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Pharmacology > Peripheral Vasodilators > Flashcards

Peripheral Vasodilators Flashcards

1
Q

List the five uses of peripheral vasodilators

A 
manage hypertensive crises
induce controlled hypotension
facilitate LV forward SV
tx pulmonary HTN
mangange angina/myocardial ischemia
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2
Q

What are the three general mechanism by which peripheral vasodilators exert their effects

A

arterial vasodilation to decr. SVR (afterload)
venous vasodilation to decr. venous return and ventricular filing (preload)
to decrease both preload and afterload

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3
Q

What is Nitric Oxide (NO) synthesized from

A

amino acid L-arginine

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4
Q

How does NO gain access to the smooth muscle cells

A

via diffusion from endothelial cells into vascular smooth muscle cells

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5
Q

What is the MOA of NO once it enters smooth muscle cells

A

activates guanylate cylase»increase in cGmp»activation of MLC phosphatase»leading to dephosphorylation of MLC and promoting vasorelaxation

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6
Q

What are the five normal physiologic CV effects of NO

A 
regulates SVR/PVR
regulates distribution of CO
released in vascular autoregulation
generated by both art/veins
negative inotropic and chronotropic effects
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7
Q

What are the three normal effects of NO on the lungs

A

bronchodilation
selective dilation of vasculature supplying well-ventilated lung segments
mediator of V/Q matching

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8
Q

What is the normal effect of NO on platelets

A

inhibits platelet activation, aggregation, and adhesion

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9
Q

What is the normal effect of NO on the nervous system

A

NT of CNS and PNS
helps with memory
modulates pain and anesthetic effects

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10
Q

What is the normal effect of NO on the immune system

A

modulates inflamation
Macrophages activate NO synthase»NO
Kills bacteria, fungi, and protozoa in high concentration

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11
Q

How is NO used to tx pulmonary HTN

A

SELECTIVE pulmonary vasodilator: diffuses from alveoli to PV smooth muscle 3-5x CO and produces only pulmonary vasodilation (not systemic) bc it rapidly binds to and is inactivated by HEMOGLOBIN

*Vasodilates only portions of the lung that is well ventilated

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12
Q

What is the therapeutic concentration range of NO

A

0.05-80 ppm

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13
Q

What is the onset of action of NO

A

1-2 minutes with rapid offset

*rapidly binds to heme moiety of hgb and gets metabolized to methemoglobin

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14
Q

What is the half-life of NO in blood

A

6 seconds

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15
Q

What are the six disadvantages of NO use

A

corrosive to metal parts
special equipment required
metabolite (nitrogen dioxide»nitric acid)»pulmoonary edema and acid pneumonitis
methemoglobinemia
epithelia hyperplasia and ciliary depletion
rebound HTN

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16
Q

Sodium Nitroprusside Dehydrate (NTP) is a PRODRUG composed of

A

ferrous (Fe2+) iron center complexed with five cyanide (CN-) moieties and nitrosyl group

  • 44% cyanide
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17
Q

In the presence of light, NTP is rapidly converted to

A

CN-

*must protect from light

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18
Q

What is the MOA of SNP

A

direct-acting, non-selective art/ven vasodilator

enters RBC and interacts with 02hgb»methemoglobin + unstable SNP radical»5 CN- + NO

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19
Q

What three options does CN- have once produced by toxic NTP radical

A

bind to methemoglobin»cyano-methgb
react with liver and kidney»thiocyanate (sulfur required)»long term toxicity
bind to P-450»acute cyanide toxicity

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20
Q

Name the three complications associated with NTP administration

A

Cyanide toxicity
Thiocyanate toxicity
Methemoglobinemia

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21
Q

What are the s/s associated with CN- toxicity

A

Tachyphylaxis
Elevated SVO2
Mental status change»seizures
Metabolic acidosis

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22
Q

Is there cyanosis associated with CN- toxicity

A

NO

*Blood arterial saturation high, but cell can’t use it

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23
Q

Name six tx measures for cyanide toxicity

A 
DC NTP
give 100% 02
Sodium thiosulfate
Sodium Nitrate
Sodium Bicarbonate 
Vitamin B12
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24
Q

What is the clinical indication for NTP

A

Acute management of HTN
Controlled hypotension
Afterload reduction

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25
Q

What are the two contraindications of NTP

A

compensatory HTN

inadequate cerebral circulation

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26
Q

Name some CV effects of NTP

A 
decreased afterload/preload
increased HR/contractility (reflex)
decreased renal perfusion>>increased renin 
increased catecholamine
intracoronary STEAL and decreased DBP
27
Q

Name some Pulmonary effect of NTP

A

causes pulmonary vasculature dilation»reduction in pulmonary artery pressure»decreased perfusion of normally ventilated alveoi»increased dead space

prevents normal vasoconstrictive response of pulmonary vasculature to hypoxia»decreased pa02»>V/Q mismatch

*Tx with PEEP

28
Q

What is the MOA of Nitroglycerin (NGT)

A

permeates vascular smooth muscle and reacts with tissue thiols to liberate NO

NO»>increased cGMP»activates MLC phosphotase»»dephosphorates MLCK»relaxation

29
Q

NGT selectively binds to

A

post-capillary veins

  • dilates capacitance vessels»decreased venous return»decreased ventricular wall tension (preload)
  • reduced myocardial O2 demand and increased endocardial perfusion
30
Q

In high doses NTG can cause arterial vasodilation resulting in

A

decreased SVR (afterload)
decreased ESP»decreased myocardial workload»02 demand
reduced LVEDP»decreased coronary perfusion pressure and reduction of myocardial 02 supply

31
Q

Does NTG increase TOTAL coronary blood flow in the presence of atherosclerotic CAD

A

NO

  • Selectively dilates large epicardial arteries increasing blood flow to ISCHEMIC areas of subendocardium
  • RobinHood effect
32
Q

What is the difference b/t NTG and NTP

A

NTG may decrease the area of myocardial ischemia

NTP may increase the area of myocardial ischemia

33
Q

IV NTG has a half-time of

A
  1. 5 minutes

* making it useful for when short decreases in BP is needed. eg. mayfield pin insertion

34
Q

Can NTG produce methemoglobinemia

A

Yes

doses> 5 mg/kg
SPO2 will read 85% regardless of Pa02
Tx with methylene blue

35
Q

What are the six indications for NTG

A 
periop HTN
CHF
Pulmonary HTN
Angina pectoris
Controlled Hypotension
Sphincter of Oddi spasm
36
Q

What are the three contraindications of NTG

A

constrictive pericarditis or pericardial tamponade

Hypotension

Increased intracranial pressure

37
Q

Does NTG effect platelet function and is bleeding time prolonged

A

No

yes,bleeding time is prolonged d/t vasodilation/venous pooling

38
Q

Nicardipine is a calcium channel blocker that

A

binds to L-type calcium channels and impairs calcium entry into smooth muscles.

  • selective for arterial smooth muscle instead of cardiac muscles like verapamil
39
Q

What are main cardiovascular effects of nicardipine

A

Significant SVR decrease (afterload goes down)

dilation of coronary arteries 1000x nifedipine

40
Q

What is the main effect that nicardipine has on the heart

A

Indirect increase in HR d/t compesatory response to vasodilation

41
Q

Nicardipine is indicated for what two reasons

A

short term tx of hypotension

periop control of bp during CV surgery

42
Q

Nicardipine is not comptible with what solutions

A

LR or NaHCO3

43
Q

Nicardipine is compatible with what solutions

A

Dextrose and saline

44
Q

What are the three main AE of nicardipine

A

H/A»>hypotension»N/V

45
Q

What are the two treatment medications for overdose of nicardipine

A

vasopressors

calcium GLUCONATE

46
Q

What is the single most important contraindication of nicardipine

A

Aortic stenosis

47
Q

Nicardipine should be used with caution in which heart patient

A

CHF

*may have negative inotropic effects

48
Q

Clevidipine is a dihydropyridine CCB similar to nicardipine, but what is different about it’s preparation

A

milky white injectable emulsion

49
Q

Clevidipine is contraindicated in what three patient populations

A

allergies to soybeans, eggs

hyperlipemia, acute pancreatitis

Severe aortic stenosis

50
Q

What is the onset, half-life and context-specific half-life of clevidipine

A

onset= 60 seconds
half-life= 15 minutes
context-specific half-life at 12 hour= < 2 minutes

51
Q

What is the MOA of Hydralazine

A

relaxes ARTERIAL smooth muscle via:
inhibits release of calcium store from SR

stimulates NO formation

hyperpolarizes vascular smooth muscles

increase cGMP

52
Q

What is the onset of action of hydralazine

A

10-20 minutes

53
Q

What is the effective half-life of hydralazine

A

2-4 hours

54
Q

What is the elimination half-time of hydralazine

A

3 hours

*effects last long, must be committed when using

55
Q

What is a major SE of hydralazine

A

produces a drug-induced LUPUS syndrome

*fever, arthralgia, arthritis, anemia, vasculitis

56
Q

What is hydralazine used to treat

A

essential HTN

pregnancy-induced HTN

57
Q

What are the three contraindications of hydralazine

A

coronary artery disease (decreased afterload, but increased HR)

mitral valve heart disease

critical aortic stenosis

58
Q

What is the negative effect of decreasing afterload with hydralazine with use in heart patients

A

greater diastolic decrease in BP»decreased coronary perfusion

decrease afterload»>increase HR, contractility, SV»>CO= WORKLOAD»>angina pectoris and MI

*increase demand with decrease supply

59
Q

Fenoldapam is a dopamine agonist that agonizes what two receptor types

A

D1

A2

60
Q

What is the effects of fenoldopam

A

rapid-acting vasodilator in coronary, renal, mesenteric, and peripheral arteries

61
Q

Can fenoldapam be used in glaucoma patients

A

NO

*increases intraocular pressure

62
Q

What are the effects of B-type NAtriuretic Peptide (BNP)

A

increase in intracellular cGMP»vascular smooth muscle relaxation

counters angiotensin/NE in setting of HF

decrease PAOP and SVR in HF patients

63
Q

What drug is used as a short term tx for pheochromocytoma

A

Phentolamine

*increase in HR (reflex), increased release of NE (paradoxical)

Pharmacology (27 decks)

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