Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Nurs 575 Anesthesia Pharmacology > Sympathomimetic drugs (week 10) > Flashcards

Sympathomimetic drugs (week 10) Flashcards

Week 10

1
Q

Where is Epinephrine synthesized, stored, & released?

A

Adrenal Medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Natural functions of Epinephrine?

A
  • Regulates contracility
  • HR
  • Vascular/Bronchial smooth muscle tone
  • Glandular Secretions
  • Metabolic processes: glycogenolysis & Lipolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What receptors does Epinephrine work on?

A
  • α-adrenergic receptors
  • β1ÂandÂβ2Âadrenergic receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What issues does epinephrine have with oral adminstration

A

Not effective

  • rapidly metabolized in GI/Liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Epinephrine is (Water or Lipid) soluble and what does this property account for?

A

Water-soluble

  • It’s poor lipid solubility = lack of CNS effects

Prevents entrance to CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Clinical uses of Epinephrine?

A
  • Anaphylaxis
  • Severe Asthma/Bronchospasm
  • Cardiopulmonary resuscitation
  • Inc. myocardial contractility & vascular resistance
  • Prolong LA duration of action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which catecholamine has the most significant effects on metabolism? What effects are these?

A

Epinephrine

  • Glycogenolysis & inhibition of insulin secretion
  • Hyperglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is coagulation affected by Epinephrine?

A

It is accelerated (hypercoaguable)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

A patient is hypercoaguable during the intra & post-operative state, what could this reflect?

A

Epinephrine release due to the stress of surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Epinephrine dosing in Adults
(Cardiac Arrest/Infusion/Bolus)

A
  • Cardiac Arrest: 1mg q3-5 min
  • Infusion: 1-16 mcg/min or 0.1-1mcg/kg/min
  • Bolus: 5-10mcg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Epinephrine dosing in Pediatrics
(Cardiac Arrest/Infusion/Bolus)

A
  • Cardiac Arrest: 0.01mg/kg q3-5 min
  • Infusion: 0.1-1mcg/kg/min
  • Bolus: 1-2mcg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where is Norepinephrine systhesized & stored?

A

Post-ganglionic sympathetic nerve endings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When is norepinephrine released?

A

SNS stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What receptors does Norepinephrine activate?

A
  • β1-adrenergic agonist
  • α1-adrenergic agonist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Norepinephrine is the first line agent to treat what?

A

Refractory HoTN in severe sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Primary utility of Norepi?

A

Potent vasoconstrictor to increase SVR/MAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Benefits of Norepi in severely HoTN septic pts?

A

Increases:

  • Sphlancnic blood flow
  • UOP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Primary S/E of Norepi?

A

Excessive vasoconstriction may lead to:
* End-organ hypoperfusion & ischemia
* Decreased Renal, sphlancnic, peripheal vascular bed blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Norepi Adult dosing?
(Bolus/Infusion)

A

Bolus: 8-16 mcg
Infusion: 0.02-1mcg/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Norepi Pediatric dosing?
(Infusion)

A

Infusion: 0.05-2mcg/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is Dopamine?

A

Endogenous catecholamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Function of Dopamine (generally)

A
  • Regulates cardiac, vascular, & endocrine function
  • Important neurotransmitter in the CNS/PNS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Hemodynamic effects of Dopamine?

A

Increases CO by increasing SV
* via β1 adrenergic agonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why must Dopamine be a continuous infusion?

A

Rapid half-life of 1-2 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Hemodynamic effects of Dopamine

A
  • Increase HR
  • Increase CO
  • Increase SBP
  • Increase UOP
    after CPBP or w/ CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Unique properties of Dopamine

A

Simultaneously Increase:
* CO
* Renal blood flow
* UOP
* GFR
* Na+ excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Between Dobutamine, epinephrine, & Dopamine which drug is associated with sinus tachycardia/ventricular arrhythmias the most?

A

Dopamine

Dose related

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Dopamine dosing for Adults/Pediatrics?
(Infusion)

A

Adults/Pediatric infusion: 2-20mcg/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the most potent sympathomimetic? How much more than Epi/Norepi?

A

Isoproterenol
* 2-3x Epi
* 100x Norepi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What receptors does Isoproternol interact with? Effects?

A
  • β1-agonist in the heart -> Increase CO
  • β2-agonist in Skeletal muscle -> Decrease MAP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Why doesn’t HR decrease w/ Isoproterenol?

A

Baroreceptor mediated reflex doesn’t occur because MAP doesn’t increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Clinical use of Isoproterenol

A

Increases HR before PPM or TPM insertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Dosing/use of Isoproterenol
(Infusion)

A

Infusion: 1-5mcg/min to increase HR 2/2 heart block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is Dobutamine

A

Synthetic catecholamine derived from Isoproterenol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What receptors does Dobutamine interact with? Effects?

A
  • Potent β1: Increased Myocardial contractility & SA/AV node automaticity
  • α1: myocardial contractility @ higher doses
  • Weak β2: peripheral vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Clinical uses of Dobutamine

A
  • Inc. CO in CHF or weaning from bypass
  • Combined with vasodilators to improve CO w/ increased SVR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Adverse effects of Dobutamine?

A

Occurence of Tachyarrhythmias
* especially in HF or pts with pre-existing arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Dosing/Half-life of Dobutamine

A

Infusion: 2-10 mcg/kg/min
Half-life: 2 min

That’s why infusion only, like dopamine/isoprotereno

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What drugs are catecholamines?

A
  • Epi
  • Norepi
  • Dopamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What drugs are synthetic catecholamines?

A
  • Isoproterenol
  • Dobutamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What drugs are synthetic non-catecholamines?

A
  • Ephedrine
  • Phenylephrine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Description of Ephderine

A

Direct & indirect sympathomimetic

43
Q

Direct & Indirect effects of Ephedrine?

A
  • Direct: stimulates β1ÂandÂα1Âreceptors
  • Indirect: Release of endogenous Norepi
44
Q

Unique benefit to Ephedrine and why does it occur?

A

Prolonged Duration
(10-60 min vs. 5-10 min of Epi)
* Slow inactivation/excretion

45
Q

Clinical use of Ephedrine

A
  • Increase SBP in SNS blockade 2/2 regional anesthesia or IV/inhaled anesthetics
  • Maternal HoTn AND bradycardia post-spinal/epidural
46
Q

Adult Ephedrine dosing

47
Q

CV effects of Ephedrine? Primary mechanism?

A

Increase in:
* SBP/DBP
* HR
* CO
Myocardial contractility via β1-receptorsÂ

48
Q

You give a second bump of that Ephedrine, but it had less of an effect, why?

A

Tachyphylaxis
* α-receptor inhibition
* Occurs with many sympathomimetics

49
Q

Mechanism of Phenylephrine?

A
  • Primarily direct α1-adrenergic stimulation
  • small indirect release of NEÂ
50
Q

True/False: Phenylephrine causes increases in SBP by arterial constriction

A

False: venoconstriction

51
Q

Dosing of Phenylephrine
(Bolus/Infusion)

A

Bolus: 50-200 mcg IV
Infusion: 20-50mcg/min

52
Q

Clinical uses of Phenylephrine

A
  • Treat SNS blockade by regional anesthetics
  • Treat vasodilation 2/2 IV/Inhaled anesthetics
  • Primary tx for Maternal HoTN 2/2 neuraxial block
53
Q

What effects do β2-selective adrenergic agonists have on tissues?

A
  • Relax brochiole & uterine smooth muscle
  • Generally lack β1Âeffects on heart
54
Q

Concentration per puff of Albuterol, Metaproterenol & Terbutaline?

A
  • Albuterol - 90 mcg/puff
  • Metaproterenol - 200 mcg/puff
  • Terbutaline - 200 mcg/puff
55
Q

β2 Selectivity of Albuterol, Metaproterenol & Terbutaline?

A
  • Albuterol - High
  • Metaproterenol - Moderate
  • Terbutaline - High
56
Q

Clinical uses of β2-adrenergic agonists?

A
  • Preferred Tx of acute asthma & exercise induced asthma
  • Given to stop premature uterine contractions (tocolytic)
57
Q

With optimal technique, where are β2 agonists delivered, and how much?

A
  • 12% makes it to the lungs
  • Other 88% goes to Mouth, pharynx, larynx
58
Q

Describe the optimal technique steps for Metered dose inhaler

A
  • Discharge inhaler while taking a slow deep breath over 5-6 seconds
  • Hold breath @ full inspiration (IRV am’i’rite) for 10 seconds
59
Q

When delivering a metered dose inhaler via ETT, what should you know?

A

Decreases 50-70% amount of drug reaching the trachea

60
Q

Side effects of systemic absorption of β2-agonists?

A
  • Tremor
  • Inc. HR (less so with selective)
  • Hyperglycemia
  • Hypokalemia & hypomagnesemia
  • Transient desaturation (relaxation of Hypoxic pulmonary vasoconstriction)
61
Q

Albuterol dosing & Timing

A
  • Two puffs 1 to 5 min apart
  • Q4-6hrs
  • No more than 16-20 puffs/day
62
Q

What effect would volatile anesthetics and albuterol have on bronchomotor tone?

A

Effects are additive

63
Q

Dosing & effects for Terbutaline

A

0.25mg SubQ

Effects similar to Epi but longer

64
Q

MoA of PDEi

A

Exert competitive inhibitory effect on phosphodiasterase enzymes

65
Q

Unique benefit of PDE3is?

A

Benefits pts who would benefit from inotropy & vasodilation

66
Q

What is Milrinone a derivative of and how does it compare?

A

Amrinone
30x the inotropic effect & less side-effect

67
Q

Milrinone dosing
(Bolus/Infusion)

A
  • Bolus: 50mcg/kg over 10 min
  • Infusion: 0.375-0.75 mcg/kg/min
68
Q

Clinical uses of Milrinone

A
  • LV dysfunction
  • Wean from CPBP
  • CHF pts w/ β1Âdownregulation
  • P. HTN
  • Vasodilation & dec. SVR > dobutamine

CPBP = cardiopulmonary bypass

69
Q

Does Milrinone cause more or less tachycardia than dobutamine?

70
Q

S/E of Milrinone

A

Rapid administration ->
* HoTN
* AV nodal enhancement -> arrhythmias

71
Q

Calcium (gluconate or chloride) may be used to treat what situations?

A

Myocardial depression caused by

  • Volatile anesthetics
  • Transfusion of citrated blood
  • Termination of CPBP
72
Q

Normal plasma iCal and what % is it of total plasma calcium?

A
  • 1-1.26mmol/L (2-2.5 mEq/L or 4-5mg/dL)
  • 45% of total plasma
73
Q

Side-effects from an α receptor blockade?

A
  • Orthostatic HoTN
  • Reflex Tachycardia (baroreceptor)
  • Impotence (unfortunate)
74
Q

Which drugs are competitive α -antagonists?

A
  • Phentolamine
  • Prazosin
  • Yohimbine
75
Q

MoA & Clinical uses of Phentolamine

A

Non-selective αÂreceptor blockade
* Acute HTN
* Manipulation/removal pheochromocytoma
* Sympathomimetic extravasation (infiltrate phento @ the site)

76
Q

Most beneficial clinical response to α-antagonist

A

Diseases w/ large cutaneous vasoconstriction
* Raynauds disease

77
Q

What is Prazosin?

A

Selective post-synapticÂα1Âantagonist

78
Q

Benefits of Prazosin’s selectivity?

A

Less likely to evoke reflex tachycardia (Baroreceptor)
* via leaving the inhibitory α2 activity on NE release

79
Q

What effect does acutely holding β-adrenergic antagonists pre-operatively do?

A
  • Upregulation of β receptors w/ chronic β blockade
  • Causes SNS Hyperactivity to surgical stimulus

So don’t hold them

80
Q

What is the principle difference in pharmacokinetics between β-blockers?

A

Elimination half-life

  • 10 min for esmolol
  • Up to hours for others
81
Q

Description & effects of Metoprolol?

A

Selective β1-adrenergic antagonist prevents
* Inotropy
* Chronotropy
* Leaves β2 receptors intact

82
Q

What happens if you give a FAT dose of metoprolol?

A

Becomes non-selective

83
Q

Description & forms of Esmolol

A

Rapid onset & short acting β1-adrenergic antagonist
IV only

84
Q

Dosing of Esmolol

A

0.5-1.5mg/kg IV over 60 seconds
w/ 50-300 mcg/kg/min infusion

85
Q

What is important to know about Esmolol’s metabolism?

A

Plasma esterases involved in metabolism are different than plasma cholinesterase
* Succinylcholine duration not prolonged

86
Q

Principle contraindication for β-receptor antagonists?

A

Pre-exisiting AV heart block
or cardiac failure not caused by Tachycardia

87
Q

Signs of β-blocker related excess myocardial depression?

A
  • Bradycardia
  • Low CO
  • HoTN
  • Cardiogenic shock
88
Q

Treatment for β-blocker related myocardial depression?

A
  • Atripine first
  • Isoproterenol continuous infusion if atropine unsuccessful
  • Glucagon 1-10mg IV bolus, 5mg/hr infusion
  • Transvenous pacemaker
89
Q

Concern with β-antagonists and airways?

A

Non-selective β-blockers increase airway resistance 2/2 bronchoconstriction due to β2-blockade

90
Q

How do non-selective β-blockers interfere with hypoglycemia recognition?

A
  • Interfere w/ glycogenolysis caused by Epi in response to hypoglycemia
  • Blunt hypoglycemia related tachycardia
  • non-selective not recommended for DM @ risk of hypoglycemia
91
Q

Coadministration of β-blockers with volatile anesthetics has mimimal myocardial depressant effects. What is the exception to this?

A

Timolol
Severe bradycardia in presence of inhaled anesthetics

92
Q

Which β-antagonists have the least effect on the CNS?

A

Atenolol & Nadolol

Less lipid soluble than other β-antagonists-> less CNS effects

93
Q

What class of drugs are recommended for pts at risk of myocardial ischemia during high-risk surgery? What kind of pts considered high risk?

A

β-adrenergic antagonists
* CAD
* Positive stress test
* DM w/ insulin
* LV hypertrophy

94
Q

Dosing for Metoprolol IV?

95
Q

Dosing for Atenolol IV?

96
Q

Dosing for propanolol IV?

97
Q

What are Propanolol & Esmolol are effective at controlling

A
  • Ventricular rate in Afib/Flutter
  • Atrial dysrhytmias post-cardiac surgery
98
Q

What drugs are β and α receptor antagonists?

A

Labetalol & Carvedilol

99
Q

β:α potency ratio for Labetalol?

A
  • 3:1 Oral
  • 7:1 IV
100
Q

CV effects of Labetalol

A
  • Decrease SVR via α1 blockade
  • No reflex tachycardia due to β blockade
  • CO unchanged
101
Q

Dosing of Labetalol

A

0.1-0.5mg/kg IV

102
Q

S/E of Labetalol

A
  • Orthostatic HoTN
  • Bronchospasm
  • Fluid retention w/ long term therapy- combine with diuretic
103
Q

Why are β-blockers ideal for laryngoscopy/intubation?

A

Prevent Excessive SNS activity
Attenuate HR & BP

Nurs 575 Anesthesia Pharmacology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions