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68 Cards in this Set

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  • Back
Most effective way to prolong QT interval pharmacologically?
Blocking K+ channels with Class III AA
What few drugs are available to treat bradycardias?
Catecholamines like isoproterenol or anti-cholinergic drugs like atropines.
What can cause delayed after depolarizations?
digoxin or catecholamines
What arrhythmic drugs decrease slope of phase 4 and phase 0?
Class II and Class IV
What drugs decrease the lope of the "funny current"
calcium channel blockers
What does Ach do to impulse generation and channels?
Ach can hyperpolarize the ligand gated K channels making it more negative and less likely the cell will fire.
What happens to threshold potential when you block Na or Ca channels?
Make it less negative and lower the rate of firing.
Digitalis (Digoxin) does what to automaticity of pacemaker cells?
Increases
Anti-arrhythmias do what do the automaticity in pacemaker cells?
decrease
How do you change potassium and calcium to increase automaticity?
Increase calcium (Ca)
Decrease potassium (K)
What triggers DADs?
Cardiac glycosides
catecholamines (increase Ca)
low K outside
low Na/high Ca
What major things determine conduction velocity?
1) upstroke velocity of phase 0
2) amplitude of phase 0
- lower RPM, higher amplitude, higher velocity
How do you treat reentery?
Potassium channel blockers to prolong AP (like Class II anti aa drugs)
OR
shorten using lidocraine (type Ib aa drug). which does something, but i don't get it
What are the major sydnromes of reentry arrhythmias in the heart?
WPW
Supraventricular AV nodal renetry
Ventricular Tachycardia
What class of aa drugs convert a reentry unidirectional block to a full (bidirectional) block?
Class IA, IC, and III (by decreasing membrane responsiveneess and decreasing conduction velocity)
What class of aa drugs eliminate a block completely by increasing its conduction velocity and responsiveness? What is the prototype?
Class IB
Prototype - lidocaine
What are the 2 MAJOR classes of aa drugs used?
1) secondary (unclassified)
2) primary (class I-IV)
Name the FIVE secondary aa drugs mentioned? What is each used for?
Cardiac Glycosides
Adenosine
Magnesium Sulfate
Atropine
Phenylephrine
How do you use cardiac glycosides as aa drugs?
Treats paroxysmal atrial tachycardia, atrial flutter, and atrial fib. It slows down AV node and prevents clot and stroke
How do you use adenosine as an aa drug?
Supraventricular ARrythmias, Torsades (used for acute phase only, must be infused)
How do you use magnesium sulfate as aa drug?
it's a natural agonist of calcium, treats refractory ventricular tachycardias, torsades
How does atropine treat aa?
It blocks Ach receptors and blocks Parasymp input. Used to treat heart blocks.
How does phenylephrine work as an aa drug?`
It is an alpha receptor agonist that causes vasoconstriciton - activates vagal reflex that slows the ventricular rate
Class IB drugs:
Lidocaine
Phenytoin
Tocainide
Mexiletine
Class IC drugs:
Flecainide
Propafenone
Moricizine
Class III drugs
Amiodarone
Sotalol
Dofetilide
Ibutilide
Class IV drugs
Verapamil
Diltiazem
Class IA drugs
Quinidine
Procainamide
Disopryamide
Moricizine
Class II drugs
Beta blockers: propranolol, Metoprolol, Sotalol, Acebutolol, Esmolol
Mechanism of Class I drugs.
Fast sodium channel blockers (phase 0) - broad spectrum for arrhythmias
Mechanism of Class II drugs
Phase 4 and beta blockers - atrial and excessive catecholamine arrhythmias
Mechanism of Class III drugs
Phase 3 and potassium channel blockers - primarily reentry arrhythmias
Mechanism of Class IV drugs
Phase 4 and Calcium channel blockers - atrial and AMI arrhythmias
How do Class IA drugs work?
1) block fast Na channels, to slow conduction and increase AP duration
2) blocks K channels - prolongs repolarization
What aa drugs can trigger a Torsade episode?
Class IA (and class I in general)
Major toxicity for Class IA drug (and class I in general)
Torsades
How do Class IA drugs look on an EKG?
They prolong QT and broaden the QRS.
Quinidine, Procainamide, Disopryamide uses
Class IA drug that causes cardiac depression and vasodilation.
Quinidine pharmacology
Interactions: Hyperkalemia enhances its action
Adverse Effect: Like all Class IA, the anticholinergic activity can cause PVA's
Also, Cinchonism, (vertigo, headache, visual), thrombocytopenia, torsades
Procainamide pharmacology
indications: less Ach block, its a metabolite drug
Adverse effect: systemic lupus like syndromes, fever, GI distress, agranulocytosis, torsades.
Disopyramide pharmacology
mostly related to anti-ach actions
How do Class IB drugs work?
block fast Na channels (ones that are mostly inactivated). They don't depress conduction much, but have modest depression of AP duration.
What do Class Ib drugs do to AP and EKG?
AP - decreased duration
QT shortened (no risk of torsades)
Class IB uses
Drug of choice for post-MI, heart surgery, and digoxin toxicity (least cardiotoxic of all antiarrhythmic drugs)
NOT useful against atrial arrhythmias
Class IB pharmacolgoy
Plasma halflife of lidocain is 10 mins, chemical halflife is 2 hours (whatever that means). It has high Volume of dist
Adverse effect: CNS related (seizures, tremor, twitching, headache, blurred vision).
Orally effective form of lidocaine.
Tocainide
How do Class IC drugs work?
block fast Na channels: severely depresses conduction, doesn't change AP duration
What do Class IC drugs do to AP and EKG?
Decrease slope of phase 0
Widen QRS
Class IC uses
chronic stable ventricular arrhythmias, especially those that do not respond to conventional aa drugs.
Class IC pharmacology.
Toxicities: Numerous drug interactions, can precipitate congestive heart failure, and can be pro-arrythmic (due to decreased conduction velocity) VERY TOXIC JUST DON'T USE UNLESS LAST RESORT DANGER DANGER
How do Class II drugs work?
block phase 4 (spontaneous depol) of pacemakers. These include the beta blockers. they inhibit SA node, and decrease AV node transmission
Class II uses
Supraventricular arrhythmias
Ventricular arrhythmias associated with excess catecholamines
Decrease incidence of suddent deaths after AMI
Class II pharmacology
Toxicities: exercise intolerance, bronchospasms, bradycardia, asystole (all beta blocker related)
How do Class III drugs work?
blocks delayed rectifier current (K), slowing phase 3. This doesn't change conduction but seriously prolongs AP (and thus ERP)
Class III drugs do to AP and EKG?
Increase AP and Increase QT
Amiodarone uses
Class III drug that has mixed modes of action, potent dilator - is effective against reentry and ventricular arrhythmias as well as atrial arrhythmias,
Amiodarone pharmacology
Class III - numerous drug interactions and toxicities, contains iodine which complicates thyroid function
Dronedarone uses
Class III - protects against EADs and side effects associated with ERP prolongation. Also associated with ERP prolongation
Sotalol uses
Class III produces both beta blockers (class ii) and Class III actions. indicated for life threatening ventricular arrythmias
Dofetilide uses
Class III indicated for atrial fib and flutter
Dofetilide pharmacology
adverse effects: prolonged QT, torsades
Ibutilide uses
indicated for atrial flutter and fib, a "pure" class III that increases slow Na current
How do class IV antiarrhythmic drugs work?
They block slow cardiac channels and decrase phase 0 and phase 4 of pacemaker cells (SA node and AV node) - block phase 2......?
Two types of Class IV drugs and how they work
1) verapamil and diltiazem which blcok Ca channels
2) Nifedipime are vascular smooth muscle, antihypertensive. Minimal effecto on heart
Class IV toxicities
heart failure, hypotension, heart block, constipation
Uses for Class IV
Supraventricular arrhytymias and ventricular arrhytmias associated with AMI
risk factors for torsades
prolonged QT (more than 500ms)
heart disease
advanced age
bradycardia
treatment for torsades
Correct hypokalemia
correct hypomagnesemia
Discontinue drug prolonging QT
Pacing or drugs to shorten QT