By Zainul Abedin

Content material:
Chapter 1 Ions channels and currents (pages 1–37):
Chapter 2 Electrophysiologic results of cardiac autonomic job (pages 38–49):
Chapter three Mechanisms of arrhythmias (pages 50–66):
Chapter four Sinus node disorder and AV blocks (pages 67–93):
Chapter five Supraventricular tachycardia (pages 94–218):
Chapter 6 Differential prognosis of huge advanced tachycardia (pages 219–225):
Chapter 7 Ventricular tachycardia and ventricular traumatic inflammation (pages 226–368):
Chapter eight surprising cardiac dying and threat stratification (pages 369–387):
Chapter nine Cardiac arrhythmias in sufferers with neuromuscular problems (pages 388–393):
Chapter 10 Syncope (pages 394–406):
Chapter eleven Pharmacologic treatment of arrhythmias (pages 407–444):
Chapter 12 electric remedy for cardiac arrhythmias (pages 445–493):

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Extra info for Essential Cardiac Electrophysiology: The Self-Assessment Approach

Sample text

T β3-adrenoceptors are desensitization-resistant and their action may exceed that of impaired, down-regulated or desensitized β1- and β2-adrenoceptors. This may result in depression of contractility and exacerbation of heart failure. t This supports the observation that nonselective beta-blockers reduce cardiac mortality in patients with recent MI and CHF. 2 Cholinergic receptors7,8 t Cholinergic receptors are nicotinic or muscarinic depending on their ability to interact with nicotine or muscarine.

T These mutations decrease HCN channel expression, decelerate If activation, or, when located in CNBDs, abolish sensitivity of HCN channels to cAMP. t HCN4 mutations cause bradycardia by reducing If and the speed of membrane depolarization during phase 4; this results in slower pacemaking rates in SAN myocytes. HCN expression in acquired diseases6 t Increased HCN expression in atrial or ventricular myocytes in pathologic conditions could initiate arrhythmia by triggering spontaneous excitation of nonpacemaker myocytes.

2 Phasic block occurs when there is sequential declined in peak current from beat to beat. t It is also called use dependent or frequency dependent block. It decreases AP upstroke and slows conduction velocity. This type of block increases with repetitive stimulation. If interval between AP is less then four times the recovery constant of the channel, block accumulates. t During phase 0 Na channels open (open state) for less than 1 millisecond then becomes inactive. t During phase 2 and 3 (plateau phase) less then one percent of sodium channels remain open (Inactivated State).

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