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2-Pharm Exam 3 > Calcium Channel Blockers (CCB) > Flashcards

Calcium Channel Blockers (CCB) Flashcards

1
Q

What is the importance of calcium ions?

A

Calcium ions play a key role in the electrical excitation of cardiac cells and vascular smooth muscle cells

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2
Q

What do calcium channel blockers interfere with?

A

CCB drugs interfere with inward movement of calcium ions across myocardial and vascular smooth muscle cells

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3
Q

What are the activities possessed by calcium channel blockers?

A

Possess vasodilating activity

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4
Q

Where do calcium channel blockers drugs bind?

A

CCB drugs bind to receptors on voltage-gated calcium ion channels (L, N, & T) – results in maintenance of these channels in an inactive/closed state

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5
Q

What is the end result of calcium channel blockers binding?

A

calcium influx is decreased and reduced intracellular calcium

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6
Q

What calcium channel blockers are selective for AV node?

A

Phenylalkylamines & benzothiazepines

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7
Q

What calcium channel blockers are selective for arteriole beds?

A

Dihydropyridines

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8
Q

What are common side effects of calcium channel blockers?

A

systemic hypotension, peripheral edema, flushing, headache

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9
Q

What are the MOA of calcium channel blockers?

A

All clinically used CCB drugs bind to a unique site on the α-1 subunit of the L-type calcium channel (slow channel) which reduces entry of calcium ions into cells

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10
Q

What is Ca++ influx through L-type calcium channels responsible for?

A

phase 2 of the cardiac action potential and excitation-contraction coupling in cardiac/vascular smooth muscle & depolarization in SA & AV nodal tissue

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11
Q

What does blockade result in?

A
  • Blockade results in slowing of heart rate
  • reduced contractility
  • decreased activity at SA node
  • decreased speed of conduction through AV node
  • vascular smooth muscle relaxation (decrease in BP)
  • treat coronary vasospasm
  • increase coronary blood flow
  • treat angina
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12
Q

Review action poteintal in pacemaker cells- automaticity.

A
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13
Q

Review smooth muscle contraction.

A
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14
Q

Review smooth muscle contraction diagram.

A
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15
Q

What are the three classifications of calicum channel blockers?

A

Phenylalkylamine, Dihydropyridines and Benzothiazepine

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16
Q

What calicum channel blockers are Phenylalkylamine?

A

Verapamil

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17
Q

What calicum channel blockers are Dihydropyridines?

A

Nifedipine, Nicardipine, Nimodipine, Isradipine, Felodipine, Amlodipine

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18
Q

What calicum channel blockers are Benzothiazepine?

A

Dilitazem

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19
Q

What is the MOA of Verapamil?

A

Binds to α1 subunit of L-type Ca++ channel when open

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20
Q

What is the effects of Verapamil?

A
  • Depresses AV node
  • neg chronotropic effect SA node
  • neg inotropic effect exaggerated in patients w/LV dysfunction
  • moderate dilation coronary arteries
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21
Q

What cardiac conditions should Verapamil be avoided in?

A
  • heart failure with bradycardia
  • SA node dysfunction
  • AV block
  • effect enhanced with β blockade
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22
Q

What is the relationship between Verapamil and Wolff-parkinson white syndrome?

A

Avoid: Wolff-Parkinson White (WPW) syndrome - can result in antegrade conduction resulting in wide-complex VT deteriorating into VF

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23
Q

What the uses of Verapamil?

A
  • SVT (AV node action)
  • essential HTN
  • vasospastic angina
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24
Q

What has replaced adenosine for Verapamil?

A

Replaced by adenosine for SVT

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25
Q

When are the pharmacological effects of Verapamil seen?

A

2-3 min after IV

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26
Q

What is the elimination half time of Verapamil?

A

6-12 hours (prolonged in liver disease)

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27
Q

What is the IV dose of Verapamil?

A

IV dose 2.5-10 mg (infusion 5 mg/h) per Nagelhout

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28
Q

What is the metabolism of Verapamil? What is produced?

A

Hepatic metabolism with active metabolite norverapamil that is renally excreted

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29
Q

What is the protein binding of Verapamil?

A

Highly protein bound (90%) and may be affected by other drugs such as lidocaine, diazepam, propranolol

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30
Q

What do Dihydropyridines prevent?

A

Prevent Ca++ entry with an extracellular modulation of L-type Ca++ channel with primary effect on peripheral arterioles and cerebral vessels

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31
Q

What Dihydropyridines have effects on your peripheral arterioles?

A

nifedipine, nicardipine, clevidipine, isradipine, amlodipine, felodipine

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32
Q

What Dihydropyridines have effects on your cerebral vessels?

A

nimodipine

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33
Q

What can acute administration of dihydropyridines can result in?

A

reflex tachycardia d/t reduced BP leading to SNS activity or baroreceptor reflex

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34
Q

What is the clinical uses of Dihydropyridines?

A

treatment of HTN

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35
Q

What is the the clinical use of nimodipine sl?

A

tx of post SAH vasospasm

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36
Q

What are other uses of Dihydropyridines?

A
  • Raynaud syndrome
  • cluster HAs
  • angina
  • certain dysrhythmias
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37
Q

What are the properties of Nifedipine?

A

Greater coronary and peripheral artery vasodilating properties than verapamil

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38
Q

What effects the offset of Nifedipine clinical properties?

A

Negative inotropic, chronotropic, chromotropic effects offset by sympathetic reflex

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39
Q

Nifedipine: Decrease in BP results in _______

A

Reflex tachycardia

40
Q

Nifedipine: What are baroreceptors?

A

stretch receptors in the large vessels of the neck and thorax which are activated when the vessel walls are stretched by increased arterial pressure sending impulses to vasomotor center (medulla oblongata) via IX, X leading to a decrease in sympathetic outflow

41
Q

Nifedipine: What is the barorecptor reflex?

A
  • The function of the baroreflex is to maintain adequate blood pressure and cardiac output in the face of changing degrees of vascular filling and vasoconstriction.
  • The efferent loop is the ANS which affects hemodynamic function by varying the myocardial contractility, HR, SV and SVR.
42
Q

What effect do vasodilator drugs have?

A
  • Vasodilator drugs decrease intravascular pressures and cause a baroreceptor mediated elevation of heart rate.
  • This response increases cardiac output and maintains arterial blood pressure.
43
Q

Nifedipine: Little effects on _______

A

SA/AV nodes

44
Q

What is the clinical use of Nifedipine?

A

stable vasospastic angina

45
Q

When should Nifedipine be avoided?

A
  • LV dysfunction (worsening myocardial depression)
  • aortic stenosis
  • hypertrophic obstructive cardiomyopathies
46
Q

What effect does Nicardipine (Cardene) have on the myocardium?

A

Lacks effects on SA/AV nodes, minimal myocardial depressant

47
Q

What does Nicardipine (Cardene) not cause?

A

Does not affect preload or HR and does not cause rebound HTN when D/C’d

48
Q

What are the properties of Nicardipine (Cardene)?

A

Greatest vasodilating effects of the CCB, mainly coronary arteries

49
Q

What is the use of Nicardipine (Cardene) in anesthesia?

A

control B/P

50
Q

What is the infusion of Nicardipine (Cardene)?

A
  • Start infusion at 0.5-5 mg/hr, titrated q 5-15 min (Nagelhout) after bolus 0.625-2.5 mg
  • *Initiate therapy at 5 mg/hour as a continuous IV infusion.
  • The initial infusion rate of 5mg/hr IV may be increased by 2.5 mg/hr every 5 minutes to a maximum of 15 mg/hr
51
Q

What can Nicardipine (Cardene) be used in conjunction with?

A

May be used in conjunction with a β-blocker to treat angina

52
Q

What is the formularies for Nicardipine (Cardene)?

A

IV form as opposed to the other dihydropyridines

53
Q

What is the side effects of Nicardipine (Cardene)?

A

similar to nifedipine: (common) flushing, vertigo, headaches

54
Q

What are the clinical uses of Nicardipine (Cardene)?

A
  • Acute HTN
  • angina
  • tocolytic (inhibit uterine contractions)
  • blunt hemodynamic responses before procedures such as ECT
55
Q

What is the solubility of Nimodipine?

A

Highly lipid soluble analog of nifedipine (can enter into CNS)

56
Q

What is the dose of Nimodipine?

A

Given 60 mg orally (OG/NG diluted with 30 ml of saline)

57
Q

What is the uses for Nimodipine?

A
  • Only on approved for SAH induced vasospasm due to intracellular influx of Ca++ that results in contraction of large cerebral arteries
  • May be used intraoperatively after a cerebral aneurysm clipping
58
Q

What is the relationship of Nimodipine and cardiac arrest/anoxic brain injury?

A

May have use in cerebral protection after cardiac arrest/anoxic brain injury to stabilize intracellular Ca++ gradients

59
Q

What is the clinical use of Amlodipine?

A

Used with β-blocker to treat ischemia, HTN, vasospastic angina,

60
Q

What is the forumlaries for Amlodipine?

A

Oral form only

61
Q

What is the onset of Amlodipine?

A

slow onset

62
Q

What is the elimination half time of Amlodipine?

A

very long elimination half time (30-40 hrs)

63
Q

What is the onset of Clevidipine?

A

Ultra-short acting IV CBB

64
Q

What is the clinical indications for Clevidipine?

A

treat acute, severe HTN (only available in IV form)

65
Q

What is the onset and duration of Clevidipine?

A

Quick onset 2-4 min and short duration 5-15 min makes it useful in intraoperative period

66
Q

What is the dose of Clevidipine?

A

0.25-0.5 mg bolus followed by infusion 1-2 mg/hr titrated to effect

67
Q

What is true about the formulation of Clevidipine?

A

Formulated in lipid emulsion

68
Q

What are side effects of Clevidipine?

A
  • hypotension
  • tachycardia
  • caution use in patients w/hyperlipidemic states
  • acute/chronic pancreatitis
  • heart failure w/reduced LVEF
69
Q

What is the metabolism of Clevidipine?

A

rapidly metabolized by plasma esterases

70
Q

What is the metabolic half life of Clevidipine?

A

1 minute & unaffected by hepatic or renal dysfunction

71
Q

What effects metabolism of Clevidipine?

A

Patients with pseudocholinesterase deficiency, metabolism is significantly delayed and half-life time increased by approx. 32%

72
Q

What is the MOA of Diltiazem?

A

Along with L-type Ca++ channel, may also work on the Na+/K+ pump to decrease the intracellular Na+ exchanged for extracellular Ca++ and may inhibit the Ca++ /calmodulin binding

73
Q

What is the clinical uses of Diltiazem?

A

blocks AV node; first-line tx of SVT’s; also used in tx of chronic essential HTN; has vasodilating properties

74
Q

What is the myocardial effects of Diltiazem?

A

Minimal myocardial depressant effects and unlikely to interact with β blockers

75
Q

What is the IV dose of Diltiazem?

A
  • IV dose 0.25-0.35 mg/kg over 2 minutes and repeated in 15 min.
  • Infusion after bolus for 24 hrs (10mg/hr)
76
Q

What is the elimination for Diltiazem and its active metabolite? When is the effects prolonged?

A
  • Elimination half time 4-6 hrs parent drug, 20 hrs for the active metabolites (prolonged with liver disease)
77
Q

Why is Diltiazem used in clinical anesthesia?

A

in anesthesia practice to control HR

78
Q

What function can Diltiazem interfere with?

A

CBB may interfere with Ca++ mediated platelet function

79
Q

What drug levels can be increased with Diltiazem?

A

Increase digoxin levels

80
Q

What drugs interfere with Diltiazem?

A

Affected by P450 inhibition of cimetidine and ranitidine

81
Q

Concerns with long term use with the _______ subclass of CCB

A

dihydropyridine

82
Q

What protective effects can be seen with Diltiazem?

A
  • CBB may aid in cyto-protection by limiting oxygen free radicals and by increasing renal blood blow for those with HTN
  • Activation of the endothelial enzyme xanthine oxidase is known to be induced by mediators of immune cells or by episodes of ischemia and reperfusion leading to cell injury/death
83
Q

Review comparison tables of CCB.

A
84
Q

Where is vasopressin produced?

A

Arginine vasopressin (antidiuretic hormone): An endogenous hormone produced in the hypothalamus

85
Q

Where is vasopressin stored?

A

stored in posterior pituitary & released from hypothalamus

86
Q

What is the function of Vasopressin?

A
  • control osmoregulation
  • stimulated by increased osmolality
  • hypovolemia
87
Q

What is the effects of Vasopressin?

A
  • Is potent vasoconstrictor (increases SVR & MAP)
  • no effect on HR or myocardial contractility
88
Q

What is the dose of Vasopressin?

A

Low-dose infusion (0.02-0.04 units/min) increases BP, UOP, & CrCl

89
Q

What is the relationship between Vasopressin and septic shock?

A

decreases the dosage of norepinephrine required to maintain BP in patients with septic shock

90
Q

What is Vasopressin often used with?

A

Used as add-on tx with catecholamine vasopressors

91
Q

What is the complications of Vasopressin?

A
  • GI ischemia
  • decreased cardiac output
  • skin or digital necrosis
  • cardiac arrest at doses > 0.04 units/min
92
Q

What is the use of Vasopressin in anesthesia?

A
  • tx of refractory hypotension (i.e., ACE-I-induced)
  • Vial: 20u/mL – dilute to 2u/mL; Give 1-2 units IV
93
Q

What are natural catecholamines?

A
  • Epinephrine: α-1, β-1, β-2 agonist effects
  • Norepinephrine: potent α-1, β-1 agonist effects
  • Dopamine: Dopaminergic receptors, α-1, β-1 agonist effects (effects are dose dependent)
94
Q

What are synthetic catecholamines?

A
  • Isoproterenol: potent β-1, β-2 agonist effects
  • Dobutamine: potent β-1 agonist, weaker β-2 , α-1 effects at higher doses
95
Q

What are Synthetic Noncatecholamines?

A
  • Ephedrine: α-1, β-1, β-2 agonist effects (direct & indirect acting)
  • Phenylephrine: α-1 agonist

2-Pharm Exam 3 (14 decks)

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