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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
Diltiazem is the only
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
26
Benzothiazepine CCBs relatively
``` 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 ```
27
HR | myocardial contractility
nodal tissue | conducting tissue
28
``` Non DHPs produce arterial vascular smooth muscle AFFECT PRELOAD Y/N ? _______Coronary vascular resistance ________ coronary blood flow _______ O2 supply myocardial and decrease demand. ```
``` arterial vascular smooth muscle DOES NOT AFFECT PRELOAD decreased Coronary vascular resistance increases coronary blood flow Increase O2 supply myocardial and decrease demand. ```
29
Verapamil is the
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.
30
**** Clinical uses of VERAPAMIL
To convert: SVTs PSVT: rapid conversion to SR, or Paroxysmal SVT To control HR in (NOT CONVERSION) Atrial fib Aflutter with RVR
31
Can decrease uterine blood flow
VERAPAMIL
32
``` Absorption is (verapamil)______% onset ______minutes PROLONGED in ________ _______protein binding CYP 450 enzymes dependent Y/N____ Dependent on liver blood flow Y/ N____ ```
``` greater than 90% onset 1-3 minutes PROLONGED in liver disease (metabolism) Highly protein binding CYP 450 enzymes dependent Dependent on liver blood flow ```
33
Active metabolite of verapamil
N-demethylation active metabolite NORVERAPAMIL may accumulate in patients with renal insufficiency (adjust dose for renal failure)
34
Verapamil dosing
5-10 mg IV , over AT LEAST 2 minutes | Repeat after 30 minutes
35
Liver patients with verapamil? | geriatric
cut the dose in half. | give over 3 minutes
36
Adverse effects of VERAPAMIL with IV dose not PO
HYPOTENSION | 2nd and 3rd AV block
37
Do not give verapamil or Cardizem with diazepam
bound highly to protein.
38
Major adverse effects of verapamil
Hypotension
39
With protein binding whatever is in the tank first
What protein bind drug is there first
40
Verapamil diazepam with local anesthetics
they also have local anesthetics activity , may be additive to local anesthetics
41
Drug to drug interactions
drugs that decrease hepatic blood flow
42
Verapamil and diazepam | Do not give with EF less than 40%
Can increase sedative effectiveness | if patient is on midazolam first, and you add verapamil will increase midazolam
43
1,4-Dihydropyridines CCB’s
Are referred to as “Arterial vascular smooth muscle selective” agents
44
Pharmacological effects dihydropyridines
these agents exhibit little to no negative | inotropic clinical effects
45
Ok to give DHPs in patients with
LV dysfunction to manage BP not HF
46
DHP do not have
negative dromotrope and chronotrope | no use dependence
47
DHPs use for anesthesia providers
* Treatment of hypertensive crisis * Hypertensive urgency – oral agents * Hypertensive EMERGENCY ALWAYS IV – IV agents (end organ emergencies) --> End Organ damage damage.
48
Emergency vs urgency
End organ damage (headaches, chest pain)
49
Nifedipine :
will be on boards, stink
50
Nifedipine is a
1st generation DHP prototype, short acting
51
Nifedipine has a greater
Has greater coronary and peripheral artery vasodilator properties than verapamil or diltiazem
52
Oral DHP nifedipine has :
lot of side effects and is not the preferred medication. \ Peripheral edema Reflex tachycardia Flushing
53
*****IMMEDIATE release nifedipine can cause
can cause life threatening Ischemia Induces reflex tachycardia Decrease coronary renal and cerebral perfusion Increased myocardial O2 demand
54
NEVER use
SL or IR nifedipine
55
Nimodipine is a
DHP agent that is available oral capsule or liquid solution
56
Unique calcium channel blocker only use in one area? why?
Nimodipine; crosses BBB and HIGHLY LIPID SOLUBLE.
57
Nimodipine has: | Only use in ?
- 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
Nimodipine you cannot
skip doses, worsens patient outcomes
59
NIMODIPINE GIVEN how frequent?
EVERY 4 hours, and INTRAOP
60
• Nimodipine Oral dose
Dose: 60 mg PO or NG/Gastric tube q 4 hours x 21 days
61
Nimodipine if unable to give IV
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
Nicardipine is a ______generation DHP and more selective for blocking ____________
2nd generation DHP , more selective for blocking vascular smooth muscle Good antihypertensive
63
Prominent coronary and cerebral vasodilating activities.
Nicardipine
64
Not associated with bradycardia or REBOUND HTN
Nicardipine (can just turn off)
65
Does nicardipine cross BBB? increase ICP?
Yes; no
66
Nicardipine undergo
Extensive first pass metabolism
67
Onset IV nicardipine
5 mns
68
Contraindications for Nicardipine
Advanced Aortic Stenosis | Since afterload reduction can be expercted to reduced myocardial oxygen delivery
69
Nicardipine with HF EF <40
Titrate slowly, use with caution in patient with LV dysfunction
70
Clevidipine and nicardipine
same effects | The first 3rd generation IV DHP CCB
71
Clevidipine is Fast /slow?
ultra fast onset and offset Arterial specific vasodilating effect Use for acute HTN
72
Clevidipine is a
racemix mixture
73
Clevidipine and all other CCB
reduce gastric emptying.
74
How does prevent gastric emptying
smooth muscle require calcium to contract | CCB block calcium therefore can impair contraction of smooth muscle.
75
Clevidipine is the _______Acting onset ______ offset of effect?
fastest acting onset 2-4 min offset of effect 15 minutes
76
Clevidipine Pharmacokinetics
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
bonus: Formaldehyde is a
carcinogen, embaulming fluid | -
78
Looks like propofol
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
Allergic to egg and soy do not give
Clevidipine
80
Severe aortic stenosis do not give
Clevidipine.
81
Clevidipine can cause
rebound HYPERTENSION | wean them off
82
Do not give clevidipine to patient with this deficiency?
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
When do you SL nifedipine?
Never | SL nifedipine, intraoperative MI when hemodynamics are normal
84
NonDHP
Can be used for
85
DHPs NEVER DECREASE
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
Mechanism of action of the 3 classes of
KNOW chart
87
DHP are more selective than the
nonDHP on arterial vascular smooth muscle better at lowering BP Adverse effects; PERIPHERAL ADVERSE EFFECT much high in NON-DHP.
88
Using DHP for clinical indications
for
89
1, 4 dihydropirine d
Decrease SVR sufficient Active baroreceptor reflex mediate increase in sympathetic tone to overcome their negative inotropic effect. No massive decrease
90
Verapamil - Drugs to drug interactions: with DIAZEPAM
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
Diazepam and midazolam
can increase sedative effect of midazolam
92
Diazepam and midazolam
can increase sedative effect of midazolam | 3-4 folds increase in concentration midazolam and half life was increase, leading to decrease clearance.
93
on what tissue does verapamil work?
Cardiac
94
CV effect of nitroglycerin are
dose dependent | at some dose you will start to arterial
95
The primary metabolites of CLEVIDIPINE are a ___________and ______which are
- carboxylic acid metabolite - formaldehyde inactive

SRNAPharmacology I (29 decks)

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