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Pharm 2 > Vasoconstrictors - Week 1 > Flashcards

Vasoconstrictors - Week 1 Flashcards

1
Q

2 hemodynamic effects of vasoconstrictors

A

Increase arterial resistance and after load (increase SVR and MAP)

Increase venous return (increase preload and CO)

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2
Q

Reflex changes of vasoconstrictors include:

A
  • decreased HR
  • decreased conduction
  • occasionally decreased contractility
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3
Q

non cardiac effects of vasoconstrictors

A
  • bronchodilation
  • glycogenolysis
  • insulin, renin, and pituitary hormone
  • CNS stimulation (low lipid solubility)
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4
Q

indications for vasoconstrictors

A
  • decreased arterial resistance (HoTN)
  • CPR
  • Anaphylactic shock
  • intracardiac R –> L shunts
  • hypovolemia
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5
Q

2 types of HoTN

A

Iatrogenic and Physiologic

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6
Q

What is the goal of using vasoconstrictors in CPR?

A

To restore perfusion pressure to vital organs (used in conjunction w other appropriate cardiac drugs)

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7
Q

Name 4 complications/contraindications for vasoconstrictors

A
  • can worsen LV failure
  • can exacerbate RV failure
  • can decrease renal blood flow
  • can mask hypovolemia
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8
Q

Epi stimulates which receptors?

A

alpha 1, Beta 1, and Beta 2

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9
Q

Epi is the most potent activator of ________ receptors. it is ______x more potent than NE.

A

Alpha 1

2-10

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10
Q

How does epidural increase the following processes:

  • lipolysis
  • glycogenolysis
  • insulin secretion
A

lipolysis - increases
glycogenolysis - increases
secretion of insulin - decreases

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11
Q

T/F Epi decreases blood sugar in response to surgical stress.

A

False - episode increases the blood sugar

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12
Q

Does epi decrease renal blood flow even in the absence of changes in systemic BP?

A

yes.

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13
Q

Name 2 renal effects of epi

A
  • potent renal vasoconstrictor (a1 effect)

- stimulates renin release (indirect effect)

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14
Q

What is the physiological effect of low doses (1-2 mcg/min) of epi?

A

Predominantly B2 stimulation

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15
Q

Compare the alpha effects to the B2 effects of low dose epi, and what is the net effect on SVR and MAP?

A

a1 receptors in skin, mucosa, and hepatorenal system are stimulated

B2 receptors in sk musc are stimulated

Net effect:

  • decreased SVR (distribution of blood to sk muscle)
  • MAP remains the same (essentially)
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16
Q

What are the physiological effects of intermediate doses of epi (4 mcg/min)

  • receptor stimulated:
  • effect on HR, contractility, and CO
  • effect on automaticity
A

Predominantly B1 stimulation

  • increased HR, contractility, and CO
  • increased automaticity (may lead to dysrhythmias)
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17
Q

What would be considered high dose epinephrine, and what receptor predominates at this dose?

A

> 10 mcg/min

Alpha 1

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18
Q

Epinephrine is the most potent activator of Alpha 1 receptors. It is a potent vasoconstrictor of the ______, ______, and ______ vascular beds with no significant effect on _______ _______. It is therefore used to maintain ________ and _______ perfusion

A

vasoconstrictor of cutaneous, splanchnic, and renal beds

little effect on cerebral arterioles

used to maintain myocardial and cerebral perfusion

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19
Q

Can reflex bradycardia occur w epinephrine?

A

Yes.

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20
Q

What is racemic epi, and what does it do?

A

moisture of levo- and dextrorotary isomers

constricts edematous mucosa

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21
Q

What are 3 indications for racemic epi?

A
  • severe croup
  • post-extubation airway edema
  • traumatic airway edema
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22
Q

Racemic epi tx lasts _______ minutes. The pt should be observed for ___ hrs after tx to watch for _____.

A

30-60 min

2 hrs

rebound

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23
Q

What are the CNS of epi?

A

There aren’t any.

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24
Q

What are 8 side effects of epi?

A
  • hyperglycemia
  • mydriasis
  • plt aggregation
  • sweating
  • HA
  • tremor
  • nausea
  • arrhythmias
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25
Q

What 5 things should be monitored on a pt who has received/is receiving epinephrine?

A
  • BG
  • RR
  • O2 sats
  • HR
  • BP
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26
Q

How does NE affect:

  • SBP
  • DBP
  • MAP
A

increases all three my adjusting SVR (alpha 1 effects)

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27
Q

NE is a potent vasoconstrictor of ______, _______, and _______ vascular beds. What are the implications for each?

A

Renal, mesenteric, and cutaneous

  • Renal - decreased RBF –> oliguria
  • Mesenteric - mesenteric infarct
  • Cutaneous - periph hypo perfusion –> gangrene of digits
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28
Q

T/F: NE is a potent alpha agonist that produces intense arterial AND venous vasoconstriction in ALL vascular beds and LACKS bronchodilating effects.

A

True

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29
Q

T/F: NE is primarily an a1 agonist, and any B1 effects are overshadowed by a1 effects.

A

True.

The B2 effects are virtually non-existent. However, it can still cause arrhythmias r/t the B1 effects.

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30
Q

How do high and low doses of NE affect CO?

A

Low doses - CO increases

High doses - CO may decrease b/c of increased after load and baroreceptor-mediated reflex bradycardia. Refractory HoTN is also a possibility.

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31
Q

How do the metabolic effects of NE compare to the metabolic effects of epi?

A

Fewer metabolic effects w NE (B/c it doesn’t have the B2 effects as much)
Larger doses of NE may have metab effects.

32
Q

What is the effect of dopamine at 5 mcg/kg/min?

A

It causes NE to be released, contributing to cardiac stimulation (precursor)

33
Q

What is the effect of dopamine at 10 mcg/kg/min?

A

alpha effects begin to predominate

34
Q

At what dose of dopamine do the Alpha receptor effects definitely predominate?

A

> 20 mcg/kg/min

35
Q

How does dopamine effect the pulm status?

A

It. doesn’t.

36
Q

What are the CNS effects of dopamine:

  • IV
  • Increased dopamine
  • Decreased dopamine
  • D2 inhibition
A
  • IV dopamine - none, it doesn’t cross the BBB
  • increased dopamine - mania
  • decreased dopamine - schizophrenia, ADHD, PD
  • D2 inhibition - decreased prolactin secretion
37
Q

What 5 things should be monitored in a pt on dopamine?

A
  • BP
  • HR
  • MAP
  • UOP
  • Mental status
38
Q

T/F: All catecholamines are sympathomimetics, but no tall sympathomimetics are catecholamines.

A

True

39
Q

What type of drug is ephedrine, and what are the clinical implications?

A

Synthetic noncatecholamine

It still works on the sympNS, but it isn’t metabolized by COMT, and it is not recycled. Therefore, it is entirely dependent on MAO for metabolism.

40
Q

Ephedrine has direct and indirect actions, but its principle effect is ______.

A

indirect

41
Q

Beta stimulation by ephedrine may evoke ________, particularly in a ________ ________.

A

Arrhythmias

Sensitized myocardium

42
Q

What is the principle mechanism of ephedrine?

A

increased myocardial contractility

43
Q

How do the Beta 1 effects of the ephedrine combine with the release of NE caused by ephedrine to increase CO?

A

Nepi: venoconstriction > arteriolar constriction –> increased preload

B1: increased HR and contractility

combination leads to increased CO

44
Q

Does ephedrine increase both SBP and DBP as a result of the increased CO?

A

Yes

45
Q

Explain how tachyphylaxis occurs w repeated dosing of ephedrine.

A

A2 in the CNS senses too much NE so it stops making NE. If NE is not available, it will not be released in response to ephedrine.

46
Q

How does ephedrine affect uterine blood flow and bronchial smooth muscle?

A

preserves or increases UBF

Bronchial smooth musc relaxant (direct effect)

47
Q

T/F: Ephedrine is similar to epinephrine, but the BP response is less intense and lasts longer.

A

True.

It lasts longer because it has no reuptake and is metabolized by MAO only. this makes it last longer than a normal catecholamine.

48
Q

Does ephedrine cross the BBB?

A

Yes. Therefore, high doses can cause psychosis.

49
Q

Side effects of ephedrine

A
  • HTN
  • insomnia
  • urinary retention
  • HA
  • weakness
  • tremor
  • palpitations
  • psychosis
50
Q

What 4 things should be monitored in a pt receiving ephedrine?

A
  • BP
  • pulse
  • UOP
  • mental status
51
Q

How are ephedrine OD and extravasation treated?

A

Supportive therapy

52
Q

What type of drug (structurally) is phenylephrine?

A

synthetic non-catecholamine

53
Q

Which does phenylephrine increase more, preload or after load?

A

preload

54
Q

Phenylephrine increases PVR when:

A

CO is adequate

55
Q

Phenylephrine may be used to improve _____ _____ _____ w/o _____ side effects

A

coronary perfusion pressure

chronotropic

56
Q

Is phenylephrine safe for preggo pts?

A

Yes.

(Neo used to be taboo, and ephedrine was the drug of choice. But Neo is actually just as good as ephedrine, if not better. Neo has also been associated w better fetal acid-base status than ephedrine)

57
Q

3 alternative uses for phenylephrine

A
  • drug induced priapism
  • mydriatic agent
  • nasal decongestant
58
Q

Phenylephrine decreases ______ and ______ blood flow and increases ______ and ______.

A

decreases renal and splanchnic

increases pulm art resist and pressure

59
Q

T/F: although phenylephrine does cause reflex bradycardia, it doesn’t not directly cause dysrhythmias.

A

True

60
Q

T/F: phenylephrine is like NE but less potent and longer lasting.

A

True.

It lasts longer because it is not reuptaken and recycled. It is only metabolized by MAO.

61
Q

What 4 things should be monitored in a pt receiving phenylephrine?

A
  • BP
  • HR
  • ABG
  • CVP
62
Q

What posterior pituitary hormones increase BP?

A

Arginine vasopressin (AVP) (Pitressin)

DDVAP (Desmopressin)

Oxytocin (Pitocin)

63
Q

What are the ratios of Antidiuretic : Vasopressor effects of the following drugs:

  • Arginine vasopressin
  • Oxytocin
  • DDAVP
A

antidiuretic: vasopressor effects
- AV 100:100
- Oxytocin 1:1
- DDAVP 1200:0.39

64
Q

Vasopressin stimulates vascular _______ receptors causing intense arterial vasoconstriction.

A

V1a

65
Q

Vasopressin increases the permeability of cell membranes resulting in the passive reabsorption of water via the _____ receptors in the renal _________.

A

V2

collecting ducts

66
Q

Vasopressin is used to preserve _________ homeostasis in pts w _______.

A

cardiocirculatory homeostasis

advanced vasodilatory shock

67
Q

Vasopressin is good for pts who:

A
  • conventional vasopressor therapy has failed or the pt is resistant to it
  • experience adverse effects of conventional vasopressor therapy
68
Q

T/F: Unlike catecholamines, effects of arginine vasopressin are preserved during hypoxia and severe acidosis.

A

True

69
Q

3 Advantages of vasopressin over epinephrine

A
  • epi increases myocardial O2 consumption, contributing to the risk of developing post-resuscitation MI and arrhythmias
  • catecholamines may not work as well in an acidic environment associated w CPR
  • in animal studies, vasopressin is associated w:
    • better blood flow to vital organs
    • better delivery of cerebral O2
    • better chance of resuscitation and better neurologic outcome
      (human data is lacking)
70
Q

T/F: Vasopressin is at least as effective as epi, may have fewer adverse effects than epi, and therefore is a reasonable alternative to epi in the tx of cardiac arrest.

A

True, esp if pt is highly acidic

71
Q

adverse effects/drug interactions of vasoconstrictors

A
  • cardiac dysrhythmias (beta stimulation)
  • pure alpha agonists can activate baroreceptor reflex mediated bradycardia and possibly decrease CO
  • antihypertensives may decrease the pressor response to indirect acting drugs or enhance the response to direct acting drugs (denervation hypersensitivity)
72
Q

How do tricyclic antidepressants and MAOI’s interact w vasoconstrictors?
What are the anesthetic implications?

A
  • increase availability of endogenous NE
  • exaggerated response w indirect acting agents
  • worse in the first 14-21 days of therapy (then down regulation of receptors occurs)
  • ok to continue these drugs in the period period
  • use a decreased dose of direct acting drugs
73
Q

How does cocaine interact w vasoconstrictors?

How is acute toxicity best managed?

A
  • interferes w re-uptake of catecholamines –> both exogenous and endogenous catecholamine effects are enhanced
  • produces central and peripheral sympathetic stim –> vasoconstriction, tachycardia, and arrhythmias
  • acute toxicity may best be managed w adrenergic blockade (Labetalol w a and B effects)
74
Q

How do natural weight loss products interact w vasoconstrictors?
How soon before surgery should a pt stop taking the product?

A
  • they may contain ma Huang (ephedra) which contains ephedrine, pseudoephedrine
  • long term use results in tachyphylaxis from depletion of endogenous catecholamines stores –> peri-op hemodynamic instability and cv collapse
  • stop product at least 24 hrs prior to surgery
75
Q

What drug should be used to treat extravasation from vasoconstrictors? How does it work?

A

Phentolamine

  • alpha 1&2 antagonist
  • peripheral vasodilator
  • treats skin necrosis 2* to NE, dopamine, and epi

Pharm 2 (7 decks)

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