Pre-period contraction extrasystole refers to all contractions outside of the normal contraction of the heart, also known as extrasystole or premature contraction. In certain pathological conditions, myocardial tissue can produce an additional excitation and contraction of the myocardium after the effective inactivity of the sinus rhythm and before the next rhythmic excitation is delivered. The myocardium has a long noncontracting period, up to the full duration of systole and the first 1/3 of diastole, so that stimuli given during this period are ineffective, while subsequent stimuli can cause contraction. Based on this property, extra-period contractions can be artificially induced. There is an abnormally long rest period between the next normal contraction, which should occur, and the next normal contraction, which is called a compensatory interval. This is due to the fact that the normal excitation from the automatic center becomes ineffective during the noncontracting period of the extrasystole. The excitation that causes ventricular extrasystole can travel backwards through the excitation conduction system and conflict with normal excitation on its way to cancel it out, so normal excitation can also be shed at times. The etiology of preterm contraction can be divided into two major categories: functional and organic, the specific causes are as follows: (1) organic heart disease: all kinds of myocarditis, cardiomyopathy, whether in the acute phase or myocarditis has recovered, can appear preterm contraction. Coronary atherosclerotic heart disease, hypertension, pulmonary heart disease, rheumatic heart valve disease, heart failure and shock, etc., due to myocardial ischemia, hypoxia and cause a variety of pre-term contraction. (2) Systemic diseases: respiratory diseases, hepatobiliary system diseases and central nervous system diseases can cause preterm contraction. Such as tonsillitis, influenza, endocrine diseases, hyperthyroidism, adrenal diseases; electrolyte disorders and acid-base imbalance, hypokalemia, hypocalcemia, acidosis and alkalosis, etc. (3) Drug factors: antimony, digitalis, quinidine, procainamide, etc. cause myocardial toxic damage, epinephrine, isopropyladrenaline, dobutamine, reserpine, etc. due to a slightly larger dose of myocardial excitation. In addition, anesthetics and other drugs can cause pre-term contraction. (4) Surgery: especially cardiac surgery or cardiac intubation surgery, anesthesia hypothermia, extracorporeal circulation, etc. (5) Functional factors: smoking, alcohol, coffee and strong tea, exertion, mental stress, insomnia, sudden changes in body position, and poor lifestyle habits such as satiety can cause preterm contraction. In addition, there are many patients with preterm contraction who are not found to have cardiac or other diseases and obvious triggers after careful examination, which may be caused by autonomic dysfunction. (1) Increased excitability (or autoregulation) of ectopic pacing sites: When the excitability of single or multiple potential ectopic pacing sites in the atria, ventricles, or atrioventricular junction is increased and significantly exceeds the autoregulation of the sinus node, the excitation is generated and propagated prematurely, rapidly, and irregularly. Or, for some reason, the ectopic pacing points may become more autoregulatory due to accelerated diastolic autodepolarization and produce preterm contractions. (2) Folded excitation: A part of the myocardium (Figure 1) has a prolonged overdue period or a unidirectional block. When normal excitation passes from p to branch b, it is blocked and cannot pass, but normal excitation passes from p to branch a at normal speed, excites the ventricular muscle (v), and then enters and crosses branch b from the ventricular muscle at an abnormally slow speed, and when it reaches the bifurcation of p, it is out of the overdue period of the previous excitation. The excitation then moves along branch a and excites the ventricular muscle again, producing a pre-term contraction. Since the folded excitation returns to its original location along a fixed pathway at a certain conduction velocity, the preterm contraction always occurs at a fixed time after the normal sinus excitation, i.e., it forms a preterm contraction with a fixed interconnection period. Giving an additional stimulus to the ventricular myocardium, if the stimulus falls after the effective ventricular nonstimulation period, can cause an additional excitation and contraction. Since this additional contraction is produced before the normal sinus contraction, it is called a preterm contraction. The preterm contraction also has its own effective inactivity period. Therefore, the excitation from the sinoatrial node immediately following a preterm contraction falls within the effective inactivity period of the preterm contraction, and as a result, the ventricle cannot be excited and contracted, and there is a “loss” that must wait until the next excitation from the sinoatrial pacing point to cause the ventricle to contract. In this way, a long period of ventricular diastole, called the compensatory interval, often follows a pre-systole. There are complete compensatory intervals and incomplete compensatory intervals. Of course, the two most common types are incomplete compensatory intervals, such as atrial premature intervals, and complete compensatory intervals, such as ventricular premature intervals. The so-called complete compensatory interval is the inter-rhythm interval plus the compensatory interval exactly equal to 2 basic cardiac cycles. In contrast, incomplete intervals are less than 2. This is mainly because the atrial premature is closer to the sinus node, it can cause the rhythm of the sinus node to reorganize, then the next issue is properly adjusted, so it is slightly shorter than 2 basic cardiac cycles, while the ventricular premature is farther away from the sinus node, so it is less likely to affect the sinus node, then the sinus node generally will not reorganize, so you should generally measure up to equal to 2 cardiac cycles. The sinoatrial node is still in rhythm with the original rhythm. However, there are exceptions, such as intermittent premature beats that do not have a compensatory cycle, and others that can have a super compensatory cycle, and there are actually various cases.