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10.1002/j.1552-4604.1991.tb03672.x http://scihub22266oqcxt.onion/10.1002/j.1552-4604.1991.tb03672.x 1753009!ä!1753009 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Pharmacol 1991 ; 31 (11): 1053-60 Nephropedia Template TP {{tp|p=1753009|t=1991. Electrophysiologic mechanisms for ventricular arrhythmias in left ventricular dysfunction: electrolytes, catecholamines and drugs |pdf=|usr=}}{{1753009}} gab.com Text Electrophysiologic mechanisms for ventricular arrhythmias in left ventricular dysfunction: electrolytes, catecholamines and drugs JO: J Clin Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=1753009 #FOAvip Cardiac arrhythmias are generated as the result of disorders of automaticity or of impulse conduction. Regardless of the mechanism, calcium is likely to be involved, although calcium antagonists are rarely useful antiarrhythmics in ventricular arrhythmias. Myocardial cells that do not ordinarily initiate action potentials may do so when they are partially depolarized, giving rise to an ectopic focus. Early afterdepolarizations (EADs) are also induced in cardiac cells by partial depolarization, whereas delayed afterdepolarizations (DADs) are induced by Ca++ overloading. EADs may be the initiating mechanism of torsade de pointes, a complication of QT prolongation associated with quinidine therapy. Both in the animal model and in humans, treatment with magnesium, isoproterenol, or pacing, all of which suppress EADs, will also suppress torsade de pointes. Ventricular tachycardia is a manifestation of ordered re-entry, and may be exacerbated by antiarrhythmics, especially class 1c drugs. In the individual patient, prediction of proarrhythmia is not possible. The risk of proarrhythmia is increased in patients with episodes of sustained ventricular tachycardia or with significant left ventricular dysfunction. Twit Text FOAVip Electrophysiologic mechanisms for ventricular arrhythmias in left ventricular dysfunction: electrolytes, catecholamines and drugs ????J Clin Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=1753009 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=1753009 #FOAvip English Wikipedia <ref>{{Cite pmid|1753009}}</ref> Electrophysiologic mechanisms for ventricular arrhythmias in left ventricular dysfunction: electrolytes, catecholamines and drugs #MMPMID1753009 Levy MN; Wiseman MN J Clin Pharmacol 1991[Nov]; 31 (11): 1053-60 PMID1753009show ga Cardiac arrhythmias are generated as the result of disorders of automaticity or of impulse conduction. Regardless of the mechanism, calcium is likely to be involved, although calcium antagonists are rarely useful antiarrhythmics in ventricular arrhythmias. Myocardial cells that do not ordinarily initiate action potentials may do so when they are partially depolarized, giving rise to an ectopic focus. Early afterdepolarizations (EADs) are also induced in cardiac cells by partial depolarization, whereas delayed afterdepolarizations (DADs) are induced by Ca++ overloading. EADs may be the initiating mechanism of torsade de pointes, a complication of QT prolongation associated with quinidine therapy. Both in the animal model and in humans, treatment with magnesium, isoproterenol, or pacing, all of which suppress EADs, will also suppress torsade de pointes. Ventricular tachycardia is a manifestation of ordered re-entry, and may be exacerbated by antiarrhythmics, especially class 1c drugs. In the individual patient, prediction of proarrhythmia is not possible. The risk of proarrhythmia is increased in patients with episodes of sustained ventricular tachycardia or with significant left ventricular dysfunction. |Anti-Arrhythmia Agents/pharmacology/therapeutic use[MESH] |Arrhythmias, Cardiac/drug therapy/*physiopathology[MESH] |Calcium/metabolism/physiology[MESH] |Catecholamines/pharmacology[MESH] |Electrolytes/pharmacology[MESH] |Electrophysiology[MESH] |Heart Conduction System/drug effects/physiopathology[MESH] |Heart Ventricles[MESH] |Humans[MESH] |Time Factors[MESH]Electrophysiologic mechanisms for ventricular arrhythmias in left vent(epmc).pdf DeepDyve Pubget Overpricing