II.

MECHANISMS FOR
ARRHYTHMIAS

Antiarrhyth.JDH 30
(MED 2/08)

A. Definition of Arrhythmias

-abnormality in rate, regularity, site of

origin, and/or sequence of activation

-they range in severity.

B. Abnormalities of Impulse Generation

Mechanisms

1. Altered Normal Automaticity

2. Triggered Impulses (afterdepolarizations)

C. Abnormality of Conduction - Re-entry

Antiarrhyth.JDH 31
(MED 2/08)

1
B. Abnormalities of Impulse Generation
1. Altered Normal Automaticity
- change in spontaneous phase 4 depolarization

Affects primarily SA node and His-Purkinje fibers but in disease states, such
as from ischemia, ventricular cells can also spontaneously depolarize.
Antiarrhyth.JDH 32
(MED 2/08)

1. Altered Normal Automaticity

Favor RAPID phase 4 Favor SLOW phase 4
Depolarization Depolarization
Sympathetic nervous system – Parasympathetic nervous
Catecholamines system – Acetycholine

Hypokalemia Hyperkalemia

Cell damage
ischemia
myocardial stretch
trauma
Drugs Drugs
atropine Class 1 antiarrhythmics -
cardiac glycosides quinidine
(His-Purkinje) verapamil
propranolol
Antiarrhyth.JDH 33
(MED 2/08)

2
B. Abnormalities of Impulse Generation
2. Triggered Impulses

– normal action potential is interrupted or

followed by an abnormal depolarization.
Early and delayed afterdepolarizations.

a. Early afterdepolarizations (EAD)

b. Delayed afterdepolarizations (DAD)

Antiarrhyth.JDH 34
(MED 2/08)

b. Delayed Afterdepolarizations (DAD)

- secondary depolarizations that occur after full repolarization
has developed.

1) Phase 0 carried by sodium with fast conduction.

2) Factors associated with DAD include:

- High intracellular Ca2+ load (ischemia, cardiac glycosides)

- Increased SNS activity – high catecholamines.
- fast heart rates
Antiarrhyth.JDH 35
(MED 2/08)

3
a. Early afterdepolarizations (EAD)
– secondary depolarizations that occur before repolarization
is complete.
1) Phase 0 may be carried by Ca2+, Na+ or mixture
of the two.
2) Factors associated with EAD include:

- Increased SNS activity - high catecholamines

- Cell damage (hypoxia, mycocardial stretch)
- slow heart rate
- hypokalemia
- More likely with Purkinje cells
** - Prolonged QT interval (delayed repolarization)
(increased in slowed HR and prolonged AP)
(drug-induced including antiarrhythmics.
antihistamines, antidepressants, others)
- Markedly prolonged QT interval predisposes to
torsade de pointes (a form of ventricular
tachycardia)
Antiarrhyth.JDH 36
(MED 2/08)

Electrocardiogram from a patient with the long QT

syndrome during two episodes of torsade de
pointes.

Antiarrhyth.JDH 37
(MED 2/08)

4
a. Early afterdepolarizations (EAD)
– secondary depolarizations that occur before repolarization
is complete.
1) Phase 0 may be carried by Ca2+, Na+ or mixture
of the two.
2) Factors associated with EAD include:

- Increased SNS activity - high catecholamines

- Cell damage (hypoxia, mycocardial stretch)
- slow heart rate
- hypokalemia
- More likely with Purkinje cells
** - Prolonged QT interval (delayed repolarization)
(increased in slowed HR and prolonged AP)
(drug-induced including antiarrhythmics.
antihistamines, antidepressants, others)
- Markedly prolonged QT interval predisposes to
torsade de pointes (a form of ventricular
tachycardia)
Antiarrhyth.JDH 38
(MED 2/08)

a. Early afterdepolarizations (EAD)

– secondary depolarizations that occur before repolarization
is complete.
1) Phase 0 may be carried by Ca2+, Na+ or mixture
of the two.
2) Factors associated with EAD include:

- Increased SNS activity - high catecholamines

- Cell damage (hypoxia, mycocardial stretch)
- slow heart rate
- hypokalemia
- More likely with Purkinje cells
** - Prolonged QT interval (delayed repolarization)
(increased in slowed HR and prolonged AP)
(drug-induced including antiarrhythmics.
antihistamines, antidepressants, others)
- Markedly prolonged QT interval predisposes to
torsade de pointes (a form of ventricular
tachycardia)
Antiarrhyth.JDH 39
(MED 2/08)

5
a. Early afterdepolarizations (EAD)
– secondary depolarizations that occur before repolarization
is complete. 1) Phase 0 may be carried by Ca2+, Na+ or mixture
Hereditary long of the two.
QT Syndromes 2) Factors associated with EAD include:

- Increased SNS activity - high catecholamines

- Cell damage (hypoxia, mycocardial stretch)

- slow heart rate
- hypokalemia
- More likely with Purkinje cells
** - Prolonged QT interval (delayed repolarization)
(increased in slowed HR and prolonged AP)
(drug-induced including antiarrhythmics.
antihistamines, antidepressants, others)
Acquired long - Markedly prolonged QT interval predisposes to
EAD -> long QT torsade de pointes (a form of ventricular
tachycardia)
Antiarrhyth.JDH 40
(MED 2/08)

II. MECHANISMS FOR ARRHYTHMIAS

A. Definition of Arrhythmias
B. Abnormalities of Impulse Generation

1. Altered Normal Automaticity

2. Triggered Impulses (EAD and DAD)

C. Abnormality of Conduction - Re-entry

Antiarrhyth.JDH 41
(MED 2/08)

6
C. Abnormality of Conduction - Re-entry
Requires an abnormal conduction pathway to form a
self-propagating circuit
1. Common properties of Re-entry arrhythmias
a. A divided conduction path (anatomical, pathological
or functional) which would normally extinguish itself
b. “Decremental” conduction in one path with complete
loss of conduction.
c. Re-activation of the extinguished pathway in the
reverse direction by the remaining and unopposed
pathway.
d. Correct timing of the conduction rate in the active
pathway and the refractory period of the cells in the
extinguished pathway.
Responsible for many cardiac arrhythmias.
Antiarrhyth.JDH 42
(MED 2/08)

Re-entry 1

Wave fronts meet and extinguish

Antiarrhyth.JDH 43
(MED 2/08)

7
C. Abnormality of Conduction - Re-entry
Requires an abnormal conduction pathway to form a
self-propagating circuit
1. Common properties of Re-entry arrhythmias
a. A divided conduction path (anatomical, pathological
or functional) which would normally extinguish itself
b. “Decremental” conduction in one path with complete
loss of conduction.
c. Re-activation of the extinguished pathway in the
reverse direction by the remaining and unopposed
pathway.
d. Correct timing of the conduction rate in the active
pathway and the refractory period of the cells in the
extinguished pathway.
Responsible for many cardiac arrhythmias.
Antiarrhyth.JDH 44
(MED 2/08)

Re-entry 2

(Ischemic) area with decremental conduction

(i.e., an area where conduction velocity
progressively slows to zero and then dies out.)
Antiarrhyth.JDH 45
(MED 2/08)

8
C. Abnormality of Conduction - Re-entry
Requires an abnormal conduction pathway to form a
self-propagating circuit
1. Common properties of Re-entry arrhythmias
a. A divided conduction path (anatomical, pathological
or functional) which would normally extinguish itself
b. “Decremental” conduction in one path with complete
loss of conduction.
c. Re-activation of the extinguished pathway in the
reverse direction by the remaining and unopposed
pathway.
d. Correct timing of the conduction rate in the active
pathway and the refractory period of the cells in the
extinguished pathway.
Responsible for many cardiac arrhythmias.
Antiarrhyth.JDH 46
(MED 2/08)

Re-entry current when the unopposed

Re-entry 3
wavefront crosses the same area out
of the refractory period

(Ischemic) area with decremental conduction

(i.e., an area where conduction velocity
progressively slows to zero and then dies out.)
Antiarrhyth.JDH 47
(MED 2/08)

9
C. Abnormality of Conduction - Re-entry
Requires an abnormal conduction pathway to form a
self-propagating circuit
1. Common properties of Re-entry arrhythmias
a. A divided conduction path (anatomical, pathological
or functional) which would normally extinguish itself
b. “Decremental” conduction in one path with complete
loss of conduction.
c. Re-activation of the extinguished pathway in the
reverse direction by the remaining and unopposed
pathway.
d. Correct timing of the conduction rate in the active
pathway and the refractory period of the cells in the
extinguished pathway.
Responsible for many cardiac arrhythmias.
Antiarrhyth.JDH 48
(MED 2/08)

Re-entry current when the unopposed

Re-entry 3
wavefront crosses the same area out
of the refractory period

Why
doesn’t
the re-
entry
current die
out too?

(Ischemic) area with decremental conduction

(i.e., an area where conduction velocity
progressively slows to zero and then dies out.)
Antiarrhyth.JDH 49
(MED 2/08)

10
Re-entry 4
Antiarrhythmic
drugs break a
re-entry circuit
by causing a
bidirectional
block.
They do this
by directly or
indirectly
modifying the
refractory
period of the
area of
damaged cells
Antiarrhyth.JDH 50
(MED 2/08)

C. Abnormality of Conduction - Re-entry

Requires an abnormal conduction pathway to form a
self-propagating circuit
1. Common properties of Re-entry arrhythmias
a. A divided conduction path (anatomical, pathological
or functional) which would normally extinguish itself
b. “Decremental” conduction in one path with complete
loss of conduction.
c. Re-activation of the extinguished pathway in the
reverse direction by the remaining and unopposed
pathway.
d. Correct timing of the conduction rate in the active
pathway and the refractory period of the cells in the
extinguished pathway.
Responsible for many cardiac arrhythmias.
Antiarrhyth.JDH 51
(MED 2/08)

11
 Re-entry: Common mechanism for Arrhythmias
1. Regions of anatomically-split pathways affected by
ischemia or other injury
2. Re-entry in AV node [paroxysmal supraventricular
tachycardia (PSVT)]
3. Developmental pathologies (Wolff-Parkinson-
White Syndrome, where an accessory pathway
bridges atria and ventricle in a way that can “short
circuits” the AV node).
4. Areas of ischemic injury (MI)
5. Functional re-entry circuit in torsade de pointe
initiated by an EAD.

Antiarrhyth.JDH 52
(MED 2/08)

IV. ANTIARRHYTHMIC DRUGS

Class 1 Class 2 Class 3 Class 4
Sodium Channel Beta Adrenergic Prolong Refractory Calcium Other
Blockers Blockers Period (Potassium Channel
Channel Blockers) Blockers
A Quinidine Propranolol* Amiodarone Verapamil
Procainamide Acebutolol Bretylium Diltiazem Adenosine
Disopyramide Esmolol Sotalol Atropine
Others Ibutilide Digoxin

B Lidocaine
Phenytoin
Mexiletine

C Flecainide
Propafenone
Moricizine
*additional mechanisms at higher concentrations (Class 1B effects)
Antiarrhyth.JDH 53
(MED 2/08)

12
Class 1 Antiarrhythmic Drugs

Sodium Channel Blockers

Class 1A Quinidine (Procainamide, Disopyramide)

Class 1B Lidocaine (Phenytoin, Mexiletine).

Class 1C Flecainide (Propafenone, Morcizine).

Antiarrhyth.JDH 54
(MED 2/08)

Class 1 Antiarrhythmic Drugs

Class 1A Depress phase 0 depolarization (conduction
velocity) in fast response cells and decreases
automaticity; prolong action potential duration and increase
refractory period. Moderate effects on conduction in
NORMAL cells.
Class 1B Depress phase 0 depolarization (conduction
velocity) in fast response cells and can decrease
automaticity. No significant effect on action potential
duration. Minimal effects on conduction in NORMAL cells
Class 1C Depress phase 0 depolarization (conduction
velocity) in fast response cells and can decrease
automaticity. Minimal effect on action potential duration.
Marked effects on conduction in NORMAL cells.

Antiarrhyth.JDH 55
(MED 2/08)

13
Class 1 Antiarrhythmic Drugs
Class 1A Depress phase 0 depolarization (conduction
velocity) in fast response cells and also can depress
automaticity; prolong action potential duration and increase
refractory period. Moderate effects on conduction in
NORMAL cells.

Class 1B Depress phase 0 depolarization (conduction

velocity) in fast response cells and can decrease
automaticity. No significant effect on action potential
duration. Minimal effects on conduction in NORMAL cells

Class 1C Depress phase 0 depolarization (conduction

velocity) in fast response cells and can decrease
automaticity. Minimal effect on action potential duration.
Marked effects on conduction in NORMAL cells.
Antiarrhyth.JDH 56
(MED 2/08)

Class 1 Antiarrhythmic Drugs

Class 1A Depress phase 0 depolarization (conduction
velocity) in fast response cells and also can depress
automaticity; prolong action potential duration and increase
refractory period. Moderate effects on conduction in
NORMAL cells.

Class 1B Depress phase 0 depolarization (conduction

velocity) in fast response cells and can decrease
automaticity. No significant effect on action potential
duration. Minimal effects on conduction in NORMAL cells

Class 1C Depress phase 0 depolarization (conduction

velocity) in fast response cells and can decrease
automaticity. Minimal effect on action potential duration.
Marked effects on conduction in NORMAL cells.
Antiarrhyth.JDH 57
(MED 2/08)

14
A. Class 1 - Sodium Channel Blockers
1. Drug binding to the sodium channel is both voltage and
use dependent. - Drug bound channels do not conduct.

USE-DEPENDENT BLOCKADE

Most drugs bind to open and inactive states of the

channel (i.e., at lower RMP).

Because of use-dependence, greater effect of the drug

when heart is beating faster.

i.e., suppress conduction more during tachycardia than

at a normal heart rate.

The degree of dependency varies with each drug.

Antiarrhyth.JDH 58
(MED 2/08)

A. Class 1 - Sodium Channel Blockers

1. (continued)

Drug-Channel interactions are reversible and

dissociation occurs as the membrane is repolarized.

Extent and rate of dissociation varies with each drug.

Antiarrhyth.JDH 59
(MED 2/08)

15
A. Class 1 - Sodium Channel Blockers
2. Comparison of Lidocaine, Quinidine and Flecainide on Normal Cells

The different subgroups of class 1 drugs bind to different

channel states or have different binding kinetics.

Drug State-Dependence tau Recovery (seconds)

Quinidine (1a) Open 3
Lidocaine (1b) Inactive > Open 0.1
Flecainide (1c) Open 11

Antiarrhyth.JDH 60
(MED 2/08)

3. Action Potentials -
Basis for conduction
from cell to cell.

Algebraic sum of
voltage over time
yields ECG.

PR Interval =
primarily AV node
conduction time

QT Interval = ventricular depolarization

-> repolarization time

Antiarrhyth.JDH 61
(MED 2/08)

16
A. Class 1 - Sodium Channel Blockers
2. Comparison of Lidocaine, Quinidine and Flecainide on Normal Cells

Antiarrhyth.JDH 62
(MED 2/08)

Class 1A - Sodium Channel Blockers

QUINIDINE
Mechanism
1. Predominant action
- blocks voltage gated sodium channels;
binds preferentially to open state of channel.
Selectivity for: a) cells at higher heart rate;
b) cells at less negative RMP;
Effect on cells is to:

decrease rate of phase 0

increase threshold for excitability;
decrease automaticity in His-Purkinje
cells (but not SA cells).
Antiarrhyth.JDH 63
(MED 2/08)

17
Class 1A - Sodium Channel Blockers
QUINIDINE

2. Blocks potassium channels - prolongs refractory period.

increase phase 3 and prolongs the QT interval

3. Alpha-adrenergic blockade

4. Atropine-like effect (anticholinergic)

Therapeutic Uses

1. Use has declined but is still used for -

2. Variety of supraventricular and ventricular tachyarrhythmias.

Antiarrhyth.JDH 64
(MED 2/08)

Class 1A - Sodium Channel Blockers

QUINIDINE
Side Effects

1. Prolongation of QT interval - increased risk of

torsades de pointes (2-8%; form of ventricular
tachycardia which can culminate in ventricular
fibrillation).
2. Hypotension due to alpha-adrenergic blockade.
3. High incidence of diarrhea (30-50%)
Other Considerations
1. Drug interaction with digoxin - increases latter's
serum level.
2. Still widely used despite side effects.

Antiarrhyth.JDH 65
(MED 2/08)

18
Class 1A - Sodium Channel Blockers
QUINIDINE
Related Drugs
(Similar to quinidine but different pharmacokinetics)

PROCAINAMIDE (Pronestyl, Procan) -

lacks vagolytic and alpha-adrenergic blockade;

60-70% become ANA positive;
25-50% develop a lupus-like syndrome

DISOPYRAMIDE (Norpace)

Antiarrhyth.JDH 66
(MED 2/08)

Class 1B - Sodium Channel Blockers

LIDOCAINE (Xylocaine)
Mechanism

Predominant action - blocks voltage gated sodium

channels; binds preferentially to inactivated state of
channel. Selectivity for:

a) ventricular cells over atrial cells;

b) cells with fast rate over cells with slow rate;
c) cells with less negative RMP > more negative RMP.

Sodium channel blockade leads to increased threshold

for excitability; decreased automaticity.

Antiarrhyth.JDH 67
(MED 2/08)

19
Class 1B - Sodium Channel Blockers
LIDOCAINE (Xylocaine)
Therapeutic Uses
1. Acute suppression of ventricular arrhythmias. (no
longer the first choice for recurrent sustained V-tach
or V-fib.)

2. Must be given parentally because of extensive first

pass effect - often as intravenous bolus and infusion.
Latter modified with liver disease and heart failure.
Side Effects
1. Central nervous system symptoms - seizures (very
rapid administration) and drowsiness, dysarthria
and dysesthesia (more gradual increase in serum
levels).
2. Depression of cardiac function.
Antiarrhyth.JDH 68
(MED 2/08)

Class 1B - Sodium Channel Blockers

LIDOCAINE (Xylocaine)

Other Considerations
Also used at local anesthetic.

Related Drugs
(Lidocaine variants not susceptible to first-pass metabolism
and can be given orally, and tend to be less selective for
“sick” cells.)

MEXILETINE (Mexitil)
TOCAINIDE

Antiarrhyth.JDH 69
(MED 2/08)

20
Class 1C - Sodium Channel Blockers
FLECAINIDE (Tambocor)
Mechanism
1. Predominant action - blocks voltage gated sodium
channels; Selectivity for cells at high heart rate but
greater depression at normal rates than class 1A and
1B.
2. Can block potassium channels (but much less or
negligible effect on QT interval ).

Therapeutic Uses

1. Variety of supraventricular tachycardias.

2. Life-threatening ventricular arrhythmias.

Antiarrhyth.JDH 70
(MED 2/08)

Class 1C - Sodium Channel Blockers

FLECAINIDE (Tambocor)
Side Effects
1. Proarrhythmic - especially in presence of
severe heart disease -> increase mortality

2. Depression of left ventricular function.

Related Drugs

PROPAFENONE (Rythmol)

Antiarrhyth.JDH 71
(MED 2/08)

21
Class 2 (Beta - blockers)
Effects primarily due to blocking beta adrenergic influences
on conducting system.

Propranolol

Acebutolol
Esmolol
Others

Antiarrhyth.JDH 72
(MED 2/08)

Class 2 - Beta Adrenergic Blockers

PROPRANOLOL (Inderal)
Mechanism
1. Predominant action - blockade of beta adrenergic
receptors (ß1 in myocardium).

Therapeutic Uses

1. Beta blockers reduce mortality in early period and

subsequently after acute myocardial infarction.

2. Chronic ventricular arrhythmias.

3. Control of ventricular rate in atrial flutter or fibrillation.

4. Paroxysmal supraventricular tachycardia (PSVT).

Antiarrhyth.JDH 73
(MED 2/08)

22
Class 2 - Beta Adrenergic Blockers
PROPRANOLOL (Inderal)
Therapeutic Uses

5. Symptomatic sinus tachycardia.

6. Catecholamine-related ventricular arrhythmias.

Side Effects See lecture on "Autonomic Drugs

Related Drugs

Esmolol Very short half-life / used i.v.

Antiarrhyth.JDH 74
(MED 2/08)

Class 3 (Potassium Channel - blockers)

Major effect is to prolong duration of action potentials

and, thus, increase refractory period.

Amiodarone

Bretylium
Sotalol
Ibutilide

Antiarrhyth.JDH 75
(MED 2/08)

23
Class 3 - Potassium Channel Blockers
AMIODARONE (Cordarone)
Chemistry
Iodinated compound related to thyroid hormone
Mechanism
1. Predominant action - prolongs action potential
duration and refractory period (block of potassium
channels?). <- class 3
2. Blocks sodium channels (phase 0). <- class 1
3. Blocks calcium channels (phase 2). <- class 4
4. Noncompetitive blockade of alpha and beta <-class 2
adrenergic receptors and muscarinic receptors.
5. Actions responsible for antiarrhythmic effects often
unclear.

Antiarrhyth.JDH 76
(MED 2/08)

Class 3 - Potassium Channel Blockers

AMIODARONE (Cordarone)
1. Functional effects:

a. Decreases SA node automaticity

b. Decrease AV node conduction velocity

c. Prolongs AV node and ventricular refractory period

d. Increases the PR and QT intervals

Antiarrhyth.JDH 77
(MED 2/08)

24
Class 3 - Potassium Channel Blockers
AMIODARONE (Cordarone)
2. Therapeutic Uses
a. FDA recommendation - only for life-threatening ventricular
arrhythmias refractory to all other available forms of therapy.
b. Powerful inhibitor of pacemaker automacitiy
c. Long-term (oral) use

1. trial fibrillation and atrial flutter

2. Supraventricular tachycardia
3. Life-threatening (sustained) ventricular tachycardia

d. i.v. use:

1. Ventricular fibrillation
2. Sustained ventricular tachycardia

Antiarrhyth.JDH 78
(MED 2/08)

Class 3 - Potassium Channel Blockers

AMIODARONE (Cordarone)

3. Side Effects (most minimized at low doses)

a. Hypotension
b. AV block
c. Arrhythmias (2%)
d. Blue-gray skin discoloration
e. Pulmonary fibrosis (potentially fatal)
f. Thyroid abnormalities (from iodine content)
g. Corneal deposits
h. Blurred vision
i. Photosensitivity
j. GI disturbances

Antiarrhyth.JDH 79
(MED 2/08)

25
Class 3 - Potassium Channel Blockers
AMIODARONE (Cordarone)
Related Drugs
Ibutilide K channel blocker
Na channel activator
Uses -> atrial fibrillation

Sotalol K channel blocker

Nonselective β blocker
Uses -> ventricular and atrial arrhythmias
Dose-dependent torsade de pointes

Antiarrhyth.JDH 80
(MED 2/08)

Class 4 (Calcium Channel - blockers)

Depresses slow response action potentials in AV and
SA nodes where depolarization is mediated primarily by
calcium influx.

Verapamil

Diltiazem

Antiarrhyth.JDH 81
(MED 2/08)

26
Class 4 - Calcium Channel Blockers
VERAPAMIL (Isoptin, Calan)
Mechanism
1. Predominant action - blocks voltage-gated L-type
calcium channels.
Therapeutic Uses
1. Control of ventricular rate in atrial flutter and fibrillation.
2. Paroxysmal supraventricular tachycardia (PSVT) due to
reentry involving the AV node.
Side Effects 1. Cardiac depression.
2. Hypotension.
3. Constipation (most common).

Related Drugs DILTIAZEM (Cardizem, Dilacor)

Antiarrhyth.JDH 82
(MED 2/08)

Other Antiarrhythmics
ADENOSINE (Adenocard)
Mechanism
1. Predominant action - acts through A1 adenosine
receptors to activate potassium channels and inhibit
effects of increased cyclic AMP. This in turn leads to:

a) hyperpolarization and slowing of SA node firing;

b) shortening of action potential of atrial cells;
c) depression of conduction velocity through AV node.

These actions break the reentry circuit allowing

resumption of normal sinus rhythm.

Antiarrhyth.JDH 83
(MED 2/08)

27
Other Antiarrhythmics
ADENOSINE (Adenocard)
Therapeutic Uses

1. Acute conversion of paroxysmal supraventricular

tachycardia (PSVT) due to reentry involving the AV
node. Highly effective.

2. Given as intravenous bolus in central line. Effects

transient (maximal within 10-20 sec).

Side Effects

1. Transient facial flushing, dyspnea and chest pressure.

Antiarrhyth.JDH 84
(MED 2/08)

Other Antiarrhythmics
ATROPINE
Mechanism
1. Predominant action - muscarinic blockade;
decreases acetylcholine-induced activation of
potassium channels through M2 receptors;
increases spontaneous phase 4 depolarization of
SA node.
Therapeutic Uses

1. Sinus bradycardia (e.g., acute myocardial infarction)

Side Effects
See lecture on "Cholinergic Systems"
Antiarrhyth.JDH 85
(MED 2/08)

28
 Other Antiarrhythmics
DIGOXIN (Lanoxin)
Mechanism
See lecture on "Drug Therapy of Congestive Heart Failure”
Increases vagal tone and suppresses AV node activity.

Therapeutic Uses
Control of ventricular rate in atrial flutter and fibrillation.

Side Effects

See lecture on "Drug Therapy of Congestive Heart Failure"

Antiarrhyth.JDH 86
(MED 2/08)

The End

Antiarrhyth.JDH 87
(MED 2/08)

29