Antiarrythmics
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| Cardiac action potential | initiated in SA node-atria depolarizes-AV node slows down the potential so the ventricle can fill-His Purkinje system-races down to apex of heart then comes back up through ventricles (contract bottom up)
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| what happens in depolarization? | sodium influx chemically and electrically from high to low concentration, inside of cell is negative and Na is positive
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| Phase of depolarization in fast ap? | phase 0
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| What happens in phase 1 of fast ap? | Ca comes into cell when potential reaches +55mV
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| What happens in phase 2 of fast ap? |
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| What happens in phase 3 of fast ap? |
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| What happens in phase 4 of fast ap? | Diastole; heart is filling
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| Na/K ATPase function and phase? |
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| Drugs that block fast sodium channels? | local anesthetics; too much will decrease conduction velocity (slope of phase 0) so much they will stop the heart
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| Drugs that block potassium channels? |
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| Slope of phase 0 is directly proportional to... | conduction velocity....affected by Na channel blockers; otherwise known as speed of depolarization
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| Effects of blocking K channels | increase duration of action potential; slows down heart rate; increases refractory period; takes longer to get potassium out and get back to phase 4
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| Where is the slow potential? | SA and AV nodes
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| What phase does slow potential not have? | Phase 1
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| What happens in phase 0 of slow ap? |
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| What happens in phase 2 of slow ap? |
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| What happens in phase 3 of slow ap? |
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| What happens in phase 4 of slow ap? |
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| What happens in phase 0 of fast ap? |
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| What happens if you block calcium channels? |
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| What affect do b1 receptors have on action potential? |
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| PR interval | Time to go from SA to AV; mostly AV time
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| QRS interval | Tells us conduction velocity through ventricles; tells his purk or vent conduction problem
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| QT interval | Ventricular repolarization; prolonged tells us there is a potassium uptake or blocking issue
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| Torsades |
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| Wide QRS = | slow ventricular conduction and slowed fast action potential
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| Prolonged PR from which drugs? |
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| Adverse affect of local anesthetic | widened QRS
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| Ectopic pacemakers | Pacemaker that starts up anywhere in the heart other than the SA node
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| Name arrythmias based on... | speed, location,
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| Class 1A action and drugs | moderate affect phase 0; quinidine, procainamide
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| Class 1B action and drugs | No change to phase 0; lidocaine
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| Class 1C action and drugs | Marked phase 0 change;
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| Class II action and drugs |
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| Class III action and drugs |
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| Class IV action and drugs |
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| Frequency dependence = |
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| Explain the h gate |
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| Explain refractory period |
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| Quinidine | Class 1A local anesthetic
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| Procainamide | Class 1A local anesthetic, increase phase 0 and action potential duration; can produce torsades
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| Lidocaine | Class 1B; only for Vtachs and only IV
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| Mexiletine | Class 1B oral version of lidocaine
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| Flecainide | Class 1C; used for Vtachs in adults; kids SVTs and atrial tachs; increases QT and causes torsades
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| CAST trial | showed adverse affects from long term local anesthetic use
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| Affects of beta blockers on heart rhythm | decrease sinus tach; block junctional arrythmias in and around the AV node; protect the ventricle in an atrial tach by slowing conduction in AV node
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| Propranolol |
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| Atenolol |
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| Timolol |
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| Esmolol |
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| Drugs that slow AV conduction are... | additive in their affects
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| Amiodarone | Na, K, Ca, and B blocker; 3 1/2 month half life
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| Sotalol | K and B blocker
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| Dronedarone | Amiodarone with shorter half life; iodine removed so half life is 24 hours; contraindicated in heart failure; produces more torsades than amiodarone
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| Dofetilide | inward rectifying potassium channel blockers; truly cardioselective; only for atrial tachs; 6% torsades occurence; maintains SR
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| Ibutilide | Class III
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| Verapamil |
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| Diltiazem |
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| Adenosine |
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| Atropine |
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| Magnesium |
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| Digitalis |
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| what is a cardiac arrhythmia? | variation in the way the action potential is formed and/or the way the action potential is propagated across the heart
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| Which parts of the heart do not have a fast cardiac ap? | SA and AV nodes
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| 3 effects of local anesthetics (Na channel blockers) on fast cardiac action potential | decrease conduction velocity, increase refractory period, and increase threshold
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