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Vasopressors Flashcards

1
Q

End organ damage occurs when map is below 50 for ___

A

1 minute

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2
Q

End organ damage occurs when MAP is below 65 for ____

A

13-28 minutes

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3
Q

What is the difference between autonomic and somatic ANS?

A

Somatic does not involve ganglia, ACH goes directly to the nicotinic receptor

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4
Q

Sympathetic innervation of the adrenal medulla

A

ACH binds to the nicotinic receptor on the adrenal medulla (instead of the post ganglionic neuron), then epinepherine is released into the blood to bind on to adrenergic receptors

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5
Q

Sympathetic innervation

A

ACH binds to the nicotinic receptor on the post ganglionic neuron which releases norepinepherine to bind to adrenergic receptors

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6
Q

Parasympathetic innervation

A

ACH binds to the nicotinic receptor on the post ganglionic neuron which releases ACH to bind to muscuranic receptors

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7
Q

Sympathetic nervous system origin

A

T1-L2
Preganglia near spinal cord
Postganglia secrete norepinepherine

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8
Q

What converts dopamine to norepinephrine?

A

Beta Hydroxylase

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9
Q

What releases NE from the synaptic vessel?

A

Action potential

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10
Q

Signal termination of NE

A

Reuptake
Metabolism by MAO and COMT
Dilution by diffusion

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11
Q

Location of adrenergic receptors

A

A1- periphery
A2- Presynaptic in the PNS, postsynaptic in the CNS
B1- heart
B2- smooth muscle

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12
Q

A1 receptor works by __

A

Increase intracellular Ca++
Smooth muscle contraction
Peripheral vasoconstriction
Bronchoconstriction
- insulin
+glycogenolysis
+gluconeogenesis
Mydriasis
GI relaxation

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13
Q

A2 works in the presynaptic PNS by ____

A

Decreases Ca++ into cell
Limits release of NE

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14
Q

A2 in the postsynaptic CNS

A

Sedation
Decreases BP
Decreases sympathetic outflow
Platelet aggregation

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15
Q

B-1 works to __

A

Increases chronotropy
Increases dromotropy
Increases inotropy

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16
Q

B2 works by __

A

Smooth muscle relaxation
Peripheral vasodilation
Decreases BP
+ insulin
+ glycogenolysis
+ gluconeogenesis
Decreases GI mobility

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16
Q

Parasympathetic nervous system origins

A

Craniosacral origin (3,7,9,10)

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17
Q

ACH

A

Activates BOTH arms of ANS
Ca++ mediated action potential
Formed by choline and acetyltransferase
Deactivated by acetylcholinesterase

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18
Q

SNS effect on GI system and bladder

A

Decreases motility
Constricts sphincter
Relaxes smooth muscle in bladder, but contracts sphincter

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19
Q

ANS effect on GI and bladder

A

Increases motility, relaxes sphincter
Contracts bladder smooth muscle, relaxes sphincter

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20
Q

Down regulation

A

Long process of destruction of receptors
Extended exposure to agonists will reduce the number of receptors
Tachyphylaxis

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21
Q

Up regulation

A

Chronic depletion of catecholamines or beta blockers will increase the amount of receptors but not their sensitivity

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22
Q

Tachyphylaxis

A

Decreased effectiveness due to chronic exposure
Happens with down regulation

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23
Q

Receptor uncoupling

A

Rapid inability of the receptor to bind to the G protein

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24
Sequestration
Slowly move receptors inside the cell
25
Pheocromocytoma
Uncontrolled release of catecholamines due to adrenal gland dysfunction
26
Uses of sympathomimetics
Positive inotropy Elevate blood pressure Treat bronchospasms Manage anaphylaxis Arrhythmia management Addition to LA to slow systemic absorbtion
27
Types of sympathomimetics
Naturally occurring catecholamines (direct) Synthetic catecholamines Synthetic non catecholamines (direct and indirect)
28
What are sympathomimetics derived from?
B Phenylethlamine
29
Catecholamines vs synthetic non catecholamines
Sympathomimetics (synthetic non catecholamines) do not have the hydroxyl group in the 3 and 4 position of benzene ring
30
Indirect acting
Synthetic non catecholamines
31
Direct acting
synthetic non catecholamines catecholamines
32
How are catecholamines metabolized or rided?
COMT- MAO- present in liver, kidneys, gi tract Reuptake
33
How are synthetic non catecholamines metabolized?
MAO only NO COMT
34
How are phenylepherine and catecholamines metabolized?
Sulfoconjugation reactions- SULT1A3 and SULT1A4 Via sulfate?
35
Vasoconstrictor non cardiac effects
Bronchodilation Glycogenolysis Increased insulin Increased renin Increased CNS stimulation Increased pituitary hormone
36
Vasoconstrictor contraindications
LV failure can be worsened RV failure can be exacerbated Poor renal blood flow can be decreased more Hypovolemia can be masked
37
What are the natural catecholamines
Epi Dopamine Norepi
38
What receptor does Epi work on?
A1, B1, B2 "all of them" Most potent A1 activator 2-10x more potent than norepi
39
Epi works by __ and for ___
Asthma, anaphylaxis, cardiac arrest, bleeding, LA to stop absorbtion Increases lipolysis Increases glycogenolysis Decreases insulin Stimulated renin and decreases renal blood flow
39
Epi at low doses
1-2mcg/min B-2 Decreases SVR but holds BP
39
NE
Catecholamine Increases systolic, diastolic, and MAP Maintains BP by adjusting SVR
40
Epi at moderate doses
4mcg/min B1 effects
41
Epi at high doses
10mcg/min A1 masks all other receptors Reflex bradycardia can occur No significant effect on cerebral arteries
42
Racemic epi
Levo and dextrorotatory isomers Used for croup and airway edema Treatment lasts for 30-60 minutes 2 hours later can experience rebound edema
43
Epi side effects
Little CNS effect Hyperglycemia mydriasis Platelet aggregation Sweating Headache nausea Skin tissue damage
44
NE side effects
Renal injury Mesenteric infart Gangrene of digits
45
NE receptors it affects
A1 B1 small and overshadowed by A1
46
NE effect on CO
Increase but may decrease at higher doses due to reflex bradycardia Refractory hypotension
47
Dopamine receptor sites
Endogenous catecholamine D at low doses Beta at moderate doses 5mcg/kg/min Alpha at high doses 10-20mcg/kg/min
48
Endogenous dopamine in the CNS
Low- schizophrenia High- manic
49
Ephederine
Synthetic non catecholamine Indirect and direct but mostly indirect A1 and B receptors to increase inotropy Venoconstriction is greater than arterioconstriction Increases Sys and diastolic BP Can lead to tachyphylaxis Increase uterine blood flow Smooth muscle relaxant
50
Ephederine dose
2.5-25mg IV or 25-50mg PO
50
How does ephederine compare to epinepherine
Ephderine is less intense but lasts longer
51
Ephedrine SE
Insomnia/ headache/ psychosis Palpatations/ HTN/ tremor Cocaine and amphetamines will exaggerate HTN due to the reuptake blockade
52
Phenyl
Synthetic non catecholamine A1 agonist Inreases preload more than afterload Can improve coronary perfusion pressure without increasing chronotropy Ok for pregnancies
53
Other used for phenyl
Priapism Mydriatic Decongestant
54
Phenyl SE
Reflex Bradycardia Decreases renal and schplanic blood flow Increases PA resistance and PAP
55
Phenyl dose and onset
50-200mcg Onset 1-2 minutes Duration- 5-10 minutes
56
Phenyl vs NE
Phenyl less effective but longer lasting
57
Onset of Epi, NE, Ephed, and Phenyl
Immediate Immediate 1-3 minutes 1-3 minutes
58
Duration of Epi, NE, Ephed, and Phenyl
5-15 5-15 15-20 15-20
59
Synthetic catecholamines
Isoproterenol Dobutamine
60
Synthetic non catecholamines
Ephedrine Phenylepherine
61
Vasoconstrictor SE
Dysrhythmias Reflex bradycardia Antihypertensives may decrease pressor response to indirect acting drugs OR they may increase to direct acting drugs
62
Vasoconstrictors and TCA / MAOI
TCA and MAOI can stop the breakdown and lead to a higher pressor effect Exaggerated response with indirect acting Worse in first 1-2 weeks of therapy (then a down regulation occurs) Ok to continue perioperatively Use decreased dose of direct activing drugs
63
Vasopressors and cocaine
Cocaine stops the reuptake Enhances pressor effect
63
Weight loss products
May contain ephedra Stop atleast 24h prior to surgery Can lead to tachyphylaxis and perioperative cardiovascular collapse
64
Phentolamine
A1 and A2 antagonist Treatment for necrosis from epi, NE, and dopamine 5-10mg injected at site Peripheral vasodilator
65
DDAVP vs vaso
DDAVP no pressor affect 1200:0 Vaso 100:100 ADH:pressor effect
66
Posterior pituitary hormones
Vasopressin 100:100 Oxytocin (Pictocin) 1:1 adh/pressor effect
67
When to use vaso
Advanced vasodilitory shock For pt who are resistance Effects of vaso are preserved in hypoxia and severe acidosis
68
Vaso receptors
V1intense arterial constriction V2 renal collecting ducts increase reabsorption of water
69
Vasopressin advantages of epi
Vaso does not increase myocardial O2 consumption Vaso has no effect on heart Epi may not work well in acidic and hypoxic patients
70
How does oxytocin work
Increases Ca++ in myometrium to increase uterine contraction strength Oxytocin receptors increase in pregnancy Used for uterine contractions and to reduce post partum hemorrhaging

AP + Phys (38 decks)

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