Ch 49: Antidysrhythmic Drugs Flashcards
Virtually all of the drugs used to treat dysrhythmias can also…
…cause dysrhythmias.
p. 534
What type of therapies are beginning to replace drugs as the preferred treatment for many dysrhythmias?
nonpharmacologic therapies such as implantable defibrillators and radiofrequency ablation
(p. 534)
What term is actually more appropriate than “arrhythmia”?
dysrhythmia
p. 534
What is the term for the electrical pathways between the SA node and AV node?
internodal pathways
p. 535
Fast potentials occur in…
…fibers of the His-Purkinje system and in atrial and ventricular muscle.
(p. 535)
Drugs that reduce calcium entry during phase 2 (of fast potentials) do not…
However, they can…
…influence cardiac rhythm.
…reduce myocardial contractility.
(p. 535)
In phase 3 (of fast potentials), rapid ______________ takes place. This is caused by…
repolarization
extrusion of potassium from the cell.
Phase 3 repolarization can be delayed by drugs that…
…block potassium channels.
p. 535
During phase 4, two types of electrical activity are possible:
1) the membrane potential may remain stable
2) the membrane may undergo spontaneous depolarization
(p. 535)
All cells which have the capacity for self-excitation (automaticity)…
…are potential pacemakers.
p. 536
Under normal conditions, ____________ cells undergo very slow spontaneous depolarization, and __________ cells do not undergo any.
His-Purkinje; myocardial
p. 536
Under pathologic conditions, significant _____ _ ______________ may occur in all of these cells, and especially in ________ ______. When this happens, a ___________ can result.
phase 4 depolarization; Purkinje fibers
dysrhythmia
(p. 536)
Slow potentials occur in cells of the…
…SA node and AV node.
p. 536
Spontaneous phase 4 depolarization in the SA node normally determines…
…heart rate.
p. 536
Phase 0 of fast potentials is caused by…
In contrast, phase 0 of slow potentials is caused by….
…a rapid influx of sodium.
…a slow influx of calcium.
(p. 537)
Slow potentials lack…
… a phase 1.
p. 537
The P wave is caused by…
…depolarization of the atria.
p. 537
The QRS complex is caused by…
…depolarization of the ventricles.
p. 537
The T wave is caused by…
…repolarization of the ventricles, and is not associated with overt physical activity of the heart.
(p. 537)
Lengthening of the PR interval indicates…
…a delay in conduction through the AV node.
p. 537
What drug depresses the ST segment?
Digoxin
p. 537
Dysrhythmias arise from 2 fundamental causes:
1) disturbances of impulse formation (automaticity)
2) disturbances of impulse conduction
(p. 537)
Dysrhythmias may be produced if tissues that do not normally express automaticity…
…develop spontaneous phase 4 depolarization.
p. 537
Excessive discharge of \_\_\_\_\_\_\_\_\_\_\_ neurons can augment automaticity to cause tachycardia; excessive \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ (\_\_\_\_\_) discharge can suppress automaticity to cause bradycardia.
sympathetic
parasympathetic (vagal)
(p. 537)
Degrees of AV block:
If impulse conduction is…
If some impulses pass through but…
If all traffic through…
….delayed, but not prevented, the block is a 1st degree.
…but others do not, the block is a 2nd degree.
…the AV node stops, the block is a 3rd degree.
(p. 537)
The phenomenon of reentrant activation can result in…
…repetitive ectopic beats.
p. 538
According to the Vaughan Williams classification scheme, which antidysrhythmic drugs are in Class I? Class II? Class III? Class IV? Other antidysrhythmic drugs?
Class I: Sodium channel blockers Class II: Beta blockers Class III: Potassium channel blockers (drugs that delay repolarization) Class IV: Calcium channel blockers Other: adenosine and digoxin
(p. 538)
What are the effects of beta and calcium channel blockers in the SA node?
AV node?
in the atria and ventricles?
..they reduce automaticity
…they slow conduction velocity
…they reduce contractility
(p. 539)
Amiodarone is an important potassium channel blocker. It works by…
It prolongs both the…
…delaying repolarization of fast potentials.
…action potential duration and the effective refractory period.
(p. 539)
Which classes of antidysrhythmic drugs cause QT prolongation?
Class IA and class III
p. 540
What are the 2 major groups of dysrhythmias?
supraventricular dysrhythmias
ventricular dysrhythmias
(p. 540)
Group I antidysrhythmic drugs block cardiac sodium channels. By doing so, they decrease…
…conduction velocity in the atria, ventricles and His-Purkinje system.
(p. 542)
What are the primary differences between Class 1A and Class 1B antidysrhythmic drugs?
Class IA agents delay polarization, and class IB agents accelerate repolarization. Class IB agents have little or no effect on the ECG.
(p. 542, 545)
Class I drugs are similar in action and structure to the…
…local anesthetics.
p. 542
Like quinine, quinidine has…
…antimalarial and antipyretic properties.
p. 543
Quinidine is strongly…
…anticholinergic (atropine-like) and blocks vagal input to the heart.
(p. 543)
To prevent excessive ventricular stimulation by quinidine, patients are usually pretreated with…
…digoxin, verapamil, or a beta blocker, all of which suppress AV conduction.
(p. 543)
Quinidine (along with fellow Class IA agents procainamide and disopyramide) have 2 pronounced effects on the ECG:
1) widening of the QRS complex
2) prolongation of the QT-interval
(p. 543)
Quinidine is a also a drug of choice for…
…severe malaria.
p. 543
Quinidine and quinine are both known as cinchona alkaloids because their natural source is the bark of the South American cinchona tree.
Cinchonism is a term for the adverse effects which can be caused by these drugs. It is characterized by…
…tinnitus, headache, nausea, vertigo, and disturbed vision.
(p. 544)
Procainamide is only weakly…
…anticholinergic, and hence is not likely to increase ventricular rate.
(p. 544)
Lidocaine is used only for…
…ventricular dysrhythmias.
p. 545
Lidocaine works by:
1) blocking ______ ______ ________ and thereby slowing…
2) it reduces ____________ in the ventricles and His-Purkinje system
3) it accelerates ______________ by shortening the action potential duration and ___
1) cardiac sodium channels; …conduction in the atria, ventricles, and His-Purkinje system
2) automaticity
3) repolarization; ERP
(p. 545)
Phenytoin is also used to treat…
…digoxin-induced dysrhythmias.
p. 545
In contrast to lidocaine and many other antidysrhythmic drugs, phenytoin…
…increases AV nodal conduction.
p. 545
What are the only two Class IC agents available right now?
flecainide and propafenone
p. 546
What effects do class IC agents have on the ECG?
widening of the QRS and prolongation of the PR
p. 546
What are the 3 members of Class II?
propranolol, acebutolol, esmolol
p. 546
Propranolol is a ____________ beta-adrenergic antagonist.
nonselective
p. 546
What are the effects of Class II agents on the ECG?
bradycardia, prolongation of the PR interval
p. 546
The reduction in AV conduction velocity translates to a…
…prolonged PR interval.
p. 546
