anti arrhythmia

Question 1

what is arrhythmia

Answer 1

Abnormal heart beat, ↑ HR (tachycardia) or ↓ HR (bradycardia), results from
abnormality in generation or conduction of action potentials.

Question 2

what are the causes of arrhythmia

Answer 2

1)Abnormality in impulse generation:

2)Abnormality in impulse conduction:

Question 3

how does abnormality in impulse generation cause arrhythmia

Answer 3

Happens when cardiac sites other than SA node show enhanced automaticity—— generate competing stimuli.
——- Called ectopic foci.
Hypoxia & hypokalemia cause cells to remain partially depolarized
during diastole—–can reach the firing threshold earlier than normal
cells.
Antiarrhythmic drugs suppress automaticity by:
-decreasing the slope of phase 4 depolarization &/or:
-raising the threshold of discharge to a less negative voltage.
 Decreased frequency of discharge.
 This effect is more pronounced in ectopic foci than in normal
cells.

Question 4

how does the abnormality in impulse conduction cause arrhythmia

Answer 4

-Reentry can occur due to unidirectional block.
-Unidirectional block can occur due to myocardial injury in an area of
the heart.
-Reentry is the most common cause of arrhythmia & can occur at any
level of the cardiac conduction system.

Question 5

how do antiarrhythmic drugs solve reentry

Answer 5

1) ↑ refractory period
 convert unidirectional block
into bidirectional block OR:
2) Slow conduction
 prevent reentry.

Question 6

what are the symptoms of arrhythmia

Answer 6

Palpitations (increased awareness of the heart beating faster). This is
often the only symptom for most people.
chest pain
shortness of breath
Pounding chest (hammering, repeated heavy blows)
Rapid breathing
light-headedness (Dizziness)
fainting
fatigue
weakness
Loss of consciousness (in serious cases)
Numbness of various body parts

Question 7

what are the different types of arrhythmia

Answer 7

1. atrial arrhythmia
   -atrial tachycardia (90-230)
   -atrial flutter ( 230-380)
   -atrial fibrillation

2.superventricular tachardias
-av node reentry
- tachycardia

3.ventricular arryhtmia
- fibrillation
-tachycardia

Question 8

how do we treat arrhythmia

Answer 8

• Arrhythmias MAY require treatment because rhythms that are too rapid,
too slow, or asynchronous can reduce cardiac output.

• Can precipitate more serious or even lethal rhythm disturbances…..In
such patients, antiarrhythmic drugs may be lifesaving.

• On the other hand, because antiarrhythmic drugs can precipitate lethal
arrhythmias in some patients, treatment of asymptomatic or minimally
symptomatic arrhythmias should be AVOIDED for this reason.

• If the dose of an antiarrhythmic is ↑, it impairs conduction in normal
tissue, resulting in drug-induced arrhythmias.

• Also: a therapeutic (antiarrhythmic) dose of a drug may become proarrhythmic (arrhythmogenic) during acidosis, hypokalemia, or ischemia.

Question 9

what are the class 1 agents

Answer 9

Na+ channel blocker,Their use has declined due to their proarrhythmic affects, esp. in patients with
left ventricular dysfunction and IHD.

3 subclasses
a– moderate block— increases ap duration
b– mild block—- decreases ap duration
c— marked block —- no changes on ap duration

Question 10

what is Quinidine (class 1A)

Answer 10

• Adverse effects:
Torsade de pointes arrhythmia.
Cinchonism (headache, dizziness, tinnitus, blurred vision, disorientation, &
psychosis).

• Use of quinidine has declined much.

Question 11

what is procainamide (class 1 A)

Answer 11

 Available IV only.
 Largely replaced by ICD and amiodarone.
• Side effects:
 Cardiac: can cause torsade de pointes arrhythmia, syncope.
 Hyperkalemia increases procainamide toxicity.
 (potential problem in HF patients?)
 Antidote for proacinamide cardiac toxicity: sodium lactate.
 Extracardiac:
 lupus erythematosus-like syndrome is frequent, arthritis & arthralgia. It
happens after long-term use.
 Long-term use of procainamide is to be avoided.

Question 12

what is lidocaine (class 1B)

Answer 12

 Largely replaced by amiodarone.
 Prophylactic use should be avoided due to increased mortality noticed.
 Only IV because it is very sensitive for first pass effect.
• Side effects: Lidocaine is generally safe at therapeutic doses.

Question 13

what is Mexiletine (class 1B)

Answer 13

Available orally because it is stable for first pass effect.

Question 14

what is flecainide (class1C)

Answer 14

 Negative inotropic effect, aggravates heart failure.
 In patients with MI, it aggravates ventricular arrhythmias, which can be
fatal.

Question 15

what is propafenone

Answer 15

β–blocking properties

Question 16

what are class 2 antiarrhythmia drugs

Answer 16

Beta blockers , increasing in use (beta 1)

Question 17

what are metoprolol and esmolol (class 2)

Answer 17

 Metoprolol is the β-blocker most widely used in the treatment of
arrhythmias. Compared with propranolol it has less risk of
bronchoconstriction.
 Esmolol has very short duration of action → IV for emergency arrhythmias
and arrhythmias during surgery.

Question 18

what are class 3 antiarrythmia drugs

no herbes that prolong QT
no hepatic enzyme inhibitors
both increases the chance of torsade de pointes

Answer 18

K+ channel blockers
Block K+-channels→ ↓ the slope of repolarization→ ↑ APD→ ↑ refractory period.

Concomitant use of antiarrhythmics (esp. class 3) with drugs or herbal
products that prolong the QT interval increases the risk of torsade de
pointes.

 Also, the use of hepatic enzyme inhibitors that accumulate these drugs
increases the risk of torsade de pointes.

 Most of these drugs should be initiated in the inpatient setting due to their
proarrhythmic effect.

Question 18

what are class 3 antiarrythmia drugs

no herbes that prolong QT
no hepatic enzyme inhibitors
both increases the chance of torsade de pointes

Answer 18

K+ channel blockers
Block K+-channels→ ↓ the slope of repolarization→ ↑ APD→ ↑ refractory period.

Concomitant use of antiarrhythmics (esp. class 3) with drugs or herbal
products that prolong the QT interval increases the risk of torsade de
pointes.

 Also, the use of hepatic enzyme inhibitors that accumulate these drugs
increases the risk of torsade de pointes.

 Most of these drugs should be initiated in the inpatient setting due to their
proarrhythmic effect.

Question 19

what are dofetilide and ibutilide (class 3)

Answer 19

 delays repolarization by blocking potassium channels and activating inward
slow sodium current during (during repolarization).
 The drug of choice for atrial flutter but supplanted with ICD.

Question 20

what is sotalol (class 2 and 3)

Answer 20

This drug is a β-blocker that also blocks K+-channels.
torsade de pointes and A/Es of β-blockers. However, it has an overall
favorable A/E profile.

Question 21

what is amiodarone (class 1,2,3,4)

Answer 21

 Contains iodine and is related structurally to thyroxine.
 Shows class 1, 2, 3, & 4 actions. Its dominant effect is ↑ APD & ↑ refractory
period.

 Amiodarone also has antianginal effects.
• Side effects:
 Many, including hyperthyroidism & hypothyroidism because amiodarone
contains iodine in its structure, neuropathy, hepatotoxicity, constipation,
weight loss, optic neuritis, pulmonary fibrosis, blue-gray skin discoloration.
 Use of low doses and close monitoring reduce toxicity

Despite its adverse effect profile, amiodarone is the most commonly
employed antiarrhythmic and thought to be the least proarrhythmic of the
class 1 and 3 antiarrhythmic drugs.

• Interactions:
 Increases the activity of digoxin and warfarin (Amiodarone inhibits the
action of the cytochrome P450).
 .
 Coadministration of amiodarone with statins increases the risk of severe
muscle toxicity, kidney failure or liver disease.
 Cordarone® is pregnancy category D and is contraindicated during breast
feeding

Pharmacokinetics:
 Amiodarone has a long t1/2 of several weeks → full clinical effects may not
be achieved until 6 weeks after initiation of treatment. Loading dose is
given initially.

Question 22

what is Dronedarone (class 1,2,3,4)

Answer 22

 Like amiodarone, it has class 1, 2, 3, and 4 actions.
 Safer than amiodarone and does not have the iodine moieties responsible
for thyroid dysfunction, but may still cause liver failure.
 Less effective than amiodarone.

Contraindications:
 Many, including: permanent AF (patients in whom normal sinus rhythm
cannot be restored) and symptomatic heart failure.

Contraindications:
 Many, including: permanent AF (patients in whom normal sinus rhythm
cannot be restored) and symptomatic heart failure.

Question 23

what is class 4 of antiaaythmia drugs (Verapamil & diltiazem)

Answer 23

Ca+2 channel blockers

• Drugs block cardiac
Ca2+-channels they
decrease activity in
regions where the
spontaneous
depolarization of
phase 4 and phase 0 is
Ca2+-dependent, like
SA & AV nodes.
• Decreases
contractility and not
used for patients with
heart failure

 These drugs block voltage-dependent Ca2+-channels & therefore:
• slow phase 4 spontaneous depolarization in SA node → ↓ heart rate, which
is beneficial in atrial flutter & atrial fibrillation.
• Also slow conduction & prolong refractory period in AV node, because
action potential in AV node is also dependent on Ca2+, which is also
beneficial in atrial flutter & atrial fibrillation.

Verapamil & diltiazem are use-dependent → effective more when the heart
rate is abnormally high.

Question 24

what is digoxin ?

Answer 24

Digoxin decreases rate of conduction in AV node

Side effects:
 Digoxin can cause ectopic ventricular beats ventricular tachycardia or
ventricular fibrillation.

Question 25

what is Adenosine

Answer 25

 A naturally-occurring nucleoside.
 At high doses, adenosine affects AV node by hyperpolarization, ↓
automaticity, ↓ conduction velocity, & ↑ refractory period, but does not
convert atrial flutter or fibrillation to normal sinus rhythm.

 It is given IV.
 Vagal maneuvers (e.g., Valsalva maneuver), may be attempted prior to
Adenocard® administration.
• Side effects:
 facial flushing (18%) and shortness of breath.

Question 26

what is magnesium sulfate

Answer 26

The drug of choice for torsade de pointes and digoxin-induced
arrhythmias

Question 27

what is an Implantable cardioverter defibrillator (ICD)

Answer 27

 A small battery-powered electrical impulse generator that is implanted in
patients who have atrial arrhythmias or are at risk of sudden cardiac death
due to ventricular fibrillation and ventricular tachycardia. The device is
programmed to detect the arrhythmia and correct it by delivering a jolt of
electricity.
 Pacemakers are more often temporary and are generally designed to
correct bradycardia, while ICDs are often permanent safeguards against
sudden arrhythmias