Lecture 6: Antiarrhythmic Classification & MOA Flashcards
LO: Antiarrhythmic Classification: Vaughan-Williams
1.) Class 1: Sodium Channel blockers
2.) Class 2: Beta Blockers
3.) Class 3: Potassium Channel Blockers
4.) Class 4: Calcium Channel Blockers
5.) Other: Adenosine, digitalis, atropine, magnesium
LO: Know which antiarrhythmic drug works in which myocardial tissue
NOTE: so when you are looking for drugs to treat a specific area you will know which drugs act where.. Atropine is use for slow arrythmia to increase conduction!
LO: Describe the different MOA for antiarrhythmic agents.
1.) Slow conduction velocity of AP
– Increase refractoriness (changes in effective refractory period and action potential duration)
– Create a two way block in reentry circuit
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2.) Change the slope of Phase 4
– Decrease (e.g. beta blockers) or increase automaticity (e.g. atropine, epinephrine)
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3.) Change the threshold potential or maximum diastolic potential
– Decrease or increase automaticity (further away from threshold = decrease automaticity/ heart rate!)
LO: Class IA MOA and how it works . . .
Class IA decrease the slope of phase 0/ slow phase 0 depolarization, which prolong action potential and slow down the conduction . Will have direct effect on the myocytes.
Drug affecting the cardiac action potential/ which part of action potential it is affecting
Class 1 agent: Na channel blocker affects phase 0, class 4 agents will affect phase 0 in SA and AV node. Class 3 agents will effect repolarization of phase 3 . class 2 agents (beta blocker) will really effect the slope of phase 4!
Drug affecting the cardiac action potential/ which part of action potential it is affecting (looking at the effects on the slope of action potential)
LO: Know which drugs effect QT and PR intervals and the overall effect on the ECG
LO: Know which drug classes increase refractoriness in myocardial tissue
Know which drugs affect AV nodal conduction (decrease or increase)
NOTE: all drug treat fast arrythmias except for atropine (slow only)
LO: Proarrhythmia (Torsades De Pointes): What is it? (general) List risk factors for developing proarrhythmic event… List the antiarrhythmic drugs that are the highest risk for proarrhythmic events!
- Rapid form of polymorphic ventricular tachycardia
- Often preceded by a prolonged QT interval (so that’s why we monitor drugs that prolong QT!)
- Often in patients with structural heart disease
- Often caused by drugs; other conditions (hypokalemia, hypomagnesemia, congenital QT syndrome, etc) may also contribute
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RISKS - AA drugs that prolong QT intervals may induce arrhythmias
- This is way we monitor the QTc interval. A prolonged QTc interval puts patients at risk for proarrhythmic event.
- Highest Risk for Proarrhythmic Events: Class IA agents, Class IC agents, ibutilide, dofetilide, sotalol.
- Lower Risk for Proarrhythmic Events: Amiodarone, lidocaine, mexiletine, Class II. (important to know! lets say you have a patient at higher risk for arrythmia - eg. patient who has structural heart disease! you want to have them on the lower risk drugs: 1st Amiodarone)
- Highest Risk Factors: Structural heart disease (low EF), CAD, baseline prolonged QTc (drug induced or congential), electrolyte disturbances (hypokalemia)
LO: Proarrhythmia (Torsades De Pointes): Know how to treat torsades de pointes
- If severely symptomatic – electrocardioversion (cardioversion, defibrillation)
- Magnesium - suppresses early afterdepolarizations (EADs) and
helps terminate the arrhythmia. Magnesium achieves this by
decreasing the influx of calcium, thus lowering the amplitude
of EADs. - Correct electrolyte imbalances if presented, remove offending
drug if presented. - Isoproterenol - accelerates AV conduction and decreases the QT interval by increasing the heart rate and reducing temporal dispersion of repolarization
Drugs associated with the development of proarrhythmia (hint: some of them are not AA!) (not LO)
What Drugs for What Arrhythmias and Effects on ECG?
1. Sinus arrhythmias
2. Sinus Bradycardia
3. Atrial fibrillation
4. AV-Node reentry tachycardia
5. AV-Block
6. Ventricular Tachycardia
- Sinus (SA) arrhythmias - beta blocker, CCB, (what about nifedipine? NO- dihy CCB wont work on SA node?) decrease HR and increase PR
. - Sinus Bradycardia - atropine
. - Atrial fibrillation - Class 3, quinidine, class IB, Class IC, (class 2 wont work! Beta Blockers cuz it only works in SA AV node), Class 3, digoxin (class 5)? NO! wont work!
. - AV-Node reentry tachycardia - IC, IB? no need to monitor, Class IA and IC? need to monitor QT ! Class 3: need to monitor QT
- AV-Block
- Ventricular Tachycardia
MORE MOVING ON TO ATRIAL FIB
YES
LO: Define AF and ventricular response rate (VRR) and the importance of AV node
Atrial fibrillation (AF) is a supraventricular (above the ventricles) tachyarrhythmia characterized by
- Uncoordinated atrial activation → deterioration of mechanical function
- A. Fib characterized by chaotic atrial activity (atrial rate *500-600 beats per minute)
- A. flutter characterized by fast regular atrial activity ( ~ 300 beats per minute)
- AV node allows some of the atrial impulses to depolarize the ventricles; ventricular (QRS) rate is irregular pattern (for a. fib) and sometimes a regular pattern (for a. flutter, e.g. 2:l block).
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NOTE:
In a normal sinus rhythm- youi have P-QRS-T waves! SA node fire and atrium will contrast and come to the AV node where it will slightly delay and then it will go down his punjikie system where it travels down towards bottom on the heart where it will excite and travel and causes contractility. In an A fib heart, what we see is maybe the area of the heart just throwing out a ton of impulses. The atrium can be contracting by itself without the signal from SA node! Contracting sooo fast! 500-600 BPM! SA node still firing but atrium doesn’t care..its firing independently. Atrium is going v fast, but ventricle is only going 150 BPM..why? what’s blocking it? thank goodness we still have the AV node to block that signal! The AV node is getting bombarded with signals/ impulses but it cannot handle all of them so it only lets like 150-160 BPM IF it was not for the AV node ventricles or if there was a bypass, it would go 600BMP = ventricular fibrillation! What are two areas you wanna hit to treat afib? atrium and AV node (slow conduction). You can also easily diagnosis a fib look at ECG! When comparing AFib to AFlutter- AFlutter is a bit more stable and ECG looks more consistent and it is only going 300BPM (1 sharp - 3 tiny hump- 1 sharp)
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Importance of AV NODE:
Without the AV-node all the impulses from the atrium (300- 600 bpm) would be conducted to the ventricle’s leading to ventricular rates of 300-600 bpm – this is not compatible with life (ventricular fibrillation!)
- Because the AV-node is there, not all atrial impulses are transmitted, usually only 120-150 impulses can get through per minute. Therefore, the ventricles are beating at a rate of 120-150 bpm (VENTRICULAR RESPONSE RATE - VRR) which most patients can tolerate, patients can generate enough cardiac output (although they may be symptomatic).
- A goal of rate control therapy in atrial fibrillation/flutter is to
decrease VRR to between 80 to 110 bpm.
Epidemiology – Why Afib is Important
- More than 200,000 cases per year.
- Incidence increased 13% over past 20 years
- In USA, 12-16 million will be affected by 2050
- Increasing obesity and increasing age are risk factors that help explain rise in incidence
LO: List the symptoms associated with AFib
EXCEPT for palpitation, all of these symptoms are due to decrease CO due to decrease SV! you don’t have time to fill vesicle and push blood out cuz heart is beating so fast! so that’s why you have lower CO. You also loss your atrial kick! so makes symp worse…Futhermore …PATIENTS CAN BE ASYMPTOMATIC! THIS IS AN ISSUE!
Definitions of AF: A Simplified Scheme
Rate Control (alone) or Rate Control + Rhythm Control
Atrial Fibrillation Decision Tree: what to do with the patient
Step 1: hemodynamic unstable? BP 70/nothing, passing out? shock them! Electricity!!!..not very common… most are stable! if they are stable? 2 things we need to start right away –> IV hep or LMWH and slow down ventricular response rate (IV - beta blocker or IV diltizem eg.)
Then step 3 (assess duration of arrhythmia!) Less than 48hrs? less likely there is no clot so just do cardioversion. if it is more than 48 hr’s or unknown time there are changes of clots! so you need to do anticoag!
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HOWEVER - if a patient is already on anticoagulation when they come in? no need to give IV hep/ LMWH cuz they are already anticoag. We need to do rate control agent!
Common drug use for rate control..notice which is IV (need to give IV inpatient) then they can switch to PO
know general table
LO: CHRONIC Rate Control for other co morbidity
Strategies for Rhythm Control in Patients with Paroxysmal and persistent AF (VW CLASS IC, III)
1.) Why does this patient have DOE and palpitations?
2.) What are patient risk factors for atrial fibrillation
3.) What additional labs do you want to draw if any?
4.) What is the greatest morbidity risk to this patient?
5.) What are your acute therapeutic recommendations for the patient?
6.) What is your therapeutic recommendation upon discharge?
1.) Why does this patient have DOE and palpitations? He’s in AFIB
2.) What are patient risk factors for atrial fibrillation: Age, HTN, obesity, alcohol use, hyperthyroidism
3.) What additional labs do you want to draw if any?: Thyroid!
4.) What is the greatest morbidity risk to this patient?: Afib-> STOKE!
5.) What are your acute therapeutic recommendations for the patient? rate control and anticoagulation-> IV heparin or LMWH, IV diltiazem (for rate control)…what about IV Beta Blocker? yes! We can! :)
6.) What is your therapeutic recommendation upon discharge?
