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CRNA Pharmacology > Sympathomimetics > Flashcards

Sympathomimetics Flashcards

1
Q

Main use of NE

A

As a potent vasoconstrictor to increase PVR and MAP

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2
Q

1st line vasopresser of choice to treat septic shock?

A

NE

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3
Q

NE dosage

A

0.01 to 3μg/kg/min OR 2 to 16μg/min

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4
Q

Why should NE be used cautiously in PTs with right ventricular failure?

A

They can’t tolerate the increase in pulmonary vascular resistance and/or increase in venous return

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5
Q

NE is a potent A1 agonist that produces intense arteriole and venous constriction in all vascular beds except_____?

A

Coranry arteries

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6
Q

Why should NE be used with caution in PTs with pulmonary HTN?

A

NE increases venous constriction in the lungs which further increases pulmonary HTN

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7
Q

NE effect on the following:

1) Afterload
2) SVR
3) DBP
4) MAP
5) SBP

A

Increases all of them

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8
Q

How can NE cause tissue hypoxia, metabolic acidosis, ischemia, and renal failure?

A

Excessive peripheral vasoconstriction and decreased perfusion of renal splanchnic beds can lead to hypo perfusion of organ and oliguria leading to renal failure.

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9
Q

How do you prevent renal failure in patients with excessive NE use?

A

Adequate fluid volume resuscitation

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10
Q

Which receptors do the following bind:

1) NE
2) EPI
3) Dopamine
4) Isoproterenol
5) Phenylephrine
6) Dobutamine

A

1) NE - A1, A2, B1
2) EPI - A1, A2, B1, B2
3) Dopamine - A1, A2, B1
4) Isoproterenol - B1, B2
5) Phenylephrine - A1
6) Dobutamine - A1, B1, B2

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11
Q

Why is NE never used just for its inotropic effect?

A

Modest B1 agonist - minimal effect is seen on HR due to activation of baroreflex response.

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12
Q

Effect of NE on coronary arteries?

A

NE (just like Epi) dilates the coronary arteries which increases coronary blood flow.

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13
Q

NE and hyperglycemia

A

NE may cause hyperglycemia but is unlikely as it is seen with use of EPI. It is only seen when large doses of NE are given.

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14
Q

Which anesthetic drugs are contraindicated with the use of Levophed, EPI and NE? Why?

A

Cyclopane and Halothane because they increase cardiac autonomic irritability causing VTACH or VFIB.

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15
Q

Why is use of NE cautioned in PTs taking MAOIs or antidepressants of the Triptyline or Imipramine type?

A

Can cause severe and prolonged HTN

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16
Q

How is NE extravasation treated?

A

Phentolamine mesylate (Regitine) 5 to 10 mg diluted in 10mL NaCl injected SQ into the area

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17
Q

MOA of Phentolamine mesylate (Regitine)

A

Phentolamine is a competitive, non-selective A1 and A2 antagonist

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18
Q

Dopamine role

A
  • Precuror to NE
  • Endogenous neurotransmitter in both the PNS and CNS
  • Regulates movement in the CNS (i.e. Parkinsons)
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19
Q

Why can’t Dopamine be administered PO?

A
  • It’s not lipid soluble (also can’t cross BBB to cause CNS effects.
  • Metabolized by liver, kidney and plasma MAO and COMT enzymes to inactive metabolites
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20
Q

Why must Dopamine be given as a continuous infusion?

A

It is rapidly metabolized:

  • onset of action = 5 mins
  • plasma half-life = 2 mins
  • duration of action < 10 mins
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21
Q

What would happen if Dopamine is given to a PT on an MAOI?

A

MAO enzymes metabolize Dopamine, if they are inhibited, the effects of dopamine will be increased.

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22
Q

2 things that inactivate Dopamine

A
  • Alkaline solutions (use D5W instead)

- Light

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23
Q

Why is Dopamine unique among the catecholamines?

A

It simultaneously increases myocardial contractility, renal blood flow, glomerular filtration rate, sodium excretion and urine output.

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24
Q

Dopamine Doses?

A
  • Dopamine dose - 0.5 to 3μg/kg/min
  • Beta dose - 3 to 10μg/kg/min
  • Alpha dose - 10 to 20μg/kg/min
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25
Q

Effects of Dopamine dose (0.5 to 3μg/kg/min) of dopamine

A
  • ↑ Renal and splanchnic blood flow = diuresis
  • ↓ SPB and DBP causing hypotension
  • ↓ Preload and afterload
  • ↑ Contractility
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26
Q

Renal Dose of Dopamine

A
  • Same as Dopamine dose (0.5 to 3μg/kg/min)

- Promotes renal blood flow, diuresis and sodium excretion via dopamine1 and dopamine2 receptors

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27
Q

Which drugs antagonize Renal Dose of Dopamine?

A

Droperidol, haloperidol, and metoclopramide because the bind and block the dopamine2 receptors

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28
Q

Can you use the Renal dose of Dopamine to protect renal PTs?

A

No! although it has diuretic effects, no evidence show a ↓ of ARF with this dosing.

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29
Q

Hypoxemia effect on Renal Dose of Dopamine?

A

Attenuates of reduces effect

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30
Q

Effects of Beta dose (3 to 10μg/kg/min) of dopamine

A
  • B1 cardiac effects predominate
  • ↑ in NE release from synaptic nerve endings
  • ↑ HR, CO, SBP and contractility
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31
Q

Why is Dopamine less reliable at ↑ CO in PTs with chronic cardiac failure?

A

Because the stores of neurotransmitters might be depleted. Dopamine can no longer stimulate release of NE because there is no more

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32
Q

Effects of Beta Dose of Dopamine on SVR

A

Usually little change is seen because B1 stimulation dominates and there is little A1 binding to cause vasoconstriction.

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33
Q

Cardiac effects of dopamine

A

Positive chrono trope, isotrope, dromotrope and lusitrope (rate of myocardial relaxation)

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34
Q

Effects of Alpha dose (10 to 20μg/kg/min) of dopamine

A
  • Predominately stimulates A1 receptors
  • ↑ Arterial and venous constriction
  • ↑ Afterload and preload
  • ↑ SVR, BP, MAP
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35
Q

Effect of High doses ( > 20 μg/kg/min) of Dopamine

A
  • Vasoconstriction compromises circulation in limbs
  • B1 cardiac effects get override
  • Reversal of renal dilation results in antidiuresis
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36
Q

GI risks of Dopamine

A
  • N and V

- Mesenteric ischemia leading to bacterial translocation and multiple organ dysfunction syndrome

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37
Q

Pulmonary/Ventilation risks of Dopamine

A
  • Depression of ventilation: monitor ABGs and ensure they do not deteriorate
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38
Q

Endocrine risks of Dopamine

A
  • Hyperglycemia possible
  • ↓ prolactin, growth, thyroid and pituitary hormone secretion
  • Prolonged infusions can deplete NE stores
  • Halogenated hydrocarbon anesthetics ↑ of ventricular arrhythmias
  • ↑intraocular pressure (be careful with glaucoma PTs)
39
Q

Isoproterenol’s potency at Beta receptors

A

Isoproterenol is the most potent activator of all sympathomimetics at Beta receptors. It is a more potent activator at B1 and B2 than Epi and NE

40
Q

How can Isoproterenol be given?

A
  • Bolus IV injection followed by a continuous infusion
  • IM
  • SQ
  • Intracardiac
  • Aerosol
41
Q

(T/F?) Isoproterenol must be protect from light?

A

True

42
Q

Metabolization of Isoproterenol

A

Metabolized primarily by COMT in the liver

43
Q

Clinical uses of Isoproterenol

A
  • Heart blocks
  • Cardiac arrest until electric shock or pacemaker available
  • Bronchospasms during anesthesia (0.01 to 0.02mg diluted in 0.5 to 1 ml NaCl) given via IV
  • Adjunct to fluid and electrolyte replacement
44
Q

Isoproterenol B1 effects @ 1 to 10μg/min continuous IV

A
  • ↑ HR, contractility, automaticity and myocardial oxygen consumption
45
Q

Isoproterenol B2 effects @ 1 to 10μg/min continuous IV

A
  • ↑ HR and contractility

- ↓ Preload and afterload, PVR, DBP, CO, renal blood flow, and MAP

46
Q

(T/F?). All sympathomimetics has the potential to cause tachyarrhythmias?

A

True

47
Q

Why should you NOT use Isoproterenol to treat septic shock patients?

A

Potent B2 agonists effects cause systemic vascular resistance to fall which ↓ DBP and impair coronary perfusion pressure.

48
Q

Classify the sympathomimetic agents based on their chemical structure?

A

1) Endogenous catecholamines - Epi, NE, and Dopamine
2) Synthetic catecholamines - Isoproterenol and dobutamine
3) Direct Acting Synthetic non-catecholamines - Phenylephrine
4) Indirect Acting Synthetic non-catecholamines - Amphetmines
5) Mixed Acting Synthetic non-catecholamines - Ephedrine

49
Q

Dobutamine recepter affinity

A

B1 > B2> A1

50
Q

Dobutamine is NOT a pure B1 adrenergic agonist! elaborate!

A

It is a racemic mixture (+) and (-)
(+) is more potent at B1 and B2, and antagonist at A1
(-) is less potent at B1 and B2 and a potent A1 agonist

51
Q

Dobutamine metabolism

A
  • Rapidly metabolized by COMT
  • Plasma half time = 2 mins
  • Need a CI at 2.5 to 20μg/kg/min for therapeutic levels
  • Onset of action 1 to 2 mins
  • Steady state achieved in 10 mins
52
Q

Why does Dopamine, EPI and Dobutamine have to be dissolved in D5W?

A

To avoid inactivation of the catecholamine that may occur in alkaline solution

53
Q

Clinical use of Dobutamine

A
  • Inotropic Support to increase CO
  • ↓ Output from organic heart disease or surgical procedures
  • Useful if HR and SVR are already increased
54
Q

When is Dobutamine used with vasodilators

A

When you want to ↓ afterload in the presence of ↑ SVR

55
Q

When is Dobutamine used with Dopamine

A

To ↑ CO and renal perfusion (dopamine)

56
Q

Cardiovascular effect of Dobutamine

A
  • Positive inotrope with mild effects on HR and BP
  • Dose dependent ↑ in CO and SV without increase in HR
  • HR ↑ only slightly if dose is < 20μg/kg/min
  • LV filling is decreased
  • ↓ in pulmonary vascular resistance
  • Doesn’t cause release of endogenous NE
57
Q

High doses ( > 10μg/kg/min) of Dobutamine

A

may cause tachyarrhythmias but are uncommon

58
Q

Effects of Dobutamine dose of 2.5 to 20μg/kg/min

A
  • ↓ Preload
  • ↓ Afterload
  • ↑ Contractility
  • Hr or ↑
59
Q

MOA of Ephedrine

A

Mixed Acting synthetic non-catecholamine

  • Direct acting - ↑ NE release from nerve terminal (Majority of ephedrine effect is this indirect method)
  • NonDirect Acting - Weak A1, A2, B1, B2 agonist
60
Q

2 drugs the block the effect of Ephedrine? How?

A

Reserpine and Guanethidine - by blocking the re-uptake of NE, which Ephedrine relies on as a mostly non-direct acting synthetic noncatecholamine

61
Q

Ephedrine characteristics

A
  • Lipid soluble
  • Potent CNS stimulant (can cross BBB)
  • Can be taken PO, IM and IV
  • Metabolized slowly by MAO but not acted on by COMT
  • Excreted in urine (t 1/2 = 3 to 6 hrs)
  • Can produce mydriasis
  • Does not cause hyperglycemia like EPI
62
Q

Clinical uses of Ephedrine

A
  • Tx hypotension in parturients (10mg to 25mg IV)
  • Tx of bronchial asthma
  • Nasal decongestant (topical)
  • Antiemetic (0.5mg/kg IM)
63
Q

Cardiovascular effect of Ephedrine

A
  • ↑ Afterload
  • ↑ Contractility
  • ↑ HR
64
Q

Effects of PT taking clonidine before they get Ephedrine

A

Oral Clonidine is an A2 agonist (just like precedex) and will enhance the presser effects of ephedrine.

65
Q

Ephedrine is subject to tachyphylaxis! Explain

A

It is an indirect act synthetic non-catecholamine that relies on the endogenous stores of NE, it will stop working after the stores are depleted

66
Q

Which medical conditions presents with already depleted stores of neuronal catecholamines?

A

Sepsis and heart transplant - ephedrine won’t work in these PTs

67
Q

Usual dose of Ephedrine

A

2.5 to 25μg/kg/min IV or 25 to 50mg IM

68
Q

Why is Ephedrine NOT a good agent to use to restore BP in women about to give birth?

A

It lowers umbilical artery pH resulting in fetal acidosis at delivery

69
Q

How long should you wait to administer Ephedrine after the PT has taken and MAOI?

A

14 days - Ephedrine is metabolized very slowly by MAOs

70
Q

(T/F?) All non-catecholamines are less potent than catecholamines?

A

True

71
Q

Can Phenylephrine activate Beta receptors?

A

Although considered and A1 agonist, it has some Beta effects at high doses.

72
Q

Clinical use of Phenylephrine

A
  • Hypotension associated with anesthetics (usual dose = 50 to 200μg IV)
  • Hypotension associated with septic shock (dose = 0.5 to 8μg/kg/min)
  • CI at 20 to 50μg/min to sustain BP during carotid endarterectomy
  • To relieve drug-induced prism (persistent erection)
  • Nasal decongestant (topical)
73
Q

Phenylephrine Cardiovascular effects

A
  • ↑ Afterload
  • Contractility
  • ↓ HR
74
Q

Uterine Effects of Phenylephrine

A
  • Uterine blood flow slightly decreased

- Higher umbilical pH and less fetal acidosis at delivery compared to ephedrine

75
Q

Amphetamie characteristics

A
  • ↑ NE, DA, and 5HT release from their storage sites in nerve terminals
  • Mainly works in CNS
  • Lipid soluble (crosses BBB)
  • CNS stimulant
  • Tachyphylaxis common
  • Weak bases (overdose tx is to acidify urine)
76
Q

Cardiovascular Effects of Amphetamines

A
  • ↑ SBP and DBP

- ↓ HR

77
Q

CNS effects of Amphetamines

A
  • Apetite supression
  • Enhances analgesia produced by opioids
  • ↑ Respiration and depth of respiration
  • Feeling awake and alert, agitated, dizzy and restless
78
Q

“Selective B2-Adrenergic Agonists” MOA

A
  • Selective B2 agonists - stimulates activity of adenyl cyclase and ↑ cAMP leading to bronchodilation and inhibition of release of mediators of hypersensitivity from mast cells.
  • Relaxation of uterine smooth muscle
79
Q

Clinical uses for Selective B2-Adrenergic Agonists

A
  • Acute episodes of bronchospasms
  • TX of asthma and COPD, chronic bronchitis and emphysema
  • Prevent exercise-induced bronchospasm
    Tocolytics (i.e. Ritodrine and Terbutaline) - stops premature labor
80
Q

(T/F?) LABAs should never be used to treat an acute asthma attack or acute bronchospastic attack?

A

Only SABAs should be used for this

81
Q

Selective B2-Adrenergic Agonists Adverse Effects

A
  • Tremor
  • Tachycardia
  • Palpitations
  • Nervousness and insomnia
  • hyperglycemia and hypokalemia
  • Arrhythmias and EKG changes
  • Parodoxical bronchospasm
82
Q

Interaction of Selective B2-Adrenergic Agonists with MAOIs and TCAs

A

Shouldn’t be administered within 2 weeks of each other because their actions potentiate each other

83
Q

2 types of Selective B2-Adrenergic Agonists

A

1) SABAs (onset - < 5 mins, duration - 3-6 hrs)
2) LABAs (onset - < 5 mins, duration > 12 hrs)
* Has nothing to do with the onset of action, only the duration

84
Q

Types of SABAs

A
  • Albuterol
  • Levalbuterol
  • Respiclick
  • Terbutaline
  • Bitolterol
  • Metproterenol
  • Perbuterol
    ALBert’s LEVel of RESpect TERminiate BITter METhodical PERsonalities
85
Q

The only 2 inhaled SABAs currently available?

A

Albuterol and Levalbuterol

86
Q

Characteristics of Albuterol

A
  • Is a racemic mixture (R and S enantiomers) only the R enantiomer can do B2 agonism
  • Available as PO tablet or syrup, MDI
87
Q

Levalbuterol Characteristics

A
  • The R enantiomer of albuterol
  • Available as MDI or solution for inhalation
  • Cause less tachycardia than Albuterol
88
Q

Types of LABAs

A
  • Salmeterol
  • Formeterol
  • Arformoterol
  • Indacaterol
  • Olodaterol
  • Vilanterol
89
Q

LABAs Characteristics

A
  • Can cause death in asthma patients

- Available as single agent products or combined with inhaled corticosteroids or inhaled anticholinergics

90
Q

Mybertiq (Mirabegron) MOA

A

Selective B3 Agonist for Tx of overactive bladder - relaxes detrusor muscle (can cause HTN)

91
Q

Midodrine

A
  • An A1 adrenergic agonist used as a vasopressor/antihypotensive to treat orthostatic hypotension.
  • It is a prodrug
92
Q

Northera (Droxidopa)

A

A synthetic amino acid precursor of NE used as an oral agent to treat neurogenic orthostatic hypotension

93
Q

Northera (Droxidopa) adverse reaction

A
  • Headache
  • Nausea
  • HTN

CRNA Pharmacology (8 decks)

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