Antiarrhythmics - SRS Flashcards
What are the Class Ia Na+ channel blockers?
Disopyramide (Norpace)
Quinidine
Procainamide
What are the class Ib Na+ channel blockers?
Lidocaine (Xylocaine)
Mexiletine
Tocainide
Class Ic Na+ channel blockers include what drugs?
Moricizine
Flecainide (Tambocor)
Propafenone (Rythmol)
What are the class II antiarrhythmics?
β-Adrenergic Receptor Blockers
Esmolol (Brevibloc)
Metoprolol (Lopressor, Toprol XL)
Propranolol (Inderal)
What are the class III antiarrhythmics?
K+ Channel Blockers
Amiodarone (Cordarone)
Bretylium
Dofetilide (Tikosyn)
Ibutilide
Sotalol (Betapace)
What are the class IV antiarrhythmics?
Ca2+ Channel Blockers
Verapamil (Calan)
Diltiazem (Cardizem)
What are the “Other” ACLS drugs?
Adenosine
Atropine
Anticoagulants
Digoxin
MgSO4
Naloxone (Narcan)
Vasopressors
Which of the shown channels are blocked by Na+ channel blocking drugs?
Middle - Activated
Right - Inactivated
channels are impacted by Na+ channel blockers
What are m gates?
The activation gates for sodium channels
What are the inactivation gates for sodium channels?
H gates
What two things cause arrhythmias?
Abnormal Impulse Generation
Abnormal Impulse conduction
Abnormal impulse generation can arise due to triggered automaticity, what phase does early afterdepolarization disrupt?
Delayed afterdepolarization?
EAD: Phase 3
DAD: phase 4
Which of the graphs shows DAD? EAD?
Abnormal impulse conduction can arise from what two types of things?
Depressed conduction
Reentry
What are examples of arrythmias resulting from depressed conduction?
Simple block
- AVnodal block
- Bundle Branch block
What does reentry describe? What is required for a reenty derived arrhythmia to occur?
Impulse reenters/excites areas of heart more than once
Must be an obstacle – establishes a circuit
Must be unidirectional block
Conduction time must be long enough that retrograde impulse does not encounter refrac
tory tissues
What are the three main things that anti-arrhythmic drugs do?
Induce arrhythmias (weigh benefits vs. risks)
Depress autonomic properties of abnormal pacemaker cell
Alter conduction characteristics of reentrant loop
By what means do antiarrhythmic drugs depress autonomic properties of abnormal pacemaker cells?
Decrease slope of phase 4
Elevate threshold potential
How do anti-arrhythmic drugs alter the conduction characteristics of reentrant loop?
Facilitate conduction (shorten refractoriness) Depress conduction (prolong refractoriness)
What drugs have the effects shown in the four graphs?
A. B-Blockers
B. Na+ channel blockers and Ca2+ channel blockers
C. Adenosine
D. K+ channel blockers
What is the predominant mechanism of Type IA ACLS?
Describe the dissociation kinetics
Na+ channel blocker
Dissociates with intermediate kinetics
What is the predominant mechanism of type IB ALCS drugs?
Describe the dissociation kinetics
Na+ channel blocker
Dissociates with rapid kinetics
What is the predominant mechanism for type IC ACLS drugs
Describe the dissociation kinetics
Na+ channel blocker
Slow kinetics
What is the predominant mechanism of type II ACLS drugs?
B-blocker
What is the predominant mechanism of the type III ACLS drugs?
K+ channel blocker
What is the predominant mechanism of the type IV ACLS drugs?
Ca2+ channel blocker
What impact do Type IA drugs have on…
Conduction velocity
Refractoriness
Autonomic properties
?
Conduction velocity - Decrease
Refractoriness - Increase
Autonomic properties - Decrease
What effect do Type IB drugs have on…
Velocity
Refractoriness
No effect on velocity
May decrease refractoriness
What effect do type IC drugs have on conduction velocity?
Refractoriness?
Decrease conduction velocity
No effect on refractoriness
What effect do Type II drugs have on conduction velocity?
Refractoriness?
Autonomic properties?
Decrease conduction velocity
Increase refractoriness
Decrease autonomic properties
What effect do Type III drugs have on refractoriness?
Action potential duration?
Increase refractoriness
Increase action potential duration
What impact do type IV drugs have on conduction velocity?
Refractoriness?
Autonomic properties?
Decreases conduction velocity
Increase refractoriness
Decrease autonomic properties
What phase of depolarization do class IA drugs slow?
Phase 0 depolarization
What are the cardiac effects of Procainamide? (4)
Extracardiac?
- Slows upstroke of action potential,
- slows conduction,
- prolongs QRS,
- prolongs action potential duration.
Ganglion-Blocking
Procainamide is metabolized to N-acetylprocainamide (NAPA), what class of activity does this metabolite have?
Class III
What are the therapeutic uses of procainamide?
Atrial and ventricular arrhythmias
Name three ADR’s for procainamide?
- Excessive APD prolongation,
- QT prolongation,
- reversible lupus erythematosus (~33%)
What are the common SLE type ADR’s seen in procainamide ADR’s?
Arthritis, Arthralgia and rarely renal effects
What type of atrial arrhythmias are class IB drugs used for?
NONE.
Ok, so what are the arrhythmias that class IB drugs are used for?
Ventricular only
What phase of the depolarization/repolarization cycle do class IB drugs impact?
Shorten phase 3 repolarization
What are the effects of lidocaine?
Decreases action potential duration
Shortens phase 3 repolarization
What is lidocaine the DOC for?
Termination of VT and prevention of VF after cardioversion in the the setting of acute ischemia
Lidocaine has relatively low cardiotoxicity, but what ADR’s should we keep in mind?
In what patients are these effects more common? At what dose do they tend to manifest?
Neurologic effects… more common in the elderly, and tend to manifest at doses greater than 9 ug/mL
- paresthesias
- tremor
- nausea
- lightheadedness
How is lidocaine administered?
IV only. If you want oral, you can use mexiletine
Class IC drugs have a high incidence of drug induced arrhythmias. In what situation are these drugs absolutely contraindicated?
Cannot be used in structural heart disease, this significantly increases mortality
What phase of the myocyte depolarization/repolarization cycle do type IC drugs work on?
Phase 0
Flecainide blocks both Na+ and K+ channels but does not…
prolong action potential or QT interval
What is the therapeutic use of Flecainide?
Supraventricular arrhythmias
What is the major ADR of flecainide?
Severe exacerbation of arrhythmia
Propafenone is similar to flecainide except in that it…
Also has B-blocking activity
What are the four major effects of the Class II drugs?
Decrease automaticity
Prolong AV conduction
Decrease heart rate and contractility
Decrease O2 demand
Riddle me seven therapeutic uses for B-blockers!
- Tachyarrhythmias
- Atrial flutter
- Atrial fibrillation
- AV nodal re-entrant tachycardia
- Hypertension
- Heart failure
- Ischemic heart disease
What are some ADR’s associated with B-blockers?
- Heart Block
- bradycardia
- worsening of reactive airway disease
- cold extremities
- fatigue
- cardiac decompensation if heart relies on sympathetic drive
The ADR’s of metoprolol are similar to other B-blockers except they have reduced risk of?
Bronchospasm and diabetes exacerbation
Esmolol, also known as Brevibloc is used when?
During surgery to control heart rate
What phase of the action potential do Class III drugs work on?
Phase 3 repolarization
How do class III drugs work?
K+ channel blockade leads to diminished outward K+ flow during repolarization, increasing the duration of the action potential and prolonging refractory period
Amiodarone has multiple MOA, what are they?
- K+ channel blockade -> prolonged action potential duration and QT interval
- Significantly blocks Na+ channels
- Weak adrenergic blockade
- Weak calcium channel blockade
The pharmacokinetics of amiodarone are unique.
In what way?
How long are the effects maintained after withdrawal?
Half life biphasic…
Rapid component (50%) is 3-10 days
Slower component is several weeks
Effects persisty 1-3 months after discontinuation of the drug
Why is it important to know about the wierdness of amiodarones biphasic half life?
It significantly increases the drug levels of statins, Digoxin and warfarin.
For instance, warfarin Digoxin and Statin doses must be decreased by 33-50% if a patient is also on amiodarone. Then, when amiodarone is discontinued you will need to monitor and increase the dosing.
What are the notable ADR’s associated with amiodarone?
- Symptomatic Bradycardia
- Heart block (in those with preexisting AV node disease)
- Accumulation in Heart, Lungs, Liver and Skin
- Pulmonary toxicity with fatal pulmonary fibrosis
- Abnormal LFTs
- Skin deposits and gray-blue discoloration due to iodine
What effect does cimetidine have on amiodarone levels?
Cimetidine is a CYP3A4 inhibitor, and leads to increased levels of amiodarone
What impact does rifampin have on amiodarone levels?
Since it is an inducer of CYP3A4, it decreases the amiodarone levels
What phase of the action potential do class IV drugs work on?
slows the phase 4 spontaneous depolarization
What ion current do class IV drugs work on?
Decrease inward Ca2+ current
Verapamil slows the SA node by direct action, and suppresses both early and delayed afterdepolarizations. What type of channels does it block?
Activated and inactivated L-type Ca++ channels
What is the extracardiac effect of verapamil?
Peripheral vasodilation
What are the 5 therapeutic uses of Verapamil?
- pSVT
- Drop ventricular rate in Atrial fibrillation
- Drop rate in Atrial Flutter
- Angina
- HTN
You walk into your fourth year cardiology rotation and the first thing you see is an attending physician tearing apart an R1. Apparently they gave a patient Verapamil after misreading the EKG. What did the R1 think the EKG indicated?
What was the actual rhytm and what likely happened to the patient?
R1 thought the patient has pSVT, for which Verapamil would be perfectly fine for.
However they misdiagnosed, and the patient actually had ventricular tachycardia.
If you give verapamil to a patient with VT, they can decompensate into ventricular fibrillation and become hypotensive.
Apart from the bit about confusing pSVT and VT, what are the other ADR’s of verapamil?
- can induce AV block
- constipation
- lassitude
- nervousness
- peripheral edema
Adenosine is a nucleoside, what does it do?
Activates the inward rectifier K+ current and inhibits Ca++ current. Resulting in marker hyperpolarization and increased refractory period.
What is the therapeutic use for adenosine?
DOC for conversion of paroxysmal SVT
What are the ADRS for Adenosine?
- Flushing
- Shortness of breath
- Chest burning
- High grade AV block
- Atrial fibrillation
- headache
- hypotension
- nausea
- paresthesias
If you give a patient who is not sedated adenosine, what must you warn them of?
They may experience a crushing heart attack like pain. Not sure why we would do this but I guess it is sometimes necessary.
Atropine blocks actions of acetylcholine at parasympathetic sites and increases CO! What are the therapeutic uses of atropine?
The ABC’s of atropine!
Anesthesia - neuromuscular blockade reversal
Bradycardia
Cholinergic poisoning
What are five ADR’s associated with atropine?
Arrhytmia
tachycardia
dizziness
constipation
urinary retention
What is the mechanism of action of digoxin?
Inhibits Na+/K+ atpase, resulting in positive inotropy. Increased intracellular Na+, decreased Ca++ expulsion, increased free Ca++.
What impact does digoxin have on:
Heart rate
Refractory period
Conduction velocity
Digoxin decreases heart rate,
Increases refractory period
Decreases conduction velocity
What are the therapeutic uses of Digoxin?
- Atrial fibrillation
- SVT
- Heart failure
What are the ADR’s for digoxin?
- Nausea
- Vomiting
- Diarrhea
- Disorientation
- visual disturbances
- Aberration of color perception
- delayed afterdepolarization
What are the types of supraventricular arrhythmias? 7
Originate above the bundle of HIS, characterised by normal QRS complexes
- Sinus bradycardia
- Sinus tachycardia
- Paroxysmal supraventricular tachycardia
- Atrial flutter
- Atrial fibrillation
- Wolff-Parkinson-White
- Premature atrial contractions
What are the ventricular arrhythmias? 3
Originate below bundle of HIS
Premature ventricular contractions
Ventricular tachycardia
Ventricular fibrillation
What are the types of blocks?
Supraventricular: 1st, 2nd, or 3rd degree AV block
Ventricular: right or left bundle branch block
What drugs would be good for an acute episode of this rhythm?
Atrial Fibrillation - IV CCB, Beta-blocker or Digoxin
What What would be good drugs for a patient with this rhythm as a chronic condition?
Atrial Fibrillation
Oral Beta-blocker and CCB
Digoxin if intolerable side effects from BB and CCB
In treating A-fib, what is the long term strategy focus we should prioritize?
- Rate control more-so than rhythm control.
- Also may need to use anticoagulation to prevent dislodgment of thrombus and consequent embolus/stroke
What type of cardioversion is best for A-fib?
What are the chemical options?
Direct current cardioversion most effective
Chemical options: ibutilide IV, propafenone PO, flecainide PO, amiodarone PO/IV, dofetilide PO
What would the acute treatment of the shown rhythm involve? 3 main options and two alternatives
pSVT
IV adenosine
Verapamil
diltiazem
Or BB or digoxin if the other three fail.
If a patient had this rhythm as a chronic problem, what would be the treatment protocol?
pSVT
radiofrequency catheter ablation potentially curative
Drugs – verapamil, diltiazem, BB, or digoxin
What drugs would you want to use on a patient with the shown strip? Which ones would you not use?
If patient is within 24 hours after MI then use B-blockers if no contraindications
If asymptomatic DO NOT USE CLASS IC AGENTS - leads to increased mortality (CAST trials)
What would you use for a stable patient with this strip? 3 options
stable VT
- procainamide
- sotalol
- amiodarone
For a hemodynamically stable patient with this strip, what would you use?
MgSO4 or, alternatively class Ib agents
