Cardiac rhythm disturbance are the result of altered in impulse generation (automaticity), altered impulse propagation, or both factors acting together. The physiological regulation of automaticity and conduction is derailed. The factors which precipitate arrhythmias include myocardial ischemia with hypoxia and pH and electrolyte abnormalities excessive stretch excessive discharge of endogenous catecholamine’s. Excessive sensitivity to autonomic regulators and excessive exposure to drugs like digitalis and other potentially cardio toxic substance.
Normally the senatorial node, the pacemaker has the highest degree of automaticity, and is responsible for normal sinus rhythm. This spontaneous electrical activity of the SA node is independent of the CNS control, but is affected both by sympathetic and parasympathetic activity of the ANS. Under certain circumstances, due to drugs or pathological changes, when the SA node is suppressed as in some bradyarrhythnias, other specialized conduction tissue with automatic properties takes up the role the pacemaker. Thus, specialized a trial fibres, atriventricular nodel tissue, the bundle of his, or the purkinje fibres develop an enhasced automaticity when the SA pacemaker fails. Such a site is known as an ectopic focus and the cells exhibit an increase tendency to depolarize during diastole.
Arrhythmias due to increase automaticity in subsidiary or latent pacemakers results from myocardial ischemia or damage, hypopotassaemia or digitalis intoxication. Circulating catecholamine also increase automaticity and induce arrhythmias. Automaticity in ectopic foci may be enhanced, causing various automatic or re-entrant tachyarrhythmias. Alterations in the rate of impulse generation may occur even when the SA node is the dominant pacemaker, causing sinus irregularities.
Electro physiologically, normally the phase 4 slope of cardiac cells other than the SA node is lesser than the SA nodal cells. Under certain conditions, the purkinje fibres or other conduction tissue cells may develop a much steeper phase 4 slopes and take over an ectopic phase 4 functions. Common arrhythmias due to entropic automaticity include premature ventricular beats, ventricular tachcardias, and ventricular escape rhythms. Nearly all antiarrhythmic drugs (except beryllium)depress ectopic automaticity by decreasing the slope of phase 4 depolarization, in addition to this , quinidine, procainamide and propranolol also increase the phenytion do not share the later property.
Some arrhythmias may be attributed to a defective transmission of the cardiac action potential. In myocardial ischemic or hypoxic states any region of the heart may transmit impulses slowly or act as a conduction block. Simple slowing in the rate of ventricular contraction follows AV blockade or bundle branch block. More complex arrhythmias like paroxysmal a trial tachycar dias, AV nodal tachycardia’s and many vermicular tachycardias are probably and many ventricular tachycardias are probably the result of retrograde transmission or re-entry mechanism.
In fact when the velocity of the propagating action potential is slowed, the likelihood of a conduction block increases, and the phenomenon of re-entry operates. For re-entry to occur, the conduction block must be unidirectional. In the time needed for re-entrant conduction, repolarization of the normal purkinje tissues occurs and the ventricular cell can be reactivated.
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