tailieunhanh - Essential Cardiac Electrophysiology Self Assessment - Part 2

Lidocaine và các đại lý lớp 1B khác ngăn chặn các thành phần làm chậm dòng natri và QT giảm ở những bệnh nhân với LQT35. • inotropy tiêu cực của thuốc chẹn kênh natri có thể là do sự tắc nghẽn của dòng kênh natri chậm | 16 Essential Cardiac Electrophysiology Lidocaine and other class 1B agents block the slow component of sodium current and decrease QT in patients with LQT35. Negative inotropy by sodium channel blockers may be due to blockage of the slow sodium channel current. Slowing of heart rate produced by class 1B agents is due to blocking of background sodium current that contributes to the phase 4 of pacemaker AP. f -Adrenergic stimulation reverses the effects of class I drugs. Proarrhythmia from class IC drugs develops during increased heart rate when sympathetic activity is enhanced. Beta blockers may reverse this phenomenon5. Angiotensin II increases the frequency of reopening of the sodium channel and increases the Na current. CALCIUM CHANNELS AND CURRENTS14-17 The process of channel opening and closing is called gating. Open channels are active. Closed channels are inactive. Calcium and sodium channels open in response to depolarization and enter the nonconducting state during repolarization a gating process known as inactivation. Alpha 1 subunit of the Ca channel contains the binding site for calcium channel blocking drugs. Calcium channels are very selective and allow Ca permeability 1000-fold faster. There are four types of calcium channels i L-type expressed on surface membrane. ii T-type expressed on surface membrane. iii Sarcoplasmic reticulum SR Ca release channel. iv Inositol triphosphate IP3 receptor channels are present on internal membrane. L-type calcium channel L Large and lasting It is a major source of Ca entry into the cell. It opens when depolarization reaches positive to -40 mV. It is responsible for excitation in sino atrial node SAN and atrio-ventricular node AVN . It produces inward current that contributes to depolarization in SAN and AVN. It produces inward current responsible for plateau of AP. Increased calcium current prolongs depolarization and increases the height of the AP plateau. Calcium channel dependent inward current is responsible