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Flashcards in Peripheral Vasodilators ppt Deck (74):
1

BP= what

CO x PVR

2

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

arterioles
Postcapillary venules
heart
Kidney

3

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

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

4

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

- Increased B/p
-(leads to) increased baroreceptor firing
-parasympathoMIMESIS

5

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

-low B/P
-reduces baroreceptor firing
-parasympathoLYSIS

6

Just for your FYI to understand the baroreceptor reflexes

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

7

where are the baroreceptors located

the carotid bodies

8

where are the chemoreceptors located

carotid and aortic bodies

9

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

the SA node

10

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

Kidneys
Cerebral Autoregulation curve shift
Venouse Capacitance

11

what is the numerical definition of HTN

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

12

what is primary HTN

not caused by other factors
(etiology unk)

13

what is secondary HTN

caused by something else
(Phenochromocytoma, coarctation of the aorta, etc)

14

Long term effects of HTN

-Vessel damage
-ACCELERATION OF ATHEROSCLEROSIS
-LVH
-D/O- CVA, IHD, HF, ESRF

15

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

DL
incision
Intraop Manipulation/Pain
Emergence
Recovery

16

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

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

17

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

Diuretics
Sympatholytics
Angiotensin inhibitors
Vasodilators

18

periphreal vasodilators are most often used in what cases

CABG
Vascular
Neuro

19

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

systemic circulation
arterial vs venous

20

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how do Arterial Vasodilators work

decrease systemic b/p by decreasing SVR

21

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how do venous vasodilators work

By decrreasing systemic venous return and CO

22

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

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

23

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what is the mother of all contraction

Ca++

24

****
NTG is what diect or indirect

indirect

25

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

Ca++

26

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

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

27

how does NTG work

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

28

*****
what is Nitric Oxide

endogenous gas
chemical messenger

29

how does NO work to decrease B/P

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

30

what is a naturally occuring potent vasodilator

NO

31

****** what is important about NO half life

ultra short (<5 sec)

32

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

it is selective pulm vasodilator
only used for pulm HTN

33

******************
other name for Sodium nitroprusside

Nipride

34

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what is a main thing to remember about Niprides discontinuation

rapid termination effect 1-3 min after discontinuation
***never just turn off b/c the rebound HTN if very drastic

35

what are the 4 main advantages for Nipride

-emergent b/p control
-hypotensive technigues
-tx of pulmm edema
-onset within seconds

36

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what does Nipride do to
preload
Afterload
PVR

direct preload
direct afterload
decreased PVR

37

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

Arterial
b/c it is primarily reduces afterload

38

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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?

-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

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

pure afterload reducers decrease preload
-this decreases myocardial work and O2 requirements
-which equals decreased potential for ischemia

40

Does nipride have direct myocardial depressive effects

Nope

41

******
what are 2 bad CV effects of Nipride

reflex tachycardia
Dilation of coranary arteries = coronary steal

42

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what is the main pulmonary effect of Nipride?

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

43

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

1-2 mcgs/kg

44

*****************
guidlines for nipride infusion
starting dose
max not to exceed
max infusion for short term
max infusion for intermediate term

- 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

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what is nipride mixed in

5% dextrose

46

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

protect from light

47

******
nipride should always be given via what?

IV pump

48

*****
with nipride how often should you monitor b/p

continuously A-line (always)

49

****
Nipride is associated with N/V why?

actute hypotension

50

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s/s of cyanide toxicity

-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

how to treat cyanide toxicity

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

52

methoglobinemia can be treated with what

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

53

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

NTG is primarily direct preload effects so works on venous.

54

MOA for NTG

relaxes smooth muscle, with venous pooling,
metabolism to NO to increase cGMP, decreases Intracellular Ca++, vascular smooth muscle relaxation

55

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

decreases it
decreases it
decreases it
increased

56

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how does NTG increase endocardial perfusion

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

other effects of NTG

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

58

what is more potent NTG or nipride

nipride

59

NTG can potentiate the effects of what musle relaxant

pancurium

60

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

short term bolus can halp B/P
long term gtt have less an effect

61

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

increase it, b/c they have no cv effects

62

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hydralazine MOA

k+ channels????
NO????

63

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hydralazine can cause what r/t heart rate

tachycardia

64

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what type of pt would benifit from hydralazine?

hypertensive bradycardic pt

65

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hydralazine
dose
onset
duration

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

66

*****
what to remember about hydralazine administration

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

67

how should you mix hydralazine

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

68

******
can u use hydralazine in PIH

does water ripple when a duck farts????
you bet your ass it does!!!!!!

69

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

adenosine

70

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how does adenosine work

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

71

adenosine affects what preload or afterload

afterload

72

*****
what is teh adenosine dose for controlled hypotension

60-120mcg/kg/min

73

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dose for adenosine

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

74

adenosine is only FDA approved for what?

SVT