Question | Answer |
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 |