The Treatment Of Cardiac Dysrhythmias

Front 1

The best antdysrhythmic drug is an _____________ drug bc ischemia causes dysthythmias.

Back 1

Antilipemic

Front 2

In general, blockage of Na channels does what two things:

Back 2

Decrease phase 4 automaticity

Increase the threshold potential

*QRS widening*

Front 3

Blockade of K+ channels prolongs ______________ in the atria and ventricles.

Back 3

Repolarization

Front 4

Slowing the rate of repolarization increases the ______ & thus prevents propagation of an abnormal electrical signal.

Back 4

ERP

Front 5

What are the Class I antidysrhythmic drugs? What do they block?

Back 5

Procainamide & Lidocaine

Na channels

Front 6

Procainamide blocks what channels?

Back 6

Na+ & K+

Front 7

Procainamide may block ganglionic ___________ receptors to cause hypotension.

Back 7

Nicotinic

Front 8

What are the therapeutic uses of Procainamide?

Back 8

Given i.v. for acute control of ventricular rate in patients with atrial flutter or fibrillation (slows AV conduction to decrease ventricular rate)

Suppress PVCs

*seldom used for outpatient therapy due to toxicity

Front 9

Procainamide is metabolized to the active metabolite _________ in the liver

Back 9

N-acetylprocainamide (NAPA)

Front 10

NAPA blocks ___ channels and contributes to prolongation of the _____ interval

Back 10

K+

QT

*slow acetylators are at the greatest risk for drug toxicity

Front 11

What are the adverse side effects of Procainamide?

Back 11

Hypotension with rapid i.v. injection

Torsade de pointes (due to QT interval prolongation)



SLE like syndrome with malar rash, arthralgia, arthritis, pericarditis, positive ANA
(occurs in 23-50% of pts during long-term therapy)

Front 12

Why is Lidocaine given i.v. only?

Back 12

High first-pass metabolism

Front 13

Lidocaine only affects the __________

Back 13

Ventricles

Front 14

What is the MOA of Lidocaine?

Back 14

Blocks Na+ channels

Decreases the ERP & APD of fast fibers--an effect probably caused by enhancement of the K+ current

Front 15

What are the cardiac effects of Lidocaine?

*KNOW THIS WELL*

Back 15

Suppress ventricular automaticity (spontaneous phase 4 depolarizations) in partially depolarized tissue (ischemic tissue/digoxin toxicity); little effect on conduction in normally polarized tissue

Abolishes ventricular tachycardia (a re-entry dysrhythmia) by causing a 2-way blockade of conduction in the areas that allow retrograde transmission b/c they exhibit one-way block

Increases threshold potential to further suppress automaticity

Front 16

What are the therapeutic uses of Lidocaine?

Back 16

V-tach in patients with healed MI's

Digoxin-induced PVC

Front 17

______________ is replacing Lidocaine for the treatment of ventricular dysrhythmias.

Back 17

Amiodarone

Front 18

What are the adverse effects of Lidocaine?

Back 18

Neurological: CNS depression & Seizures

Front 19

What are the Class II antidysrhythmic drugs?

Back 19

*beta-blockers*

Atenolol
Propanolol
Esmolol

Front 20

What are the cardiac effects of the Class II drugs?

Back 20

Decrease the rate of discharge of the SA node

Suppress catecholamine-induced automaticity

Reduce conduction velocity & increases the ERP of the AV node: P-R interval is increased

Increase the ERP in fast fibers when the ERP has been shortened by stimulation of beta-adrenoceptors

Front 21

What are the therapeutic uses of the Class II drugs?

Back 21

Reduces post-MI sudden death by 25-40% by preventing fatal vent dysrhythmias--probably V Tach

Prevents PVCs triggered by physical or emotional stress

Suppresses the tachycardia caused by hyperthyroidism

Reduces ventricular rate in patients w/ A fib or A flutter

Front 22

Because of its short half-life (9 min), __________ (i.v.) is used to control ventricular rate in patients with A fib or A flutter or sinus tachycardia during cardiac catherization

Back 22

Esmolol

Front 23

What are the adverse cardiac effects of the Class II drugs?

Back 23

Negative inotropic effect

Bradycardia & AV block

Front 24

What drug is a combines class II & class III drug?

Back 24

Sotalol

Front 25

What is the MOA of Sotalol?

Back 25

L-isomer causes a non-selective, competitive blockade of beta-adrenoceptors in both slow (SA & AV) nodes & fast fibers

D & L isomers block potassium channels & inhibit the rapid component of this outward potassium repolarization current; this effect delays repolarization & thus increases both the APD & ERP in the atria, ventricles, & AV node

Front 26

The _____________ is responsible for the termination of the plateau portion of the cardiac action potential in fast fibers of the atria & ventricles.

Back 26

Outward potassium rectifier current (IKr)

Front 27

What are the cardiac effects of L-sotalol caused by blockade of beta-receptors?

Back 27

Decrease heart rate

Decreased AV conduction due to decreased conduction velocity & increased ERP

APD increased everywhere in the heart, therefore so is the ERP

Decreases catecholamine-induced automaticity everywhere in the heart

Front 28

What are the cardiac effects caused by the blockade of outward repolarizing potassium current by both d- & l- Sotalol?

Back 28

Additional increase in the APD & ERP in fast fibers OVER & ABOVE that caused by beta1-adrenoreceptor blockade

An additional increase in the ERP of the AV node

Delayed ventricular depolarization increases the Q-T interval

Front 29

What is Q-Tc interval?

Back 29

Q-T interval corrected for heart rate as calculated using the Bazett formula

Front 30

What are the therapeutic uses of Sotalol?

Back 30

Cardioversion of atrial fibrillation & atrial flutter to sinus rhythm; delays repolarization and increases the ERP so that the circus rhythm is broken (gets rids of excitable gap)

Reduce ventricular rate in patients with persistent atrial fibrillation

Chronic therapy is used to prevent life-threatening V tach & V fib
*Sotalol is used BEFORE Amiodarone b/c Sotalol causes less long-term toxicity*

Front 31

What are the adverse cardiac effects of Sotalol?

Back 31

Potassium channel blockade can precipitate torsade de pointes, especially when serum potassium is low

Decreased ventricular contractility in heart failure associated with systolic dysfunction via beta1-adrenoceptor blockade

AV block via beta1-adrenoreceptor blockade

Front 32

What drugs are Class III antidysrhythmic drugs?

Back 32

Amiodarone
Dronedarone
Dofetilide

Front 33

What is the MOA of Amiodarone?

Back 33

Blocks inward sodium channels & outward potassium channels

NON-COMPETITIVE alpha and beta adrenoceptor blockade

Front 34

How is Amiodarone administered?

Back 34

i.v. or p.o.

Front 35

What are the cardiac effects of Amiodarone?

Back 35

Extremely effective in suppressing automaticity via blockade of sodium channels

Blockade of potassium channels delays repolarization & thus prolongs the APD & the ERP in the atria & ventricles

Prolongs the ERP in the AV node; reduces the transmission of depolarizations through the AV node

Prolongs the P-R, QRS, and Q-T intervals

Reduces the firing rate of the SA node

Front 36

What are the therapeutic uses of Amiodarone?

Back 36

Cardioversion of A flutter and A fib to sinus rhythm

Reduce ventricular rate in patients w/ persistent A flutter or A fib

Terminate life-threatening V tach and V fib (i.v. administration)

Chronic therapy used to prevent life-threarening V.tach and V.fub

Front 37

What is the first-line drug for recurrent V. tach & V. fib?

Back 37

Sotalol

Front 38

Amidarone is probably ____________ than Sotalol in preventing the reoccurrence of V. tach/Vfib but is more toxic.

Back 38

MORE effective

Front 39

What device is superior to medical treatment with Sotalol or Amiodarone especially when the patient is symptomatic or has a low EF?

Back 39

ICD

Front 40

What drug can be used with an ICD in "hybrid" therapy?

Back 40

Sotalol

*NOT Amiodarone b/c it inc. the energy required for defibrillation by as much as 50%

Front 41

What are the adverse cardiac effects of Amiodarone?

Back 41

Severe bradycardia or AV block

Despite the prolongation of the Q-T interval, Amidarone seldom causes torsade de pointes

Minimal suppression of myocardial contractility in patients with HF

Front 42

What are the other adverse effects of Amiodarone?

Back 42

Pneumonitis which may progress to pulmonary fibrosis

Corneal microdeposits which cause halos in the peripheral vision

Photodermatitis

Slate gray, blue, or purple skin from cutaneous deposits

Peripheral neuropathy with weakness of the proximal muscles

Hypothyroidism or Hyperthyroidism

Front 43

What is the difference between Amiodarone & Dronedarone?

Back 43

Dronedarone does NOT contain Iodine

Front 44

What is the MOA & cardiac effects of Dronedarone?

Back 44

Same as Amiodarone

Front 45

What are the therapeutic uses of Dronedarone?

*KNOW THIS WELL*

Back 45

Prevents recurrent (paroxysmal) A fib & A flutter

Reduces the ventricular rate in patients with persistent A fib or A flutter

Front 46

What are the adverse cardiac effects of Dronedarone?

Back 46

Severe bradycardia

Despite prolongation of Q-T interval, Dronedarone has NOT been reported to cause torsade de pointe

Suppression of myocardial contractility in patients with HF (BLACK BOX WARNING)

Front 47

What are the other adverse effects of Dronedarone?

Back 47

Does not cause thyroid, pulmonary, neurological, dermal, or ocular toxicity

Major adverse effects are nausea & diarrhea

*Amiodarone is more effective for maintaining sinus rhythm in patients with recurrent A fib, but Dronedarone has fewer adverse effects

Front 48

Dofetilide is structurally-related to Sotalol but has no ___________ activity.

Back 48

Beta-blocking activity

*Pure class III

Front 49

What is the MOA of Dofetilide?

*Keeton said probably no ?s over this drug*

Back 49

Blocks outward repolarizing potassium current

Delayed repolarization increases APD & ERP in fast fibers

Front 50

What are the cardiac effects of Dofetilide?

Back 50

Produces a dose-related increase in the Q-Tc interval

No effect on AV conduction

No effect on the P-R interval or the width of the QRS

Front 51

What are the therapeutic effects of Dofetilide?

Back 51

Cardioversion of A fib and A flutter of short duration

More effective than amidarone or sotalol, but also more likely to cause dysrhythmias (tordade de pointes)

No negative effect on mortality after MI or in patients with CHF

Front 52

What are the adverse effects of Dofetilide?

Back 52

Torsade de points

No effect on BP or cardiac contractility

Front 53

The Class IV antidysrhythmic drugs are ___________

Back 53

Calcium channel blockers

Verapamil / Diltiazem

Front 54

What is the MOA of Verapamil & Diltiazem?

Back 54

Blockade of calcium channels in slow fibers, especially the AV node

Front 55

What are the cardiac effects of Verapamil & Diltiazem?

Back 55

Cardiac effects:
1. Decreased heart rate
2. Decreased conduction velocity in the AV node = inc. PR int.
3. Increased ERP in the AV node
4. Decreased contractility (dp/dt)

*DRUGS ARE BIG NO NO FOR PPL W HEART FAILURE*

Front 56

What are the therapeutic uses of Verapamil & Diltiazem?

Back 56

Reduce ventricular rate in patients with A fib or A flutter

Converts AVNRT to sinus rhythm by blocking the re-entry pathways in or near the AV node

*see diagram on pg. 329*

Front 57

What is the mechanism by which Verapamil/Diltiazem & beta-blockers annihilate AVNRT?

Back 57

Slow conduction in the fast pathway of the AV node so that signals from the two sides arrive at the bundle branches at the same time & AV nodal re-entry is thus prevented

Front 58

What are the ECG findings with regards to the QRS & P wave in AVNRT?

Back 58

Narrow QRS

P wave lost in the QRS b/c atria and and ventricles are depolarized @ the same time

Front 59

What are the adverse effects of Verapamil/Diltiazem?

Back 59

Hypotension
Sinus bradycardia
Heart block

Front 60

What is the MOA of Digoxin?

Back 60

Acts centrally to increase efferent vagal nerve activity & to decrease sympathetic outflow

Increases dp/dt via partial inhibition of the Na+/K+ ATPase

Front 61

What are the cardiac effects via increased efferent vagal activity?

Back 61

Decreased heart rate

Decreased conduction velocity in the AV node

Increased ERP in the AV node

Front 62

What does the increase in contractility caused by Digoxin's partial blockade of the Na/K ATPase do to SV?

Back 62

Increases via increased dp/dt

Front 63

What are the therapeutic uses of Digoxin?

Back 63

Reduce ventricular rate in patients with atrial tachycardias (A fib/ flutter) in the presence of heart failure caused by systolic dysfunction

Increase dp/dt in patients w/ HF from systolic dysfunction

Front 64

What are the adverse effects of Digoxin at serum concentrations above the therapeutic window?

Back 64

Inhibition of the Na+/K+ ATPase & increased Ca2+ can elicit automaticity in fast fibers resulting in PACs and PVCs

Sympathetic activity is increased

The APD & ERP are decreased in the presence of excessive intracellular calcium leading to delayed afterdepolarizations

Sinus bradycardia

AV block

Front 65

What is the MOA of Adenosine?

Back 65

Increases potassium conductance to hyperpolarize the AV node

Inhibits the ability of sympathetic stimulation to increase calcium conductance in the AV node

Front 66

What is the half-life of Adenosine in the circulation?

Back 66

10 seconds

Front 67

What are the cardiac effects of Adenosine?

Back 67

Decreased conduction velocity & increased ERP in the AV node

AV conduction momentarily ceases; the heart stops; resets the AV node

Front 68

What are the therapeutic uses of Adenosine?

Back 68

Diagnosis of AV nodal re-entry tachycardia (PSVT)

Conversion of AVNRT to normal sinus rhythm (90+% effective)

Produce coronary vasodilation during a radionuclide scan in patients who cannot exercise

Front 69

What are the adverse effects of Adenosine?

Back 69

Transient asystole
A short-lived, intense burning sensation in the chest
Flushing
Dyspnea

Front 70

Patients with AF are at very high risk for an ____________ and must be treated daily with _______________ and/or an antiplatelet drug such as ________, ________.

Back 70

Ischemic stroke

Warfarin

Aspirin, Clipidogrel

Front 71

The use of drugs to convert AF to sinus rhythm and to maintain sinus rhythm does what to the incidence of stroke versus just controlling ventricular rate?

Back 71

Does not decrease the incidence of stroke

*Increases the risk of potentially fatal ventricular dysrhythmias and adverse drug effects

Front 72

What drugs are suitable for use to control ventricular rate in patients with A fib/flutter that also have heart failure?

Back 72

Amiodarone

Digoxin