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Antiarrhythmics
FA Classes I-IV
Question | Answer |
---|---|
On which phase of the action potential do sodium channel blockers work? | Phase 0 |
Which "kind" of cells are more attractive for sodium channel blockers? | Depolarized cells |
Arrange antiarrhythmic strength in the three classes of Na-channel blockers? | IC > IA > IB |
Which are the Class IA sodium channel blockers? | Quinidine, Procainamide, and Disopyramide |
What are the effects on the ventricular action potential caused by Class IA sodium channel blockers? | ↑ AP duration and ↑ effective refractory period (ERP) |
How are Sodium channel blockers represented in an EKG? | ↑ QT interval |
What are the shared adverse effects of Class IA Na-channel blockers? | Thrombocytopenia, and Torsade de pointes due to ↑ QT interval |
What is the main adverse effect of Quinidine? | Cinchonism |
What is the associated adverse effect of Procainamide? | SLE-like syndrome |
What is the associated adverse effect of Disopyramide? | Heart failure |
Which class of sodium channel blockers have a weak profile? | Class IB |
Which are the Class IB sodium channel-blockers? | Lidocaine, Phenytoin, and Mexiletine |
Which class of sodium channel blockers preferentially affect ischemic or depolarized Purkinje and ventricular tissue? | Class IB |
What class of antiarrhythmic is Phenytoin? | Class IB |
Is AP duration increased or decreased by Class IB Sodium channel blockers? | ↓ AP duration |
Which Na+ channel blockers are often used in Digitalis-induced arrhythmias? | Class IB |
What are the main adverse effects of Class IB Sodium channel blockers? | CNS stimulation/depression, CV depression |
Which class IB antiarrhythmic is associated with GI intolerance? | Mexiletine |
Which class of Na+ channel blockers have the STRONGEST effect? | Class IC |
What is the main mechanism of action of Class IC Na channel blockers? | Significantly prolongs ERP in AV node and accessory bypass tracts |
What class of sodium channel blockers is contraindicated in HF patients or post-MI patients? | Class IC |
Which are the Class-IC antiarrhythmics? | Flecainide and Propafenone |
On which phase of the action potential do ß-blockers work on? | Phase 4 |
What is the mechanism of action of ß-blockers? | 1. Decrease SA and AV node activity by ↓ cAMP, ↓ Ca2+ currents 2. Suppress abnormal pacemakers by ↓slope of phase 4 |
Which node, AV or SA, is most susceptible to beta blockers? | AV node --> ↑ PR interval |
Which are common arrhythmias treated with ß-blockers? | SVT, ventricular rate control of AFIB and A-FLUTTER |
Why are beta blockers not used in diabetic patients? | They mask the signs of hypoglycemia |
What are some general adverse effects of ß- blockers? | Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, HF), CNS effects (sedative, sleep alteration) |
What is a specific adverse effect of Metoprolol? | Dyslipidemia |
Which beta blocker is known to cause exacerbation of vasospasms in vasospastic angina? | Propranolol |
Which are the non-selective beta blockers? | Carvedilol and Labetalol |
What is the problem of all beta blockers, except those that are non-selective? | May cause unopposed α1-agonism (vasoconstriction) |
How is B-blocker toxicity treated? | Saline, atropine, and glucagon |
What are some common B-blockers? | Metoprolol, Propranolol, esmolol, timolol, and carvedilol |
Which B-blocker is the shortest acting? | Esmolol |
What are the class III antiarrhythmics? | Potassium channel blockers |
Which are the class III antiarrhythmics? | Amiodarone, Ibutilide, Dofetilide, and Sotalol |
What are the effects of class III K+ blockers on the AP and EKG? | ↑ AP duration, ↑ ERP, and ↑ QT interval |
What is the associated adverse effect of Sotalol? | Torsade de Pointes and excessive ß-blockade |
Which fatal arrhythmia is associated with most Potassium channel blockers? | Torsade de Pointes |
What are the most significant adverse effects of Amiodarone? | 1. Lungs --> pulmonary fibrosis 2. Liver --> Hepatotoxicity 3. TH gland --> hypo/or hyperthyroidism Acts as a hapten --> corneal deposits, blue/gray skin deposits in skin CV --> bradycardia, HF, and heart block |
Why does Amiodarone have class I, II, III, and IV effects? | Due to its lipophilic structure |
What are the two main Calcium antiarrhythmics? | Diltiazem and Verapamil |
What is the MOA of Calcium channel blockers? | Decrease conduction velocity, ↑ERP, ↑ PR interval |
What are common adverse effects of calcium channel blockers? | Constipation, flushing, edema, CV effects (HF, AV block, sinus node depression) |
What is the drug of choice for terminating SVT? | Adenosine |
MOA of adenosine | ↑ K+ out of cells ==> hyperpolarizing the cell and ↓ intracellular calcium --> decreasing AV node conduction |
What substances may affect and blunt the effect of Adenosine? | Caffeine and Theophylline |
Which are common uses for Magnesium as an antiarrhythmic? | Torsade de Pointes and Digoxin toxicity |
Which IV drug selectively inhibits the "funny" sodium channels? | Ivabradine |
Which is the DOC in patients that cannot tolerate ß-blockers? | Ivabradine |
What are associated adverse effects of Ivabradine? | Luminous phenomena/visual brightness, HTN, and bradycardia |