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Anesthesia Pharmacology II > Antihypertensive > Flashcards

Antihypertensive Flashcards

1
Q

What do calcium channel blockers do?

A

Selectively inhibit Ca++ ions at L type Ca channnels
Reduce myocardial O2 demand by decreasing afterload and coronary vasodilation
Also decrease HR

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2
Q

What are the pharmacologic effect of Ca++ channel blockers?

A 
↓ Contractility
↓ Heart Rate
↓ SA Node Activity
↓ AV Node Conduction
↓ Systemic BP
-2º vascular smooth muscle relaxation
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3
Q

What are clinical effects of calcium channel blockers?

A 
Peripheral Vasodilation
-Decreases afterload
Depression of myocardial contractility
Improving myocardial ischemia
-decrease demand
Electrophysiologic conduction
-Verapamil at the AV node(slows conduction)
-Significant for anti-arrythmic effects
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4
Q

What are the clinical uses of calcium channel blockers?

A

Coronary artery spasm
Stable angina
Cerebral vasospasm
HTN

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5
Q

What are verapamil’s effects?

A 
Derivative of papavarine
*AV node depression*
Sa node-chronotrope
Negative inotrope
vasodilator
Also works on fast sodium channel (potentiates local)
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6
Q

What are the clinical uses of verapamil?

A

SVT tx
stable angina
Essential HTN
Maternal and fetal tachydysrhythmias ( will cross placenta)
Intra-arterial injection for cerebral vasospasm

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7
Q

What are the effects of nifedipine?

A

Vasodilator
negligible SA/AV node effects
TAchycardia
NO Myocardial depression

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8
Q

What are the clinical uses of nifedipine?

A

Angina

HTN emergencies

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9
Q

What effects does nifedipine have on conduction?

Myocardial depression?

A

No effects on either

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10
Q

NIfedipine is sensitive to light. T/F

A

T

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11
Q

Nifedipine has been associated with peripheral _______.

A

edema

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12
Q

Which calcium channel blocker causes the most vasodilation (especially on coronary arteries)?

A

Nicardipine

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13
Q

What are teh clinical uses of nicardipine?

A

perioperative HTN
Improves LV function during ishemia
Coronary Spasm

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14
Q

What is halflife of nicardipine?

A

14 minutes

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15
Q

What is different about nimodipine compared to nifedipine? what is it used to treat?

A

Lipid soluble so it will cross BBB

used to treat cerebral vasospam

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16
Q

What is bolus and infusion dose of nicardipine?

A

100-200 mcg

infusion 5mg/hour

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17
Q

What are the effects of diltiazem?

A

Slows AV node function–antiarrhythmic
coronary vasodilation
minimal myocardial depression

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18
Q

What are the clinical uses of diltiazem?

A

SVT including afib and flutter
essential HTN
Used similar to verapamil

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19
Q

What drugs do calcium channel blockers interact with?

A 
Anesthetic drugs
NMB
Local anesthestic
K containing solution
Dantrolene
Platelet function
Digoxin ( may increase plasma concentration)
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20
Q

What class is clevidipine?

A

it is the first third generation dihydropyridine

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21
Q

HOw is clevidipine cleared?

A

plasma choliesterases

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22
Q

what is the halflife of clevidipine?

A

1 minute

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23
Q

What is the effect of clevidipine?

A

Arterial specific vasodilating effects

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24
Q

What are the peripheral vasodilators?

A 
Sodium Nitroprusside (SNP)
Nitroglycerin (NTG)
Hydralazine
Papavarine
Trimethaphan
Adenosine
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25
When should you give a peripheral vasodilator?
``` Treat HTN crisis Maintain controlled hypotension Improve LV stroke volume -CHF -Regurgitant valves ```
26
How do nitrovasodilators work?
Increase NO production which leads to increased cGMP
27
What are the functions of NO
Maintains CV tone, platelet aggregation, and CNS signalling | Aids in GI relaxation and immune functions
28
how is NO inactivated?
hemoglobin
29
What is the duration of NO?
5 seconds
30
NO is synthesized from ___________
l-arginine
31
Which generates more NO, arteries or veins?
arteries
32
``` HOw are each of the following related to NO: Essential HTN Hypotension-septic shock atherosclerosis Vasospasm (after SAH) ```
Essential HTN: decrease in NO production Septic shock: surge in NO Atherosclerosis: decrease in NO leading to an increase in platelet production Vasospasm: decrease in NO
33
How is NO used clinically?
to tx pulmonary HTN heart and lung transplant -20-40 ppm; FGF must be > than MV ARDS
34
Does sodium nitroprusside (SNP) work on arterial or venous?
nonselective: arterial=venous | decereases both preload and afterload
35
How does the chemical struture of SNP relate to its toxicity?
Iron center with 5 CN and 1 NO hanging off
36
What is the infusion dose of SNP. Where do you start to run into trouble
0.3-10mcg/kg/min | CN accumulation at >2mcg/kg/min
37
What is the duration of SNP?
1 minute
38
At low doses SNP causes a greater decrease in ________ than ________
afterload, preload
39
SNP does not cause pulmonary vasodilation. t/f
f
40
What are negative effects of SNP?
``` Toxicity -cyanide, thiocyanate, Methemoglobinemia Light sensitive Reflex tachycardia vascular steal Ischemia in HTN pts Rebound HTN Risk of increase ICP Inhibits platelet function N/V (from hypotension) ```
41
What is the treatment for cyanide toxicity
1. Turn off SNP 2. increase O2 3. Bicarb if acidotic
42
What are the effects of cyanide toxicity?
Tissue anoxia Anaerobic metabolism lactic acidosis
43
What are the symptoms of thiocyanate toxicity?
fatigue Tinnitis N/V
44
Why would thiocyanate toxicity occur?
impaired renal clearance
45
What is the tx for thiocyanate toxicity?
dialysis
46
When would you use SNP?
``` controlled hypertension hypertensive emergencies Cardiac Disease -Decrease LV afterload -Treat CHF Aortic surgery -manipulate BP during cross clamp ```
47
SNP inhibits hypoxic pulmonary vasoconstriction. T/F
t
48
With SNP cerebral blood flow is ________ and platelet aggregation is _________.
increased, decreased
49
What is a side effect of NTG?
cerebral vasodilator-headache
50
Nitroglycerin only dilates veins. T/F
F. if enough is given it will dilater arteries as well
51
How does NTG decrease ventricular wall tension?
less volume returns
52
What are the routes of administration for NTG?
Sublingual, transdermal. IV | Not PO--takes too long and too much 1st pass metabolism
53
What is the emlimination half time of NTG?
90 sec
54
what effects does NTG have on the Pulmonary system? | Gi?
Cebrebral vasodilator-headache Pulm vasodilaor GI relaxation
55
What are the clinical uses of NTG?
Angina pectoris Cardiac failure Acute HTN Controlled hypotension
56
Hydralizine is principally a _______ vasodilator
arterial
57
What is the onset/duration of hydralazine?
onset 15-20 minutes, IV dose lasts hours
58
What is the dose for hydralizine?
2.5-5 mg q 15 minutes
59
What are the side effects fo hydralazine?
``` Reflex tachycardia headache Angina Flushing Rash (when on hydralazine chronically) coronary steal ```
60
Why might hydralazine be preferred in OB
Maintains uterine BF
61
Who would use papavarine?
Mostly vascular surgeons | you can give phenylephrine or norepi to fix it if it causes to much hypotension
62
What are the uses of adenosine?
Endogenous nucleotide potent coronary vasodilator 0.6-1.5 sec half life use for PSVT
63
What is trimethaphan?
Ganglionic blocker 10-200 mcg/kg/min causes mydriasis
64
How do ace inhibitors work?
Block conversion of Ang I → Ang II Prevent Ang II vasocontriction and stimulation of sympathetic system Ang II responsible for secretion of aldosterone
65
What is the advantage to ACE inhibitors?
No CNS effects like other drugs
66
What are the side effects of ACE inhibitors?
Cough Angioedema Contraindicated for pts with renal artery stenosis
67
What is the protocol for ACE inhibotors and surgery?
Continue normal regimen up to surgery and being again ASAP Pt on chronic ACE inhibitor may exhibit exaggerated HYPOtension with GA (there is some new evidence suggesting that withholding drugs for 12 hrs preop will decrease) Hypotension normally responds to fluid or pressor therapy
68
What type of drug is losartan?
ARB
69
Ace inhibitors are contraindicated for which patients?
renal artery stenosis

Anesthesia Pharmacology II (11 decks)

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