1 --- 2 title: "Lippincott Illustrated Reviews Pharmacology (Lippincott" 3 isbn: "9781975170561" 4 block: 2 5 total_blocks: 5 6 prev_block: ./9781975170561_block1.md 7 next_block: ./9781975170561_block3.md 8 pages: "396-738" 9 --- 10 11 12 13 a minor effect on the duration of the action potential and refractoriness. Automaticity is reduced by an increase in the threshold potential, rather than a decrease in slope of phase 4 depolarization. Flecainide also blocks K+ channels, leading to increased duration of the action potential. Propafenone [proe-PAF-e-none], like flecainide, slows conduction in all cardiac tissues but does not block K+ channels. It possesses weak β-blocking properties. 14 15 16 17 18 ![A diagram illustrates an action potential with labeled phases, ion channels, and currents across a cell membrane.](https://cdn.orris.care/cdss_images/bc4397c83bd62d5963cd194d31fcf989fefe90f5bccb3cd78a5682cf3663d19d.png) 19 20 21 22 Figure 11.8 Schematic diagram of the effects of class IC agents.I_Na and I_K are transmembrane currents due to the movement of Na⁺ and K⁺, respectively. 23 24 2. Therapeutic uses: Flecainide is useful in the maintenance of sinus rhythm in atrial flutter or fibrillation in patients without structural heart disease and in treating refractory ventricular arrhythmias. Use of propafenone is restricted mostly to atrial arrhythmias, such as rhythm control of atrial fibrillation or flutter and paroxysmal supraventricular tachycardia prophylaxis in patients with AV reentrant tachycardias. 25 26 3. Pharmacokinetics: Flecainide is well absorbed after oral administration and is metabolized by CYP2D6 to multiple metabolites. The parent drug and metabolites are mostly eliminated renally. Propafenone is metabolized to active metabolites primarily via CYP2D6 and also by CYP1A2 and CYP3A4. The metabolites are excreted in the urine and the feces. 27 28 4. Adverse effects: Flecainide is generally well tolerated, with blurred vision, dizziness, and nausea being the most frequent unwanted side effects. Propafenone has a similar side-effect profile but may also cause bronchospasm, and it should be avoided in patients with asthma. Propafenone is also an inhibitor of P- glycoprotein. Both drugs should be used with caution with potent inhibitors of CYP2D6. 29 30 31 ## IV. CLASS II ANTIARRHYTHMIC DRUGS 32 33 Class II agents are β-adrenergic antagonists, or β-blockers. These drugs diminish phase 4 depolarization and, thus, depress automaticity, prolong AV conduction, and decrease heart rate and contractility. Class II agents are useful in treating tachyarrhythmias caused by increased sympathetic activity. They are also used for atrial flutter and fibrillation and for AV nodal reentrant tachycardia. In addition, β-blockers prevent life-threatening ventricular arrhythmias following a myocardial infarction. 34 35 Metoprolol [me-TOE-pro-lol] is the most widely used β-blocker for the treatment of cardiac arrhythmias. Compared with nonselective β-blockers, such as propranolol [pro-PRAN-oh-lol], it has a reduced risk of eliciting bronchospasm. It is extensively metabolized by CYP2D6 and has CNS 36 37 38 39 penetration (less than propranolol but more than atenolol [a-TEN-oh-lol]). Esmolol [ES-moe-lol] is a very [... Output truncated due to length. 4426 tokens/17330 characters removed ...]