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Anesthesiology > Vasopressors > Flashcards

Vasopressors Flashcards

1
Q

What are the general effects of alpha-1 adrenergic receptor agonists?

A

Sympathetic regulation (decreased insulin release, vasoconstriction, mild inotropy, negative chronotropy)

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2
Q

What receptors do epi and norepi target?

A

Epi: alpha 1, alpha 2, beta 1, and beta 2
Norepi: alpha 1, alpha 2, beta 1

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3
Q

How is the change in BP different when using norepi vs epi?

A

With epi, you have alpha-1 and beta-2 effects (constrict and dilates) so you have a more pronounced increase in SBP and minimal changes in DBP; Norepi increases both equally

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4
Q

How does norepi affect HR?

A

Increased SVR -> baroreceptor mediated bradycardia (countered by beta-1 chronotropic effect) = no real change in HR

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5
Q

What pressor is best for renal preservation with severe sepsis?

A

Norepi (raises BP and preserves CO)

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6
Q

What receptors does dobutamine target?

A

Beta-1&raquo_space;> beta-2, alpha-1

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7
Q

First line pressor for hypotension? If CO is still low? If that doesn’t work? Still not working?

A

NE -> dobutamine -> vasopressin -> epi

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8
Q

What is the primary advantage of a NE gtt vs dopamine gtt?

A

Lower rate of arrhythmias (in particular tachyarrhythmias)

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9
Q

How are catecholamines metabolized in the liver vs. neurons? Final product of metabolism?

A

Liver: First by COMT, then MAO
Neurons: First by MAO, then COMT
Final product: Vanillymandelic acid (VMA)

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10
Q

What effects do you get of low-dose dopamine?

A

Significant DA1 agonist (renal artery vasodilation) and weak adrenergic receptor effects -> minimal increase in HR and contractility + diuresis

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11
Q

Are low-dose dopamine drips renal protective?

A

No, same number of kidneys fail with or without the drip

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12
Q

What effects do you get of medium-dose dopamine (5-10mcg/kg/min)? High dose (>10 mcg/kg/min)?

A

Medium: beta > alpha (vasodilation, increased HR, increased contractility)
High: alpha-1 + beta-1 and beta-2 (increased SVR)

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13
Q

What receptors do dopexamine target?

A

Beta-2&raquo_space;> Beta-1 and potent DA effects (opposite of dobutamine)

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14
Q

What receptors do isoproterenol target?

A

Beta 1 and beta 2 roughly equally

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15
Q

What is dromotropy?

A

The conduction speed of electrical impulses within the heart

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16
Q

What is lusitropy?

A

Ability of the heart to relax in diastole

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17
Q

Mechanism of action of ephedrine?

A

Increased post-synaptic NE release and/or decreased NE reuptake

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18
Q

What happens when you activate beta receptors?

A

G-protein couple receptors -> adenylate cyclase -> ATP to cAMP -> activates PKA (protein kinase A) -> increased intracellular Ca++ from sarcoplasmic reticulum

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19
Q

What is the mechanism of action of milrinone?

A

Phosphodiesterase 3 inhibitor: decrease the degradation of cAMP which increases intracellular Ca++

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20
Q

What happens when you activate alpha receptors?

A

G-protein coupled receptor -> phospholipase C -> splits phosphatidyl inositol -> release of Ca++ from sarcoplasmic reticulum

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21
Q

What cardiac effects do you see with milrinone?

A

Increased intracellular cAMP -> increased contractility, increased HR, arterial and venous vasodilation

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22
Q

How does nitric oxide work?

A

Lowers PA pressures by being a direct vasodilator; stimulates guanylate cyclase -> increased cGMP -> relaxation of smooth muscles

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23
Q

What receptors does fenoldopam target?

A

Purely DA1 agonist (systemic vasodilation and increased renal blood flow)

24
Q

How is sildenafil (Viagra) important in PA pressures?

A

Phosphodiesterase (PDA 5) inhibitor which is what breaks down cGMP (more cGMP -> more smooth muscle relaxation -> lower PA pressures)

25
Q

What is a side effect of NO (nitric oxide)?

A

Methemoglobinemia

26
Q

How does nesiritide work?

A

Recombinant BNP -> stimulates guanylate cyclase -> increases cGMP -> vasodilation (decreases afterload)

27
Q

When would you use nesiritide?

A

Severe decompensated heart failure by decrease afterload and encouraging forward flow

28
Q

During ACLS, what dose of vasopressin can be used instead of epi?

A

40 units

29
Q

Forumula for SVR and PVR?

A

SVR: (MAP - CVP) / CO
PVR: (PAP - PWP) / CO
(both multiplied by 80)

30
Q

Does vasopressin affect contractility?

A

No, only affects vascular tone

31
Q

How does phentolamine work?

A

Alpha-1 and alpha-2 antagonist

32
Q

How does prazosin work?

A

Alpha-1 antagonist

33
Q

How does labetalol work?

A

Non-selective beta blocker with alpha-1 antagonism

34
Q

Side effects of sodium nitroprusside?

A

Met-Hb and cyanide toxicity

35
Q

What effects do you see from cyanide toxicity?

A

Uncoupling of the electron transport chain -> increased anaerobic metabolism -> lactic acidosis

36
Q

Treatment for cyanide toxicity?

A
  1. Sodium nitrite (increase met-Hgb) to pick up cyanide and become cyanmet-Hgb, followed by methylene blue
  2. Sodium thiosulfate (binds cyanide producing thiocyanate)
  3. Vitamin B12
37
Q

Why would a patient with ARDS on sodium nitroprusside therapy have a sudden profound desaturation?

A

Sodium nitroprusside vasodilates pulmonary vasculature -> counteracts hypoxic pulmonary vasoconstriction -> increases blood flow to poorly oxygenated alveoli -> increased V/Q mismatch

38
Q

What medication can redistribute coronary blood flow to the subendocardium during ischemia?

A

Nitroglycerin

39
Q

Mechanism of action of nitroglycerin?

A

Decreases preload (venodilator) and wall tension, coronary artery vasodilator

40
Q

What are the beta-1 actions in the heart?

A

Increase inotropy, chronotropy, and dromotropy

41
Q

What are the primary effects of beta-2 action?

A

Systemic and pulmonary arteriolar vasodilation

42
Q

How does levosimendan work?

A

Calcium sensitizer without increasing Ca++, inotrope

43
Q

Common inotrope used following cardiac transplantation to maintain an elevated HR and CO?

A

Isoproterenol

44
Q

Which inotrope improves diastolic relaxation?

A

Milrinone

45
Q

Low dose epinephrine vs. higher doses?

A

Low-dose: beta-1 effect (alpha-1 offset by beta-2)

Higher-doses: alpha-1 effect predominates

46
Q

How are the catecholamines synthesized (order of compounds)?

A

Tyrosine -> DOPA -> Dopamine -> NE -> Epi

47
Q

Inotrope of choice in early cardiogenic shock with low BP and s/s of end-organ compromise?

A

Dopamine (alpha-1 effects will correct organ perfusion pressure) over dobutamine (beta-2 effect would worsen perfusion)

48
Q

Type of shock with elevated CO? Increased delivery of O2? Increased CVP? Decreased SVR?

A

Elevated CO: Distributive
Increased DO2: Distributive
Increased CVP: Cardiogenic & obstructive
Decreased SVR: Distributive

49
Q

What is another name for ADH?

A

Vasopressin

50
Q

What vasopressor is preferred in patients with aortic stenosis or HOCM?

A

Phenylephrine (from the reflexive bradycardia)

51
Q

How does sodium nitroprusside work?

A

SNP consists of 5 cyanide groups and a NO group: the NO diffuses out and stimulates guanylate cyclase -> increased cGMP -> smooth muscle relaxation

52
Q

What cardiovascular effects do you see with sodium nitroprusside?

A

Decreased SVR (arterial vasodilator), reflexive tachycardia, increased contractility, decreased preload (venodilator)

53
Q

What does sodium nitroprusside do to platelets?

A

Decreases the number and aggregation 1-6 hours after infusion; returns to normal 24 hours after infusion

54
Q

Why can you use phenylephrine in a hypotensive patient after induction with propofol who has coronary artery disease?

A

Phenylephrine will increase SVR, improving coronary perfusion (aortic diastolic pressure - LVEDP), and decreases HR (increases time for filling)

55
Q

What state of iron does methemoglobin have?

A

Ferric (3+)

Anesthesiology (21 decks)

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