Electrocardiogram (ECG) is one of the major diagnostics tools for Cardiac Arrhythmias (CA). ECG interpretation is more important to provide specific treatment of different arrhythmic myocardial regions. In this article the aim is to focus on detailed normal and abnormal ECG interpretation with different myocardial regions. Contraction and Relaxation Process (CRP) during cardiac cycle generates complex ECG with addition of each conduction node electrical vector activity in cardiac conduction system. Epinephrine stimulates Beta1 adrenergic receptors to produce more G stimulation proteins and thus leads to increase calcium level in the cell that provides frequent production of Action Potential (AP) like sinus tachycardia, Early Afterdepolarization (EAD) and Delayed Afterdepolarization (EAD). Myocardial scar regions, AP cannot move because of blockage, in turns moving rapidly around the dead area in a circular way to lead reentrant arrhythmias. On the other hand of respiration cycle, vagus outflow fluctuates (inspiration) the Sinus Node (SN) to increase heart rate (R-R distance will decrease, more P wave and QRS complex will be produced) and to decrease heart rate during expiration (R-R distance will be more). Finally conclude that different myocardial dysfunction regions are the major cause of multi-classified cardiac arrhythmias.

Cardiac arrhythmias is one of the cardiovascular diseases that cause more death in today’s industrial world. Among the generation of arrhythmias in cardiac myocytes, Early Afterdepolarization (EAD) and Delayed Afterdepolarization (DAD) is most significant one. Sodium -Calcium Exchanger (Na+- Ca2+ X) dysfunction is one of major source of DAD and EAD. Na+- Ca2+ X which exact mechanism is responsible for promoting EAD and DAD still not derived clearly from any cardiac models investigation. It is very important to understand the electrophysiological characteristics of Na+- Ca2+ X and its role in cardiac arrhythmias to clearly detect such arrhythmias effects. In this research article the aim is to build a strong fundamental foundation of Na+- Ca2+ X mechanism in terms of electrophysiological molecular segment (internal structure) arrangements and various Na+- Ca2+ X investigations on cardiac arrhythmias. Na+-Ca2+X is one which belongs to low chemical attraction, high transport capacity and energetically driven by the Na+ ions. The second is an L-type Ca2+ channel, which has a high affinity to Ca2+. Na+-Ca2+X eject nearly thirty (30%) of Ca2+ is required to activate the myofilaments in rabbit, guinea pig and human ventricles and a very small amount (7%) of Ca2+ is required in rat and mouse ventricles. Na+-Ca2+X transport Ca2+ up to 5000 per second (≈6μM/L), which is much greater than SR Ca2+ ATP Ca2+ transport (100 to 150 per second at ≈0.3μM/L). By using voltage patch clamp, Na+-Ca2+X current is measured in guinea pig ventricular myocyte, from that density of Na+-Ca2+X is to be found, 250 to 400 Na+-Ca2+X/μm2 . Na+-Ca2+X current (INaCa) at level [Ca2+]o = 0.50mM, Na+-Ca2+X mechanism of Ca2+ ions removal is very quickly, why because Calcium Induced Calcium Release (CICR) process does increase the cytosolic Ca2+ concentration very early. Enhanced activity of Na+-Ca2+X or increased Na+-Ca2+X channel current reduces the Action Potential (AP) and AP Duration (APD), and triggers rapid firing within cardiac pulmonary veins. Minimum intracellular calcium levels in SR is responsible for systolic dysfunction in failure heart. Similarly it increases the inward Na+-Ca2+X current, life threatening arrhythmias like DAD happen by sudden release of calcium in SR. Finally increased or enhanced or hypertrophy conditions of Na+-Ca2+X is produces EAD and DAD.