Pathophysiology of Arrhythmias and Antiarrhythmic Drugs Flashcards
(45 cards)
What are the three types of enhanced automaticity?
- Enhanced Normal
- Enhanced Abnormal
- Triggered
What type of arrhythmia results from Digoxin Toxicity?
• what conditions will exacerbate this arrhythmia?
- Digoxin causes INCREASED INTRACELLULAR Ca2+
- Results in DELAYED AFTERDEPOLARIZATION
- Exacerbated by: HYPOKALEMIA, CATECHOLAMINES
What triggers Torsade de Pointes?
• what type of arrhythmia is caused?
•What conditions will exacerbate this arrhythmia?
- Prolonged QT interval leaves people susceptible to…
- EARLY Afterdepolarization
- Exacerbated by: HYPOKALEMIA and LOW HEART RATES
What areas of the heart may be affected by re-entry currents?
• Rate?
• Properties changed to end re-entry circuits
Areas
• Atrium = Flutter, Fibrillation
• AV node = Paroxymal Supraventricular Tachycardia
•Ventricle = Ventricular Tachycardia
Rate: typically more than 140 bpm
Properties:
• Conduction Velocity
• Refractory Period
• Convert Unidirectional Block to Complete block
What are the classes I through IV of Antiarrythmics?
• Drugs in each class?
- Na+ channel Blockers
• Procainamide, Lidocaine - Beta adrenoreceptor Blockers
• Metoprolol, Atenolol - K+ Channel Blockers
• Amiodarone, Sotolol - Ca+ Channel Blockers
• Verapamil, Diltiazem
Class I antiarrhythmic agents
• How do they work?
• Cells that they act on?
• Net effect on AP?
MOA:
- Na+ channels are blocked
- Less Na+ allowed in the cell during depolarization
- INCREASED REFRACTORY PERIOD
Cells:
• Sodium Channel Dependence means only works on MYOCYTES in atria and ventricle
AP Effect:
• DECREASED phase 0 rise
Differentiate between class IA, IB, and IC? • what is the root cause of these differences? • Drugs in each of these classes
Differences rooted in DIFFERENCES IN RATE OF DISSOCIATION from the Receptor - LONGER the drug is on the receptor the SHALLOWER the phase 0 slope
Class IA (intermediate dissociation const.): • also has K+ channel blocking properties that prologue AP drugs: procaineamide, quinidine, disopyramide
Class IB (FAST dissociation const.): • good for antitachycardia drugs: Lidocaine
Class 1C (SLOW dissociation const.): drugs: Flecanide
What are the ONLY drugs that both prolong phase 0 and prolong the overall AP?
• Class 1A sodium channel blockers
drugs: procaineamide, quinidine, disopyramide
How do Beta Blockers (class II antiarrhythmics) work as Antiarrhythmics?
• Slow ENHANCED AUTOMATICITY related to catecholamines and ischemia
these work really well to treat arrhythmias in patients with Coronary Heart Disease and Improves Survival
What arrhythmias are Beta Blockers used to treat?
- Ventricular Pre-Mature Beats
- EXCERCISE-INDUCED increases in VENTRICULAR rate and ATRIAL Fibrillation: slows AV nodes by blocking positive influence of Catecholamines
How do the Class III work?
• Arrythmia type?
• Risk?
MOA:
- K+ channel blockage
- less K+ escapes on depolarization
- LONGER EFFECTIVE REFRACTORY period
* *Blockage in the SLOW conducting limb of the re-entry circuit**
Arrhythmia:
• Ectopic Pacemakers in Atria and Ventricles targeted
Risk:
• Prolonged QT => TORSADE DE POINTES
How do class IV antiarrythmics work? • Arrythmia type? • NAME THEM
Verapamil and Diltiazem (non-dihyropyridines)
MOA:
- Ca2+ channel blocked
- PACEMAKER cells can’t depolarize as easily
Arrythmia treated:
• blocks SA nodal AUTOMATICITY and AV nodal conduction
Risk:
• SA/AV BLOCK, impaired heart contractility
Class IV adverse effects and contraindications.
• Name them
Verapamil and Diltiazem
Risk:
• Complete SA or AV block
• Impaired Heart Contratility
• Hypotension
Contraindications:
• DO NOT GIVE TO PEOPLE WITH CHF, bradycardia, or AV block
How does digoxin work as an antiarrhythmic?
• Arrythmias treated?
•what patients is it most beneficial in?
In addition to effects of Na+/K+ channel inhibition leading to intracellular Ca2+ increases, DIGOXIN ALSO STIMULATES VAGAL ACTIVITY.
Effect:
•Reduction in SA nodal activity and AV nodal conductivity
Most beneficial in a CHF patient with Atrial Fibrillation
How does Adenosine work as an antiarrythmic?
• Arrythmias Treated
• Adverse Effects
MOA:
• HYPERPOLARIZATION of SA and AV nodes prevents heartbeat
Arrythmias Treated:
• Paroxysmal Supraventricular Tachy. (PSVT) by blocking AV node
You can make a DDx of two conditions using Adenosine. What two conditions does this include?
• why does this work?
DDx of Atrial Fibrillation/ Atrial Flutter vs. Paroxysmal Supraventricular Tachycardia
Adenosine ONLY works on SA/AV nodes - PSVT is a re-entry mechanism involving AV node while A. Fib. and A. Flutter are re-entry mechanisms involving only MYOCARDIAL tissue
If fibrillation doesn’t stop with adenosine then the arrhythmia was rooted in the SA or AV nodes
Procainamide • Class/MOA • Tissues Affected • SIDE EFFECTS • METABOLISM and excretion • ADMINISTRATION
Procainamide
Class IA Na+ channel blocker, decreases phase 0 slope
MYOCARDIAL (atrial and ventricular tissues only affected)
Side Effects:
• DRUG INDUCED LUPUS
•TORSADES DE POINTES
**Hepatic Acetylation and Renal Excretion
***IV Administered b/c long term use give a HUGE chance of experiencing side effects
Why is there such a high risk of drug induced lupus for procainamide?
• Arrythmias treated
• 50% of the population are slow Acetylators putting them at a MUCH higher risk of Torsades de Pointes or Drug induced Lupus
***SHORT TERM TREATMENT FOR ATRIAL AND VENTRICULAR ARRYTHMIAS
A patient presents with arthralgia, skin rash, pleural and pericardial effusion. They were placed on an antiarrhythmic medication a few months ago. What is the name and MOA of the drug that caused this?
• What type of arrythmia were they probably being treated for?
Procainamide: • Class 1A sodium channel blocker (since its class 1A it also blocks some K+ channels)
• Quinidine, Disopyramide
A patient develops a low grade fever and petechiae over their extremities as a result of an antiarrhythmic, what drug is likely the cause?
• how does it work?
Qunidine • Class 1A sodium channel blocker (since its class 1A it also blocks some K+ channels)
• Procainamide and Disopyramide are the drugs in this class
Quinidine
• Class/MOA
• Side effects
• Arryhthmias Treated
Qunidine • Class 1A sodium channel blocker (since its class 1A it also blocks some K+ channels) - works by slowing phase 0 depolarization
• Cause QT prolongation
Arryhthmias treated:
• Myocardial tissue based (a. fib, v. fib. etc)
Side Effects:
• DIARRHEA - severe and common
• AUTOIMMUNE THROMBOCYTOPENIA
Disopyramide
• Class/MOA
• Side effects**
• Other drugs in class
Qunidine • Class 1A sodium channel blocker (since its class 1A it also blocks some K+ channels) - works by slowing phase 0 depolarization
• Cause QT prolongation
Side effects (IMPORTANT):
•PROMINENT VAGOLYTIC - atropine-like effects: URINARY retention, Dry Mouth, Blurred Vision
• May precipitate Heart failure
A patient suffers a stoke as a result of atrial fibrillation. Would you use lidocaine to treat this patient?
NO, lidocaine is highly effective at treating v. fib. but NOT a. fib.
Lidocaine • Class/MOA*** • Side effects • Administration • Arrythmias Treated
Class 1B
• 1B’s bind and block Na+ channels TRANSIENTLY
• Rapid dissociation means it has its GREATEST EFFECT ON ARRYTHMIC tissue due to rapid Kd
Side Effects:
• CNS (agitation, confusion, seizures)
Administration:
• MUST be given IV (b/c of 1st pass metabolism)
ONLY V. FIB treated
