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Anesthesia Pharm II > Peripheral Vasodilators ppt > Flashcards

Peripheral Vasodilators ppt Flashcards

1
Q

BP= what

A

CO x PVR

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2
Q

what 4 thins create the resistance for b/p (PVR) (looking for what organs and/or body parts

A

arterioles
Postcapillary venules
heart
Kidney

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3
Q

What causes the short term (minute to minute) b/p regulation in our bodies
and what type of innervation is it

A

the ANS -> baroreceptor relfex-> in the carotid bodies

parasympathetic innervartion

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4
Q

if the baroreceptors sense INCREASED stretch what does this mean?
what occurs?
what what PNS regulation occurs?

A
  • Increased B/p
  • (leads to) increased baroreceptor firing
  • parasympathoMIMESIS
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5
Q

if the baroreceptors sense REDUCED stretch what does this mean?
what occurs?
what what PNS regulation occurs?

A
  • low B/P
  • reduces baroreceptor firing
  • parasympathoLYSIS
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6
Q

Just for your FYI to understand the baroreceptor reflexes

A

the barorecptor is regulated by the PNS, so the “feed and breed” stage. so if you stimulate it (increased stretch) it kicks in high gear. this causes increased PNS sstimulation that results in parasympathomimesis. or the activation of the PNS so everything slows and lowers. the oppisite occurs with reduced stretch or reduced stimulation, less stimulation = less barorecptor activity whch = less PNS activation so you get the SNS reaction

for a good pic the baroreceptors work on the same pathway as the valsalva maneuver

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7
Q

where are the baroreceptors located

A

the carotid bodies

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8
Q

where are the chemoreceptors located

A

carotid and aortic bodies

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9
Q

with the chemoreceptors if it senses low b/p what is stimulated

A

the SA node

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10
Q

what 3 things are responsible for LONG term regulation of B/P

A

Kidneys
Cerebral Autoregulation curve shift
Venouse Capacitance

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11
Q

what is the numerical definition of HTN

A

sustained SBP B/P > 140 mmHg or DBP >90mmHg

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12
Q

what is primary HTN

A

not caused by other factors

etiology unk

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13
Q

what is secondary HTN

A

caused by something else

Phenochromocytoma, coarctation of the aorta, etc

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14
Q

Long term effects of HTN

A
  • Vessel damage
  • ACCELERATION OF ATHEROSCLEROSIS
  • LVH
  • D/O- CVA, IHD, HF, ESRF
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15
Q

When do we need to control HTN in the OR (the more common times, we cause HTN)

A 
DL
incision
Intraop Manipulation/Pain
Emergence
Recovery
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16
Q

Almost always if a pt is hypertensive on induction what will occur on emergence

A

htn
(so anticipate this and have drugs ready)
he states hydrolazine would be good for this

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17
Q

what are the 4 major drug categories for differing sites of action for treatment of HTN

A

Diuretics
Sympatholytics
Angiotensin inhibitors
Vasodilators

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18
Q

periphreal vasodilators are most often used in what cases

A

CABG
Vascular
Neuro

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19
Q

Periphreal vasodilators anct on what? and speparate into what two categories

A

systemic circulation

arterial vs venous

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20
Q

how do Arterial Vasodilators work

A

decrease systemic b/p by decreasing SVR

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21
Q

how do venous vasodilators work

A

By decrreasing systemic venous return and CO

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22
Q

Hydralazine although we don’t know the exact mechanism of action we know that it does effect what?

A

K+ channels, it probally closes the channels leading to a hyperpolazization of the cell, which means it can’t depolorize, Ca++ cannot enter contractions decrease

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23
Q

what is the mother of all contraction

A

Ca++

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24
Q

NTG is what diect or indirect

A

indirect

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25
Q

No matter what drug you are using for vasodilation they all come down to what someway or another

A

Ca++

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26
Q

In you open up a K+ channel as with hydralazine what happens to K+

A

it comes out of the cell (this is not how hydralazine works it somehow increases K+ in cell

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27
Q

how does NTG work

A

leads to Nitric Oxide, makes cell + increases Guanylate cyclase causing increased cGMP causing reuptake of Ca++ from the SR, leading to Ca++ mixing with calmodulin leading to MLCK causing a contraction

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28
Q

what is Nitric Oxide

A

endogenous gas

chemical messenger

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29
Q

how does NO work to decrease B/P

A

NO -> guanylactecyclase (increased cGMP) then cGMP causes vasodilation

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30
Q

what is a naturally occuring potent vasodilator

A

NO

31
Q

**** what is important about NO half life

A

ultra short (<5 sec)

32
Q

what is important about inhaled NO, and what is it used for

A

it is selective pulm vasodilator

only used for pulm HTN

33
Q

other name for Sodium nitroprusside

A

Nipride

34
Q

what is a main thing to remember about Niprides discontinuation

A

rapid termination effect 1-3 min after discontinuation

***never just turn off b/c the rebound HTN if very drastic

35
Q

what are the 4 main advantages for Nipride

A
  • emergent b/p control
  • hypotensive technigues
  • tx of pulmm edema
  • onset within seconds
36
Q 
**********************
what does Nipride do to 
preload
Afterload
PVR
A

direct preload
direct afterload
decreased PVR

37
Q

Nipride is primarily a what dilator (venous or arterial) why?

A

Arterial

b/c it is primarily reduces afterload

38
Q

if you had a pt with an 99% occluded Left circ would you give a Direct afterload reducer (a drug that primarily affect arteries) drug? why/why not? what drug is a direct afterload reducer you would not want to give?

A
  • the LAD would dilate gets great flow (really didn’t need it)
  • now the left circ will not dilate and all flow goes down LAD
  • boom!! killed him now ischemic inleft circ MI dead
39
Q

how do pure afterload reducers work in the body. basically say how it will decrease the potential for ischemia?

A

pure afterload reducers decrease preload

  • this decreases myocardial work and O2 requirements
  • which equals decreased potential for ischemia
40
Q

Does nipride have direct myocardial depressive effects

A

Nope

41
Q

what are 2 bad CV effects of Nipride

A

reflex tachycardia

Dilation of coranary arteries = coronary steal

42
Q

what is the main pulmonary effect of Nipride?

A

May prevent the normal response of the pulm vasculature to hypoxia (HPV) by dilating the pulm arteries

43
Q

a bolus of nipride of how much has been shown effective to blunt the HTN response to DL/intubation

A

1-2 mcgs/kg

44
Q 
*****************
guidlines for nipride infusion
starting dose
max not to exceed
max infusion for short term
max infusion for intermediate term
A
  • start small 0.5mcg/kg/min
  • **rarely exceeds 3 mcg/kg/min
  • 10 mcg/kg/min should not be used for more than 10-15 min
  • 2mcg/kg/min should not be administerd for more than 1-3 hours
45
Q

what is nipride mixed in

A

5% dextrose

46
Q

*** what must you do the the bottle of nipride

A

protect from light

47
Q

nipride should always be given via what?

A

IV pump

48
Q

with nipride how often should you monitor b/p

A

continuously A-line (always)

49
Q

Nipride is associated with N/V why?

A

actute hypotension

50
Q

s/s of cyanide toxicity

A

-Tachyphylaxis (describing an acute (sudden) decrease in the response to a drug after its administration)
-methemoglobinemia
-increased MVO2 content
- tachycardia
- increased ICP
Metabolic Acidosis

51
Q

how to treat cyanide toxicity

A
  • discontinue gtt
  • give O2
  • treat met acidosis
  • sodium thiosulfate 150mg/kg over 15min
  • 3% sodium nitrate-5mg/kg over 5min
52
Q

methoglobinemia can be treated with what

A

methylene blue 1-2 mg/kg of 1% solution over 5 min

53
Q

what is the main difference b/t Nipride and NTG?

A

NTG is primarily direct preload effects so works on venous.

54
Q

MOA for NTG

A

relaxes smooth muscle, with venous pooling,

metabolism to NO to increase cGMP, decreases Intracellular Ca++, vascular smooth muscle relaxation

55
Q 
**************
what does NTG do to 
preload?
LEDP (wedge pressure)?
Myocardial O2  demand?
endocardial perfusion
A

decreases it
decreases it
decreases it
increased

56
Q

how does NTG increase endocardial perfusion

A

decreases the size of LV (stretch) sine the cononary arteries fill during diastole this decreased stretch allows increased filling of steries and thus increased endocrdial perfusion

57
Q

other effects of NTG

A
  • releives coranary spasm
  • redistributes coronary blood flow to ischemic areas
  • relaxes bronchial smooth muscle
  • provides uterine relaxation
  • relaxes sphincter of oddi
58
Q

what is more potent NTG or nipride

A

nipride

59
Q

NTG can potentiate the effects of what musle relaxant

A

pancurium

60
Q

what is the difference b/t bolus and infusion gtts of NTG

A

short term bolus can halp B/P

long term gtt have less an effect

61
Q

All drugs that are direct acting on b/p do what to HR and why?

A

increase it, b/c they have no cv effects

62
Q

hydralazine MOA

A

k+ channels????

NO????

63
Q

hydralazine can cause what r/t heart rate

A

tachycardia

64
Q

what type of pt would benifit from hydralazine?

A

hypertensive bradycardic pt

65
Q 
*****************
hydralazine
dose
onset
duration
A

5-20 mg
up to 15 min
2-4 hrs

66
Q

what to remember about hydralazine administration

A

dont get the urge to re bolus give it time to work you cant take it back

67
Q

how should you mix hydralazine

A

20mg in 1cc so mix in 3cc to get 5mg/cc

68
Q

can u use hydralazine in PIH

A

does water ripple when a duck farts????

you bet your ass it does!!!!!!

69
Q

what periphreal vasodilator drug is endogenous to all cells of the body? it is the MOST potent vasodilator released by cardiac cells

A

adenosine

70
Q

how does adenosine work

A

opens K+ channels, hyperpolarizing nodal tissue an dmaking it less likely to fire-
leads to an av block and slows sinus rate

71
Q

adenosine affects what preload or afterload

A

afterload

72
Q

what is teh adenosine dose for controlled hypotension

A

60-120mcg/kg/min

73
Q

dose for adenosine

A

6mg 1-2 sec
12mg 1-2 sec
may repeat once

74
Q

adenosine is only FDA approved for what?

A

SVT

Anesthesia Pharm II (19 decks)

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