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with the dynamics of cardiac action potentials by blocking a certain ion channel or block the sympathetic
effects of the autonomic nervous system on the heart to slow down heart rate
1a 1b and 1c- these subclasses differ in the strength of sodium channel blockage and in their effect on
the
duration of action potentials and the effective refractory period (erp) while subclass 1c has
no effect on ERP 1a prolongs and 1b shortens ERP respectively changes in ERP may
have different outcomes for different types of arrhythmias a longer ERP generally reduces
cardiac excitability but prolonged repolarization z' may increase the risk of tor sada point
a type of tachycardia caused by after depolarizations
class 2 beta blockers – These drugs bind to beta-1 adrenergic receptors and block the sympathetic
influences that act through these receptors sympathetic nerves release catecholamines (norepinephrine
and norepinephrine) which act to increase SA node firing rate and cardiac conduct ability especially at the
AV node these activities may precipitate arrhythmias beta blockers suppress sympathetic effects thereby
decreasing heart rate and slowing down conduction through the AV node the latter is particularly useful
and treatment of tachycardias that originate upstream of the AV node known as super ventricular
tachycardias or SVT note should be taken however that beta blocker treatment may cause AV blocks
class-3 potassium channel blockers- these agents block the potassium channels responsible for the
repolarizing phase the result is a slowed repolarization hence a prolonged duration of action potentials
and refractory period this reduces the heart's excitability and suppresses reentrant tachycardia however
these drugs may also cause arrhythmias because slowly polarizations are associated with longer QT
intervals and increased risk of torus odd to point
class 4 calcium channel blockers these drugs block calcium channels that are responsible for
depolarization in SA and AV nodal cells blocking these channels results in a lower sinus rate and slower
conduction through the AV node however because calcium is also involved in cardiac myocyte
contraction these agents also reduce contractility of the heart and should not be used in case of systolic
heart failures