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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

***************
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

*******************************
how do Arterial Vasodilators work

decrease systemic b/p by decreasing SVR

21

******************
how do venous vasodilators work

By decrreasing systemic venous return and CO

22

****************************************
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

***************************
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