Pharm Antiarrhythmic Drugs

Front 1

Cardiac arrhythmias commonly occurs with, and the most common cause of death from? They are also associated with?

Back 1

Cardiac arrhythmias commonly occur in presence of prexisting heart disease. They are the common cause of death in a MI or terminal heart failure. They often occur with anesthesia, hyperthyroidism, and electrolyte disorders.

Front 2

What is torsade de pointes, what is caused by, and its characteristics?

Back 2

It is a ventricular arrhythmia that is often induced by antiarrhythmic and other drugs. The QRS amplitude is often waxing and waning. It is associated with a long QT syndrome, a heritable abnormal prolongation of the QT interval by mutations in the K/Na ion channel proteins.

Front 3

What occurs during phase 0?

Back 3

The SA and AV nodes: Upstroke of Ca channels (there are no fast Na channels.

Purkinje or ventricular cardiac cells: rapid upstroke of Na fast channels.

Front 4

What occurs with phase I

Back 4

The SA and AV nodes:

Purkinje or ventricular cardiac cells: inactivation of Na channels. K channels begin to open.

Front 5

What occurs with phase 2?

Back 5

The SA and AV nodes:

Purkinje or ventricular cardiac cells: Ca influx which balance K efflux. More Ca influx than K efflux.

Front 6

What occurs with phase 3?

Back 6

The SA and AV nodes: Ca channels close, and K efflux

Purkinje or ventricular cardiac cells: Ca channels close, and K efflux

Front 7

What occurs with phase 4?

Back 7

The SA and AV nodes: slow diastolic depolarization from Na (accounts for automaticity of SA and AV node.

Purkinje or ventricular cardiac cells: is the resting membrane potential.

Front 8

The refractory period of most cardiac cells (Na-dependent cells) is dependent on?

Back 8

How rapidly Na channels recover from inactivation, the membrane potential, extracellular K concentration,and actions of drugs that bind to the sodium channel (ie, Na channel blockers).

Front 9

Antiarrhythmic drugs act on?

Back 9

3 major currents (I^Na, I^Ca, I^K) or on the beta adrenoceptors that modulate currents.

Front 10

Duration of recovery in the Ca-dependent AV node, the duration of refractory is dependent on?

Back 10

The rate of recovery form inactivation of Ca-channels.

Front 11

What are the four classes of antiarrhythmic agents?

Back 11

1: Na Channel blockers; 2: Beta-adrenoceptor blockers; 3: K-channel blockers; 4: Ca-channel blockers

Front 12

Class 1 antiarrhythmic agents are subdivided based on what? And give examples the drugs involved.

Back 12

Group 1A prolong the AP; Group 1B shorten the AP; Group IC have no effect on AP duration

1A: procainamide; 1B: lidocaine; IC: flecainide

Front 13

Since ion channels in arrhythmic state spend more time open or inactivated states than normal tissue, what does the term "use dependent" or "state dependent" refer to with Class 1?

Back 13

Class 1 selectively depress tissue that are frequently deploarizing (eg, during a fast tachycardia or relatively depolarized during rest from hypoxia).

They bind to receptors that are either open or inactivated.

Front 14

What is the MOA of procainamide, a group IA, and its ECG effects?

Disopyramide and Quinidine are also class IA

Back 14

It blocks I^Na, which slows conduction velocity in the atria, Purkinje fibers, and ventricular cells. Reduce ventricular conduction results in increased QRS duration.

Increase in: QRS duration and QT interval

Blocks I^K and slow repolarization (phase 3 is delayed); this generates an increase in QT interval by increasing the AP. The refractory period will also be increased.

Front 15

What is the SE of group 1A drugs: quinidine, procainamide, and disopyramide?

Back 15

Procainamide: drug-induced lupus, hypotension, and psychosis.

Quinidine: cinchonism (vertigo, headache, tinnitus), psychosis, GI disturbances and similar to procainamide.

Disopyramide: antimuscarinic effets (constipation, double vision, urinary retention), and heart failure (muscarinc receptors decrease sympathetic, contractility, and SA node firing)

All class IA can cause cardiac arrhythmias (including torsades de pointes)

Front 16

What is the MOA of lidocaine, a Class IB (also mexiletine). What else can lidocaine be used for?

Back 16

Selectively affects ischemic or depolarized Purkinje and ventricular tissue (little affect on atrial tissue)--highly selective use and state-dependent I^Na block. It also decreases the AP.

Lidocaine can also be used as a local anesthetic.

PR interval, QRS duration, and QT interval is NOT affected.

Front 17

What are the SE of lidocaine and other class IB?

Back 17

CNS sedation or excitation (convulsions)

Front 18

All Class I (e.g., A, B, C) can cause as its SE?

Back 18

Cardiac arrhythmias.

Front 19

What are class IA, IB, and IC mainly used for?

Back 19

IA: for all types of arrhythmias: atrial and ventricular arrhythmia, especially after an MI.

IB: acute ischemic ventricular arrhythmias, such as post MI and digoxin-induced arrhythmias.

IC: refractory arrhythmia and supraventricular arrhythmias

Front 20

What is the MOA of flecainide, group IC

Back 20

They are powerful depressants of Na current, and can markedly slow conduction velocity in atrial and ventricular cells. They do not effect QT interval and they increase QRS and prolong phase 0.

Increase in: QRS duration and slightly long PR interval.

Front 21

What is the SE of flecainide, group IC?

Back 21

Exacerbate or induction of life-threatening arrhythmias (more likely to induce compared to other antiarrhythmic); heart failure exacerbation (avoid in PTs with decreased ejection fractions).

This drug causes greater mortality than placebo. This drug is restricted to use in persistent arrhythmias that fail to respond to other drugs.

Front 22

What are the class 2 drugs, and give examples and their MOA.

Back 22

They are beta-blockers. Propranolol, esmolol,and metoprolol. They reduce cAMP, which results in reduction of both Na and Ca currents and the suppression of abnormal pacemakers.

Front 23

What is the main purpose of class 2 drugs?

Back 23

Although these PTs are more likely to have depression of cardiac output than normal hearts, however, they can reduce progression of chronic heart failure and reduces incidence of potentially fatal arrhythmias.

Front 24

What are the SE of group 2?

Back 24

Bronchospasm, cardiac depression, AV block, hypotension.

Front 25

What is the MOA of sotalol, ibutilide, and dofetilide, group 3?

Back 25

Strong I^K block produces marked prolongation of AP and refractory period, and thus decreasing the contractile frequency of the cell.

Increase in: QT interval.

Front 26

What is the purpose of group 3 drugs? Their MOA? And their SE?

Back 26

To treat atrial arrhythmias.

MOA: By blocking the flow of K ion channels, phase 3 repolarization is prolonged (which prolongs QT interval) and consequently, the entire duration of the AP as well (the hallmark feature). By increasing the refractory period, it reduces the ability of the heart to respond to rapid tachycardias.

SE: Torsade de pointes

Front 27

What is amiodarone MOA (considered group 3 because it blocks the same K and prolongs AP duration)

Back 27

Considered the most efficacious of all antiarrhythmic drugs. It blocks Na, Ca, and K channels and beta adrenoceptors.

Front 28

Because of amiodarone SE, what is it mainly used for and what are its SE?

Back 28

For arrhythmias (atrial and ventricular tachycardias) that are resistant to other drugs.

It causes thyroid abnormalities, pulmonary fibrosis, hepatotoxicity, microcrystalline deposits in the cornea and skin,

Front 29

What is the MOA of verapamil and diltiazem, class 4? Its SE?

Back 29

They block calcium channels of cardiac and smooth muscles. They are effective in arrhythmias that must traverse Ca-dependent cardiac tissue (AV node); therefore, supraventricular tachycarida (e.g., atrial fibrillation, AV nodal reentry [AV arrhythmias]). By blocking Ca channels in the SA and AV nodal cells, they act to slow phase 4 spontaneous depolarization.

Prolonged stage 4 for results in: prolonged PR interval.

SE: Cardiac depression; constipation, hypertension, heart block.

Front 30

What is the MOA of adenosine, its use, and SE?

Back 30

Increases K efflux out of the cells of SA and AV node, thereby, hyperpolarizing the cell. Use for treatment of acute nodal tachycardias.

SE: Flushing, bronchospasm, hypotension, heart block.

Front 31

What is the MOA of K, its use, and SE?

Back 31

Increases the threshold for a cardiac AP, therefore, reducing the rate of cardiac myocyte excitation. It is used for digoxin toxicity and to suppress ectopic pacemakers.

SE: cardiac arrest, arrhythmogenic, paralysis

Front 32

What is the MOA of magnesium, its use, and SE?

Back 32

Increase Na/K ATPase activity. Used for digitalis arrhythmias and to treat torsades de pointes.

SE: muscle weakness, hypotension, and severe increase can cause respiratory paralysis.

Front 33

Question from book: When used as an antiarrhythmic drug, lidocaine typically?

Back 33

Reduces abnormal automaticity in the ventricles. It does not alter resting potential or AP duration, and does not increase contractility.

Front 34

Question from book: What drug is most suitable for therapy of an acute arrhythmia in a PT with thyrotoxicosis?

Back 34

Beta blockers (esmolol, propranolol)

Front 35

Question from book: A 16 year old girl has paroxysmal attacks of rapid heart rate with palpitations and shorteness of breath. These episodes occasionally terminate spontaneously but often require a visit to the emergency department of the local hospital. Her ECG during these episodes reveals an AV nodal tachycardia. The antiarrhythmic of choice in most cases of acute AV nodal tachycardia is?

Back 35

Although CCB are effective in supraventriuclar AV nodal tachycardias; however, adenosine is just as effective in most acute nodal tachycardias and less toxic due to its extremely short duration of action.

Front 36

Question from book: A 55 yr old man is admitted to the ER and is found to have an abnormal ECG. Overdoes of an antiarrhythmic drug is considered. Which of the following drugs is correctly paired with its ECG effects?

Back 36

Class IA: Increase QRS and prolonged QT interval.

Class IC: Increase QRS interval

Class II: prolonged PR interval

Class III: prolonged QT interval.

Class IV: increased PR interval.

Front 37

Question from book: What drug consistently reduce the potassium (I^K)-repolarizing current?

Back 37

All 1A drugs and class 3 agents reduce K current during phase 3 and prolong the AP.

Adenosine increases the current.

Front 38

Question from book: Recognize adverse effects of procainamide, quinidine, and amiodarone include?

Back 38

Procainamide: Lupus-like syndrome

quinidine: cinchonism and thrombocytopenia

amiodarone: pulmonary fibrosis and thyroid abnormalities.

Front 39

Question from book: A 60 year old man comes to the emergency department with severe chest pain. ECG reveals ventricular tachycardia with occasional normal sinus beats, and ST-segment changes suggestive of ischemia. A diagnosis of MI is made, and the man is admitted to the cardiac intensive care unit. His arrhythmia should be treated immediately with?

Back 39

Lidocaine has limited applications as an antiarrhythmic drug, but emergency treatment of MI arrhythmiasis is one of the most important. It is also useful in digoxin-induced arrhythmias.

Afterwards, beta-blockers are used for 2 years or more to prevent sudden death arrhythmias.

Front 40

Question from book: Which of the following drugs is used by the oral route, blocks Na channels, and decreases AP duration in ischemic tissues?

Back 40

Mexiletine.

Group IB (lidocaine and mexiletine) both due, but mexiletine is orally available.

Front 41

Question from book: What drug slows conduction through the AV node and has its primary action directly on L-type calcium channels?

Back 41

CCB, such as diltiazem and verapamil.

Front 42

Question from book: What drug has the longest half-life of all antiarrhythmic drugs?

Back 42

Amiodarone (1/2 life is weeks)

Front 43

Question from book: What drug slows the upstroke of the AP and prolongation of repolarizaiton or AP duration?

Back 43

Group IA: procainamide, disopyramide, quinidine

Front 44

Question from book: An elderly PT with rheumatoid arthritis and chronic heart disease is being considered for treatment with procainamide. She is already receiving digoxin, hydrochlorothiazide, and K supplements for her cardiac condition.

In making a decision to treat with procainamide, what is true about it?

If the Pt should take an overdose and manifest severe acute procainamide toxicity with markedly prolonged QRS, rational therapy would entail the immediate administration of ?

Back 44

Since it prolongs the QT interval, it may precipitate torsade de pointes arrhythmia.

Hyperkalemia should be avoided since it facilities procainamide toxicity.

Treat with Sodium lactate: it increases sodium current and reduce drug-receptor binding by alkalinizing the tissue.

Front 45

What is effective refractory period?

What drugs prolong the effective refractory period?

Back 45

The time that must pass after the upstroke of a conducted impulse in a part of the heart before a new AP can be propagated in that cell or tissue.

Group IA, 3, and 4.

Therefore, they will have a longer QT interval; however, CCB wont because they don't act on K channels, but they delay Ca at the AV node to produce a longer PR interval.