ANS Pharm: CCBs Flashcards

1
Q
A

Diltiazem’s effects:

  • SA node: (-) chronotrope
  • AV node: (-) dromotrope
  • ♡ muscle: (-) inotrope
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2
Q

CCBs

Aside from (-) chronotropy & inotropy, what effects do they have?

A
  • (-) dromotrope (AV)
  • vasodilate
  • depress baroreceptors

some also dilate coronaries & inhibit coronary spasm

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3
Q
A
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4
Q

T/F:
CCBs cause more relaxation in veins than arteries.

A

False

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5
Q

Which CCBs are Class IV anti-arrhythmics?

A

verapamil
&
diltiazem

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6
Q

When do Ca channels open and close?

A

closed during relaxation

open via voltage gated or receptor mechanism

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7
Q
A
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8
Q

Heart & vascular
-the 2 types of Ca Channels
-which one does CCB work on?

A

Transient (T) & Long (L)

L

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9
Q

Aside from HTN and arrhythmias, what can CCBs treat?

A
  • PVD
  • cerebral vasospasm
  • angina
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10
Q

Which agents are best for:
-HR control
-contractility preservation
-HTN control

A

HR: verapamil & diltiazem

contractility: avoid verapmil; diltiazem ✅

HTN: nifedipine, nicardipine

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11
Q

coronary antispasmodic

A

nicardipine

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12
Q

CCBs that impair contractility greatest to least

A
  1. verapamil
  2. nifedipine
  3. diltiazem
  4. nicardipine

In a patient with decreased contractility, diltiazem is a better choice than verapamil.

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13
Q

the only CCB provn to reduce morbidity & mortality from cerebral vasospasm

A

nimodipine

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14
Q

T/F:
CCBs reduce preload and afterload.

A

False
preserve preload while reducing LV afterload

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15
Q

CCBs & baroreceptors

A

verapamil & diltiazem = (-) chronotropes
but
other CBs may increase HR due to baroreceptor reflex-mediated tachycardia
(often give w/ beta-1 antagonist)

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16
Q

highest degree of myocardial depression

A

verapamil

(angina, MI)

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17
Q

T/F:
Aside from verapamil & diltiazem, CCBs have little effect on SA & AV node suppression.

A

True

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18
Q

not a potent arterial vasodilator, but strong depressor of automaticity (chronotropy), conductivity (dromotropy), and myocardial contraction (inotropy).

A

verapamil

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19
Q

does not provoke increases in HR secondary to its vasodilator effect due to its depression of automaticity and conductivity.

20
Q

If an MI/angina patient cannot tolerate a B1B, what can we give?

21
Q

What EKG change would you expect with verapamil? why?

A

prolong PR

decreases SA discharge rate & AV conduction

22
Q

What rhythms can verapamil & diltiazem treat?

A
  • SVT
  • AFIB
  • Aflutter
23
Q

This CCB used with a B1B can cause complete heart block/profound depression

24
Q

verapamil dose

A

2.5 - 10 mg over 2 minutes

titrate!
significant patient variability

25
Q

Diltiazem triggers the baroreceptor response but HR still drops. Why?

A

potent negative chronotropic and dromotropic effects on SA and AV nodes

26
Q

diltiazem dose

A

0.25 - 0.35 mg/kg over 2 minutes

titrate!
significant patient variability

27
Q

This CCB is highly selective for arterial smooth muscle without negative
chronotropic or inotropic effects.

A

Clevidipine

no effect on preload
may increase CO

28
Q

clevidipine
HL

29
Q

T/F:
Expect reflex increase in HR with Clevidipine.

30
Q

Clevidipine
uses

A
  • IV short term BP control
  • acute HTN (pheochromocytoma & intracerebral hemorrhage)
  • controlled hypotension
31
Q

Dosing of clevidipine

A

highly variable,
but 1 - 2 mg/hr is common

HL is 2 mins so gtt

32
Q

This CCB is more lipophilic than others and crosses the BBB = cerebral arterial vasodilation

A

Nimodipine

33
Q

T/F:
Nimodipine can reverse cerebral vasospasm.

A

False

reduces manifestations of cerebral vasospasm
&
may reduce cerebral arteriolar
resistance and enhance collateral blood flow

34
Q

Reflex tachycardia is possible with these CCBs

A

nifedipine
nicardipine
clevidipine

35
Q

Nifedipine is used for essential HTN and dilates (arteries/veins/both)

A

arteries

no effect on venous tone

36
Q

best CCB for Raynaud’s

A

Nifedipine

37
Q

Can we give Nifedipine to an acute MI patient?

A

no

may worsen mortality

although its depressant effects are not seen at clinical doses

38
Q

give this CCB with a B1B to prevent reflex tachycardia

A

nifedipine

39
Q

T/F:
Most CCBs show patient variability, so titrate doses carefully.

40
Q

Nifedipine dose

A

0.5 mg/hr

titrate d/t varying response

41
Q

which has longer doA?
Nifedipine or nicardipine

A

nicardipine

*why its used for chronic HTN

42
Q

Dosing of nicardipine

A

5 mg/hr,

titrate (patient variability)

nifedipine: 0.5 mg/hr

43
Q

T/F:
Nicardipine dilates coronaries without negative inotropy.

A

True
very little/no depression

44
Q

Which CCB has least increase in coronary flow?

45
Q

T/F:
Nicardipine depresses the AV node

46
Q

Does diltiazem depress the myocardium?

47
Q
A

clevidipine