Medical Pharmacology Topics
Arhythmias are abnormalities in the rate, regularity or site of origin of the cardiac impulse, or in the conduction of thet impulse such that the nermal sequence of activation of the atria and ventricles is altered. They are caused by conditions like acute myocardial ischemia, infarction, cardiomyopathy, congenital or vascular heart isease, electrolyte imbalance, hypoxia, trauma, septicemia or drugs.
The physiological mechanisms that lead to arhythmias can be categorized as either abnormalities of impulse formation or abnormalities of impulse conduction.
Abnormalities of Impulse Formation
Abnormalities of impulse formation may be due to alteration of automaticity (enhanced or depressed), development of abnormal automaticity (ectopic pacemakers), or triggere activity (early or delayed after-depolarizations). Automaticity can be modulated by changing one of three factors:
Abnormal automaticity develops
when damage or ischemic myocardioal cells, which are not usually automaticv,
become depolarized and develop automaticity. Since more of the fast Na
channels are inactivated as the resting potential becomes more depolarized,
the appearance and character of the resulting action potential becomes like
that of a slow action potential.
Early after-depolarizations (EAD) are interruptions of phase 3 repolarization (relative refractory period) that may appear when the cardiac action potential is markedly prolonged (?). The EAD may then trigger one or more bizarre action potentials whose exact origin is not clear. This type of triggered activity is most commenly seen under conditions of very slow heart rate, low extracellular K+ and treatment with drugs (often anti-arhythmics) that prolong the duration of the action potential.
EADs are throught to be responsible for Torsade de Pointe, an arhythmia caused by many antiarythmic drugs. Torsade de Pointe is usually self-limiting, resulting in brief runs of ventricular tachycardia (and syncope) that spontaneously revert to sinus rhythm. However, in some cases may progress to ventricular fibrilation.
Delayed after-depolarizations
(DAD) ae oscillations in ionic conductance and membrane potential that occur
shortly after return to resting membrane potential following a cardiac action
potential. They may be sufficient to bring the cell to threshold and trigger
an action potential, or a succession of action potentials. DADs are sometims
seen under conditions of intracellular Ca
overload in sick or damaged cardiac tisue, or in normal myocardium exposed to
drugs like digitalis, or under high sympathetic tone, particularly when heart
rate is very high.
Abnormalities of Impulse conduction
Abnormalities of impulse conduction may be due to conduction delay or block, or to reentry. The same factors that provide for physiological slowing of the cardiac impulse in the AV node makes it a common site for pathological delay or complete block of the cardiac impulse. Slowed down conduction - and in extreme cases unidirectional or bidirectional block - is commonly seen in sick or damaged myocardium.
Reentry refers to a case where a single cardiac impulse reenters a portion of the myocardium that the impulse has already passed through and exited at least once. This is thought to require unidirectional block and slowed conduction through a portion of the normal conduction path for the cardiac impulse. Under normal conditions, an impulse that spreads in two or more directions will eventually encounter itself or another impulse traveling towards it. Then the two impulses will cancel each other and allow a refractory period for the tissue to repolarize and start over. If there is a block impeading the passage of the initial impulse in one direction but not the others, the impulse will propagate only in one direction and eventually travel back to the place it was initiated, without being cancelled by another impulse branch. This condition is known as reentry because the tissue where the impulse already passed had time to repolarize and as the impulse reenters the same tissue it will continue uninpeeded.
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