Peripheral Vasodilators ppt Flashcards
BP= what
CO x PVR
what 4 thins create the resistance for b/p (PVR) (looking for what organs and/or body parts
arterioles
Postcapillary venules
heart
Kidney
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
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
if the baroreceptors sense REDUCED stretch what does this mean?
what occurs?
what what PNS regulation occurs?
- low B/P
- reduces baroreceptor firing
- parasympathoLYSIS
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
where are the baroreceptors located
the carotid bodies
where are the chemoreceptors located
carotid and aortic bodies
with the chemoreceptors if it senses low b/p what is stimulated
the SA node
what 3 things are responsible for LONG term regulation of B/P
Kidneys
Cerebral Autoregulation curve shift
Venouse Capacitance
what is the numerical definition of HTN
sustained SBP B/P > 140 mmHg or DBP >90mmHg
what is primary HTN
not caused by other factors
etiology unk
what is secondary HTN
caused by something else
Phenochromocytoma, coarctation of the aorta, etc
Long term effects of HTN
- Vessel damage
- ACCELERATION OF ATHEROSCLEROSIS
- LVH
- D/O- CVA, IHD, HF, ESRF
When do we need to control HTN in the OR (the more common times, we cause HTN)
DL incision Intraop Manipulation/Pain Emergence Recovery
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
what are the 4 major drug categories for differing sites of action for treatment of HTN
Diuretics
Sympatholytics
Angiotensin inhibitors
Vasodilators
periphreal vasodilators are most often used in what cases
CABG
Vascular
Neuro
Periphreal vasodilators anct on what? and speparate into what two categories
systemic circulation
arterial vs venous
how do Arterial Vasodilators work
decrease systemic b/p by decreasing SVR
how do venous vasodilators work
By decrreasing systemic venous return and CO
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
what is the mother of all contraction
Ca++
NTG is what diect or indirect
indirect
No matter what drug you are using for vasodilation they all come down to what someway or another
Ca++
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
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
what is Nitric Oxide
endogenous gas
chemical messenger
how does NO work to decrease B/P
NO -> guanylactecyclase (increased cGMP) then cGMP causes vasodilation
what is a naturally occuring potent vasodilator
NO
**** what is important about NO half life
ultra short (<5 sec)
what is important about inhaled NO, and what is it used for
it is selective pulm vasodilator
only used for pulm HTN
other name for Sodium nitroprusside
Nipride
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
what are the 4 main advantages for Nipride
- emergent b/p control
- hypotensive technigues
- tx of pulmm edema
- onset within seconds
********************** what does Nipride do to preload Afterload PVR
direct preload
direct afterload
decreased PVR
Nipride is primarily a what dilator (venous or arterial) why?
Arterial
b/c it is primarily reduces afterload
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
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
Does nipride have direct myocardial depressive effects
Nope
what are 2 bad CV effects of Nipride
reflex tachycardia
Dilation of coranary arteries = coronary steal
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
a bolus of nipride of how much has been shown effective to blunt the HTN response to DL/intubation
1-2 mcgs/kg
***************** 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
what is nipride mixed in
5% dextrose
*** what must you do the the bottle of nipride
protect from light
nipride should always be given via what?
IV pump
with nipride how often should you monitor b/p
continuously A-line (always)
Nipride is associated with N/V why?
actute hypotension
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
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
methoglobinemia can be treated with what
methylene blue 1-2 mg/kg of 1% solution over 5 min
what is the main difference b/t Nipride and NTG?
NTG is primarily direct preload effects so works on venous.
MOA for NTG
relaxes smooth muscle, with venous pooling,
metabolism to NO to increase cGMP, decreases Intracellular Ca++, vascular smooth muscle relaxation
************** what does NTG do to preload? LEDP (wedge pressure)? Myocardial O2 demand? endocardial perfusion
decreases it
decreases it
decreases it
increased
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
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
what is more potent NTG or nipride
nipride
NTG can potentiate the effects of what musle relaxant
pancurium
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
All drugs that are direct acting on b/p do what to HR and why?
increase it, b/c they have no cv effects
hydralazine MOA
k+ channels????
NO????
hydralazine can cause what r/t heart rate
tachycardia
what type of pt would benifit from hydralazine?
hypertensive bradycardic pt
***************** hydralazine dose onset duration
5-20 mg
up to 15 min
2-4 hrs
what to remember about hydralazine administration
dont get the urge to re bolus give it time to work you cant take it back
how should you mix hydralazine
20mg in 1cc so mix in 3cc to get 5mg/cc
can u use hydralazine in PIH
does water ripple when a duck farts????
you bet your ass it does!!!!!!
what periphreal vasodilator drug is endogenous to all cells of the body? it is the MOST potent vasodilator released by cardiac cells
adenosine
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
adenosine affects what preload or afterload
afterload
what is teh adenosine dose for controlled hypotension
60-120mcg/kg/min
dose for adenosine
6mg 1-2 sec
12mg 1-2 sec
may repeat once
adenosine is only FDA approved for what?
SVT
