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CVPR - CV Unit 1 > Arrythmias & Anti-arrhythmia drugs > Flashcards

Arrythmias & Anti-arrhythmia drugs Flashcards

1
Q

Class I drugs - Mechanism

A

Class I anti-arrhythmic drugs block cardiomyocyte Na+ channels and are use-dependent, such that they preferentially block over-active channels

Act to decrease conduction velocity and increase refractory period thereby blocking re-entry arrythmias

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2
Q

Class Ia drugs - Example

A

Procainamide

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3
Q

Class Ia drugs - mechanism

A

Moderate class I action (use-dependent Na+ channel blocking) with a moderately slowed upstroke (extended phase 1)

Some class III action - block K+ channels leading to slower repolarization and longer Na+ channel inactivation, leading to a longer refractory period (extended phase 2)

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4
Q

Class Ib drug - Example

A

Lidocaine

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5
Q

Class Ib drugs - mechanism

A

Mild Class I action

No significant slowing of Na+ dependent upstroke - no effect on conduction

Increases refractory period

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6
Q

Class Ic drugs - 2 examples

A

Propafenone

Flecainide

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7
Q

Class Ic drugs - mechanism

A

Pronounced Class I effect (use-dependent blocking of Na+ channels) producing significantly slowed upstroke (extended phase I)

Mild prolongation of phase 2

Net effect is decreased conduction speed and prolongation of tissue refractory period

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8
Q

Class II drugs - 1 examples

A

Beta blockers:

Metoprolol

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9
Q

Class II drugs - mechanism

A

Block signaling through the B-adrenergic receptor; decreases L-type Ca2+ current, If, and Iks leading to reduction in rate of diastolic depolarization in pacing cells, reduced upstroke rate, and slowed repolarization in AV nodal cells

Net effect is slowed pacing (decreased HR) and decreased conduction through AV node

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10
Q

Uses of B-blockers in treating arrythmia

A

Arrythmias that involve AV nodal re-entry

Controlling ventricular rate during atrial fibrillation

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11
Q

Class III drugs - 2 examples

A

Amiodarone

Ibutilide

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12
Q

Class III examples - mechanism

A

Block K+ channels leading to prolongation of phase 2 (extended duration of repolarization) as well as elongated refractory period via increased inactivation of Na+ channels

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13
Q

Amiodarone

A

Class III drug

Blocks K channels (Class III mechanism) but also decreases conduction velocity and increases refractory period by blocking Na+ channels; also decreases rate of diastolic depolarization (phase 4) in automatic cells, reducing pacing rate

Risk of prolonged QT interval / Torsades
Treatment of Ventricular Tachycardia

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14
Q

Sotalol

A

Class III drug

Blocks K+ channels (Class III mechanism) but also has some B-blocker activity

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15
Q

Class IV drugs - 2 examples

A

Verapamil

Diltiazem

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16
Q

Class IV drugs - mechanism

A

Use-dependent blockers of L-type Ca2+ channels, especially in nodal cells

Blockage of Ca2+ channels in nodal cells causes slowed upstroke and reduced pacing; indirectly causes slower repolarization (increased refractory period) because reduced AP amplitude activates fewer K+ channels

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17
Q

Adenosine - mechanism

A

Adenosine acts via the A1 receptor at the AV node; the A1 receptor is Gq-linked, which down regulates adenylyl cyclase and cAMP activity; decreased PKA-mediated phosphorylation increases K1 current which hyperpolarizes the AV node, and decreases phase 0 Ca2+ current

Inhibits AV nodal conduction with increased refractory period

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18
Q

Procainamide - Details

A

Class Ia drug

Side effects: Lupus syndrome (1/3 of all patients on long-term therapy)

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19
Q

Lidocaine - Details

A

Class Ib drug

Least cardiotoxic agent of all Class I drugs

Side effects: paresthesia, tremors, seizures, agitation, confusion

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20
Q

Esmolol - Details

A

Class II

Half life of 10 minutes

Side effects: hypotension, bronchospasm, impotenence

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21
Q

Amiodarone - Details

A

Class III

Long and highly variable half life (13-100 days)

Side effects: bradycardia, heart block, thyroid dysfunction, corneal deposits, pulmonary fibrosis, skin discoloration

22
Q

Verapamil - Details

A

Class IV

Half life of 7 hours

Side effects: hypotension, negative cardiac inotropy

23
Q

Adenosine - Details

A

Half life of 10 sec; given as IV bolus

Side effects: flushing, chest burning and SOB

24
Q

Long QT Syndrome - Definition

A

Prolongation of the ventricular depolarization/repolarization cycle - can lead to arrythmias and sudden death

25
Q

Torsades de pointes

A

Ventricular tachycardia caused by prolongation of phase 2 of the ventricular myocyte AP; often stimulated by an abrupt increase in sympathetic tone (excitement, fright, exercise)

Can degenerate into ventricular fibrillation followed by syncope and sudden death

26
Q

Romano-Ward Syndrome (RWS)

A

Autosomal dominant form of familial long QT syndrome - genetically heterogenous, caused by mutations in the slow cardiac K+ channel, the rapid cardiac K+ channel, and the cardiac Na+ channel

27
Q

LQT1 Syndrome

A

Caused by mutations that reduce the number of slow cardiac K+ channels

Reducing the size of the K+ current that helps return the membrane to resting potential during diastole

28
Q

LQT2 Syndrome

A

Caused by mutations in the rapid cardiac K+ channels

Reduces the size of the K+ current that helps return the membrane to resting potential during diastole

29
Q

LQT3 Syndrome

A

Caused by mutations that prevent Na+ channels from inactivating completely (gain of function) thereby prolonging phase 2 of the AP

30
Q

Jervell-Lange Nielson Syndrome (JLNS)

A

Autosomal recessive form of long QT syndrome

Homozygous mutation in the slow cardiac K+ channel, also associated with deafness

Heterozygotes are asymptomatic

31
Q

Brugada syndrome

A

Caused by heterogenous mutations in the cardiac Na+ channel; end result is reduction in magnitude of L-type Ca2+ current (decreased duration of plateau) with shortened QT interval

Only 40% survival by 5 years due to ventricular fibrillation

32
Q

Early Afterdepolarization (EAD)

A

Caused by re-activation of L-type Ca2+ channels in response to elevated Ca2+ concentrations within the cell

Prolongation of phase 2 (long QT) contributes to elevation of inward Ca2+ current, resulting in EADs

33
Q

Delayed afterdepolarization (DAD)

A

Initiated by elevated inward Ca2+ current which activates the NCX channel, bringing in more depolarizing Na+ current; if this current allows the cell to reach threshold it can initiate another AP, usually during early phase 4

34
Q

2 conditions of re-entrant arrythmias

A
  1. Uni-directional conduction block in a functional circuit

2. Conduction time around the circuit must be longer than the refractory period just proximal to the blocked portion

35
Q

2 strategies for treating re-entrant arrythmias

A
  1. Convert a unidirectional block to a bi-directional block
  2. Prolong refractory period of tissue proximal to the block so that the conduction velocity around the circuit is faster than the refractory period
36
Q

Brady-Tachy

A

Intermittent episodes of slow and fast rates from the SA node

Treated by withdrawal of causative agent (i.e. sometimes Beta Blockers) or pacemaker

37
Q

1st Degree AV Block

A

All P waves conduct to QRS waves but the conduction is delayed with a PR interval > 0.2 s

Caused by disease in the AV node or His-Purkinje system

38
Q

Second degree AV block - Mobitz I

A

AKA Wenckebach

Progressive prolongation of PR interval until finally a P wave occurs which is not followed by QRS; the QRS is “dropped”

Block usually occurs within the AV node

39
Q

2nd degree AV block - Mobitz II

A

Some but not all P waves are followed by QRS; PR interval is of constant length

Block is usually below the AV node in the His-Purkinje system; this is a less stable rhythm than Mobitz I

40
Q

3rd degree (complete) AV block

A

No association between P and QRS waves; both have a regular rate and rhythm but they are not coupled and P rate > QRS rate

Ventricular escape rhythm may be too slow to support adequate CO, indicating treatment with dopamine or isoproterenol (AV chronotropes) or pacemaker

41
Q

Atrial flutter

A

Prototypical re-entrant arrhythmia caused by re-entry around the cavotricuspid isthmus

P waves flutter at a rate of 240-320 bpm in a “saw tooth” pattern; ventricle contracts rapidly at a ratio of 2:1, 3:1, or 4:1 atrial contractions per ventricular contraction

Treated with electrical cardioversion (50% recurrence rate over 12 months) or ablation (98% success rate)

42
Q

Atrial fibrillation

A

Most common arrhythmia in the US

Characterized by irregularly irregular QRS waves without P waves; may show undulating baseline

Treatment: anticoagulation, rate control with B-blockers or Verapamil/Diltiazem, cardioversion, ablation

Treated with B-blocker, Ca2+ channel blocker with negative chronotropic effects (Verapamil, Diltiazem), or Digoxin to slow rapid ventricular rate and improve diastolic LV filling

Patients are at risk for atrial clot - must be anti-coagulated!

43
Q

Premature Ventricular Contraction (PVC)

A

Occasional early, wide QRS complexes are present without preceeding P wave

44
Q

Ventricular Tachycardia

A

Caused by an ectopic ventricular focus conducted by contractile ventricular myocytes

Wide, regularly, usually fast QRS mostly without visible P waves

Ventricular fill time is insufficient leading to loss of CO; may deteriorate into ventricular fibrillation

45
Q

Ventricular fibrillation

A

No consistent QRS or P waves are present; represents no coordinated contraction of the heart - this pulse has no blood pressure

ECG shows wavy baseline only

Requires emergency electrical cardioversion

46
Q

Atrial premature beats

A

Occasional early QRS complexes are present and preceeded by an abnormal P wave

Usually benign

47
Q

Atrial tachycardia

A

Abnormal, fast P waves (160-220/min) that are followed by QRS complexes

Treatment: Adenosine, vagal maeuver, Beta blocker, Verapamil/Diltiazem, ablation

48
Q

Junctional Rhythm

A

No P waves but QRS complexes are present with a regular rhythm and flat baseline

49
Q

Mechanism of cardiac glycoside action in anti-arrhythmia

A

Digitalis enhances vagal tone and reduces sympathetic activity; as a result, it decreases the frequency of transmission of atrial impulses through the AV node to the ventricles

Beneficial in reducing the rate of ventricular stimulation in patients with rapid SVTs (atrial fibrillation, atrial flutter)

50
Q

Chronotropic agents

A

Atropine
Dopamine
Epinephrine

Useful for treatment of AV block by increasing phase 0 slope in nodal tissue

51
Q

Appropriate use of B-blockers in CHF

A

Started after patient is stable on ACEI - low dose titrated to goal dose

Antagonizes effect of SNS plus anti-remodeling effect

Relative to ACE inhibitors, may exacerbate heart failure in the short term but long-term improvement in LV function and survival are dose-dependent

CVPR - CV Unit 1 (13 decks)

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