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AP + Phys > Vasopressors > Flashcards

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
Q

Sequestration

A

Slowly move receptors inside the cell

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25
Q

Pheocromocytoma

A

Uncontrolled release of catecholamines due to adrenal gland dysfunction

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26
Q

Uses of sympathomimetics

A

Positive inotropy
Elevate blood pressure
Treat bronchospasms
Manage anaphylaxis
Arrhythmia management
Addition to LA to slow systemic absorbtion

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27
Q

Types of sympathomimetics

A

Naturally occurring catecholamines (direct)
Synthetic catecholamines
Synthetic non catecholamines (direct and indirect)

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28
Q

What are sympathomimetics derived from?

A

B Phenylethlamine

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29
Q

Catecholamines vs synthetic non catecholamines

A

Sympathomimetics (synthetic non catecholamines) do not have the hydroxyl group in the 3 and 4 position of benzene ring

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30
Q

Indirect acting

A

Synthetic non catecholamines

31
Q

Direct acting

A

synthetic non catecholamines
catecholamines

32
Q

How are catecholamines metabolized or rided?

A

COMT-
MAO- present in liver, kidneys, gi tract
Reuptake

33
Q

How are synthetic non catecholamines metabolized?

A

MAO only
NO COMT

34
Q

How are phenylepherine and catecholamines metabolized?

A

Sulfoconjugation reactions- SULT1A3 and SULT1A4
Via sulfate?

35
Q

Vasoconstrictor non cardiac effects

A

Bronchodilation
Glycogenolysis
Increased insulin
Increased renin
Increased CNS stimulation
Increased pituitary hormone

36
Q

Vasoconstrictor contraindications

A

LV failure can be worsened
RV failure can be exacerbated
Poor renal blood flow can be decreased more
Hypovolemia can be masked

37
Q

What are the natural catecholamines

A

Epi
Dopamine
Norepi

38
Q

What receptor does Epi work on?

A

A1, B1, B2
“all of them”
Most potent A1 activator
2-10x more potent than norepi

39
Q

Epi works by __ and for ___

A

Asthma, anaphylaxis, cardiac arrest, bleeding, LA to stop absorbtion
Increases lipolysis
Increases glycogenolysis
Decreases insulin
Stimulated renin and decreases renal blood flow

39
Q

Epi at low doses

A

1-2mcg/min
B-2
Decreases SVR but holds BP

39
Q

NE

A

Catecholamine
Increases systolic, diastolic, and MAP
Maintains BP by adjusting SVR

40
Q

Epi at moderate doses

A

4mcg/min
B1 effects

41
Q

Epi at high doses

A

10mcg/min
A1 masks all other receptors
Reflex bradycardia can occur
No significant effect on cerebral arteries

42
Q

Racemic epi

A

Levo and dextrorotatory isomers
Used for croup and airway edema
Treatment lasts for 30-60 minutes
2 hours later can experience rebound edema

43
Q

Epi side effects

A

Little CNS effect
Hyperglycemia
mydriasis
Platelet aggregation
Sweating
Headache nausea
Skin tissue damage

44
Q

NE side effects

A

Renal injury
Mesenteric infart
Gangrene of digits

45
Q

NE receptors it affects

A

A1
B1 small and overshadowed by A1

46
Q

NE effect on CO

A

Increase but may decrease at higher doses due to reflex bradycardia
Refractory hypotension

47
Q

Dopamine receptor sites

A

Endogenous catecholamine
D at low doses
Beta at moderate doses 5mcg/kg/min
Alpha at high doses 10-20mcg/kg/min

48
Q

Endogenous dopamine in the CNS

A

Low- schizophrenia
High- manic

49
Q

Ephederine

A

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
Q

Ephederine dose

A

2.5-25mg IV or
25-50mg PO

50
Q

How does ephederine compare to epinepherine

A

Ephderine is less intense but lasts longer

51
Q

Ephedrine SE

A

Insomnia/ headache/ psychosis
Palpatations/ HTN/ tremor
Cocaine and amphetamines will exaggerate HTN due to the reuptake blockade

52
Q

Phenyl

A

Synthetic non catecholamine
A1 agonist
Inreases preload more than afterload
Can improve coronary perfusion pressure without increasing chronotropy
Ok for pregnancies

53
Q

Other used for phenyl

A

Priapism
Mydriatic
Decongestant

54
Q

Phenyl SE

A

Reflex Bradycardia
Decreases renal and schplanic blood flow
Increases PA resistance and PAP

55
Q

Phenyl dose and onset

A

50-200mcg
Onset 1-2 minutes
Duration- 5-10 minutes

56
Q

Phenyl vs NE

A

Phenyl less effective but longer lasting

57
Q

Onset of Epi, NE, Ephed, and Phenyl

A

Immediate
Immediate
1-3 minutes
1-3 minutes

58
Q

Duration of Epi, NE, Ephed, and Phenyl

A

5-15
5-15
15-20
15-20

59
Q

Synthetic catecholamines

A

Isoproterenol
Dobutamine

60
Q

Synthetic non catecholamines

A

Ephedrine
Phenylepherine

61
Q

Vasoconstrictor SE

A

Dysrhythmias
Reflex bradycardia
Antihypertensives may decrease pressor response to indirect acting drugs
OR they may increase to direct acting drugs

62
Q

Vasoconstrictors and TCA / MAOI

A

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
Q

Vasopressors and cocaine

A

Cocaine stops the reuptake
Enhances pressor effect

63
Q

Weight loss products

A

May contain ephedra
Stop atleast 24h prior to surgery
Can lead to tachyphylaxis and perioperative cardiovascular collapse

64
Q

Phentolamine

A

A1 and A2 antagonist
Treatment for necrosis from epi, NE, and dopamine
5-10mg injected at site
Peripheral vasodilator

65
Q

DDAVP vs vaso

A

DDAVP no pressor affect 1200:0
Vaso 100:100 ADH:pressor effect

66
Q

Posterior pituitary hormones

A

Vasopressin 100:100
Oxytocin (Pictocin) 1:1
adh/pressor effect

67
Q

When to use vaso

A

Advanced vasodilitory shock
For pt who are resistance
Effects of vaso are preserved in hypoxia and severe acidosis

68
Q

Vaso receptors

A

V1intense arterial constriction
V2 renal collecting ducts increase reabsorption of water

69
Q

Vasopressin advantages of epi

A

Vaso does not increase myocardial O2 consumption
Vaso has no effect on heart
Epi may not work well in acidic and hypoxic patients

70
Q

How does oxytocin work

A

Increases Ca++ in myometrium to increase uterine contraction strength
Oxytocin receptors increase in pregnancy
Used for uterine contractions and to reduce post partum hemorrhaging

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