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