Catecholamines ventricular fibrillation

Halothane exerts a pronounced hypotensive effect, to which a negative inotropic effect contributes. Enflurane and isoflurane cause less circulatory depression. Halothane sensitizes the myocardium to catecholamines (caution serious tachyarrhythmias or ventricular fibrillation may accompany use of catecholamines as antihypotensives or toco-lytics). This effect is much less pronounced with enflurane and isoflurane. Unlike halothane, enflurane and isoflurane have a muscle-relaxant effect that is additive with that of nondepolarizing neuromuscular blockers. 

Cocaine, which blocks the uptake of catecholamines, produces dose-dependent effects, initially causing euphoria, vasoconstriction, and tachycardia, and in toxic doses, convulsions, myocardial depression, ventricular fibrillation, medullary depression, and death. Cocaine is able to block nerve conduction and currently is used only for topical anesthesia. 

Another cardiac response to catecholamine release is Increased vulnerability to ventricular fibrillation. Recent studies (13) have shown that bromocriptine produced an increase of 50% in the ventricular fibrillation threshold In anesthetized dogs, and that pretreatment with the peripheral D-2 dopamine antagonist domperidone abolished this effect. This suggests that adrenergic induced cardiac arrhythmia may be inhibited by peripheral presynaptic dopamine agonists. 

Chronic skin irritation occurs as a result of defatting of the skin. Ventricular fibrillation is due to the direct sensitization of the myocardium to endogenous catecholamines. 

May precipitate cardiac dysrhythmias, esp ventricular fibrillation, due to increased myocardial sensitivity to circulating catecholamines... 

Vasopressin levels in patients with vasodilatory shock are inappropriately low, and such patients are extraordinarily sensitive to the pressor actions of vasopressin. The combination of vasopressin and norepinephrine is superior to NE alone in the management of catecholamine-resistant vasodilatory shock. Although the efficacy of vasopressin in the resuscitation of patients with ventricular fibrillation or pulseless electrical activity is similar to that of epinephrine, vasopressin followed by Epi appears to be more effective than Epi alone in the treatment of patients with asystole. 

B. Pulmonary edema or ventricular fibrillation has occasionally occurred shortly after naloxone administration in opioid-intoxicated patients. Pulmonary edema has also been associated with postanesthetic use of naloxone, especially when catecholamines and large fluid volumes have been administered. Pulmonary edema has been reported after IV nalmefene. 

Propranolol. Propranolol hydrochloride, considered the prototype of the P-adrenoceptor blocking agents, has been in use since 1964. It is a nonselective, highly Hpid-soluble P-adrenoceptor blocker having no ISA. It is a mixture of (+) and (—) enantiomers, and the (—) enantiomer is the active moiety. The local anesthetic effects of propranolol are equipotent to those of Hdocaine [137-58-6] C 4H22N20, (see Anesthetics). Therapeutic effects include termination of catecholamine-induced arrhythmias, conversion of SA nodal tachycardias (including flutter and fibrillation) and AV nodal tachyarrhythmias to normal sinus rhythm, digitahs-induced arrhythmias, and ventricular arrhythmias (1,2). The dmg also has cardioprotective properties (37,39). 

A variety of cardiac arrhythmias have been described in patients receiving levodopa, including tachycardia, ventricular extrasystoles and, rarely, atrial fibrillation. This effect has been attributed to increased catecholamine formation peripherally. The incidence of such arrhythmias is low, even in the presence of established cardiac disease, and may be reduced still further if the levodopa is taken in combination with a peripheral decarboxylase inhibitor. 

Drugs that block beta-1 receptors on the myocardium are one of the mainstays in arrhythmia treatment. Beta blockers are effective because they decrease the excitatory effects of the sympathetic nervous system and related catecholamines (norepinephrine and epinephrine) on the heart.5,28 This effect typically decreases cardiac automaticity and prolongs the effective refractory period, thus slowing heart rate.5 Beta blockers also slow down conduction through the myocardium, and are especially useful in controlling function of the atrioventricular node.21 Hence, these drugs are most effective in treating atrial tachycardias such as atrial fibrillation.23 Some ventricular arrhythmias may also respond to treatment with beta blockers. 

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