Term
| Name the 3 Class IA antiarrhythmia drugs |
|
Definition
1. Quinidine 2. Disopyramide 3. Procainamide |
|
|
Term
| List the characteristics of class 1A antiarrhythmic drugs |
|
Definition
1. block fast sodium channels 2. block channels in the open/activated state 3. Increases AP duration 4. Increases effective refractory period 5. blocks K channels (prolong repolarization) |
|
|
Term
| Antiarrhythmic durgs ____ the heart |
|
Definition
|
|
Term
| List the major side effect common to all Class IA antiarrhythmias |
|
Definition
1. Prolongs QT interval and leads to Torsade de pointes 2. Depresses SA node 3. Antimuscarinic -Inhibit vagal input |
|
|
Term
| Quindine is ___ bound to ____ |
|
Definition
|
|
Term
| List the adverse effects of Quindine |
|
Definition
1. GI: Nausea, vomiting, diarrhea 2. Cinchonism (GI, tinnitus, ocular dysfunction & CNS excitation) 3. Displaces digitalis from tissue binding site leading to toxicity 4. Syncope |
|
|
Term
| What is cinchonism? What drug is it associated w/ it |
|
Definition
GI dysfunction, Tinnitus, ocular dysfunction & CNS excitation Associated w/ Quinidine |
|
|
Term
| When would you not give Quinidine |
|
Definition
1. Sick Sinue syndrome 2. bradycarrdia |
|
|
Term
| When would you use Quinidine |
|
Definition
| Maintain normal sinus rhythm in atrial flutter or fibrillation |
|
|
Term
| What increases quinidine toxicity? Why? |
|
Definition
Antacids increases it's absorption due to quinidine being a weak base |
|
|
Term
| When would you use Disopyramide |
|
Definition
| Only when quinidine & procainamide are poorly tolerated |
|
|
Term
| Which drug is most likely to have the greatest anti-muscarinic effect? Which one the least? |
|
Definition
|
|
Term
| Procainamide is metabolized via ___________ to __________ it's active form |
|
Definition
1. N-acetyltransferase 2. N-acetyl procainamide |
|
|
Term
| When would you use Procainamide |
|
Definition
| second choice after quinidine for ventricular arrhythmias after an acute MI |
|
|
Term
| Give the adverse effects of Procainamide |
|
Definition
1. Lupus like 2. CV effects (torsades) |
|
|
Term
| Name the characteristics common to all Class 1B drugs |
|
Definition
1. Block fast sodium channels 2. Perfer inactive channels (depolarized) results in increase threshold of excitation of hypoxic heart |
|
|
Term
| Name the 2 class IB drugs |
|
Definition
1. Lidocaine 2. Mexiletine |
|
|
Term
| Lidocaine is used for __ use only because of _____ metabolism |
|
Definition
|
|
Term
| Lidocaine has the greatest effect on _____ tissue so it's used in Post MI |
|
Definition
|
|
Term
| Name the uses for Lidocaine |
|
Definition
1. Post-MI 2. Open heart surgery 3. Digoxin toxicity |
|
|
Term
| Lidocaine is the ______ of all the antiarrythmias |
|
Definition
|
|
Term
| The effects of Mexiletine are the same as ____, the difference is that it's in _____ form |
|
Definition
|
|
Term
| Give the side effects of Mexiletine |
|
Definition
Neurologic 1. Tremor 2. Nausea 3. blurred vision |
|
|
Term
| What are the characteristics of 1C antiarrythmias |
|
Definition
1. Binds fast sodium channels 2. No effect on Refractory period 3. No ANS effect |
|
|
Term
| Flecainide is a ____ ____ ______ blocker |
|
Definition
|
|
Term
| Name the 1C antiarrythmia |
|
Definition
|
|
Term
| Why does Flecainide have limited use? |
|
Definition
| there's an increase in sudden death post MI |
|
|
Term
| In what situation would you use flecainide |
|
Definition
| Supraventricular arrhythmias w/ a normal heart |
|
|
Term
| Name 4 Class II "Beta blockers" |
|
Definition
1. Propanolol 2. Atenolol 3. Metoprolol 4. Esmolol |
|
|
Term
| Give the characterstics common to all Beta blockers |
|
Definition
1. Prevent beta receptor activation leading to decrease cAMP 2. Decrease SA & AV node activity 3. Decrease Phase 4 4. Blocks catecholamine |
|
|
Term
| Have effect does catecholamines have on the heart |
|
Definition
| Make the heart more excitable & less stable |
|
|
Term
| Propanolol is a _______ beta blocker |
|
Definition
|
|
Term
| Atenolol, esmolol & metoprolol are _____ beta blockers |
|
Definition
|
|
Term
| What are the adverse effects of Propanolol |
|
Definition
1. Asthma 2. Negative inotropic 3. Heart failure |
|
|
Term
| Beta blockers are for prophylaxis in ____ __ & in SVT |
|
Definition
|
|
Term
| Give the characteristics of Class III: Potassium blockers |
|
Definition
| decreases Ik (delayed retifier current) slowing phase 3 (repolarization) of AP |
|
|
Term
| Name the 5 K channel blockers |
|
Definition
1. Amiodarone 2. Bretylium 3. Sotalol 4. Ibutilide 5. Dofeilide |
|
|
Term
List the MO of Amiodarone HINT: 5 |
|
Definition
1. Blocks K channels 2. Blocks Sodium channels (inactive) 3. Inhibitor of abnormal automaticity 4. slows SA & AV nodal conduction 5. Increases refractory period |
|
|
Term
| What's the high life of amiodarone |
|
Definition
|
|
Term
Name the side effect of Amiodarone HINT 4 |
|
Definition
1. Pulmonary fibrosis 2. heart block and failure 3. blue pigmentation (smurf skin) 4. Deposits in organs |
|
|
Term
| Amiodarone is the most effective drug at ? |
|
Definition
| preventing atrial fibrillation, ventricular tachycardia or fibrillation |
|
|
Term
| Amiodarine can be used for ___ arrythmias |
|
Definition
|
|
Term
| When would you use Bretylium |
|
Definition
| In the ER after al methods failed |
|
|
Term
| give the 5 Cardiac effects of Sotalol |
|
Definition
1. Decreases SA + AV nodes 2. Increases PR interval 3. Increases QT interval 4. Increases RP in depolarized cells 5. Decrease ectopic pacemaker |
|
|
Term
| A major side effect of sotaolol is |
|
Definition
|
|
Term
| when would you use sotaolol |
|
Definition
| Supraventricular & life threatening arrhythmias |
|
|
Term
| Name the two Class IV: Calcium blockers |
|
Definition
|
|
Term
| Calcium blockers are limited to |
|
Definition
|
|
Term
| What effect does verapamil have on digoxin |
|
Definition
| Suppresses abnormal automaticity caused by digoxin |
|
|
Term
| What 2 phases do calcium blockers affect |
|
Definition
|
|
Term
| The adverse effects of verapamil are |
|
Definition
1. Constipation 2. AV block 3. Sinus arrest |
|
|
Term
| When do you use verapamil |
|
Definition
| Supraventricular tachycardia |
|
|
Term
|
Definition
| AV nodal conduction & cAMP calcium influx |
|
|
Term
| What's the half life of Adenosin |
|
Definition
|
|
Term
| When do you use adenosine |
|
Definition
| Paroxysmal supraventricular tachycardia |
|
|
Term
| The uses for magnesium is |
|
Definition
|
|
Term
| What's the side effects for adenosine |
|
Definition
| Flushing, sedation & dyspnea |
|
|
Term
| What's the treatment for torsades de pointes |
|
Definition
1. Correct hypokalemia 2. Correct hypomagnesemia 3. Discontinue drugs that prolong QT interval |
|
|
Term
| How do you treat Wolff-Parkinson-White syndrome |
|
Definition
|
|
Term
| What don't you want to do in Wolff-Parkinson-White |
|
Definition
1. Slow AV conduction 2. Avoid digoxin, beta blocks, Ca channel blocker & adenosin |
|
|
