Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D04052 (Xylocaine)
 213 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The following results were obtained in an experimental study in the dogs in general pentobarbital anaesthesia: Lidocaine type antiarrhythmics (lidocaine, Xylocaine ASTRA, Ethmozin USSR) administered shortly before artery ligation have a pro-fibrillation effect. This effect is indirectly proportional to the ischaemic focus development. A 3rd-generation beta blocker with intrinsic sympathetic activity (celiprolol, Selectol Chemie-Linz) had the same electrostabilizing effect on the ventricles in the acute phase of ischaemia as a 1st-generation beta blocker (metipranolol, Trimepranol SPOFA). The 3rd-generation blocker, however, stopped short of provoking a drop in the heart rate invariably associated with the 1st-generation beta blocker. The analgesic fentanyl (G. Richter) in combination with benzodiazepine (m,idazolam, Dormicum Hoffmann-La Roche) inducs analgosedation. In this way the dose of the analgetic can be reduced and yet the analgesia and electrostability of the heart remain the same. Due to the lower dose of the analgesic there is a lesser decrease in the heart rate and blood pressure. Analgosedation can be discontinued by administering an antagonist-agonist of benzodiazepines (flumazenil, Anexate Hoffmann-La Roche) or an antagonist of potent analgesics (butorphanol, Beforal SPOFA) without the risk of eliminating, at the same time, the electrostabilizing effect of analgosedation on the ischaemically damaged ventricles of the heart. For the prevention of sudden coronary death due to ventricular fibrillation in the acute phase of local myocardial ischaemia we can, on the basis of our experimental results, recommend analgosedation and the use of beta blockers with intristic sympathetic action. The use of lidocaine antiarrhythmics may lead to a reduction in the electric stability of the heart ventricles the ischaemic focus is developing under a certain "critical" blood level of the antiarrhythmics.
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PMID:Prevention of sudden coronary death. 167 65

Initial assessment of widecomplex tachycardias (WCTs) should begin with patient history and physical examination. If there is a history of remote myocardial infarction, WCT should be considered as ventricular tachycardia until proved otherwise. In most cases, WCT is subsequently shown by electrophysiologic evaluation to be ventricular tachycardia. The presenting symptoms and degree of hemodynamic compromise should not be used to distinguish ventricular tachycardia from supraventricular tachycardia. A 12-lead electrocardiogram (ECG) should be carefully reviewed by looking for signs of ventricular tachycardia (atrioventricular dissociation, captured and fusion beats, certain QRS shapes and concordance). If the surface ECG is inconclusive, changing the position of V1 or use of a transesophageal lead may allow assessment of atrial activity. When more QRS than P waves are documented, the diagnosis is ventricular tachycardia. Cardioversion-defibrillation is required in patients with WCT who are in unstable condition. Atrioventricular node blockers are the agents of choice for arrhythmias that are atrioventricular node-dependent, but they may cause hemodynamic collapse if administered to patients with ventricular tachycardia or with atrial fibrillation and preexcitation. Lidocaine hydrochloride (Xylocaine HCl IV), preferred for ventricular tachycardia, has been reported to cause ventricular fibrillation in patients with atrial fibrillation and preexcitation. When there is doubt about the diagnosis, elective electrical cardioversion may be considered. Medical therapy should consist of intravenous magnesium sulfate and procainamide hydrochloride (Pronestyl). A beta blocker may also be considered if more aggressive blockade of the atrioventricular node becomes necessary.
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PMID:Wide-complex tachycardias. The importance of identifying the mechanism. 879 58