Adrenergic Agonist Medications Flashcards
(85 cards)
1
Q
List drugs in the Sympathomimetic Amines class
A
- Epinephrine
- Norepinephrine
- Dopamine
- Isoproterenol
- Dobutamine
2
Q
Direct Acting Alpha Agonists
A
Phenylephrine
3
Q
Other Inotropes
A
- Vasopressin
- Milrinone
4
Q
Mixed Function Agonists
A
•Ephedrine
5
Q
Alpha 2 Agonists
A
•Clonidine
6
Q
Beta 2 Agonists
A
•Albuterol
7
Q
Class of Epinephrine & Route
A
Class: Endogenous catecholamine, adrenergic agonist
Route: IV, IM, Inhalational
8
Q
Mechanism of Action of Epinephrine
A
Agonizes B1, B2 , A1 and A2 receptors, triggering a G protein response to increased cAMP which increases Ca, resulting in increase BP, CO , bronchial relaxation, & stabilization of mast cells
9
Q
Clinical Use and Dosing of Epinephrine
A
Cardiac arrest, shock: 1 mg
Anaphylaxis: 100-500 mcg
Infusion: 2 – 20 mcg/min
- Low dose infusion – beta agonism predominates
- Medium dose infusion – equal beta and alpha agonism
- High dose infusions – alpha agonism predominates
Mixed with local anesthetics to decrease systemic absorption 1:200,000 (5mcg/mL of epinephrine)
10
Q
Onset and DOA of Epinephrine
A
Onset: 1 minute
Duration: 5 – 10 minutes
11
Q
Metabolism and Excretion of Epinephrine
A
Metabolism: MAO, COMT
Elimination: Renally excreted
12
Q
Epinephrine may cause ___
A
tachycardia, arrythmias, angina, hypertension, decrease perfusion to splanchnic organs and uterus, and gangrene in digits
13
Q
Avoid adding epinephrine to ____.
A
peripheral nerve blocks
14
Q
Caution the use of Epinephrine in patients with ____
A
CAD, hyperthyroidism and pheochromocytoma
15
Q
Class of Norepinephrine
A
Endogenous catecholamine, adrenergic agonist
16
Q
Mechanism of Action of Norepinephrine
A
•Agonizes A1, A2 and weakly B1 receptors, triggering a G protein response to increase cAMP which increases Ca, resulting in increased BP and decreased perfusion to splanchnic organs
17
Q
Clinical Use and Absorption of Norepinephrine
A
Clinical Use: First-line vasopressor for septic shock
Absorption: IV
18
Q
Dosing, Onset and DOA of Norepinephrine
A
Infusion: 1 – 20 mcg/min
Onset: 1 minute
DOA: 2 – 10 minutes
19
Q
Metabolism and Excretion of Norepinephrine
A
Metabolism: MAO, COMT
Elimination: Renally excreted
20
Q
Norepinephrine may cause ____.
A
bradycardia (baroreceptor reflex), hypertension, profound decrease perfusion to splanchnic organs and uterus
21
Q
Avoid adding norepinephrine to ___.
A
peripheral nerve blocks
22
Q
Caution giving norepinephrine to patients with ___.
A
hyperthyroidism, pheochromocytoma and without central IV access d/t extravasation
23
Q
Class of Isoproterenol
A
Synthetic catecholamine, Non-selective beta-adrenergic agonist
24
Q
Mechanism of Action of Isoproterenol
A
Agonizes beta receptors to acts on G proteins to increase cAMP, resulting in an influx of Ca++ causing clinical effects
25
Clinical Use of Isoproterenol & Route
β1 effects increase heart rate, contractility, and cardiac output.
β2 stimulation causes bronchodilation and a decrease in peripheral vascular resistance and diastolic blood pressure
Route: IV
26
Dosing of Isoproterenol
Infusion: 0.015–0.15 mcg/kg/min
27
Onset and DOA of Isoproterenol
Onset: 1 minute
DOA: 1 – 5 minutes
28
Metabolism and Excretion of Isoproterenol
Metabolism: COMT
Elimination: Renally excreted (50% unchanged)
29
Isoproterenol is a poor inotropic choice in most situations because \_\_\_.
myocardial oxygen demand increases while oxygen supply falls
30
Caution use of Isoproterenol in patients with what conditions?
CAD, hypertrophic cardiomyopathy, hyperthyroidism, pheochromocytoma
31
Class of Dopamine
endogenous nonselective adrenergic and dopaminergic agonist, direct and indirect acting
32
Mechanism of Action of Dopamine & Route
dopamine stimulates D receptors, β-receptors, and α-receptors in a dose-dependent manner because of differing receptor affinities.
Route: IV
33
Renal Dosing of Dopamine
Not scientifically supported (urine output increases, but long-term morbidity and mortality do not improve)
34
Dosing of Dopamine
Dopaminergic receptors: 2 mcg/kg/min
β receptors: 2 to 5 mcg/kg/min
α receptors: greater than 10 mcg/kg/min
35
Onset and DOA of Dopamine
Onset: 2 – 4 minutes
DOA: 10 minutes
36
Metabolism and Excretion of Dopamine
Metabolism
•MAO and COMT ►75% inactive and 25% NE
Elimination: Renally excreted
37
Considerations for Dopamine
**Dopamine also inhibits aldosterone**, resulting in an increase in sodium excretion and urine output.
Caution in patients on MAOI and TCA, tachycardia, arrythmias
r/f extravasation
38
Class and Mechanism of Action of Dobutamine
**Class**: Synthetic catecholamine, selective beta 1 adrenergic agonist
Mechanism of Action
* synthetic analog of isoproterenol
* Acts on B1, G proteins to increase cAMP, influx of Ca causing increasing contractility & CO
* Some B2 (vasodilation, decreases SVR) & A1 (min);
39
Clinical Use and Route of Dobutamine
Clinical Use: Cardiogenic and septic shock, treat mild CHF, cardiac stress tests
Route: IV
40
Dosing of Dobutamine
Infusion: 2 to 20 mcg/kg/min
41
Onset and DOA of Dobutamine
Onset: 1 minute
DOA: 10 minutes
42
Metabolism & Excretion of Dobutamine
Metabolism: MAO, COMT
Elimination: Renally excreted
43
Caution use of dobutamine in patients with what conditions?
tachycardia, CAD, hypertrophic cardiomyopathy
44
Dobutamine can cause \_\_
Decrease SVR, platelet inhibition
45
Class and Clinical Use of Phenylephrine
**Class**: Alpha 1 adrenergic agonists
**Clinical Use**: Vasodilatory shock, hypotension (with a normal heart rate), s/p spinal anesthesia
46
Mechanism of Action of Phenylephrine & Route
Agonizes A1 receptors, activates IP3 which increases intracellular Ca and increases BP
**Route**: IV, intranasal, ocular
47
Dosing of Phenylephrine
Small boluses of 40-80 mcg
Infusion: 20 – 50 mcg/min
48
Onset and DOA of Phenylephrine
Onset: 1 minutes
DOA: 15 – 20 minutes
49
Metabolism and Excretion of Phenylephrine
Metabolism: MAO
Elimination: Renally excreted
50
Considerations for Phenylephrine
* **Reflex bradycardia** mediated by the vagus nerve can reduce cardiac output
* Caution in patients with **bradycardia, hyperthyroidism, pheochromocytoma**
* Phenylephrine must be diluted from a 1% solution (10 mg/1-mL ampule), usually to a 100 mcg/mL solution and titrated to effect
51
When would you administer phenylephrine instead of ephedrine?
If they have a normal HR
(If they are hypotensive AND bradycardic, give ephedrine instead)
52
Class, Clinical Use and Route of Vasopressin
**Class**: Exogenous antidiuretic peptide & vasopressor
**_Clinical Use_**
Septic shock, post–cardiopulmonary bypass shock state
ACE Inhibitor related hypotension
**Route**: IV
53
Mechanism of Action of Vasopressin
Vasoconstrict: stim V1 receptors on vascular smooth muscle, glomerular mesangial cells, & vasa recta; ADH (activate V2 receptors)
54
Dosing of Vasopressin
Bolus: 1 – 20 units
infusion: 0.01-0.04 units/min
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Onset and DOA of Vasopressin
Onset: 1 – 5 minutes
DOA: 10 – 30 minutes
56
Metabolism and Excretion of Vasopressin
Metabolism: Tissue peptidase metabolism
Elimination: Renally excreted
57
Complications of vasopressin include \_\_\_.
gastrointestinal ischemia, decreased cardiac output, skin or digital necrosis, and cardiac arrest (especially at doses greater than 0.04 units/min)
58
Class, Clinical Use & Route of Milrinone
**Class**: Phosphodiesterase 3 Inhibitor
**Clinical Use**
Cardiogenic shock, right heart failure, dilates pulmonary artery
Inotropy in the setting of beta blockade
_Route_: IV
59
Mechanism of Action of Milrinone
Inhibition of (PDE) III degrades cAMP which decreases hydrolysis of cAMP & cGMP in myocardium & vascular smooth muscle
Myocardium: increase cAMP whichincreases intracellular Ca & increases contractile activation
Vascular smooth muscle: increase cAMP works to cause vasodilation & decrease PVR
60
Class, Clinical Use & Route of Ephedrine
**Class**: Synthetic noncatecholamine, indirect and direct acting
_Clinical Use_
Treat hypotension with bradycardia
Used w/ GA or SNS blockade to increase BP, brady after spinal,
Like epinephrine, but weaker action and lasts 10x longer
**Route**: IV, IM
61
Dosing of Ephedrine
Small Bolus: 5 - 10 mg
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Onset and DOA of Ephedrine
Onset: 1 minute
DOA: 10 – 60 minutes
63
Metabolism and Excretion of Ephedrine
Metabolism: Resistant to MAO since lacks catecholamine
Elimination: Renally excreted (40% unchanged)
64
Considerations for Ephedrine use
Avoid in patients with CAD, tachycardia, hypertension and patients taking MAOIs, TCAs & cocaine
* Caution in trauma because subsequent doses are increased to offset the development of tachyphylaxis, which is probably due to depletion of norepinephrine stores.
* Ephedrine is available in 1-mL ampules containing 25 or 50 mg of the agent
65
Class and Clinical Use of Clonidine
**Class**: Alpha 2 adrenergic agonist
_Clinical Use_
Sedation, antihypertensive, postoperative shivering, alcohol withdrawal symptoms, and the treatment of acute postoperative pain and some chronic pain syndromes
Peripheral anesthesia – prolongs the duration of a block
66
Mechanism of Action of Clonidine
Selectively activates α2 – adrenergic receptors & thereby inhibits sympathetic outflow from medulla which causes decreases HR, contractility, & vasomotor tone
Analgesia: α2 adrenergic receptor in dorsal horn produces anti-nociceptive state by inhibiting release of sub P & nociceptive neuron firing produced by painful stimuli.
67
Dosing of Clonidine
**Intravenous**: 1–3 mcg/kg
68
Metabolism and Excretion of Clonidine
**Metabolism**: ~50% of drug is metabolized in liver
**Elimination**: Renally excreted (~ 50% unchanged)
69
Consideration of Clonidine
Clonidine potentiates anesthetic effects of other volatile or injectable anesthetics
Continuing the medication throughout the perioperative period is essential to avoid rebound hypertension
70
Class, Clinical Use and Route of Albuterol
**Class**: Selective B2 agonists
**Clinical Use**: Bronchodilation
**Route**: Inhalation
71
Mechanism of Action of Albuterol
Acts directly on b2 receptors,which when coupled to G protein, activates adenylyl cyclase which increases cAMP & decreases Ca+, increases K+ conductance causing smooth muscle relaxation & bronchodilation
72
Dosing of Albuterol
90 mcg per puff
73
Onset and DOA of Albuterol
Onset: 5 minutes
DOA: 4 hours
74
Metabolism and Excretion of Albuterol
Metabolism: MAO
Elimination: Renally excreted (30 % unchanged)
75
Albuterol can cause \_\_\_\_.
Tremors, tachycardia, hypokalemia
76
If spetic shock, treated with \_\_\_.
norepinephrine and vasopressin (due to the fact that you're dealing with peripheral vasiodilation from sepsis)
- Epinephrine is the third line
Dopamine is inferior due to causing more arythmias
No phenylephrine becuase it decreases CO from ans increase in SVR
77
If cardiogenic shock, pt needs \_\_\_\_.
**Inotropy**
If they're hypotensive, give epinephrine
If they have poor CO but they're not hypotensive, give dobutamine or milrinone
78
If hemorrhagic shock, treat with \_\_\_.
rescuscitation instead of vasopressors
79
Describe what's going on with aortic stenosis, what is the goal? What is the treatment?
Aortic stenosis = heart pushing against fixed defect
Goal is to lower the HR because need time for LV to fill and push out against stenotic valve
USE PHENYLEPHRINE, alpha 1 causes systemic vasoconstriction with reflex bradycardia
80
Pharmacological treatment of tamponade
Keep HR fast with increased inotropy
Use epinephrine
81
Treatment of pulmonary hypertension with systemic hypotension
Use vasopressin alone because it is the only vasopressor that doesn't affect the pulmonary vascular resistance
82
If hypotensive with arrythmias, give\_\_\_.
Phenylephrine or vasopressin because they do not have beta agonism
\*If the patient is hypotensive because of an arrythmia, think about cardioversion rather than vasopressors.
83
Dose of Milrinone
Dosing (IV)
* Loading dose: 50 mcg/kg over ten minutes
* Infusion: 0.375–0.75 mcg/kg /min
84
Onset and Elimination of Milrinone
Distribution
•Onset: 5 – 15 minutes
Elimination
•Renally excreted (80% unchanged)
85
Caution use of Milrinone in patients with \_\_\_\_
hypotension, renal failure
•Side effects include arrythmias
