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CRNA Pharmacology > Calcium Channel Blockers > Flashcards

Calcium Channel Blockers Flashcards

1
Q

Phenylalkylamines

A

Verapamil

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2
Q

Benzothiazepines

A

Diltiazem

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3
Q

1,4-Dihydropyridines

A 
Nifedipine (Procardia®)
Nicardipine (Cardene® I.V.,Cardene® SR) Nimodipine (Nimotop®)
Felodipine (Plendil®)
Isradipine (DynaCirc®)
Nisoldipine (Sular®)
Amlodipine (Norvasc®)
Clevidipine (Cleviprex®)
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4
Q

Calcium Channel Blockers

Class Adverse Effects

A

hypotension, peripheral edema, flushing, headache, dizziness, fatigue and gingival hyperplasia

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5
Q

Non-dihydropyridine agents can also cause

A

– bradycardia, AV block, systolic heart failure

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6
Q

Dihydropyridine agents can also cause –

A

reflex tachycardia

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7
Q

How are CCBs classified

A

into different groups based upon their chemical structure with each group differing in their pharmacology

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8
Q

Calcium Channel Blockers

Mechanism of Action

A

ALL CCB’s bind to their own unique receptor site on the α1 subunit of “L-Type” voltage-gated calcium channels and inhibit the transmembrane influx of calcium into cells through these slow voltage-gated calcium channels and thus decease intracellular calcium

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9
Q

How do CCBs differ in their tissue selectivity

A

CCB’s differ in their tissue selectivity, binding-site locations on the α1 subunit, and their mechanism of calcium conductance blockade

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10
Q

Non-Dihydropyridine calcium channel blockers MOA

A

nhibit the transmembrane influx of calcium ions into arterial vascular smooth muscle, cardiac muscle cells and cardiac conducting cells (SA/AV nodal tissue) BUT are more selective for myocardial tissue calcium channels (especially in AV nodal tissue)

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11
Q

1,4-Dihydropyridine calcium channel blockers MOA

A

Inhibit the transmembrane influx of calcium ions into arterial vascular smooth muscle and cardiac muscle cells, with a far greater effect on arterial vascular smooth muscle cells than on cardiac muscle cells

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12
Q

Verapamil MOA

A

Binds to the intracellular portion of the “L-type” channel α1 subunit preferentially when it is “OPEN” and occludes the channel

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13
Q

“Use-Dependence” or “Frequency-Dependence” of Verapamil

A

calcium channel blockade by verapamil is ENHANCED as the frequency of stimulation increases 9works better at higher HRs

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14
Q

Verapamil Characteristics

A

1) Is relatively selective for inhibiting the transmembrane influx of Ca2+ in the SA/AV nodal tissue and cardiac muscle; especially in AV nodal tissue
2) Less potent as a peripheral vasodilator than 1,4- Dihydropyridine class CCB’s but is more potent as a vasodilator than Diltiazem
3) Is a more potent negative chronotropic, inotropic and dromotropic agent than diltiazem
4) Reflex sympathetic tachycardia is blunted by verapamil

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15
Q

Verapamil causes peripheral vasodilation which …

A

⇓ 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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16
Q

Diltiazem MOA

A

Binds to the inner surface of the cell membrane of the “L- type” channel α1 subunit (binds at a different site than verapamil does) and blocks the channel mostly from the inside surface of the membrane by entering the channel preferentially when it’s “OPEN”

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17
Q

Use-Dependence” or “Frequency-Dependence of diltiazem

A

means that calcium channel blockade by diltiazem is ENHANCED as the frequency of stimulation increases (works better at higher HRs)

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18
Q

Dilatiazem Characteristics

A
  • Is relatively selective for inhibiting the transmembrane influx of Ca2+ in the SA/AV nodal tissue and cardiac muscle; especially in AV nodal tissue
  • Less potent as a peripheral vasodilator than 1,4- Dihydropyridine class CCB’s and Verapamil
  • Is a less potent negative chronotropic, inotropic and dromotropic agent compared to verapamil
  • Reflex sympathetic tachycardia is blunted by diltiazem
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19
Q

Diltiazem causes peripheral vasodilation which ___

A

⇓ blood pressure which triggers the baroreceptor reflex response but the reflex tachycardia is blunted by the DIRECT negative chronotropic effects of diltiazem

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20
Q

Non-DHPs Pharmacological Effect

A
  • SA/AV node depolarization is dependent largely on Ca2+ movement
  • Non-DHP’s decrease the rate of phase 4 spontaneous depolarization and slow the rate of phase 0 depolarization in SA & AV nodes
  • Suppress (⇓) the automaticity of the SA node by reducing Ca2+ influx and decreasing rate of recovery of the channel in SA node (⇓ impulse generation - neg chromotrope)
  • Suppress (⇓) the conduction velocity through the AV node and prolongs AV node refractoriness (⇑ its functional refractory period) by reducing Ca2+ influx and decreasing rate of recovery of the channel in AV nodal tissue - neg dromotrope which results in increased PR interval
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21
Q

The most marked effect of verapamil & diltiazem on nodal tissue is

A

⇓ the conduction velocity through the AV node and to ⇑ its functional refractory period. Verapamil & diltiazem are effective in automatic and re-entry tachyarrhythmias due to their ability to slow AV nodal conduction time and prolong AV nodal refractoriness

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22
Q

Cardiac Muscle Cell Pharmacologic Effects of Non-DHPs

A

Within the cardiac muscle cell, Ca2+ binds to troponin which eventually leads to actin and myosin interacting to cause cardiac muscular contraction. Therefore, blockade of the slow “L-Type” calcium channels results in decreased myocardial contractility
• Negative inotropic effect
• CCB’s alter the plateau phase (Phase 2) of the cardiac muscle cell action potential

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23
Q

Non DHPs effect of artery

A

-arterial vascular smooth muscle relaxation and cause little effect on venous resistance vessels at concentrations that produce arteriolar vasodilation
-Arterial vasodilation ⇓ afterload and ⇓ systemic vascular resistance which ⇓ systolic and diastolic blood pressure
- ⇓ coronary vascular resistance via coronary vasodilation,
which ⇑ coronary blood flow and ⇑ myocardial O2 supply
- ⇓ myocardial O2 demand
- Relax coronary artery vasospasms & ⇑ blood flow through fixed coronary obstructions

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24
Q

Verapamil, The “prototype” non-dihydropyridine CCB that is a synthetic derivative of ___ ?

A

Papervine

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25
Q

as a racemic mixture

A

• L-enantiomer of verapamil is a specific & potent “L-type”
calcium channel blocker
• D-enantiomer of verapamil is devoid of calcium channel blocking activity but posses’ blockade of fast Na+ channels, accounting for the local anesthetic effects of verapamil

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26
Q

Verapamil

Clinical Uses

A
  • Supraventricular tachyarrhythmia’s
  • Vasospastic angina (as effective as beta-blockers)
  • May be useful in the treatment of maternal and fetal tachyarrhythmia’s as well as premature labor, however, it may ⇓ uterine blood flow so it should be used with extreme caution
  • Symptomatic hypertrophic cardiomyopathy
  • Essential hypertension
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27
Q

Verapamil contraindicated in in which SVTA rhythms?

A

1) Wolff-Parkinson-White and Lown-Ganong-Levine syndromes

2)

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28
Q

Verapamil Pharmacokinetics

A
  • Onset IV Effect is 1-3 minutes
  • Protein binding: 90% (High)
  • Metabolism occurs in the liver via multiple CYP 450
  • Has an activate metabolite
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29
Q

Verapamil

Dosing

A
  • 5-10mgIV(0.075-0.15mg/kg)overatleast2min
  • may give additional 10 mg IV after 30 min if no response or response is not adequate
  • Liver disease: give 20 - 50% of normal dose
  • Geriatrics: give slower IV over at least 3 minutes
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30
Q

Verapamil Cardiovascular

Adverse Effects

A
  • Hypotension – The major adverse effect of IV verapamil
  • Bradycardia
  • 2nd or 3rd degree AV block
  • Heart failure
  • Neg inotrope
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31
Q

Other Verapamil Adverse Effects

A
  • Constipation, peripheral edema, nausea

* Headache, dizziness

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32
Q

Diltiazem

Clinical Uses

A

Same as Verapamil

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33
Q

Diltiazem

Pharmacokinetics

A
  • Absorption: Well absorbed but is subject to extensive hepatic first-pass metabolism
  • Peak Effect: ~15 min IVP
  • t1/2 = ~4 hours
  • Liver disease can prolong t1/2, thus necessitating diltiazem dosage reductions in liver disease
  • Protein Binding: 70-80%
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34
Q

Diltiazem Metabolism

A
  • Via CYP450

- 2 active metabolites: desacetyldiltiazem and desmethyldiltiazem

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35
Q

Diltiazem Dosing

A

1) IV Bolus - Initial: 0.25 mg/kg over 2 min; may repeat after 15 min if
response is inadequate
• Second: 0.35 mg/kg over 2 min
2) Continuous Infusion - Start immediately following bolus for continued reduction of heart rate (for up to 24 hours) in patients with atrial fibrillation or atrial flutter
• 5 - 15 mg/hour continuous infusion rate

36
Q

The major adverse effect of IV Diltiazem and IV Verapamil

A

Headache

37
Q

Verapamil and Diltiazem Drug-Drug Interactions

A

1) CYP3A4 Inhibitors
2) ↑ Digoxin concentrations (↑ bradycardia)
3) ↑ neg chrontropic, dromotropic and inotropic effect when added to BBs
4) + Dantrolene = CV collapse and hyperkalemia

38
Q

What happens if Verapamil, Diltiazem or Midazalam is given with Diazapem

A

Since Diazepam is a highly protein bound drug, it will compete for that protein leaving more of the unbound pharmacologically active version of the drug, which increases the drug’s effect.

39
Q

What happens if Verapamil or Diltiazem is given with Local anesthetics

A

Since Verapamil and Diltiazem have local anesthetic properties, this will increase the risk of local anesthetic toxicity

40
Q

What happens if you give Verapamil or Diltiazem with a drug that decreases hepatic flow? give an example.

A

I.e. Cimetidine - decreases hepatic flow, which will decrease clearance and increase plasma concentrations

41
Q

What happens if Verapamil or Diltiazem is given with Midazolam?

A

Causes increase in sedative effects of Midazolam

42
Q

Which PT population should you take caution when giving Verapamil or Diltiazem plus inhaled anesthetics and why?

A

Its with LV dysfunction or hypovolemia, because both drugs and inhaled anesthetics depress contractility, conductivity, automaticity and vasodilator at the same time.

43
Q

What happens if Verapamil or Diltiazem is given with Neuromuscular blocking agents?

A

They potentiate each other, the dose of Verapamil/Diltiazem should be lowered as well as the dose of the NMB agent.

44
Q

Verapamil and Diltiazem Contraindications

A

1) Sever hypotension, cariogenic shock or bradycardia
2) Sick sinus syndrom, 2nd or 3rd degree AV block
3) Sever CHF
4) Afib/Aflutter and WPWS
5) Wide complex Vtac

45
Q

1,4-Dihydropyridine CCBs MOA

A

Binds A1 subunit of L-type voltage gated calcium channel and inhibits transmembrane influx of ca ions into smooth muscle and cardiac cells

46
Q

Why are 1,4-Dihydropyridine CCBs referred to as “Arterial smooth muscle selective agents”?

A

Because they have a far greater effect on arterial vascular smooth muscle cells than on cardiac muscle cells and cause little effect on venous resistance vessels

47
Q

1,4-Dihydropyridine CCBs coronary effects

A

1) Increase coronary blood flow and myocardial O2 supply and decreases myocardial O2 demand
2) Relaxes coronary artery vasospasm and increases flow through fixed coronary obstructions

48
Q

Effects of 1,4-Dihydropyridine CCBs on baroreflex

A
  • Due to their potent peripheral vasodilation effect, they elicit a baroreceptor mediated ↑ in sympathetic discharge resulting in:
    Reflex tachycardia, dizziness, headache, flushing and peripheral edema
49
Q

1,4-Dihydropyridine CCBs cardiac effects

A

1,4-Dihydropyridine CCBs has little to no negative inotropic clinical effects, no dromotropic and chronotropic effects

50
Q

Do 1,4-Dihydropyridine CCBs agents exhibit “Use Dependence”?

A

No

51
Q

Adverse Effects of 1,4-Dihydropyridine CCBs agents

A

1) Main Side Effects - peripheral edema, dizziness, flushing, hypotension, headache, reflex tachycardia, and palpitations
2) Othe Side Effects - weakness, fatigue, N/V, and gingival hyperplasia

52
Q

gingival hyperplasia

A

Overgrowth of gum tissue around teeth

53
Q

1,4-Dihydropyridines CCB’s

Clinical Uses

A

1) Hypertensive crisis
2) Chronic HTN
3) Mgmt of BP in PTs with systolic HF
4) Chronic stable angina and vasopastic angina (Prinzmetal’s or Variant Angina)

54
Q

Nifedipine Characteristics

A

1st generation 1,4-dihydropyridine CCB that is short acting

55
Q

Nifedipine available dosage forms?

A

SL or PO

56
Q

Nifedipine has a high incidence of which side effects?

A

1) Peripheral edema
2) Hypotension
3) Reflex tachy
4) Flushing
5) Headache
6) Vertigo
7) Dizziness
8) Skeletal muscle weakness

57
Q

Why should you NEVER use SL or immediate release Nifedipine?

A

It can be assoc. with reflex tachycardia, ↓ coronary, renal and cerebral perfusion, and ↑ myocardial O2 demand

58
Q

*Nimodipine Characteristics

A

1) A 1,4-dihydropyridine CCB agent
2) Highly lipid-soluble and crosses BBB
* 3) Has a greater effect on cerebral arteries than arteries elsewhere in the body
4) Dilates small resistance cerebral vessels and prevents cerebral vasospasms
4) Capsules may be used during anesthesia or surgery

59
Q

Nimodipine Dosage Forms

A

Available in oral capsule or liquid solution

60
Q

Nimodipine’s Unique Clinical Use

A

Used for improvement of neurological outcome by ↓ ischemic deficits in PTs with subarachnoid hemorrhage from ruptured berry aneurysms.

61
Q

Nimodipine Dosage

A
  • 60mg PO or NG tube q4 hrs x 21 days

- Start within 96 hours after subarachnoid hemorrhage

62
Q

Should Nimodipine be continued if the PT is scheduled for surgery?

A

Yes, administration of nimodipine should be continued to complete the 21 day period

63
Q

How do administer Nimodipine to PTs who cannot take oral meds?

A

Contents have to be extracted and placed in a syringe to be administered via an NG or gastric tube

64
Q

Nimodipine Black Box Warning

A

Death will occur due to inadvertent IV administration, - Nimodipine is a PO agent only

65
Q

*Nicardipine Characteristics

A

1) 2nd generation 1,4-dihydropyridine CCB agent
2) Has the greatest vasodilating properties of ALL CCB’s
*3) Prominent coronary and cerebral vasodilating activities
4) ↑ CO
5) Not assoc. with bradycardia of rebound HTN
Lipophilic (crosses BBB)
6) Does NOT ↑ ICP

66
Q

Nicardipine available dosage forms?

A

PO and IV

67
Q

Nifedipine Clinical Uses

A

1) Hypertensive emergencies
2) Acute ischemic stroke
3) Mgmt of spontaneous intracerebral hemmirrhage
4) Mgmt of Aneural subarachnoid hemorrhage

68
Q

Nicardipine

Pharmacokinetics

A
  • Oral absorption is complete but undergoes extensive first- pass hepatic metabolism
  • Onset (IV): 5-15 min
  • Protein Binding: > 95% (High)
  • Metabolism
  • Extensively metabolized in liver via CYP 450
  • Excretion
  • < 1% of intact drug is detected in the urine
69
Q

Nicardipine

Contraindications/Warnings

A

1) Contraindication - Advanced aortic stenosis, since after load reduction reduces myocardial O2
2) Warning - patients with heart failure

70
Q

Nicardipine

Adverse Effects

A

1) Headache
2) Hypotension
3) N/V
4) Reflex tachycardia

71
Q

Clevidipine (Cleviprex®) Characteristics

A

1) 3rd generation IV-only 1,4- dihydropyridine CCB agent
2) Has an ultrafast onset
3) Is a racemic mixture of 2 enetomers

72
Q

Clevidipine (Cleviprex®) Clinical Use

A

1) Reduction of BP when oral therapy is not feasible i.e. hypertensive emergency or preoperative HTN
2) To reduce gastric emptying

73
Q

Clevidipine (Cleviprex®) Pharmacokinetics

A
  • After IV administration, clevidipine is rapidly distributed and metabolized
  • Onset of Effect: 2-4 min
  • Peak: < 10 min
  • Offset of effect: 5-15 minutes
  • Full recovery of blood pressure is achieved after the infusion is stopped in most patients within 5-15 minutes
  • Very short t1/2
  • Initial Phase: 1 min (accounts for 85-90% of elimination) • Terminal: 15 minutes (accounts for the remainder)
  • Protein binding: > 99.5% (High)
74
Q

Clevidipine (Cleviprex®) Metabolization and excretion

A

1) 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
2) The primary metabolites are a carboxylic acid metabolite and formaldehyde, which are inactive

75
Q

Available Clevidipine (Cleviprex®) dosage forms?

A

a water-insoluble drug that is available only as a lipid emulsion dosage form

76
Q

Clevidipine (Cleviprex®) Contraindications

A

1) Allergies to soybeans, soy products, eggs, or egg products
2) Defective lipid metabolism seen in conditions such as pathologic hyperlipemia, lipoid nephrosis, or acute pancreatitis if it is accompanied by hyperlipidemia
3) Severe aortic stenosis

77
Q

Clevidipine (Cleviprex®) Adverse Effects

A

1) Most common - Headache, flushing and N/V

2) Least Common - Hypotension and reflex tachy

78
Q

PTs whose infusion of Clevidipine is stopped, should be monitored for which condition?

A

Rebound HTN, if they haven’t been switched to another antihypertensive

79
Q

Clevidipine in PTs with a Pseudocholinesterase difficiency

A

Patients with pseudocholinesterase deficiency have reduced clearance and prolonged recovery from clevidipine

80
Q

CCBs and fluid requirements

A

CCB’s increase the volume of fluids required during the perioperative period

81
Q

CCB’s and anesthetic requirements

A

CCB’s decrease anesthetic requirements by 25%

82
Q

H2 antagonists + CCB’s interaction

A

Cimetidine and ranitidine by inhibiting hepatic enzyme activity and/or decreasing hepatic blood flow may increase the plasma concentrations of certain CCB’s

83
Q

Verapamil and Diltiazem should not be given to PTs with an EF less than ______?

A

40%

84
Q

Can 1,4-Dihydropyridine CCBs be safely given to PTs with EF less than 40%?

A

Yes

85
Q

Which drug should be given to a stroke PT with a Hypertensive crisis?

A

Nicardipine because it does NOT cause ↑ ICP

CRNA Pharmacology (8 decks)

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