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Antiarrythmics

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