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63 Cards in this Set
- Front
- Back
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How are Class 1 and Class 3 drugs different from Class 2, Class 4 and others?
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Class 1 and Class 3 are specifically targeted toward the cardiac action potential
- Have direct effects on atrial and ventricular cells - Can be more useful, but more dangerous Class 2, Class 4 and others have their primary action directed toward modulating the SA and AV node |
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What are the classes of Antiarrhythmic drugs?
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Class 1: Sodium Channel Blockers
Class 2: Beta Blockers Class 3: Potassium Channel Blockers Class 4: Calcium Channel Blockers Other: Adenosine, Digoxin |
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What is the affect of Sodium Channel Blockers on Action Potential and EKG?
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- Slows upstroke of Phase 0 – rapid depolarization
- Prolongs QRS duration (not always noticeable on EKG) |
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How do Sodium Channel Blockers work?
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- Fewer Na+ channels are available for conduction
- Raise the threshold for initiation of action potention - May also decrease slope of phase 4 in cells with abnormal automaticity |
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What is the effect of Sodium Channel Blockers on automaticity?
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- Takes a larger stimulus to excite each cell
- Slows or terminates automaticity > May slow enough that sinus node now becomes dominant rhythm (“fastest one wins”) - Sinus node automaticity not usually affected unless already have sinus node dysfunction |
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What is the effect of Sodium Channel Blockers on conduction velocity?
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- Na+ channel blockade causes each cell to activate a bit more slowly
- Cumulative effect is to slow conduction through the affected tissue |
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What are Sodium Channel Blockers effects on reentry?
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Good
- Convert unidirectional block to bidirectional block at critical heart rate - Slow the “slow pathway” so much that it no longer conducts at all Bad - Slow either pathway just enough to make the reentrant circuit virtually incessant - This is the primary danger of type 1 antiarrhythmic drugs – incessant VT - Patients with prior myocardial infarction should not take type 1 drugs unless they already have an ICD (defibrillator) |
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Class 1A
Antiarrhythmic |
(Quinidine, Procainamide, Disopyramide)
- Prolongs QRS and QT - Lots of Side Effects |
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Class 1B
Antiarrhythmic |
(Lidocaine, Mexiletine)
- Only work in ventricle - Preferentially target ischemic cells - Shorten QT |
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Class 1C
Antiarrhythmic |
(Flecainide, Propafenone)
- Most potent of subclasses - Prolong QRS the most - No direct effect on QT - Negative inotropes (bad in heart failure) |
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Actions of Class 1A antiarrythmics
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Also block K+ channels
- These older drugs are not “clean” Na+ blockers - QT prolongation can cause arrhythmias -->“Torsades de pointes” (aka Polymorphic Ventricular Tachycardia) Lots of noncardiac side effects - Not well-tolerated by patients |
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Quinidine
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Class 1A
Major GI side effects - Nausea and vomiting - Diarrhea in up to ⅓ of patients CNS side effects - “cinchonism” = tinnitus, confusion, visual disturbance, etc. Autoimmune thrombocytopenia Major interaction with digoxin - Raises digoxin level |
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Procainamide
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Only 1A drug used intravenously
Breakdown product = NAPA (N-acetyl procainamide) - An active metabolite; Metabolism depends on rate of acetylation; Pts can be “slow” or “rapid” acetylators - Blood level = check both Procainamide + NAPA Lupus-like syndrome in up to ⅓ of patients - Fever, rash, arthralgias, etc. - Requires stopping the drug On ACLS protocol for V Tach |
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Disopyramide
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Strong anticholinergic effect
- Dry mouth, urinary retention, constipation, exacerbation of glaucoma Negative inotrope - unlike procainamide and quinidine, which are not negative inotropes - Has been used as a “good side effect” in patients with hypertrophic cardiomyopathy Use if pt has A-fib and hypertrophic cardiomyopathy |
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Mexiletine
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Class 1B
- Oral only - Practically speaking, probably okay to consider this an oral form of lidocaine - Not very effective, but mixes well with certain other antiarrhythmics when needed |
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Lidocaine
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Class 1B
Intravenous only Cleared by liver, so careful in: - Liver disease (obviously) - Heart failure means less hepatic perfusion CNS side effects - Can be serious if levels get too high - Confusion --> seizures If prolonged infusion needed, must check levels frequently |
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Lidocaine and Mexiletine
Action |
Shorten the QT interval
- Not usually enough to be noticeable on EKG Target ventricular cells only - No effect on atrium Preferentially affect ischemic tissue - Can be useful for ventricular arrhythmias in AMI Can increase mortality if used during AMI |
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Class 1C Antiarrhythmics
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The MOST POTENT Na+ channel blockers
Markedly decrease upstroke of phase 0 “Clean” drugs – no effect on K+ channels - No direct effect on QT interval - Can cause bad arrhythmias, but not Torsades Negative inotropes - contraindicated in systolic heart failure Primarily used for atrial arrhythmias (AFib) - Also can be used to “shut down” accessory pathways (i.e. Wolff-Parkinson-White syndrome) |
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Flecainide
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Class 1C
Side effects are common, but not usually severe enough to stop the drug if it’s working - Fatigue is very common - Visual disturbances fairly common (Complaints are vague but consistent) |
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Propafenone
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Class 1C
HAS BETA BLOCKING PROPERTIES - How much depends on individual patient’s metabolism Mild CNS symptoms - Dizziness |
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Use-dependence
and Sodium Channel Blockers |
Na+ channel blocking drugs bind preferentially to open channels
- The more the channels are open (being used), the greater the blockade - This means that Na+ channel blockers are even more effective at faster heart rates During atrial fibrillation, atrial rates are very fast (300-400 bpm) - This is one reason why Na+ channel blockers can actually stop AFib (convert it to sinus rhythm) |
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Sotalol
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Class 3
Also has beta blocker activity - Can be good or bad depending on patient Cleared by the kidney - Can accumulate in renal failure and cause Torsades (I’ve seen this quite a few times) QT must be monitored periodically (q 6 months) |
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Ibutilide
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Class 3
- Intravenous - Given IV to convert Afib... Torsades occurs in up to 10%, but can be partially prevented by giving IV magnesium first -QT must be monitored periodically |
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Dofetilide
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Class 3
- Oral administration - is cleared by liver and kidney (renal clearance is important) - is relatively safe in heart failure (b/c not a negative inotrope) - QT must be monitored periodically |
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Amiodarone
Dangerous for your ... |
- has A LOT of iodine in it... iodine plays a major role in its noncardiac toxicities
- Eyes – corneal deposits; rare optic neuropathy - serious - Hypothyroidism – common, easily remedied - Hyperthyroidism – rare, can be serious - Hepatic injury - Pulmonary toxicity – irreversible, but usually only after several years, takes 10 years to develop - Skin photosensitivity – bluish discoloration of skin only after years of fairly high-dose therapy - Major interaction with warfarin NOT A DRUG NOT YOUNG PEOPLE |
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Amiodarone
Drug for your Heart |
Prolongs QT but very rarely causes Torsades
- Not usually thought of as a risk for Torsades - Don’t need to monitor QT Almost never causes ventricular arrhythmias - But also can’t be counted upon to prevent them - Only ICDs have been shown to improve mortality in patients at risk for fatal arrhythmias |
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Amiodarone
Actions |
Class 3
- has some properties of all four antiarrhythmic drug classes - Some Na+ channel blocking properties - Some β-blocking properties - A lot of K+ blocking properties - Some Ca++ channel blocking properties ... can be used for just about every arrhythmia |
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Dronedarone
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Class 3
Supposedly this is just like amiodarone except: Without the iodine Without the awful toxicities May not be as protected from Torsades - QT does have to be monitored - Torsades risk is probably low Interferes with creatinine secretion – raises serum creatinine level, but GFR is actually not affected |
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Amiodarone
Dangerous for your ... |
- has A LOT of iodine in it... iodine plays a major role in its noncardiac toxicities
- Eyes – corneal deposits; rare optic neuropathy - serious - Hypothyroidism – common, easily remedied - Hyperthyroidism – rare, can be serious - Hepatic injury - Pulmonary toxicity – irreversible, but usually only after several years, takes 10 years to develop - Skin photosensitivity – bluish discoloration of skin only after years of fairly high-dose therapy - Major interaction with warfarin NOT A DRUG NOT YOUNG PEOPLE |
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Amiodarone
Drug for your Heart |
Prolongs QT but very rarely causes Torsades
- Not usually thought of as a risk for Torsades - Don’t need to monitor QT Almost never causes ventricular arrhythmias - But also can’t be counted upon to prevent them - Only ICDs have been shown to improve mortality in patients at risk for fatal arrhythmias |
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Amiodarone
Actions |
Class 3
- has some properties of all four antiarrhythmic drug classes - Some Na+ channel blocking properties - Some β-blocking properties - A lot of K+ blocking properties - Some Ca++ channel blocking properties ... can be used for just about every arrhythmia |
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Which antiarrhythmics are okay to use in systolic heart failure?
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- Beta blockers, just don’t give too much
- Amiodarone - Dofetilide - Sotalol, but its beta blocking properties might be a problem - Dronedarone, but contraindicated in severe CHF - Digoxin |
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Which antiarrhythmics are relatively contraindicated to use in systolic heart failure?
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Verapamil and diltiazem
- Due to negative inotropy - Sometimes you have no choice but to use them |
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Which antiarrhythmics are definitely contraindicated to use in systolic heart failure?
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Any type 1 antiarrhythmic, unless already have ICD
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Which antiarrhythmics are okay to use with a prior MI and scar but without systolic heart failure?
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- Beta blockers
- Amiodarone - Dofetilide - Sotalol - Dronedarone - Digoxin - Verapamil and diltiazem, but beta blockers are better |
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Which antiarrhythmics are okay to use with healthy ventricles?
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- Everything is okay (hooray!)
- Type 1 antiarrhythmics (especially 1C – flecainide and propafenone) may actually be safer than type 3 drugs in patients with a structurally normal ventricle |
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Name the Cardioselective Beta Blockers
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Atenolol
Metoprolol Esmolol Bisoprolol Acebutolol* * Intrinsic Sympathomimetic Activity |
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Name the non-selective Beta Blockers
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Propranolol
Labetalol# Carvedilol# Pindolol* Nadolol # Also blocks Alpha receptors * Intrinsic Sympathomimetic Activity |
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When does cardioselective vs. Nonselective matter?
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Asthma
- Nonselective beta blockers block β-2 receptors, can cause bronchospasm (rarely can be life-threatening) • Peripheral vascular disease and Raynaud’s Severe PVD and Raynaud’s syndrome can be exacerbated by nonselective beta blockers (Sometimes even selective β-blockers are a problem) Additional alpha blockade (Labetalol) can be helpful useful in hypertensive emergencies |
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How do beta blockers work?
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- Block the effects of Catecholamines… block the effects of the sympathetic nervous system (which would be increasing HR)
- have no effect on the cardiac action potential - The ONLY antiarrhythmic drugs that actually improve survival in patients with heart disease |
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What are the effects of beta blockers?
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Negative chronotropic effect
- Slows automaticity in sinus node and AV node by SLOWING PHASE 4 DEPOLARIZATION - Slows sinus rhythm and slows junctional escape rhythm Negative dromotropic effect - SLOWS VELOCITY OF CONDUCTION THROUGH AV NODE - Especially useful to slow ventricular response rate during atrial tachyarrhythmias Negative inotropic effect |
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What are the adverse effects of beta blockers?
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Negative chronotropic effect
- Sinus bradycardia Negative dromotropic effect - AV block Negative inotropic effect - Can worsen patients who are already having severe, acutely decompensated heart failure - In most heart failure patients, beta blockers are a good thing When beta blockers make a heart failure patient worse, negative inotropy usually isn’t the reason - The problem is usually bradycardia (negative chronotropic and dromotropic effects) |
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Name the class 3 antiarrythmics
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Sotalol
Dofetilide and Ibutilide Amiodarone Dronedarone |
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What are the affects of potassium channel blockers on Action Potential and EKG?
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Prolong Phase 3 – Repolarization
- This prolongs the Effective Refractory Period of the cell - Makes the cell unable to sustain faster heart rates Prolong QT |
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What are the risks associated with prolonging the QT interval with potassium channel blockers?
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Torsades (polymorphic VT) is a risk with most (exception = amiodarone)
Torsades is more likely when: - Too much drug on board (renal or hepatic failure, depending on drug) - Hypokalemia - Bradycardia and especially sinus pauses Despite all this, K+ channel blockers can be used in patients with prior AMI |
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Reverse Use Dependence and Potassium Channel Blockers
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K+ channel blocking drugs have a greater effect during slower heart rates
This makes them less useful in terminating atrial fibrillation (when atrial rates are very fast) Also means that bad arrhythmias such as Torsades are more likely during slower heart rates if the QT is prolonged - “pause-dependent Torsades” = Polymorphic VT occurring after a sinus pause |
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What are the classes of Calcium Channel Blockers?
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Dihydropyridine (DHP)
- Nifedipine, Amlodipine, Felodipine…. - Have no clinically relevant effects… such potent vasodilators that no one can take a high enough dose to actually affect the cardiac Ca++ channels Nondihydropyridine (non-DHP) - Diltiazem - Verapamil |
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How do nondihydropyridines work?
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Block the L-type calcium channels
Only affect Sinus and AV nodal cells - AV node is affected most |
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What are the effects of nondihydropyridines?
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- Negative Chronotropic Effect on SA and AV Node
- Negative Dromotropic Effect on AV node - Negative Inotropic effect |
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What are the adverse effects of nondihydropyridines?
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- Too much negative chronotropy (Sinus node dysfunction, “shut down” a junctional escape rhythm)
- Too much negative dromotropy (AV block) - Too much negative inotropy (Systolic heart failure) - Hypotension - Peripheral edema - Various drug interactions |
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Calcium Channel Blockers
and Negative Chronotropic Effect on SA and AV Node |
Sinus Node
- Usually do not cause significant sinus bradycardia unless patient already has sinus node dysfunction - If patient does have sinus node dysfunction, the effect can be profound AV node - Can “shut down” a junctional escape rhythm |
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Calcium Channel Blockers
and Negative Dromotropic Effect on AV node |
PRIMARY USE FOR THESE DRUGS
Especially useful to slow ventricular response rate during atrial tachyarrhythmias - Atrial fibrillation, Atrial flutter, Atrial tachycardia… Can interrupt any reentrant loop that uses the AV node as part of the circuit - AV Node Reentry - AV Reentrant Tachycardia |
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Calcium Channel Blockers
and Negative Inotropic effect |
Unlike beta blockers, this really is a PROBLEM
These drugs are relatively contraindicated in patients with systolic heart failure |
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Digoxin
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• Is a form of digitalis
• Is a cardiac glycoside |
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How does Digoxin compare to Verapamil and Diltiazem?
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- Similar AV nodal effects
- No hypotension - Digoxin is a (mildly) positive inotrope - Much less effective in slowing AV nodal conduction than verapamil and diltiazem - Narrow therapeutic index – much easier to reach toxic levels - Almost never the best first choice for any arrhythmia – especially bad in elderly patients o Usually an add on to beta blocker… they counter each others SNS/PNS activity |
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Digoxin
and Positive Inotropic Effects |
1. Digoxin poisons the Na+-K+ pump
2. Increases Na+ concentration inside the cell 3. Na+-Ca++ exchanger keep more Ca++ in the cell to try to get ride of Na+ 4. More Ca++ enters Sarcoplasmic Reticulum --> more Ca++ available for contraction |
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Digoxin
as a Antiarrhythmic |
Primary effect on cardiac rhythm is through AUGMENTATION OF VAGAL TONE
Primarily affects SA and AV nodes - Like verapamil and diltiazem, sinus node is not usually affected, but can be profoundly suppressed in patients with pre-existing sinus node dysfunction - AV node is the primary target (slows conduction velocity throught the AV node) |
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What is Digoxin Toxicity?
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- Nausea / vomiting, visual disturbances (seeing yellow-green halos around things)
- High-grade AV block along with atrial tachycardias - Ventricular tachyarrhythmias due to delayed afterdepolarizations - Digoxin is cleared by the kidney, so must keep track of renal function |
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How do you treat Digoxin Toxicity?
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Severe toxicity may need digibind (an antibody that binds Digoxin) and dialysis (because the digoxin and digibind-digoxin complexes need to be cleared)
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What is important to know about Adenosine?
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- It is a natural substance
- It is given as a rapid IV push - It is cleared very quickly after administration (Half-life = about 10 seconds) - Can precipitate bronchospasm in asthmatics (Bronchospasm may continue even after adenosine has been eliminated) - Rarely can precipitate atrial fibrillation occurs with large doses - Not common with usual doses (6 mg to 12 mg) |
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What is Adenosine’s primary purpose?
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To cause AV nodal block:
- Great for terminating any reentry involving AV node – usually the first-line drug for this - It also usually slows the sinus node a bit - It has no noticeable effect on ventricular cardiac cells |
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When is re-entry possible?
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- at least two pathways are available for impulse conduction
- unidirectional block is possible - slow (i.e. relatively slower) conduction is possible in at least one of the available pathways ... the slow pathway is the reentrant loop |
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Wolff-Parkinson-White Syndrome
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- Accessory conduction pathway from atria to ventricle (bundle of Kent), bypassing AV node.
- As a result ventricles begin to partially depolarize earlier, giving rise to characteristic DELTA wave on ECG. - May result in reentry current leading to supraventricular tachycardia. - AVRT |
