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Clinicals > Vasopressors and Vasodilators > Flashcards

Vasopressors and Vasodilators Flashcards

1
Q

What can sympathomimetic agents lacking B1 specificity cause?

A

-cause intense vasoconstriction
-reflex-mediated bradycardia–aka, the phenylephrine effect

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2
Q

What is the MOA of sympathomimetics?

A

-either directly or indirectly activate beta or alpha adrenergic G-protein coupled receptors
-Increases cAMP–enhances calcium influx to the cytosol (actin and myosin interact more forcefully)

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3
Q

Direct vs indirect acting sympathomimetics:

A

-direct: Epi, NE, Phenylephrine, Dopamine

-indirect: ephedrine is the main one! Evoke the release of NE from postganglionic sympathetic nerve endings—then the NE acts on the adrenergic receptor

(phenylephrine has a lil bit of a indirect action)

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4
Q

Epinephrine:

A

“the prototype catecholamine”
-Alpha and Beta sitm, increases CO the HR the MOST, no real effect on PVR

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5
Q

Dose of Epinephrine:

A

1-2 mcg IVP

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6
Q

Phenylephrine:

A

-alpha1 agonist, tx hypotension
-VERY useful in CAD and AS b/c NO TACHYCARDIA!!
-venous constriction> arterial constriction
-mimics NE, but less potent and longer-lasting

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7
Q

What’s a big thing to look out for with Phenylephrine?

A

-REFLEX BRADYCARDIA: more of this the higher the dose of Neo ya give!

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8
Q

Dose of Phenylephrine:

A

50-100 mcg IVP (on hand: 10 mg/mL)

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9
Q

What should you give if you want to increase CO without increasing HR?

A

Vasopressin (per Dr. Kane)

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10
Q

Ephedrine:

A

-indirect acting, released NE acts on agonist receptor
-BP response is less intense and lasts 10x longer than epi
-tachyphylaxis develops QUICK
-can give IM (50 mg) for longer effect (ex: spinal anesthesia)

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11
Q

Which sympathomimetic is DOC for women in labor?

A

-Ephedrine!
-tx hypotension d/t SAB
-NO effect on uterine blood flow! Doesn’t put the baby at risk

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12
Q

Dose of ephedrine:

A

5-10 mg (on hand: 50 mg/mL)

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13
Q

True or False: Ephedrine has a little positive effect on PVR

A

True!

Epinephrine has no effect, Ephedrine has a little effect, Phenylephrine has a huge effect, and Vasopressin is in between ephedrine and Phenylephrine

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14
Q

Vasopressin:

A

-stimulates vascular V1 receptors to cause ARTERIAL vasoconstriction

-also increases renal-collecting duct permeability, increases water absorption

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15
Q

Which sympathomimetic is effective in reversing catecholamine-resistant hypotension?

A

Vasopressin!

(also treats ACE-I resistant hypotension)

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16
Q

What are the side effects of Vasopressin?

A

-CV: coronary artery vasoconstriction (so DON’T give to CAD pts)

-GI: stimulate GI smooth muscle…abd pain, N&V

-decreases platelet counts and antibody formation

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17
Q

Vasopressin Dose:

A

1-2 units

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18
Q

Nitric Oxide:

A

-chemical messenger for cGMP: inhibits calcium entry into smooth muscle-increases uptake at endoplasmic reticulum (relaxes muscle tone)

19
Q

What is the first line drug for pulmonary HTN in neonates?

A

Nitric Oxide!

20
Q

What all is nitric oxide involved in?

A

-CV tone relaxation
-platelet regulation
-CNS neurotransmitter
-GI smooth muscle relaxation
-immune modulation
-pulmonary artery vasodilation

21
Q

So how does NO release actually lower BP?

A

-decreases SVR: arterial vasodilators

-decrease venous return: venous vasodilators

22
Q

Is sodium nitroprusside an arterial or venous vasodilator?

A

-arterial vasodilator > venous

23
Q

Is Nitroglycerin an arterial or a venous vasodilator?

A

Venous vasodilator

24
Q

Sodium nitroprusside:

A

-relaxes arteries more than veins, but still both

-immediate onset, transient duration-requires continuous administration

-REQUIRES invasive arterial monitoring!!
**

25
Q

What is the dose of sodium nitroprusside?

A

-0.3 mcg/kg/min, titrated to 2 mcg/kg/min

26
Q

What are types of surgeries sodium nitroprusside is good or?

A

-pheochromocytoma
-case where you need immediate response b/c don’t wanna rupture an aortic suture line! (aortic surgery)
-spine surgery

27
Q

Which vasodilator can cause cyanide toxicity?

A

Sodium nitroprusside

-with higher doses-CN accumulates due to insufficient amount of sulfur donors/methemoglobin exhaustion

28
Q

When to worry about CN poisoning?

A

-when tachyphylaxis is developing with sodium nitroprusside and giving larger doses
-increased mixed venous sats
-metabolic acidosis
-CNS dysfunction, change in LOC

STOP DRUG!!

29
Q

Nitroglycerin:

A

-acts on venous capacitance vessels
(mostly) and large coronary arteries as well

-causes venous pooling: decreases CO b/c of decreases preload

30
Q

When can you hit tachyphylaxis with nitroglycerin?

A

60-100 mcg/min

dose dependent and duration dependent (within 24 hours) limits vasodilation

31
Q

Initial dose of nitroglycerin:

A

5-10 mcg/min infusion and titrate up d/t tachyphylaxis

32
Q

What are common uses for nitroglycerin?

A

-acute MI: relieves pulmonary congestion, decreases O2 requirements, limits MI size

-sphincter of Oddi spasm: give after glucagon!

-retained placenta: inhibits calcium release-placenta turns loose of the uterus

33
Q

Hydralazine:

A

-direct, systemic arterial vasodilator
-decreases ITP, decreases Calcium release
-causes EXTREME hypotension, rebound tachycardia

34
Q

What is the onset of hydralazine?

A

peak plasma concentration at 1 hr

35
Q

What is the initial dose of hydralazine?

A

2.5 mg IV

36
Q

1/2 life of Hydralazine:

A

3-7 hours**
slow starting but long-lasting!

37
Q

What are the different types of calcium channel blockeres?

A

-phenyl alkylamines: selective for AV node

-benzothiazepines: selective for AV node

-dihydropyrimidines: selective for arterial beds**the ones that cause vasodilation!!!

38
Q

How do CCB’s work? (MOA)

A

bind to receptors on voltage-gated calcium ion channels (L type, main pathway) and decrease calcium influx…inhibits excitation-contraction coupling

39
Q

What 2 things are decreased with CCB’s?

A

-decreased vascular smooth muscle contractility (decreased SVR and systemic blood pressure, increased coronary blood flow)

-decreased speed of conduction through the AV node

40
Q

Nicardipine:

A

-aka Cardene
-greatest at coronary artery dilation!!
-short term control of hypertension
-great effects with minimal side effects
-NO change in HR!

41
Q

Dose of Nicardipine:

A

5 mg/hr, can increase by 2.5 mg/hr 4 times, MAX dose of 15 mg/hr

42
Q

True or False: Nicardipine is a quick onset and offset drug

A

True!

50% drug decrease 30 minutes after D/C

43
Q

Which vasodilator can worsen PaO2?

A

Sodium Nitroprusside d/t affected hemoglobin

44
Q

Which drug would be the first intervention for HTN post-CEA?

A

cardene drip b/w won’t increase HR and causes arterial dilation

Clinicals (8 decks)

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