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normal BP:
SP< 120

*AND*

DP <80
prehypertensive:
SP = 120-139

OR

DP = 80-89
Stage I Hypertensive:
SP = 140-159

OR

DP = 90-99
Stage II Hypertensive:
SP = 160 or greater

OR

DP = 100 or greater
BP =
CO x TPR
TPR is affected by (4):
1. hematocrit

2. local tonal factors

3. SNS/PNS stimulation

4. hormones like ADH
if hematocrit increases, so does
viscosity

thereby increasing R
hematocrit isn't that big a deal, though, b/c
it's relatively constant
endothilin =
constrictor
adenosine =
major dilator
CO is affected by delta HR, due to
hormones from SNS/PNS
CO is also affected by delta SV, due to: (3)
1. contractility (ionotropic state)

2. preload

3. afterload
preload =
EDV
how does preload affect SV?
putting more or less blood into the heart => more or less force against ventricular walls => more or less contractile force in *response*
in other words, as EDV increases,
contraction force increases,

so SV increases
injection of EPI => increase in
*force* of contraction => inc. in SV
Afterload =
the resistance the left ventricle has to overcome in order to eject blood
tested by continuing to increase the pressure of a clamp against the
aorta
speed decreases as afterload
increases
higher BP => higher
afterload
higher afterload =>
lower SV,

b/c speed of shortening decreases
adding EPI => increase of speed at
every point of afterload chart, even zero afterload
factors that contribute to BP:
1. sympathetic signals from brain
(inc. HR, CO)

2. blood vessel tone
(factors, SNS/PNS)

3. the kidney
(via renin or ADH)

4. baroreceptors
kidneys' effect on BP: loss of water/volume =>
dec. Pressure =>

(dec. P or [Na+] => release of renin)

renin => angiotensinogen from liver => A1 => A2 (via ACE)
(ACE =
angiotensin converting enzyme)
A2 => (2)
1. vasoconstriction (which inc. BP)

2. release of aldosterone (inc. reabsorption of Na+ => inc. BP due to water following)
*renin is always on, just
regulated up or down
where are baroreceptors found?
at the aortic and carotid sinuses

(carotid sinus at bifurcation of internal and external carotids)
as BP increases, baroreceptors increase signals, which
increase ParaNS stimulation

but decrease SNS stimulation
a MAP below 50
doesn't register,

baroreceptors don't fire

b/c they can't detect anything
a MAP greater than 150 =>
baroreceptors always ON, not useful at all
what are 95% of hypertension cases?
Essential Hypertension
***there are no specific ______ of EH, so there is no ____ ***
causes

cure,

only treatments
EH is caused by a combo of
marginal (high-normal) factors which, by themselves, aren't a big deal
2 things that lead to EH:
genetic factors (blacks have highest risk)

systemic factors (taken together)
5 systemic factors that can lead to EH:
1. slow leak of EPI from adrenal cortex

2. slightly higher release of renin from kidneys

3. desensitized baroreceptors

4. slight inhibition of tonal *factors* (=> less dilation)

5. obesity (adipose secretes check)
with desensitized baroreceptors, high BP is seen as
normal BP
5% of Hypertension cases is:
Secondary Hypertension
SH is recognized by:

(8)
1. sudden onset

2. other conditions (which then cause SH)

3. no family history

4. caused by some medicine, alcohol, cocaine

5. renal disease (don't absorb Na+)

6. renal vascular disease

7. coarction

8. compromised endocrine function (e.g. EPI is overmade)
renal vascular disease: stenosis of renal arteries =>
high BP right before narrowing, but very low BP after it

=> kidneys only sense low BP, release LOTS of renin

=> huge inc. in BP
coarction explained: congenital narrowing of aorta =>
high BP before it, low BP after it

=> high BP in upper body desensitizes b.r.'s

while low BP in lower body stimulates release of renin
what's the key difference between pacemaker cells and all other cells?
depolarization is a result of Calcium, \

not Na+
the heart repolarizes ...
at once
ST segment ~
the plateau
prolonged P-R interval = problem with
conducting tissue between SA and AV nodes
complete heart block => atrium and ventricle beating
independently
aortic pressure will vary between
80 and 100 mm HG
gravity helps get blood back into heart, at least in the
upper body
vWF ~ platelet
*adhesion*
hemophilia A =
factor 8 deficiency
serum =
plasma without clotting factors
endo releases antithombins, heparin, etc. to prevent
clotting
endothilin 1 is released when endo is
compromised
**what releases ROS?**
**endo**
what's the affect of glycation LDL, and why does it happen?
=> foreign LDL's,

diabetes
what's the biggest factor affecting tone of coronary arteries, and thus of blood flow through them?
**the local environment**
what's the most important factor of the local environment?
adenosine

**always around b/c you're always breaking down ATP, esp. as the heart works harder**
acute coronary syndrome is diagnosed by
EKG
what's the relationship between ACS and plaque?
ACS often occurs *when* a plaque is *ruptured*
3 forms of ACS:
1. unstable angina

2. non-STEMI

3. STEMI
1. small clot => unstable angina; pain occurs, but no
biomarkers
2. non-STEMI = just like
unstable angina, but has biomarkers
3. STEMI
serious, has biomarkers
symptoms of MI: (4)
1. persistent pain that radiates out

2. nausea

3. vomit

4. dyspnea
propranitol =
antagonist of EPI
SH is generally a result of
kidney disease (increased Na+ reabsorption)
to treat hypertension: (2)
1. diet

2. exercise

*helps both during and after*
CAD may lead to ACS, which comes in
3 forms