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8 Cards in this Set

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MECHANISM
Group 1 Antiarrhythmics (Local Anesthetics)
Drugs with Group 1A Action
All group 1 drugs slow or block conduction in ischemic and depolarized cells and slow or abolish abnormal pacemakers wherever these processes depend on sodium channels

They block INa, and therefore slow conduction velocity in the atria, Purkinje fibers, and ventricular cells. At high doses they also slow AV conduction.
The reduction in ventricular conduction results in increased QRS duration in the ECG. In addition, the 1A drugs block IK and slow repolarization. Therefore, they increase AP duration and the effective refractory period (ERP) in addition to slowing conduction velocity and ectopic pacemakers. The increase in AP duration generates an increase in QT interval
MECHANISM
Group 1 Antiarrhythmics (Local Anesthetics)
Drugs with Group 1B Actions
Useful sodium channel-blocking drugs bind to their receptors much more readily when the channel is open or inactivated than when it is fully repolarized and recovered from its previous activity

Lidocaine selectively affects ischemic or depolarized Purkinje and ventricular tissue and has little effect on atrial tissue; the drug reduces AP duration in some cells, but because it slows recovery of sodium channels from inactivation it does not shorten (and may even prolong) the effective refractory period.
MECHANISM
Group 1 Antiarrhythmics (Local Anesthetics)
Drugs with Group 1C Action
As a result, antiarrhythmic sodium channel blockers are use dependent or state dependent in their action (ie, they selectively depress tissue that is frequently depolarizing, eg, during a fast tachycardia; or tissue that is relatively depolarized during rest, eg, by hypoxia).

These drugs have no effect on ventricular AP duration or the QT interval. They are powerful depressants of sodium current, however, and can markedly slow conduction velocity in atrial and ventricular cells. They increase the QRS duration of the ECG.
MECHANISM
Group 2 Antiarrhythmics (Beta Blockers)
Their mechanism in arrhythmias is primarily cardiac -adrenoceptor blockade and reduction in cAMP, which results in the reduction of both sodium and calcium currents and the suppression of abnormal pacemakers. The AV node is particularly sensitive to blockers and the PR interval is usually prolonged by group 2 drugs
MECHANISM
Group 3 Antiarrhythmics (Potassium IK Channel Blockers)
The hallmark of group 3 drugs is prolongation of the AP duration. This AP prolongation is caused by blockade of IK potassium channels that are responsible for the repolarization of the AP (Figure 14–5). AP prolongation results in an increase in effective refractory period and reduces the ability of the heart to respond to rapid tachycardias
MECHANISM
Group 4 Antiarrhythmics (Calcium Channel Blockers)
These agents cause a state- and use-dependent selective depression of calcium current in tissues that require the participation of L-type calcium channels . AV conduction velocity is decreased and effective refractory period increased by these drugs. PR interval is consistently increased
MECHANISM
Adenosine
Adenosine is a normal component of the body, but when it is given in high doses (6–12 mg) as an intravenous bolus, the drug markedly slows or completely blocks conduction in the atrioventricular node (Table 14–1), probably by hyperpolarizing this tissue (through increased IK1) and by reducing calcium current. Adenosine is extremely effective in abolishing AV nodal arrhythmias,
MECHANISM
Magnesium Ion
Magnesium appears to have similar depressant effects as potassium on digitalis-induced arrhythmias. Magnesium also appears to be effective in some cases of torsade de pointes arrhythmia.