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CRAAB 3 > Nordgren: K and Ca Channel Blockers > Flashcards

Nordgren: K and Ca Channel Blockers Flashcards

1
Q

What is the goal of antiarrhythmic drugs?

A

To restore normal sinus rhythm and conduction or when that’s not possible prevent more serious arrhythmias.

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2
Q

How do antiarrhythmic drugs achieve the goal of restoring normal sinus rhythms?

A
  1. Decrease or increase conduction velocity (how fast membrane depolarizes)
  2. Alter the excitability of cardiac cells by changing the duration of the ERP (how long the AP)
  3. Suppress abnormal automaticity (spontaneous depolarization, pacemaker potential.)
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3
Q

What are class III drugs?

A

K channel blockers

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4
Q

What do K channel blockers specifically block?

A

The inward rectifier K channels (Kr)

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5
Q

Where do K channel blockers act on the AP?

A

Phase 3 (repolarization)

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6
Q

What does blocking phase 3 K channels do?

A

SLOWS repolarization thereby increasing the AP duration and the ERP

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7
Q

What does prolonging repolarization do to the QT interval?

A

Lengthens it! This prolongs the time that the cell is UNEXCITABLE.

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8
Q

Class III drugs are useful for what type of arhythmias?

A

Reentry arrhythmias

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9
Q

What is important to know about when thinking about contraindications Class III drugs?

A

Proarrhythmic as well as being antiarrhythmic

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10
Q

Why are class III drugs contraindicated in pts w/ long qt syndrome?

A

Prolonging the QT interval can produce torsades de pointes.

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11
Q

What drug is contraindicated in pts with heart block or SA node dysfunction? Why?

A

Amiodarone, because it has class IV effects that can cause bradycardia and AV block.

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12
Q

What are Class IV drugs?

A

Ca channel blockers

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13
Q

Where do class IV drugs act?

A

Bind to L type Ca channels on vascular smooth muscle, cardiac myocytes and SA/AV nodes.

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14
Q

What effect does Ca binding to channels located on vascular smooth muscle have?

A

Increases the influx of Ca into muscle cells–> stimulates smooth muscle contraction and cardiac myocyte contraction.

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15
Q

What does blocking Ca entry do to vascular smooth muscle?

A
  1. smth muscle relaxation (vasodilation)

2. decreased myocardial contractility.

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16
Q

What effect do class IV drugs have in cardiac myocytes?

A

Ca in flux slows the repolarization of the AP (plateau)

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17
Q

What does blocking Ca entry do in cardiac myocytes?

A
  1. shortens phase 2 of AP

2. Reduces force of contraction (less Ca available to bind troponin)

18
Q

What effect do Class IV drugs have in nodal cells?

A

L type Ca channels play an important role in pacemaker currents and in phase 0 of the AP.

19
Q

What does blocking Ca entry do in nodal cells?

A
  1. decreases HR

2. Decreases conduction velocity

20
Q

What are therapeutic indications for Class IV drugs?

A

Hypertension
Angina
Arrhythmias

21
Q

How do class IV drugs help hypertension?

A

Decrease systemic vascular resistance (TPR) through smooth muscle relaxation.

  1. Lowers arterial bp
  2. Primarily affects arterial vessels (pressure reservoir) rather than venous vessels (volume reservoir)
22
Q

What is the formula for resistance?

A

Resistance= 8Lη / πr4

23
Q

What is angina?

A

chest pain often d/t ischemia of the heart muscle

24
Q

Why are class IV drugs used for angina?

A

Cause vasodilation and decrease HR

25
Q

How does systemic vasodilation relieve angina?

A
  1. It reduces arterial P, which reduces the ventricular afterload, thus decreasing oxygen demand.
  2. A decrease in HR and contractility lead to decreased myocardial oxygen demand.
  3. Dilating coronary arteries and prevent/reverse coronary vasospasm, thereby increasing oxygen supply to the myocardium.
26
Q

Why are class IV drugs good for arrhythmias?

A
  1. Decrease pacemaker depolarization rate > good for ectopic foci that are causing aberrrant AP firing
  2. Decrease conduction velocity and prolong repolarization at the AV node (helps to block reentry mechanisms, which can cause SVT)
27
Q

How do subclasses of class IV differ?

A

In the specificity for cardiac vs. vascular L type Ca channels

28
Q

What are dihydropyridines?

A
  1. Smooth muscle selective class

2. Primarily used to reduce systemic vascular resistance and arterial pressure

29
Q

What are dihydropyridines used to treat and NOT used to treat?

A

Good for hypertension.

NOT good for angina b/c the vasodilator and P lowering effects can lead to reflex cardiac stimulation (tachycardia and increased contractility), which can dramatically increase myocardial oxygen demand.

30
Q

What are verapamil and diltiazem?

A

Non-dihydropyridines

31
Q

What is verapamil good for?

A

Relatively selective for myocardium, less effective as a systemic vasodilator drug.

*impt in treating angina nad arrhythmias by reducing myocardial oxygen demand and reversing coronary vasospasm.

32
Q

What is diltiazem good for?

A

An intermediate between verapamil and dihydropyridines its selective for vascular Ca channels. By having both cardiac depressant and vasodilator actions, it can reduce arterial pressure w/ out producing the same degree of reflex cardiac stimulation caused by dihyropyridines.

33
Q

What are the SE of dihydropyridines?

A
  1. Flushing, HA, excessive hypotension, edema and reflex tachycardia
  2. Activation of sympathetic reflexes and lack of direct cardiac effects (poor choice for angina)
34
Q

Why are long acting dihydropyridines safer antihypertensive drugs than anti-hypertensive drugs?

A

Because they have reduced reflex responses.

35
Q

What are the SE of non-dihydropyridine?

A

Excessive bradycardia, impaired electrical conduction (AV block), depressed contractility

36
Q

Pts w/ pre-existing bradycardia, conduction defects or heart failure caused by systolic dysfunction should NOT be given what drugs?

A

Ca channel blockers–especially the cardiac selective (non-dihydropyridines)

37
Q

Why should class IV drugs NOT be administered to pts being treated with a beta blocker?

A

Because those also depress cardiac electrical and mechanical activity–> augments effects of Beta blockade.

38
Q

What do K channel blockers do?

A

Class III

Increase AP duration and ERP

39
Q

What do Ca channel blockers do?

A

Class IV- Dihydropyridines vs. non

Promote vasodilation and delay depolarization of pacemaker cells

40
Q

What are two misc antiarrhythmics?

A

adenosine and digitalis

CRAAB 3 (7 decks)

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