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心律不正Cardiac Arrhythmias

时间:2016-03-20 16:35来源:www.ukassignment.org 作者:anne 点击:
Cardiac Arrhythmias心律不正
 
在正常人的心脏跳动,每个起源于窦房结,称为正常窦性心律,NSR。心脏跳动70次,休息一分钟。放慢心率是指心动过缓,心率加快,称为心动过速。在睡眠和加速的情绪,运动,发烧,和许多其他刺激的速度减慢。在健康的年轻人在一个正常的呼吸率、心率和呼吸的阶段变化,即在吸气呼气加速减速,特别是如果呼吸深度增加。这种窦性心律失常是一种正常现象,主要是由于副交感神经输出到心脏的波动。吸气时,从肺牵张受体在迷走神经冲动抑制延髓的心抑制区。保持心率减慢的强直性迷走神经放电,心率上升。
In the normal human heart, each beat originates in the SA node, known as the normal sinus rhythm, NSR. The heart beats about 70 times a minute at rest. The slowed heart rate is refer to bradycardia, and the accelerated heart rate is known as tachycardia. The rate is slowed during sleep and accelerated by emotion, exercise, fever, and many other stimuli. In healthy young individuals breathing at a normal rate, the heart rate varies with the phases of the respiration, that is it accelerates during inspiration decelerates during expiration, especially if the depth of breath is increased. This sinus arrhythmia is a normal phenomenon and is due to primarily to fluctuations in parasympathetic output to the heart. During inspiration, impulses in the vagi from the stretch receptors in the lungs inhibit the cardioinhibitory area in the medulla oblongata. The tonic vagal discharge that keeps the heart rate slow decreases, and the heart rate rises.
Disease processes affecting the sinus node lead to marked bradycardia accompanied by dizziness and syncope (sick sinus syndrome). In the United States more than 850,000 people are hospitalized for an arrhythmia each year.
 
Abnormal Pacemakers异常的心脏起搏器
 
房室结和传导系统的其他部分可以在异常情况下成为心脏起搏器。此外,患病的心房和心室肌纤维可以减少重复和膜电位放电。
在导通系统的其它部分的放电率更为快速,这就是为什么在模拟节点通常控制的心脏速率。当从心房到心室的传导完全中断,第三度心脏传导阻滞的结果,也被称为完全性心脏传导阻滞,和心室打率低(室性自主节律)独立的心房。块可能是由于房室结疾病(房室传导阻滞)或传导系统下方的节点(结下块)The AV node and other portions of the conduction system can in abnormal situations become the cardiac pacemaker. In addition, diseased atrial and ventricular muscle fibers can have their membrane potentials reduced and discharge repetitively.
The discharge rate of the SA node is more rapid than that of the other parts of the conduction system, and this is why the SA node normally controls the heart rate. When conduction from the atria to the ventricles is completely interrupted, third-degree heart block results, also known as complete heart block, and the ventricle beat at low rate (idioventricular rhythm) independently of the atria. The block may be due to disease in the AV node (AV nodal block) or in the conducting system below the node (infranodal block). In patients with AV nodal block, the remaining nodal tissue becomes the pacemaker and the rate of idioventricular rhythm is approximately 45 beats/min. In patients with infranodal block due to disease in the bundle of His, the ventricular pacemaker is located more peripherally in the conduction system and the ventricular rate is lower; it averages 35 beats/min, but in individual cases it can be as low as 15 beats/min. In such individuals, there may also be periods of asystole lasting a minute or more. The resultant cerebral ischemia causes dizziness and fainting (Stroke-Adams syndrome). Causes of third-degree heart block include septal myocardial infarctian and damage to the bundle of His during surgical correction of congenital interventricular septal defects.
When conduction between the atria and ventricles is slowed but not completely interrupted, in complete heart block is present. In the form called first-degree heart block, all the atrial impulses reach the ventricles but the PR interval is abnormally long. In the form called second-degree heart block, not all atrial impulses are conducted to the ventricles. For example, a ventricular beat may follow every second or every third atrial beat (2:1 block, 3:1 block, etc). In another form of incomplete heart block, there are repeated sequences of beats in which the PR interval lengthens progressively until a ventricular beat is dropped (Wenckebach phenomenon). The PR interval of the cardiac cycle that follows each dropped beat is usually normal or only slightly prolonged.
Sometimes one branch of the bundle of His is interrupted, causing right or left bundle branch block. In bundle branch block, excitation passes normally down the bundle on the intact side and the sweeps back through the muscle to activate the ventricle rate is therefore normal, but the QRS complexes are prolonged and deformed. Block can also occur in the anterior or the condition called hemiblock or fascicular block. Left anterior hemiblock produces abnormal left axis deviation in the ECG, whereas left posterior hemiblock produces abnormal right abnormal right axis deviation. It is not uncommon to find combinations of fascicular and branch blocks (bifascicular or trifascicular block). The bundle of His electrogram produce detailed analysis of the site of block when there is a defect in the conduction system.
 
Implanted Pacemakers植入心脏起搏器
 
When there is marked bradycardia in patients with sick sinus syndrome or third-degree heart block, an electronic pacemaker is frequently implanted. These devices which have become sophisticated and reliable, are useful in patients with sinus node dysfunction, AV block, and bifascicular or trifascicular block. They are useful also in patients with severe neurogenic syncope in whom carotid sinus stimulation produces pauses of more than 3 seconds between heartbeats.
 
Ectopic Foci of Excitation异位异位灶
 
Normally, myocardial cells do not discharge spontaneously, and the possibility of spontaneous discharge of the bundle of His and Purkinje system is low because the normal pacemaker discharge of the SA node is more rapid than their rate of spontaneous discharge. However, in abnormal conditions, the His-Purkinje fibers or the myocardial fibers may discharge spontaneously. In these conditions, increased automaticity of the heart is said to be present. If an irritable ectopic focus discharges once, the result is a beat that occurs before the expected next normal beat and transiently interrupts the cardiac rhythm (atrial, nodal, or ventricular extrasystole or premature beat). If the focus discharges repetitively at a rate higher than that of the SA node, it produces rapid, regular tachycardia (atrial, ventricular, or nodal paroxysmal tachycardia or atrial flutter).
 
Re-entry重新进入
 
A more common cause of paroxysmal arrhythmias is defect in conduction that permits a wave of excitation to propagate continuously within a closed circuit (circus movement). For example, if a transient blocks is present on one side of a portion of the conducting system, the impulse can go down the other side. If the block then wears off, the impulse may conduct in a retrograde direction in the previously blocked side back to the origin and then descend again, establishing a circus movement. If the re-entry is in AV node, the re-entrant activity depolarizes the atrium, and the resulting atrial beat is called an echo beat. In addition, the re-entrant activity in the node propagates back down to the ventricle, producing paroxysmal nodal tachycardia. Circus movements can also become established in the atrial or ventricular muscle fibers. In indibiduals with an abnormal extra bundle of conducting tissue connecting the atria to ventricles, the circus activity can pass in one direction through the AV node and in the other direction through the bundle, thus involving both the atria and the ventricles.
 
Atrial Arrhythmias房性心律失常
 
Excitation spreading from an independently discharging focus in the atria stimulates the AV node prematurely and is conducted to the ventricles. The P waves of atrial extasystoles are abnormal, but the QRST configurations are usually normal. The excitation may depolarize the SA node, which must repolarize and then depolarize to the firing level before it can initiate the next normal beat. Consequently, a pause occurs between the extrasystole and the next normal beat that is usually equal in length to the interval between the normal beats preceding the extrasystole, and the rhythm is “reset”.
Atrial tachycardia occurs when an atrial focus discharges regularly or there us re-entrant activity producing atrial rates up to 220/min. Sometimes, especially in digitalized patients, some degree of atrioventricular block is associated with the tachycardia (paroxysmal atrial tachycardia with block).
In atrial flutter, the atrial rate is 200-350/min. In the most common form of this arrhythmia, there is large counter clockwise circus movement in the right atrium. This produces a characteristic saw tooth pattern of flutter waves due to atrial contractions. It is almost always associated with 2:1 or greater AV block because in adult, the AV node cannot conduct more than about 230 impulses per minute.
In atrial fibrillation, the atria beat very rapidly (300-500/min) in a completely irregular and disorganized fashion. Due to the AV node discharges at irregular rate, usually 80-160/min. The condition can be paroxysmal or chronic, and in some cases there appears to be a genetic predisposition. The cause of atrial fibrillation is still a matter of debate, but in most cases it appears to be due to multiple concurrently circulating re-entrant excitation waves in both atria. However, some cases of paroxysmal atrial fibrillation seem to be produced by discharge of one or more ectopic foci. Many of these foci appear to be located in the pulmonary veins as much as 4 cm from the heart. Atrial muscle fibers extend along the pulmonary veins and are the origin of these discharges.


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