Peripheral Vasodilators Flashcards by hassan gonzales

List the five uses of peripheral vasodilators

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

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

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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What is Nitric Oxide (NO) synthesized from

amino acid L-arginine

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How does NO gain access to the smooth muscle cells

via diffusion from endothelial cells into vascular smooth muscle cells

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

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

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What are the five normal physiologic CV effects of NO

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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What are the three normal effects of NO on the lungs

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

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What is the normal effect of NO on platelets

inhibits platelet activation, aggregation, and adhesion

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What is the normal effect of NO on the nervous system

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

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What is the normal effect of NO on the immune system

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

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How is NO used to tx pulmonary HTN

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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What is the therapeutic concentration range of NO

0.05-80 ppm

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What is the onset of action of NO

1-2 minutes with rapid offset

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

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What is the half-life of NO in blood

6 seconds

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What are the six disadvantages of NO use

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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Sodium Nitroprusside Dehydrate (NTP) is a PRODRUG composed of

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

44% cyanide

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In the presence of light, NTP is rapidly converted to

CN-

*must protect from light

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What is the MOA of SNP

direct-acting, non-selective art/ven vasodilator

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

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

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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Name the three complications associated with NTP administration

Cyanide toxicity
Thiocyanate toxicity
Methemoglobinemia

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What are the s/s associated with CN- toxicity

Tachyphylaxis
Elevated SVO2
Mental status change»seizures
Metabolic acidosis

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Is there cyanosis associated with CN- toxicity

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

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Name six tx measures for cyanide toxicity

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

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What is the clinical indication for NTP

Acute management of HTN
Controlled hypotension
Afterload reduction

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What are the two contraindications of NTP

compensatory HTN | inadequate cerebral circulation

Name some CV effects of NTP

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

Name some Pulmonary effect of NTP

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

What is the MOA of Nitroglycerin (NGT)

permeates vascular smooth muscle and reacts with tissue thiols to liberate NO NO>>>increased cGMP>>activates MLC phosphotase>>>>dephosphorates MLCK>>relaxation

NGT selectively binds to

post-capillary veins * dilates capacitance vessels>>decreased venous return>>decreased ventricular wall tension (preload) * reduced myocardial O2 demand and increased endocardial perfusion

In high doses NTG can cause arterial vasodilation resulting in

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

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

NO * Selectively dilates large epicardial arteries increasing blood flow to ISCHEMIC areas of subendocardium * RobinHood effect

What is the difference b/t NTG and NTP

NTG may decrease the area of myocardial ischemia NTP may increase the area of myocardial ischemia

IV NTG has a half-time of

1. 5 minutes | * making it useful for when short decreases in BP is needed. eg. mayfield pin insertion

Can NTG produce methemoglobinemia

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

What are the six indications for NTG

``` periop HTN CHF Pulmonary HTN Angina pectoris Controlled Hypotension Sphincter of Oddi spasm ```

What are the three contraindications of NTG

constrictive pericarditis or pericardial tamponade Hypotension Increased intracranial pressure

Does NTG effect platelet function and is bleeding time prolonged

No yes,bleeding time is prolonged d/t vasodilation/venous pooling

Nicardipine is a calcium channel blocker that

binds to L-type calcium channels and impairs calcium entry into smooth muscles. * selective for arterial smooth muscle instead of cardiac muscles like verapamil

What are main cardiovascular effects of nicardipine

Significant SVR decrease (afterload goes down) dilation of coronary arteries 1000x nifedipine

What is the main effect that nicardipine has on the heart

Indirect increase in HR d/t compesatory response to vasodilation

Nicardipine is indicated for what two reasons

short term tx of hypotension periop control of bp during CV surgery

Nicardipine is not comptible with what solutions

LR or NaHCO3

Nicardipine is compatible with what solutions

Dextrose and saline

What are the three main AE of nicardipine

H/A>>>hypotension>>N/V

What are the two treatment medications for overdose of nicardipine

vasopressors calcium GLUCONATE

What is the single most important contraindication of nicardipine

Aortic stenosis

Nicardipine should be used with caution in which heart patient

CHF *may have negative inotropic effects

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

milky white injectable emulsion

Clevidipine is contraindicated in what three patient populations

allergies to soybeans, eggs hyperlipemia, acute pancreatitis Severe aortic stenosis

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

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

What is the MOA of Hydralazine

relaxes ARTERIAL smooth muscle via: inhibits release of calcium store from SR stimulates NO formation hyperpolarizes vascular smooth muscles increase cGMP

What is the onset of action of hydralazine

10-20 minutes

What is the effective half-life of hydralazine

2-4 hours

What is the elimination half-time of hydralazine

3 hours *effects last long, must be committed when using

What is a major SE of hydralazine

produces a drug-induced LUPUS syndrome *fever, arthralgia, arthritis, anemia, vasculitis

What is hydralazine used to treat

essential HTN pregnancy-induced HTN

What are the three contraindications of hydralazine

coronary artery disease (decreased afterload, but increased HR) mitral valve heart disease critical aortic stenosis

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

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

Fenoldapam is a dopamine agonist that agonizes what two receptor types

D1 A2

What is the effects of fenoldopam

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

Can fenoldapam be used in glaucoma patients

NO *increases intraocular pressure

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

increase in intracellular cGMP>>vascular smooth muscle relaxation counters angiotensin/NE in setting of HF decrease PAOP and SVR in HF patients

What drug is used as a short term tx for pheochromocytoma

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