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SRNAPharmacology I > Calcium Channel Blockers > Flashcards

Calcium Channel Blockers Flashcards

1
Q

Negative chronotrope

A

Esmolol
Verapamil
Metoprolol

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2
Q

Negative DROMOTROPE

A

Esmolol
Verapamil
Diltiazem

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3
Q

Will cause Coronary vasodilation

A 
Verapamil
Clevidipine
Diltiazem
Nisoldipine
Nifedipine
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4
Q

Most likely to cause both hypotension and reflex tachycardia

A

Nifedipine

Nicardipine

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5
Q

Verapamil and diltiazem slow HR by working on what phase of the SA node action potential?

A

phase 4 depolarization of the SA node action potential

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6
Q

Calcium channel blockers work on what phase of ventricular action potentials?

A

phase 2 (plateau phase)

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7
Q

Calcium channel blockers are grouped these agents

A

Structurally unrelated drugs that have fundamental differences.

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8
Q

Calcium ions play a key role in

A

electrical excitation of cardiac conducting cells (Sa/AV nodes)
Contractility of cardiac myocytes, smooth msucel (Vascular smooth muscle tone ) and skeletal tone.

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9
Q

except for _____ and _____

A

Diltiazem
NIfedipine
all currently available are given as racemic mixtures.

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10
Q

Chemical structure classification

A

Non-dyhydropyridines (Non-DHP)

Dihydrophyridine (DHP)

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11
Q

Non DHP everything else DHP

A

Verapamil

Diltiazem

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12
Q

All CCB can cause

A

Hypotension
Peripheral EDEMA
GINGIVAL HYPERPLASIA

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13
Q

Non DHP cause in addition to All CCB effect

A

Bradycardia
AV block
Systolic HF.

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14
Q

DHP can cause

A

REFLEX TACHYCARDIA

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15
Q

DHP will never cause what?

A

BRADYCARDIA

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16
Q

ALl CCB have their one binding site of

A

on the alpha 1 subunit “L-type” voltage gated calcium channels and inhibit the trans-membrane influx of calcium into cells through the slow voltage-gated calcium channels and thus DECREASE INTRACELLULAR CALCIUM

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17
Q

***** MECHANISM Of ACTION (MEMORIZE) what dictates pharm response

A

Non DPH
Inhibit transmembrane influx of calcium into arterial vascular smooth muscle cardiac muscle cells and cardiac conduction cells (SA/AV nodal tissue( but are more selective for myocardial tissue calcium channels (especially in AV Nodal tissue)

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18
Q

***** MECHANISM Of ACTION (MEMORIZE) what dictates pharm response

A

DPH
Inhibit the transmembrane influx of calcium ions into arterial smooth muscle and cardia muscle cells, with a far greater effect on arterial vascular smooth muscle cells than on CARDIAC muscle cells
DO NOT ACT on nodal CELLS/tissues

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19
Q

Can you use non-DHP in HF decreased EF

A

Yes/NO

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20
Q

Non DHP CCBs

A 
Verapamil
Diltiazem (class IV antiarrhythmics)
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21
Q

**Verapamil is the _______Agent
Binds to where ?
What is meant by use dependence?

A

ONLY phenylalkylamine agent

binds to intracellular portion of the L type channel alpha 1 subunit preferentially when it is open and occludes the channel
USE dependence or frequency dependence –: which means that calcium channel blockade by verapamil is enhanced as the frequency of stimulation increase.

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22
Q

Verapamil is the most potent and is

A

relatively selective for inhibiting the transmembrane influx of Ca2 in the Sa/AV nodal tissue and cardiac muscle

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23
Q

****Verapamil and diltiazem

A

verapamil more potent negative chronotropic, inotropic and dromotropic agents than diltiazem

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24
Q

What is blunted by verapamil?

A

Reflex sympathetic tachycardia (verapamil causes peripheral vasodilation which decrease blood pressure which triggers the baroreceptor reflex response but the reflex tachycardia is blunted by the direct negative chronotropic effects of verapamil

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25
Q

Diltiazem is the only

A

Benzothiazepine agent
binds to inner surface o the cell membrane of the l type channel alpha 1 subunit (BINDS TO A DIFFERENT SITE THAN VERAPAMIL DOES)
Much better blockade is enhanced as the frequency of alpha increases

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26
Q

Benzothiazepine CCBs relatively

A 
Relatively selective for inhibiting the transmembrane influx of CA2+ in the SA/AV node tissue and cardiac muscle, especially in AV nodal tissue
LESS POTEN as a peripheral vasodilator than 1, 4 dihydropyridine class CCBs and verapamil
Less potent drom, chrono, and inotropic agents
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27
Q

HR

myocardial contractility

A

nodal tissue

conducting tissue

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28
Q 
Non DHPs produce 
arterial vascular smooth muscle
AFFECT PRELOAD Y/N ?
\_\_\_\_\_\_\_Coronary vascular resistance
\_\_\_\_\_\_\_\_ coronary blood flow
\_\_\_\_\_\_\_ O2 supply myocardial and decrease demand.
A 
arterial vascular smooth muscle
DOES NOT AFFECT PRELOAD
decreased Coronary vascular resistance
increases coronary blood flow
Increase O2 supply myocardial and decrease demand.
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29
Q

Verapamil is the

A

prototype non dhp
L-enantimor of verapamil is a specific and potent L type CCB
D-enantiomer is devoid of CCB activitly but posees blockage of fast NA channels,
Weak alpha blocking agents.

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30
Q

** Clinical uses of VERAPAMIL

A

To convert:
SVTs
PSVT: rapid conversion to SR, or Paroxysmal SVT

To control HR in (NOT CONVERSION)
Atrial fib
Aflutter with RVR

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31
Q

Can decrease uterine blood flow

A

VERAPAMIL

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32
Q 
Absorption is  (verapamil)\_\_\_\_\_\_%
onset \_\_\_\_\_\_minutes 
PROLONGED in \_\_\_\_\_\_\_\_
\_\_\_\_\_\_\_protein binding 
CYP 450 enzymes dependent Y/N\_\_\_\_
Dependent on liver blood flow Y/ N\_\_\_\_
A 
greater than 90%
onset 1-3 minutes
PROLONGED in liver disease (metabolism)
Highly protein binding
CYP 450 enzymes dependent
Dependent on liver blood flow
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33
Q

Active metabolite of verapamil

A

N-demethylation
active metabolite NORVERAPAMIL
may accumulate in patients with renal insufficiency (adjust dose for renal failure)

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34
Q

Verapamil dosing

A

5-10 mg IV , over AT LEAST 2 minutes

Repeat after 30 minutes

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35
Q

Liver patients with verapamil?

geriatric

A

cut the dose in half.

give over 3 minutes

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36
Q

Adverse effects of VERAPAMIL with IV dose not PO

A

HYPOTENSION

2nd and 3rd AV block

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37
Q

Do not give verapamil or Cardizem with diazepam

A

bound highly to protein.

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38
Q

Major adverse effects of verapamil

A

Hypotension

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39
Q

With protein binding whatever is in the tank first

A

What protein bind drug is there first

40
Q

Verapamil diazepam with local anesthetics

A

they also have local anesthetics activity , may be additive to local anesthetics

41
Q

Drug to drug interactions

A

drugs that decrease hepatic blood flow

42
Q

Verapamil and diazepam

Do not give with EF less than 40%

A

Can increase sedative effectiveness

if patient is on midazolam first, and you add verapamil will increase midazolam

43
Q

1,4-Dihydropyridines CCB’s

A

Are referred to as “Arterial vascular smooth muscle selective” agents

44
Q

Pharmacological effects dihydropyridines

A

these agents exhibit little to no negative

inotropic clinical effects

45
Q

Ok to give DHPs in patients with

A

LV dysfunction to manage BP not HF

46
Q

DHP do not have

A

negative dromotrope and chronotrope

no use dependence

47
Q

DHPs use for anesthesia providers

A
  • Treatment of hypertensive crisis
  • Hypertensive urgency – oral agents
  • Hypertensive EMERGENCY ALWAYS IV – IV agents (end organ emergencies) –> End Organ damage damage.
48
Q

Emergency vs urgency

A

End organ damage (headaches, chest pain)

49
Q

Nifedipine :

A

will be on boards, stink

50
Q

Nifedipine is a

A

1st generation DHP prototype, short acting

51
Q

Nifedipine has a greater

A

Has greater coronary and peripheral artery vasodilator properties than verapamil or diltiazem

52
Q

Oral DHP nifedipine has :

A

lot of side effects and is not the preferred medication. \
Peripheral edema
Reflex tachycardia
Flushing

53
Q

*****IMMEDIATE release nifedipine can cause

A

can cause life threatening Ischemia
Induces reflex tachycardia
Decrease coronary renal and cerebral perfusion
Increased myocardial O2 demand

54
Q

NEVER use

A

SL or IR nifedipine

55
Q

Nimodipine is a

A

DHP agent that is available oral capsule or liquid solution

56
Q

Unique calcium channel blocker only use in one area? why?

A

Nimodipine; crosses BBB and HIGHLY LIPID SOLUBLE.

57
Q

Nimodipine has:

Only use in ?

A
  • greater effect on cerebral arteries than on arteries elsewhere.
  • To improve neurological outcomes with patient with SAH or other brain injuries (craniotomy)
  • Prevent further BRAIN DAMAGE
58
Q

Nimodipine you cannot

A

skip doses, worsens patient outcomes

59
Q

NIMODIPINE GIVEN how frequent?

A

EVERY 4 hours, and INTRAOP

60
Q

• Nimodipine Oral dose

A

Dose: 60 mg PO or NG/Gastric tube q 4 hours x 21 days

61
Q

Nimodipine if unable to give IV

A

In patients who cannot take oral medications, the contents of the nimodipine capsules have to be extracted and placed in a syringe and administered via nasogastric or gastric tube

62
Q

Nicardipine is a ______generation DHP and more selective for blocking ____________

A

2nd generation DHP , more selective for blocking vascular smooth muscle
Good antihypertensive

63
Q

Prominent coronary and cerebral vasodilating activities.

A

Nicardipine

64
Q

Not associated with bradycardia or REBOUND HTN

A

Nicardipine (can just turn off)

65
Q

Does nicardipine cross BBB? increase ICP?

A

Yes; no

66
Q

Nicardipine undergo

A

Extensive first pass metabolism

67
Q

Onset IV nicardipine

A

5 mns

68
Q

Contraindications for Nicardipine

A

Advanced Aortic Stenosis

Since afterload reduction can be expercted to reduced myocardial oxygen delivery

69
Q

Nicardipine with HF EF <40

A

Titrate slowly, use with caution in patient with LV dysfunction

70
Q

Clevidipine and nicardipine

A

same effects

The first 3rd generation IV DHP CCB

71
Q

Clevidipine is Fast /slow?

A

ultra fast onset and offset
Arterial specific vasodilating effect
Use for acute HTN

72
Q

Clevidipine is a

A

racemix mixture

73
Q

Clevidipine and all other CCB

A

reduce gastric emptying.

74
Q

How does prevent gastric emptying

A

smooth muscle require calcium to contract

CCB block calcium therefore can impair contraction of smooth muscle.

75
Q

Clevidipine is the
_______Acting
onset ______
offset of effect?

A

fastest acting
onset 2-4 min
offset of effect 15 minutes

76
Q

Clevidipine Pharmacokinetics

A

Metabolism & Excretion
• Rapidly metabolized by hydrolysis of the ester linkage, primarily by nonspecific esterase’s in blood and extravascular tissues, making its elimination unlikely to be affected by hepatic or renal dysfunction
• The primary metabolites are a carboxylic acid metabolite and formaldehyde, which are inactive

77
Q

bonus: Formaldehyde is a

A

carcinogen, embaulming fluid

-

78
Q

Looks like propofol

A

Clevidipine
Is a water-insoluble drug that is available only as a lipid
emulsion dosage form
• Certain patients with disorders of lipid metabolism can not
receive this drug or the drug needs to be used with extreme
caution

79
Q

Allergic to egg and soy do not give

A

Clevidipine

80
Q

Severe aortic stenosis do not give

A

Clevidipine.

81
Q

Clevidipine can cause

A

rebound HYPERTENSION

wean them off

82
Q

Do not give clevidipine to patient with this deficiency?

A

pseudocholinesterase deficiency
Esterase enzyme that breaks down clevidipine, therefore the patient with this genetic disorder will not be able to metabolize and clear clevidipine.

83
Q

When do you SL nifedipine?

A

Never

SL nifedipine, intraoperative MI when hemodynamics are normal

84
Q

NonDHP

A

Can be used for

85
Q

DHPs NEVER DECREASE

A

HR; Only block L type in arterial vascular smooth muscle, BUT TO a LESSER degree cardiac muscle cells.
Inhibit transmembrane influx of calcium ions into arterial vascular smooth muscle

86
Q

Mechanism of action of the 3 classes of

A

KNOW chart

87
Q

DHP are more selective than the

A

nonDHP on arterial vascular smooth muscle better at lowering BP
Adverse effects; PERIPHERAL ADVERSE EFFECT much high in NON-DHP.

88
Q

Using DHP for clinical indications

A

for

89
Q

1, 4 dihydropirine d

A

Decrease SVR
sufficient Active baroreceptor reflex mediate increase in sympathetic tone to overcome their negative inotropic effect.
No massive decrease

90
Q

Verapamil - Drugs to drug interactions: with DIAZEPAM

A

What drug is bound first (which was bound to the protein first)
- if patient on verapamil or diltiazem already, and you give diazepam –> Diazepam will start to compete with diltiazem, increase unbound portion then lead to increase effect of diltiazem or verapamil.

  • if patient on diazepam already, and you give diltiazem or verapamil doses, can kick of diazepam off binding site, –> prolonged effect of diazepam.
91
Q

Diazepam and midazolam

A

can increase sedative effect of midazolam

92
Q

Diazepam and midazolam

A

can increase sedative effect of midazolam

3-4 folds increase in concentration midazolam and half life was increase, leading to decrease clearance.

93
Q

on what tissue does verapamil work?

A

Cardiac

94
Q

CV effect of nitroglycerin are

A

dose dependent

at some dose you will start to arterial

95
Q

The primary metabolites of CLEVIDIPINE are a ___________and ______which are

A
  • carboxylic acid metabolite
  • formaldehyde

inactive

SRNAPharmacology I (29 decks)

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