441-antiarrhythmics only

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jgiantess
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124290
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441-antiarrhythmics only
Updated:
2011-12-18 03:41:38
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drugs
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pharmacology
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  1. Quinidine
    • Class IA antiarrhythmic: Na+ Channel Blocker
    • blocks Na+ channel @ open and activated state.
    • also blocks K+ channel to prolong AP.
    • overall, increases refractory period, decreases re-entry.
    • SE: cinchonism, diarrhea, ab cramps, N/V, hypotension, Torsades de Pointes, aggravation of underlying HF, conduction disturbances or ventricular arrhythmias, fever, hepatitis, thrombocytopenia, hemolytic anemia.

  2. Procainamide
    • Class IA antiarrhythmic: Na+ Channel Blocker
    • blocks Na+ channel @ open and activated state.
    • also blocks K+ channel to prolong AP.
    • overall, increases refractory period, decreases re-entry.
    • SE: systemic lupus erythematosus, diarrhea, nausea, vomiting, Torsades de Pointes, aggravation of underlying HF, conduction disturbances or ventricular arrhythmias, agranulocytosis.

  3. Disopyramide
    • Class IA antiarrhythmic: Na+ Channel Blocker
    • blocks Na+ channel @ open and activated state.
    • also blocks K+ channel to prolong AP.overall, increases refractory period, decreases re-entry.

  4. Lidocaine
    • Class IB antiarrhythmic: Na+ Channel Blocker
    • major block Na+ channel @ open and INactivated
    • minor block Na+ channel @ open and activated
    • shortens depol, quickens repol, and shortens AP
    • overall: decreases refractory period, and decreases re-entry.
    • SE: dizziness, sedation, slurred speech, blurred vision, paresthesia, muscle twitching, confusion, N/V, seizures, psychosis, sinus arrest, aggravation of underlying conduction disturbances.

  5. Mexiletine
    • Class IB antiarrhythmic: Na+ Channel Blocker
    • major block Na+ channel @ open and INactivated
    • minor block Na+ channel @ open and activated
    • shortens depol, quickens repol, and shortens AP
    • overall: decreases refractory period, and decreases re-entry.
    • SE: dizziness, sedation, anxiety, confusion, paresthesia, tremor, ataxia, blurred vision, N/V, anorexia, aggravation of underlying conduction disturbances or vent arrhythmias.

  6. Tocainide
    • Class IB antiarrhythmic: Na+ Channel Blocker
    • major block Na+ channel @ open and INactivated
    • minor block Na+ channel @ open and activated
    • shortens depol, quickens repol, and shortens AP
    • overall: decreases refractory period, and decreases re-entry.

  7. Propafenone
    • Class IC antiarrhythmic: Na+ Channel Blocker
    • most significant effect on Na+ channels @ open & activated
    • mild effect on Na+ channels @ open & inactivated
    • 0 effect on K+ and repol, no change in ERP
    • but refractory period of AV node increased.
    • for Atrial flutter and fibrillation and VT/VF.
    • SE: dizziness, fatigue, bronchospasm, headache, taste disturbances, N/V, bradycardia or AV block, aggravation of underlying HF, conduction disturbances or ventricular arrhythmias.

  8. Flecainide
    • Class IC antiarrhythmic: Na+ Channel Blocker
    • most significant effect on Na+ channels @ open & activated
    • mild effect on Na+ channels @ open & inactivated
    • 0 effect on K+ and repol, no change in ERP
    • but refractory period of AV node increased.
    • for Atrial flutter and fibrillation and VT/VF.
    • SE: blurred vision, dizziness, dyspnea, headache, tremor, nausea, aggravation of underlying HF, conduction disturbances or ventricular arrhythmias.

  9. Esmolol
    • Class II antiarrhythmic: B-adrenoceptor antagonist
    • blocks B1 receptor and SNS stimulation, decreases cAMP
    • @ pacemaker cells:
    • 1) decrease slope of Phase 4: opposes adrenaline effect at transient Ca2+ channels
    • 2) decrease slope of Phase 0: inhibits slow L-type Ca2+ channels, decrease HR
    • @ nonpacemaker cells:
    • at Phase 0, blocks inward Na+ current - increase ERP, decrease conduction.
    • Antihypertensive: B1 selective blocker at low doses
    • therefore, less effect on bronchioles
  10. Propranolol
    • Class II antiarrhythmic: B-adrenoceptor antagonist
    • blocks B1 receptor and SNS stimulation, decreases cAMP
    • @ pacemaker cells:
    • 1) decrease slope of Phase 4: opposes adrenaline effect at transient Ca2+ channels
    • 2) decrease slope of Phase 0: inhibits slow L-type Ca2+ channels, decrease HR
    • @ nonpacemaker cells:
    • at Phase 0, blocks inward Na+ current - increase ERP, decrease conduction.
    • Antihypertensive: non-cardioselective beta-adrenoceptor antagonist
    • blocks B1R - less CO, less renin release so fall in angiotensin II levels and decrease in tubular Na reabs.
    • block B2R - presynaptically, reduce NE overflow. Also - (bad) - increases risk of bronchoconstriction, peripheral VC, masking of compensatory response ass'd with hypoglyc...etc.
  11. Metoprolol
    • Class II antiarrhythmic: B-adrenoceptor antagonist
    • blocks B1 receptor and SNS stimulation, decreases cAMP
    • @ pacemaker cells:
    • 1) decrease slope of Phase 4: opposes adrenaline effect at transient Ca2+ channels
    • 2) decrease slope of Phase 0: inhibits slow L-type Ca2+ channels, decrease HR
    • @ nonpacemaker cells:
    • at Phase 0, blocks inward Na+ current - increase ERP, decrease conduction.
    • Antihypertensive: B1 selective blocker at low doses
    • therefore, less effect on bronchioles
  12. Atenolol
    • Class II antiarrhythmic: B-adrenoceptor antagonist
    • blocks B1 receptor and SNS stimulation, decreases cAMP
    • @ pacemaker cells:
    • 1) decrease slope of Phase 4: opposes adrenaline effect at transient Ca2+ channels
    • 2) decrease slope of Phase 0: inhibits slow L-type Ca2+ channels, decrease HR
    • @ nonpacemaker cells:
    • at Phase 0, blocks inward Na+ current - increase ERP, decrease conduction.
    • Antihypertensive: B1 selective blocker at low doses
    • therefore, less effect on bronchioles
  13. Amiodarone
    • Class III antiarrhythmic: K+ channel blocker
    • blocks K+ in plateau phase & blocks repolarization
    • prolongs AP, increases ERP, more risk of TdP
    • Amiodarone has characteristics of all Vaughan Williams classes:
    • 1) Na+ channel blocker
    • 2) non-comp, non-sel B-blocker
    • 3) K+ channel blocker
    • 4) small degree of Ca2+ blocker activity
    • initial action: B-blockade (by blocking Ca2+ currents, block AP initiation by SA)
    • chronic: K+ effect, prolonged repolarization.
    • SE: tremor, ataxia, paresthesia, insomnia, corneal microdeposits, optic neuropathy/neuritis, nausea, vomiting, anorexia, constipation, TdP, brady or AV block, pulmonary fibrosis, liver fxn test abnorms, hepatitis, hypothyroidism, hyperthyroidism, photosensitivity, blue-gray skin discoloration, hypotension (IV), phlebitis (IV)

  14. Dronedarone
    • Class III antiarrhythmic: K+ channel blocker
    • blocks K+ in plateau phase & blocks repolarization
    • prolongs AP, increases ERP, more risk of TdP

  15. Sotalol
    • Class III antiarrhythmic: K+ channel blocker
    • blocks K+ in plateau phase & blocks repolarization
    • prolongs AP, increases ERP, more risk of TdP
    • Antihypertensive: non-cardioselective beta-adrenoceptor antagonist
    • blocks B1R - less CO, less renin release so fall in angiotensin II levels and decrease in tubular Na reabs.
    • blocks B2R - presynaptically, reduce NE overflow. Also - (bad) - increases risk of bronchoconstriction, peripheral VC, masking of compensatory response ass'd with hypoglyc...etc.
    • SE: dizziness, weakness, fatigue, N/V, diarrhea, brady, TdP, bronchospasm, aggravation of underlying HF

  16. Dofetilide
    • Class III antiarrhythmic: K+ channel blocker
    • blocks K+ in plateau phase & blocks repolarization
    • prolongs AP, increases ERP, more risk of TdP
    • SE: headache, dizziness, TdP

  17. Ibutilide
    • Class III antiarrhythmic: K+ channel blocker
    • blocks K+ in plateau phase & blocks repolarization
    • prolongs AP, increases ERP, more risk of TdP
    • SE: headache, TdP, hypotension

  18. Verapamil
    • Class 4 Antiarrhythmic: Ca2+ Channel Blocker
    • blocks voltage sensitive Ca2+ current during Phase 2 plateau of non-pacemaker myocytes
    • also decreases automaticity and conduction velocity in both SA and AV nodes.
    • Calcium Channel Blocker - primary action at the heart muscles (myocardium), some in conducting tissue.
    • Decrease Calcium entry into heart muscle, decrease cardiac output.

  19. diltiazem
    • Class 4 Antiarrhythmic: Ca2+ Channel Blocker
    • blocks voltage sensitive Ca2+ current during Phase 2 plateau of non-pacemaker myocytes
    • also decreases automaticity and conduction velocity in both SA and AV nodes.
    • Antihypertensive. Calcium Channel Blocker: primary action on conducting tissues.
    • Decreases flow of Calcium through transmission of nerve impulses. Slows generation of action potentials at SA node, slows conduction of action potentials through AV node.
    • decreases conduction, decrease force of contraction.

  20. adenosine (purinergic agonist)
    • acts on A1 receptor of AV node
    • decreases cAMP levels, therefore blocks Ca2+ current due to decreased phosphorylation of Ca2+ channel.
    • Enhances K+ conductance, causes hyperpolarization
    • decreases conducton velosity, increases ERP in AV node
    • slows rate of rise of pacemaker potential
    • SE: flushing and hypotension, paresthesias, SOB, chest pain (bronchospasm)

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