General clinical Considerations On Arrhythmias
Excitability Of The P Cells
The myocardial cells have the property of spontaneous excitability (automaticity). This is responsible for the pacemaking function of the heart. The sinoatrial (SA) node which has the fastest rate of excitability controls the heart rate. The S-A node contains specialized electrically active cells known as P cells which have got the highest rate of excitability. The rate of impulse production and conduction are controlled by various physiological, pharmacological and pathological processes. In normal adults, the heart rate varies between 60 and 100/min.
The Calcium Channel
The cardiac action potential is generated by movement of charged ions across the cell membrane through various channels. The action potential has two major phases- the spike and the plateau. A large fast inward movement of Na++ through the fast sodium channel is responsible for the early spike and a slower steady influx of Ca++ through a separate set of slow channels account for the plateau phase. The SA node and the AV node contain cells whose action potential is dominantly mediated by the slow calcium channels. In contrast, the Purkinje cells and the working myocardial cells have both fast and slow channels.
The exact structural details of the calcium channels in the sarcolemmal membrane are not known. It is believed that each ionic channels is a specific protein that floats in a lipid bilayer matrix with a water filled central pore for ion movement. These channels have a selective filter which determines the nature of ion passing through them. In addition, the channels are also influenced by intracellular voltage variations and hence they are also called “voltage-dependent channels”.
The slow response type of action potential seen mainly in the SA node and AV node is mediated by the slow channels. Although there are various types of slow channels, the calcium-mediated slow channel is most widely recognized. Compared to the fast channels, these channels are not only kinetically slower, but they also operate at a less negative to a more depolarized voltage range. A variety of agents block the slow channels. Local anesthetics, volatile general anesthetics etc, produce a nonspecific blockade of both fast and slow channels. In contrast, drugs like verapamil, nifedipine, diltiazem, bepridil, etc, produce a selective direct blocking action on the slow channels. The result is blockade of calcium entry into the cell. Calcium channel blockers are extensively used in the treatment of arrhythmias and hypertension.
From the sinus node, the impulse traverses through the atria to the atrioventricular node (A-V node). There are three specialized pathways in the atria which conduct impulses from the sinus node to the A-V node. There are the anterior, middle and posterior intermodal tracts. The anterior tract connects the two atria also. From the A-V node, the impulse travels through the bundle of His, bundle branches and the Purkinje system to reach the ventricular musculature.
In general, arrhythmias may be caused by abnormalities of automacity, and/or abnormalities of conduction. When the main pacemaker is suppressed, the lower centers become active and take up the pacemaking function. This gives rise to escape rhythms such as junctional escape or ventricular escape. For the same reason, enhanced automaticity of ectopic foci may occur and this leads to the development of ectopic rhythms and ectopic tachycardias (junctional arrhythmia and junctional tachycardia). Abnormality in the conduction of impulses may give rise to “re-entry phenomenon” which is considered as one of the commonest mechanisms of tachyarryhthmias. When the normal conducting pathway becomes refractory, an incoming impulse may take a different course and pass down. By the time it reaches lower down, the refractioriness of the distal end of the normal pathway, would have passed off and it may become capable of conduction. Hence the abnormal impulse gets into it and it is conducted in a retrograde direction. This is designated as re-entry phenomenon and this is responsible for perpetuating ectopic tachycardias.
© 2014 Funom Theophilus Makama