Action potential of cardiac muscles can be broken down into five phases: * Phase 0: Sodium channels open, resulting in the entrance of Na+ into the cells; this results in the<unk> polarization of the cardiac muscles. * Phase 1: Sodium channels close; this stops<unk> polarization. Potassium channels open, leading to an outward current of K+ out of the cells. * Phase 2: Potassium channels remain open (outward current of K+), and calcium channels now also open (inward current of Ca++), resulting in a plateau state. * Phase 3: Calcium channels close (inward Ca++ stops), but potassium channels are still open (outward K+ current); this persists until the cells gain back normal polarization (repolarization achieved). Please note that phase 0 leads to a net gain of Na+, while phases 1–3 lead to a net loss of K+. This imbalance is corrected by the Na+/K+-ATPase channel that pumps K+ into the cell and sodium out of the cell; this does not change polarization of the cells, but does restore ionic content to its initial state. * Phase 4: Exciting triggers (e.g. sinus node) will cause minor<unk> polarization in the cells; this will result in increasing permeability of sodium channels, which trigger the opening of sodium channels. Repolarization of the cardiomyocytes occurs in phases 1–3, and is caused predominantly by the outward movement of potassium ions. In<unk> , however, the repolarization is prolonged; this can be due to electrolyte disturbances (hypokalemia, hypomagnesemia, hypocalcemia), bradycardia, certain drugs (disopyramide, sotalol, amiodarone, amitriptyline, chlorpromazine, erythromycin) and/or congenital syndromes. The prolongation of repolarisation may result in subsequent activation of an inward<unk> polarisation current, known as an early after-depolarisation, which may promote triggered activity. Re-entry, due to a dispersion of refractory periods, is also possible; this is because M Cells (found in the mid myocardial layer) show a more prolonged repolarization phase in response to potassium blockage than other cells. In turn, this produces a zone of functional refractoriness (inability to<unk> polarize) in the mid myocardial layer. When new action potential is generated, the mid myocardial layer will remain in a refractory period, but the surrounding tissue will<unk> polarize. As soon as the mid myocardial layer is no longer in a refractory period, excitation from nearby tissue will cause a retrograde current and a reentry circuit that will result in a positive chronotropic cycle, leading to tachycardia.
Torsades de pointes
Ventricular fibrillation
Pre-excitation syndrome
Brugada syndrome
Pacemaker syndrome
Takotsubo cardiomyopathy
Sudden arrhythmic death syndrome
Unstable angina