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Anesthesia Pharmacology > 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
Q

When should you give a peripheral vasodilator?

A 
Treat HTN crisis
Maintain controlled hypotension
Improve LV stroke volume
-CHF
-Regurgitant valves
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26
Q

How do nitrovasodilators work?

A

Increase NO production which leads to increased cGMP

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27
Q

What are the functions of NO

A

Maintains CV tone, platelet aggregation, and CNS signalling

Aids in GI relaxation and immune functions

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28
Q

how is NO inactivated?

A

hemoglobin

29
Q

What is the duration of NO?

30
Q

NO is synthesized from ___________

A

l-arginine

31
Q

Which generates more NO, arteries or veins?

32
Q 
HOw are each of the following related to NO:
Essential HTN
Hypotension-septic shock
atherosclerosis
Vasospasm (after SAH)
A

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
Q

How is NO used clinically?

A

to tx pulmonary HTN
heart and lung transplant
-20-40 ppm; FGF must be > than MV
ARDS

34
Q

Does sodium nitroprusside (SNP) work on arterial or venous?

A

nonselective: arterial=venous

decereases both preload and afterload

35
Q

How does the chemical struture of SNP relate to its toxicity?

A

Iron center with 5 CN and 1 NO hanging off

36
Q

What is the infusion dose of SNP. Where do you start to run into trouble

A

0.3-10mcg/kg/min

CN accumulation at >2mcg/kg/min

37
Q

What is the duration of SNP?

38
Q

At low doses SNP causes a greater decrease in ________ than ________

A

afterload, preload

39
Q

SNP does not cause pulmonary vasodilation. t/f

40
Q

What are negative effects of SNP?

A 
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
Q

What is the treatment for cyanide toxicity

A
  1. Turn off SNP
  2. increase O2
  3. Bicarb if acidotic
42
Q

What are the effects of cyanide toxicity?

A

Tissue anoxia
Anaerobic metabolism
lactic acidosis

43
Q

What are the symptoms of thiocyanate toxicity?

A

fatigue
Tinnitis
N/V

44
Q

Why would thiocyanate toxicity occur?

A

impaired renal clearance

45
Q

What is the tx for thiocyanate toxicity?

46
Q

When would you use SNP?

A 
controlled hypertension
hypertensive emergencies
Cardiac Disease
-Decrease LV afterload
-Treat CHF
Aortic surgery
-manipulate BP during cross clamp
47
Q

SNP inhibits hypoxic pulmonary vasoconstriction. T/F

48
Q

With SNP cerebral blood flow is ________ and platelet aggregation is _________.

A

increased, decreased

49
Q

What is a side effect of NTG?

A

cerebral vasodilator-headache

50
Q

Nitroglycerin only dilates veins. T/F

A

F. if enough is given it will dilater arteries as well

51
Q

How does NTG decrease ventricular wall tension?

A

less volume returns

52
Q

What are the routes of administration for NTG?

A

Sublingual, transdermal. IV

Not PO–takes too long and too much 1st pass metabolism

53
Q

What is the emlimination half time of NTG?

54
Q

what effects does NTG have on the Pulmonary system?

Gi?

A

Cebrebral vasodilator-headache
Pulm vasodilaor
GI relaxation

55
Q

What are the clinical uses of NTG?

A

Angina pectoris
Cardiac failure
Acute HTN
Controlled hypotension

56
Q

Hydralizine is principally a _______ vasodilator

57
Q

What is the onset/duration of hydralazine?

A

onset 15-20 minutes, IV dose lasts hours

58
Q

What is the dose for hydralizine?

A

2.5-5 mg q 15 minutes

59
Q

What are the side effects fo hydralazine?

A 
Reflex tachycardia
headache
Angina
Flushing
Rash (when on hydralazine chronically)
coronary steal
60
Q

Why might hydralazine be preferred in OB

A

Maintains uterine BF

61
Q

Who would use papavarine?

A

Mostly vascular surgeons

you can give phenylephrine or norepi to fix it if it causes to much hypotension

62
Q

What are the uses of adenosine?

A

Endogenous nucleotide
potent coronary vasodilator
0.6-1.5 sec half life
use for PSVT

63
Q

What is trimethaphan?

A

Ganglionic blocker
10-200 mcg/kg/min
causes mydriasis

64
Q

How do ace inhibitors work?

A

Block conversion of Ang I → Ang II
Prevent Ang II vasocontriction and stimulation of sympathetic system
Ang II responsible for secretion of aldosterone

65
Q

What is the advantage to ACE inhibitors?

A

No CNS effects like other drugs

66
Q

What are the side effects of ACE inhibitors?

A

Cough
Angioedema
Contraindicated for pts with renal artery stenosis

67
Q

What is the protocol for ACE inhibotors and surgery?

A

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
Q

What type of drug is losartan?

69
Q

Ace inhibitors are contraindicated for which patients?

A

renal artery stenosis

Anesthesia Pharmacology (25 decks)

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