Anti-Anginals

Cards (18)

  • Congestive Heart Failure (CHF)

    When the heart muscle (myocardium) weakens & enlarges, it loses its ability to pump blood through the heart & into the systemic circulation
  • Cardiac Glycosides
    • Positive inotropic action increases myocardial contraction stroke volume
    • Negative chronotropic action decreases heart rate
    • Negative dromotropic action decreases conduction of heart cells
  • Cardiac-altered functions that can contribute to digoxin-induced ventricular dysrhythmias
    • Suppression of AV conduction
    • Increased automaticity
    • Decreased refractory period in ventricular muscle
  • Digoxin-immune Fab
    Binds with digoxin to form complex molecules that can be excreted in the urine, thus digoxin is unable to bind at the cellular site of action
  • Beta Blockers
    • Selective beta blockers are the group of choice for controlling angina pectoris
    • Block the beta1- & beta2-receptor sites
    • Decrease the effects of the sympathetic nervous system by blocking the action of the catecholamines, epinephrine & norepinephrine, decreasing the HR & BP
    • Used as antianginal, antidysrhythmic & antihypertensive drugs
    • Effective as antianginals because by decreasing the HR & myocardial contractility they reduce the need for oxygen consumption & consequently reduce anginal pain
    • Most useful for classic (stable) angina
  • Selective beta blockers
    • Block the beta1- & beta2-receptor sites
    • Decrease the effects of the sympathetic nervous system by blocking the action of the catecholamines, epinephrine & norepinephrine
    • Decrease the HR & BP
  • Calcium channel blockers

    Verapamil, nifedipine, and diltiazem
  • Calcium channel blockers

    • Use for the treatment of stable and variant angina pectoris, certain dysrhythmias & hypertension
    • Relax coronary artery spasm (variant angina) & relax peripheral arterioles (stable angina), decreasing cardiac oxygen demand
    • Decrease cardiac contractility
  • Cardiac dysrhythmia (arrhythmia)

    Any deviation from the normal rate or pattern of the heartbeat
  • Dysrhythmia (disturbed heart rhythm)

    Arrhythmia (absence of heart rhythm) are used interchangeably
  • Antidysrhythmic (antiarrhythmic) drugs

    • Action is to restore the cardiac rhythm to normal
  • Four classes of antidysrhythmic drugs

    • Sodium (fast) channel blockers IA, IB, IC
    • Beta blockers
    • Potassium channel blockers
    • Calcium (slow) channel blockers
  • Class I: Sodium channel blockers
    • Decreases sodium influx into cardiac cells
    • Decreases conduction velocity in cardiac tissues; suppression of automaticity, which decreases the likelihood of ectopic foci & increased recovery time (repolarization or refractory period)
  • MOA: Class 1(Sodium Channel Blockers)
    • Class 1 A - Quinidine, Procainamide, Disopyramide, Moricizine
    • Class 1 B - Lidocaine, Mexiletine, Tocainide
    • Class 1 C - Encainide, Flecainide, propafenone
  • Class II: Beta blockers
    • Decrease conduction velocity, automaticity & recovery time (refractory period)
    • More frequently prescribed for dysrhythmias than are sodium channel blockers
  • Class III: Potassium channel blockers

    • Sotalol, bretylium, amniodarone
  • Class III: Potassium channel blockers
    • Prolong repolarization & are used in emergency treatment of ventricular dysrhythmias when other antidysrhythmics are ineffective
    • Amiodarone increases the refractory period (recovery time) & prolongs the action potential duration (cardiac cell activity)
  • Class IV: Calcium channel blockers
    • Verapamil & Diltiazem
    • Slow (calcium) channel blocker that blocks calcium influx decreasing the excitability & (negative inotropic) contractility of the myocardium
    • Increases the refractory period of the AV node which decreases ventricular response
    • Contraindicated for patients with AV block or HF