Anti-Arrhythmics Part 2 Flashcards
Where are reentry circuits most common?
In the ventricle (CHD)
What’s happening during Phase 0 of the ventricular myocyte depolarization?
The voltage-gated Na+ channels are open.
What does the slope of the Phase 0 portion of the depolarization curve tell you?
Conduction velocity Smaller slope = smaller velocity
Why is the depolarization curve relatively flat in Phase 2?
The influx of Ca++ equals effluent of K+
What do the funny channels affect?
Phase 4 or the rate of automaticity
What does the PR interval reflect?
index of conduction velocity + delay at the AV node
What does the QT interval reflect
Duration of ventricular AP
What kind of rhythm is flutter (atrial or ventricular)
organized tachycardia - 180-349 bpm
What kind of rhythm is fibrillation (atrial)?
disorganized tachycardia >350 bpm
What are the four causes of tachycardias?
- ectopic pacemakers 2. re-entry circuits 3. Early After Depolarizations (EADs) 4. Delayed after Depolarizations (DADs)
How does CHD lead to re-entry circuits?
hypoxia leads to decreased ATP generation, which in turn leads to less Na+/K+ ATPase and less depolarization. That creates a localized area with an increased refractory period
Which direction is the myocardium perfused
epicardium to endocardium
Where is the heart most at risk from CHD?
endocardium because muscle contraction reduces flow to to endocardium
What are the three requirements for a re-entry circuit?
- multiple conduction pathways 2. unidirectional conduction block 3. Conduction Time > Effective Refractory Period
What is an ectopic pacemaker? Where is it commonly located?
Cells that are acting as pacemakers that run faster than the SA node. The pulmonary vein has striated cardiac muscle that often forms an ectopic pacemaker.
What is the primary means of control in long-standing a fib?
Rate control - anesthetize the AV node and screw the P wave
How does rhythm control work in a fib?
abolish a fib with pharmacologic cardioversion and restore normal sinus rhythm
What drugs (class and name) are used for rate control in a fib?
Class II (beta blocker) - metoprolol Class IV (Ca 2+ channel blockers) - verapamil, digoxin
What drugs are used in rhythm control in a fib?
Class III (K+ blocker) - amiodorone Class IC (Na+ blocker) - flecainide
Who gets anticoagulation with a fib?
high risk of stroke CHADS-VASc score > or equal to 2
What anticoagulants can be used for A fib?
Warfarin RivaroXaban ApiXaban DabigaTran
what to drugs that treat tachyarrythmias do?
- decrease automaticity
- reduce conduction velocity for AV node
- increase AP duration (or ERP)
- Interfere with the sympathetic regulation of heart rate at SA and AV nodes
What part of the ventricular depolarization does each class of drugs effect?
Class I drugs block which type of channel and do they block all of them?
Na+ channels
fraction are blocked - 100% block = asystole
What is “use-dependent blockade”?
the channel must be open for the drug to bind to the site and block the channel
Class I more selective for “diseased tissue” - activated or unactivatable state - NOT resting
Na+ channel blockers _______(increase or decrease) conduction velocity which _________(increases or decreases) the PR interval and the QRS?
decreases conduction velocity
increases PR interval
Increases QRS (AP), which also increases refractory period
*overall, decreases channels available so you need lower resting potential to activate
Where are ectopic pacemakers usually located?
in the atria
Can ectopic pacemakers conduct directly to the ventricles?
No - there is fibrous tissue between the atria and ventricles, so the impulse must go through the AV node
How does the AV node act as a brake?
It can only handle 250 bpm max, so it prevents tachycardia out of control
If you block Na+ in inactivatable state, what happens to ERP?
Increases it to longer than the AP
How do Class I drugs effect ectopic pacemakers?
by blocking Na+ Phase 4 funny channels, thereby making the cells less excitable
Class IA also blocks which channels and increases the AP duration?
K+ out
increase the time to repolarize
Class IB also keeps which channels open longer and decreases the AP duration?
K+ out increased
Of the Class I drugs, what is the duration of the ERP from longest to shortest?
1C > 1A > 1B
Which drug is best post-MI?
1B
1B is Best
Lidocaine I.V. acute VT post-MI
Mexiletine used to treat Long QT syndrome
Why are 1B drugs best post-MI?
They are highly selective for diseased tissue (ischemic)
What is flecainide used for?
VTs and SVT if no Hx of ischemic disease
THIS IS RHYTHM CONTROL
it is a very potent sodium channel blocker
What is an important side effect of 1C drugs?
ataxia because they effect Na+ channels in the cerebellum
Class 1A drugs are also what?
Anaesthetics
They also block sodium channels on pain and sensory neurons
Other than blocking Na+ channels, what is a secondary effect of Class 1A drugs?
anticholingeric, so they decrease vagal influences on the SA and AV nodes
in other words, they increase nodal conduction velocity and automaticity
What’s the danger with quinidine for a fib?
If you use it and lower the atrial tachyardia below the AV node rate “brake,” now the ventricles will beat much faster
solution: lower AV node conduction first with Ca 2+ blocker or Beta blocker
What arrhythmia can Class IA cause?
Torsades de Pointes
contraindicated in incomplete AV block - excessive Na+ channel block can lead to asystole
QT prolongation leads to torsades females > males
When is Class 1A drugs contraindicated?
Inherited Long QT Syndrome
What channel mutation is seen in the most common form of prolonged QT Syndrome?
K+ channel mutation is “rectifying,” which means it takes longer to repolarize, prolonging the QT interval. Treat with Beta-blocker
How do you treat Na+ channel inherited Long QT?
Class 1B - mexiletine
What symptom should make you concerned about Long QT?
syncope
How does amiodarone work?
blocks K+ efflux during Phase 3
also blocks Na+ channels
increases ERP
What is amiodarone first line for at low doses?
rhythm control in atrial fibrillation
what is amiodarone first line for in high doses?
VTs in structurally abnormal hearts
(especially VT post MI, post cardioversion for V-fib)
What is the major risk with amiodarone?
prolonged QT - Torsades
Amiodorone toxicity is a _________?
BITCH
Bradycardia/Blue Man
Interstitial Lung Disease
Thyroid (hypo/hyper)
Corneal/Cutaneous
Hepatic/Hypotension when IV (due to solvents)
How does sotalol work?
Blocks K+ efflux during Phase 3, increases APD
What is the first line use of sotalol?
Use for SVT and VT in patients with implanted ICD to reduce mortality and chance of shock
What is ibutalide used for?
cardioversion of SVT
(blocks K+ efflux, increases APD)
Summary table of Rx for Ventricular Arryhthmias
In what disease are rate control drugs contraindicated?
WPW
All rate control drugs decrease AV conduction velocity, but in WPW the accessory pathway will allow AP to still enter the ventricle, creating potential for retrograde conduction, leading to AV reentrant tachycardia
What do Calcium channel blockers do?
Block Ca++ channels in the AV node (selective for it, because no Na+ channels here)
decreases pacemaker current
increases ERP
decrease conduction velocity
What are Ca 2+ blockers primarily used for?
SVTs (fibrillation or flutter)
When is use of Ca++ blockers dangerous?
CHF - because they reduce contractility
What are beta blockers used for?
SVTs
What is the mechanism for beta blockers?
They block Beta 1 adrenergic receptors on the heart
They slow AV node conduction (rate control)
The decrease excitability (ectopic pacemakers)
lesser extent (due to Ca++ channel effects):
decrease SA node rate
decrease contractility
What is the best choice in CHF?
Digoxin
What is the mechanism of action for digoxin?
Inhibits Na+/K+ ATPase
lowers resting potential
lowers conduction velocity
Increases vagal activity, which causes:
decreased pacemaker activity
increased refractory period
decreased AV node conduction
What’s the danger with digoxin?
toxicity because low TI
severe bradycardia
How does adenosine work?
purine nucleoside acts at receptors on the hear
Increases K+ efflux, hyperpolarizes and causes less Ca2+ to come in
decreases: AV node conduction, SA pacemaker, automaticity
What’s the 1/2 life of adenosine?
seconds
What is adenosine used for?
diagnosis and acute termination of SVT
AV-node dependent narrow complex tachycardia
Summary Table for Treatment of Arrhythmias
