, Mcguirk S M 1990 Treatment of atrial fibrillation in horses by intravenous administration of quinidine. Journal of the American Veterinary Medical Association 197 1607-1610... 

Epinephrine usually Is administered slowly by Intravenous (IV) Injection to relieve acute asthmatic attacks not controlled by other treatments. Intravenous Injection produces an Immediate response. Use of EPI with drugs that enhance cardiac arrhythmias (digitalis or quinidine) Is not recommended. Tricyclic antidepressants and MAO Inhibitors will potentiate the effects of EPI on the heart. Epinephrine should be used with caution In Individuals suffering from hyperthyroidism, cardiovascular disease, hypertension, or diabetes. Adverse effects Include palpitations, tachycardia, sweating, nausea and vomiting, respiratory difficulty, dizziness, tremor, apprehension, and anxiety. 

Quinidine is more potent than quinine in its action on the cardiovascular system. Overdoses may cause loweriug of blood pressure. Gastric effects are lower thau quiuiue. Toxicity is lower relative to quiuiue subcutaueous lethal dose in mice is 400 mg/kg against 200 mg/kg for quinine. 

A. Cardiovascular. Anticholinergic effects may produce tachycardia. Alpha-adrenergic blockade may cause orthostatic hypotension. With very large overdoses of some agents, quinidine-llke membrane-depressant effects on the heart may occur. Many agents can cause QT prolongation and torsade de pointes (see p 14). 

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