Cardiac Arrhythmias: Difference between revisions

 

 

= General Introduction =

The cardiac action potential is a result of ions flowing through different ion channels. Ion channels are passages for ions (mainly Na⁺, K⁺, Ca²⁺ and Cl^-) that facilitate movement through the cell membrane. Changes in the structure of these channels can open, inactivate or close these channels and thereby control the flow of ions into and out of the myocytes. Due to differences in the type and structure of ion channels, the various parts of the heart have slightly different action potential characteristics. Ion channels are mostly a passive passageway, where movement of ions is caused by the electrochemical gradient. In addition to these passive ion channels a few active trigger-dependent channels exist that open or close in response to certain stimuli (for instance acetylcholine or ATP). The changes in the membrane potential due to the movement of ions produce an action potential which lasts only a few hundreds of milliseconds. Disorders in single channels can lead to arrhythmias, as seen in the section [[Primary_Arrhythmias]]. The action potential is propagated throughout the myocardium by the depolarization of the immediate environment of the cells and through intracellular coupling with gap-junctions.<cite>Kleber</cite>  

During phase 4 of the action potential intracelullair and extracellulair concentrations of ions are restored. Depending on cell type the resting membrane potential is between -50 to -95 mV. Sinus node and AV nodal cells have a higher resting membrane potential (-50 to -60 mV and -60 to -70 respectively) in comparison with atrial and ventricular cardiomyocytes (-80 to -90 mV). Sinus node cells and AV nodal cells (and to a lesser degree Purkinje fibers cells) have a special voltage dependent channel I_f, the funny current. Furthermore they lack I_K1, a K⁺ ion channel that maintains the resting membrane potential in atrial and ventricular tissue. The I_f channel causes a slow depolarization in diastole, called the phase 4 diastolic depolarization, which results in normal automaticity. The frequency of the sinus node discharges are regulated by the autonomous nerve system and due to the relative high firing frequency (60-80 beats per minute) the sinus node dominates other potential pacemaker sites.

The cardiac conduction system (Figure 2) consist of specialized fast conducting tissue though which the electric activity of the heart spreads from the atria to the ventricles. The characteristics of the different parts of the conduction system are a result of the different characteristics of the individual myocytes. On a larger level, function is controlled predominantly by the autonomic nervous system (both vagal and sympathetic nerve system). Especially the sinus node and atrioventricular node are responsive to the autonomic nerve system. The ganglionic plexi, a conglomeration of both vagal and sympathetic nerves, form the intrinsic cardiac nerve system and innervate through a network of nerve fibers the atria and ventricles. The vagal and sympathetic nerve system are both continually active in the heart, but vagal activity dominates the tonic background stimulation of the autonomic nerve system. Moreover the heart is more susceptible to vagal stimulation. Vagal stimulation provokes a rapid response and the effect dissipates swiftly in contrast to sympathetic stimulation which has a slow onset and offset. Vagal stimulation results in a reduction in sinus node activation frequency and prolongs AV nodal conduction. These effects can occur simultaneously or independent of each other.  Sympathetic stimulation exerts reverse effects, accelerating the sinus node firing frequency and improving AV nodal conduction. The autonomic nerve system has a small effect on cardiomyocytes. Vagal stimulation tends to prolong the refractory period and decrease the myocardial contractility. Sympathetic stimulation has the opposite effect on the cardiac tissue. The physiological modulation of cardiac conduction is vital to adaptation of the heart to rest and exercise. However the autonomic nervous system can contribute as a modifier is certain to facilitate the occurrence of certain arrhythmias.<cite>Braunwald</Cite>

===Venticle===

The ventricle is activated through the dense network of Purkinje fibers originating from the bundle branches. They penetrate the myocardium and are the starting point of the ventricular activation. The left ventricular areas first excited are the anterior and posterior paraseptal wall and the central left surface of the interventricular septum. The last part of the left ventricle to be activated is the posterobasal area. Septal activation starts in the middle third of the left side of the interventricular septum, and at the lower third at the junction of the septum and posterior wall. Activation of the right ventricle starts near the anterior papillary muscle 5 to 10 msec after onset of the left ventricle.<cite>Durrer</cite>

Structural abnormalities or electric changes in the cardiomyocytes can impede impulse formation or change cardiac propagation, therefore facilitating arrhythmias. Arrhythmogenic mechanisms can arise in single cells (automaticity, triggered activity), but other mechanisms require multiple cells for arrhythmica induction (re-entry).  We briefly discuss the pathofysiological mechanisms of the main causes of arrhythmia. <Cite>Coronel</Cite>

Triggered activity is activity of a cell triggered by a preceding activation. Due to early or delayed afterdepolarizations the membrane potential depolarizes and, when reaching a threshold potential, activates the cell. These afterdepolarizations are depolarizations of the membrane potential initiated by the preceding action potential. Depending on the phase of the action potential in which they arise, they are defined as early or late afterdepolarizations (figure 3).  

* A disturbance of the balance in influx and efflux of ions during the plateau phase (phase 2 or 3) of the action potential is responsible for the early afterdepolarizations. Multiple ion currents can be involved in the formation of early after depolarizations depending on the triggering mechanism. Early afterdepolarizations can develop in cells with an increased duration of the repolarization phase of the action potential, as the plateau phase is prolonged.

Conduction block or conduction delay is a frequent cause of bradyarrhythmias, however tachyarrhythmias can also result from conduction block when this block produces a re-entrant circuit. Conduction block can develop in different (physiological) conditions.  

Important criteria for the development of re-entry are a circular pathway with an area in this circle of unidirectional block and a trigger to induce the re-entry movement. Re-entry or circus movement can arise when an activation front is conducted through an unidirectional (slow conducting) pathway thereby still propagating the activation while the rest of the surrounding myocardium depolarizes. When the surrounding myocardium has recovered from the refractory state, and can be stimulated again, the impulse that exits the area of unidirectional block can reactivate this recovered myocardium. This process can repeat itself and thus form the basis of a reentry tachycardia.  Slow conduction and/or a short refractory period facilitate re-entry. The reason of unidirectional block can be anatomical (atrial flutter, AVNRT, AVRT) or functional (myocardial ischemia) or a combination of both.<Cite>deBakker,Janse</Cite>