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M2 Cardiovascular > Antiarrhythmics - Kwok > Flashcards

Antiarrhythmics - Kwok Flashcards

1
Q

What potassium current in particualr sets the resting potential?

A

Inward rectifying current (IK1)

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2
Q

During an AP, which channel opens first: Na+ or Ca2+? Which stay open longer?

A

First: Na+

Longer: Ca2+

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3
Q

Which part of the heart normally has the slowest rate of depolarization?

A

The SA node - the slow rate is the pacemaker!

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4
Q

Which part of the heart responds to rate-modifiers like catecholamines and ACh?

A

The SA node. Take home point: These compounds affect the pacemaker rate, but the rest of the heart propagates the action potential at the essentially the same speed.

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5
Q

Which cell type has a shorter Effective Refractory Period (ERP), Ventricular or SA Nodal?

A

Ventricular - the slow-response SA nodal cells have a delayed recovery.

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6
Q

Name the three main mechanisms of arrhythmias.

A

1) Increased automaticity (pathologically excitable cells)
2) Triggered automaticity (normal AP interrupted or followed by abnormal afterdepolarization)
3) Reentry (abnormal impulse conduction)

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7
Q

What three changes in the AP could one see with increased automaticity?

A

1) Phase 4 slope increased (faster rate of depolarization)
2) Threshold potential is more negative
3) Maximum diastolic potential is more positive (higher resting potential)

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8
Q

What are the two types of triggered automaticities?

A

1) Early afterdepolarizations (EADs) - interrupt repolarization
2) Late afterdepolarizations (DADs) - occur after repolarization

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9
Q

What factors exacerbate EADs?

What can occur from said exacerbation?

A

Exacerbated by slow rate, long QT syndrome (slow repolarization).

Can result in Torsades de Pointes

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10
Q

What factors exacerbate DADs?

What are common sources of these factors?

A

Exacerbated by fast rates, high intracellular Ca2+

Results from digitalis toxicity, catecholamines, ischemia

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11
Q

What factors of a heart block are critical in causing a reentry arrhythmia?

A

1) A unidirectional block

(allows retrograde but not orthograde propagation)

2) Critical timing & the ERP of the normal tissues

(for a reentry loop to propagate, the retrograde AP must have the proper timing so that it reaches the normal tissue when it is in an excitable state)

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12
Q

What are four ways in which antiarrhythmic drugs reduce spontaneous discharge in autonomic tissues.

A

1) Decreased phase 4 slope
2) Increased threshold potential
3) Increased maxmimum diastolic potential (resting potential)
4) Increased action potential duration

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13
Q

What is the action of Class I antiarrhythmic drugs?

What are the differences between Class 1A, 1B, and 1C?

A

Sodium channel blockers

1A, 1B, and 1C vary by their effects on 1) phase 0, 2) speed of conduction, and 3) speed of repolarization

1A: MODERATE phase 0 depression & slowed conduction. PROLONG repolarization.

2A: MINIMAL phase 0 depression & slowed conduction. SHORTEN repolarization.

3A: MARKED phase 0 depression & slowed conduction. LITTLE EFFECT on repolarization.

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14
Q

Name 3 Class 1A drugs, one Class 1B drug, and one Class 1C drug.

A

1A: Quinidine, Procainamide, Disopyramide

1B: Lidocaine

1C: Flecainide

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15
Q

What is the action of Class II antiarrhythmic drugs?

Name some examples.

A

Beta-adrenergic blockers.

Propanolol, esmolol, metoprolol

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16
Q

What is the action of Class III antiarrhythmic drugs?

Name three examples.

A

Potassium channel blockers (prolong repolarization)

Amiodarone, sotalol, dofetilitde

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17
Q

What is the action of Class IV antiarrhythmic drugs?

A

Calcium channel blockers

Verapamil, Diltiazem

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18
Q

What type of cells do Class I drugs target?

A

Fast-response cells that rely on Na+ influx for the AP (aka not nodal cells)

19
Q

What effects on the AP are common to all subtypes of Class I antiarrhythmics?

A

1) Increased AP threshold
2) Decreased Vmax

20
Q

What are Class 1A drugs used to treat?

What are major side effects of Class 1A drugs? (esp. Quinidine)

A

Treat: Atrial flutter & fibrillation, prevention of Vent. tachy & fibrillation

S/E: Delayed repolarization can cause EADs (contraindications for pts with elongated QT)

Vagolytic effect (inhibit vagus nerve regulation of heart)

Can be proarrhythmic!

Severe diarrhea, cramps

P450 inhibition

Increases plasma digitalis levels (reduces renal clearance)

21
Q

What are Class 1B drugs used to treat?

What are major side effects of Class 1B drugs?

A

Treat: Vent. tachy, digitalis-induced arrhythmias

S/E: Dizziness, seizures

Note: Decreases ERP, so safe for pts with long QT

22
Q

What are Class 1C drugs used to treat?

What are major side effects of Class 1C drugs?

A

Only used in life-threatening situations when the arrhythmia has proven refractory to other drugs

Flecainide was shown to be markedy pro-arrhythmic in the CAST trial, especially in pts with structual heart diseases. The drug has largely fallen out of use.

23
Q

What is the main action of Class II agents on the AP?

A

Slow the rate of diastolic depolarization (phase 4), so reaching the threshold potential is delayed. In this way, they directly oppose the actions of endogenous catecholamines.

24
Q

What are the kinetic and administration differences between propanolol and esmolol?

A

Propanolol: Long acting. Given orally.

Esmolol: Short acting. Given IV.

25
Q

What conditions are Class II agents used to treat?

A

ALL atrial arrhythmias, ventricular tachycardia and fibrillation.

26
Q

How safe are Class II agents?

What side effects do they have?

A

Best safety record and wide clinical applications make beta blockers the most useful antiarrhythmic drugs available. Also do not prolong repolarization, so safe for pts with Long QT.

S/E: Negative inotropic effect. Heart block, bradycardia, bronchospasm.

27
Q

Which potassium channel is the most common target for Class III agents?

How do these agents affect the AP?

What is an obvious side effect of this?

A

Channel: IKr (hERG channel)

AP: Prolongs repolarization (& thus overall AP duration)

S/E: Increased ERP (risk for EADs)

28
Q

Compare Amiodarone and Sotalol. Both have multiple actions - which drugs blocks what?

A

Ami: Potent K+ blocker, modest Na+, Ca2+, and beta blocker.

Sot: Major effect is K+ blocker, some beta blocking.

29
Q

Compare Amiodarone and Sotalol. What are their uses?

A

Ami: Vent. tachyarrhythmias & fibrillation, PREVENTION of recurrent paroxysmal atrial fibrillation & flutter

Sot: Vent. tachyarrhythmias & fibrillation, also supraventricular tachycardias, atrial fibrillation

30
Q

Compare Amiodarone and Sotalol. What are the side effects of each?

A

Ami:

Triggered arrhythmias (EADs), but RARELY with Torsades de Pointes.

Inhibits T4→T3: hypothyroidism.

Often irreversible pulmonary fibrosis.

Sot:

Triggered arrhythmias (EADs), WITH Torsades de Pointes!

31
Q

What is a U wave on ECG thought to represent? Under what conditions are prominent U waves sometimes seen?

A

Thought to represent repolarization of papillary muscles or Purkinje fibers.

Seen in hypokalemia, hypercalcemia, Long QT syndrome, and sometimes during use of digitalis, epinephrine, Class IA agents, and Class III agents.

32
Q

What are the major effects of Class IV agents on the AP?

Again, what cells are expected to be affected by calcium channel blockers?

A

AP: Increase threshold, increase refractory period, depress conduction velocity

Cell type: SA and AV nodal cells

33
Q

What is the major antiarrhythmatic use of Class IV agents?

What are they rarely ever used for?

A

Major use: Atrial tachycardias, esp. paroxysmal supraventricular tachycardia

Rarely ever: Ventricular tachycardias

34
Q

Class IV agents have several side effects. Name 4 that are specific to the cardiovascular system.

A

1) Negative chronotrope → decrease SA automaticity → bradycardia
2) Negative inotrope (Decreased Ca2+ influx during plateau phase of ventricular AP)
3) Hypotension (Decreased Ca2+ influx into vascular SMCs)
4) Direct interactions with digitalis to slow conduction velocity in the AV node → HEART BLOCK (mostly Verapamil & Diltiazem)

35
Q

Class IV agents have several side effects. Name 3 that affects systems OTHER than the cardiovascular system.

A

1) Peripheral edema (mostly Nifedipine-type)
2) Constipation (decreased Ca2+ influx into intestinal SMCs) (especially Verapamil)
3) Increase plasma digitalis levels by competing for RENAL excretion (Verapamil & Diltiazem)

36
Q

What is the mechanism of action of Adenosine as an antiarrhythmic? What is its major use?

A

VERY RAPIDLY activates K+ channels to slow phase 4 depolarization at the AV node

BLOCKS cAMP-enchanced Ca2+ channel activity in AV node

Use: Supraventricular tachycardia (slows AV conduction & HR)

37
Q

What is the half life of adenosine?

A

Under 10 seconds (!)

38
Q

What type of drug is digoxin?

What is its mechanism of action?

What is it used to treat?

A

Type: Digitalis Glycoside

Mechanism: Enchances Vagal parasympathetic activity (Vagal tone) to slow conducion in the AV node.

Use: Atrial fibrillation & supraventricular tachycardia

39
Q

What type of arrhythmia is often indicated by an irregularly irregular heart rhythm?

A

Atrial fibrillation

40
Q

What would the a good drug choice for treating AV nodal reentrant tachycardia?

A

Adenosine, but other options are possible

41
Q

What does AV nodal reentrant tachycardia appear like on EKG?

A
  • No P waves (QRS→T→QRS→T→QRS→etc.)
  • Vfib
  • Regular rhythm
42
Q

In general, what classes of antiarrythmics are the best choices for a patient with long QT syndrome?

A

Class II - Beta blockers! They do not increase ERP and thus do not increase the risk of EADs.

Class 1B drugs may also be useful depending on the arrhythmia being treated, because they decrease the ERP

43
Q
A

M2 Cardiovascular (40 decks)

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