Exam 2: Ch 18 Blood Pressure Disorders Flashcards
aneurysm
abnormal dilation and outpouching of an artery
most common in aorta (any part)
berry aneurysm
spherical dilation at bifurcation
Circle of Willis
dissecting aneurysm
tear in intima allows blood to enter vessel wall
False aneurysm
1/2 of people with an aortic aneurysm
have HTN
if an aortic aneurysm is above the kidneys…
must cut off kidney blood supply to fix
symptoms of an aortic aneurysm
depends on size and location
AAA most common and 90% below renal arteries
can be asymptomatic
pain
diagnosis of aortic aneurysms
ultrasound
felt as pulsitile mass
treatment of aortic aneurysm
surgical resection
endovascular vs. open is the same chance of success
aortic dissecting aneurysm
acute and life threatening
seen in conn tissue disease (marfan’s)
Excruciating pain
H&P most critical
lower BP and correct surgically
blood pressure
rapid rise in pressure during ejection of blood from left ventricle up aorta
dicrotic notch
closure of aortic valve
pulse pressure
SBP - DBP
Difference between systolic and diastolic pressures
mean arterial pressure
DBP + PP/3
Average pressure in arterial system during ventricular contraction and relaxation
calculate BP
CO x PVR
calculate CO
SV x HR
SV = (blood ejected per beat)
PVR
peripheral vascular resistance
reflects changes in the radius of arterioles
systolic BP
size and velocity of SV
compliance of large elastic arteries
systolic HTN
less compliance of large elastic arteries
stiff aorta
diastolic BP
properties of large arteries and size of SV
resistance of arterioles
competency of aortic valve
diastolic HTN
higher PVR slows runoff
pulse pressure
high when SV is high
low in hypovolemic shock (low SC and high PVR)
hypovolemic shock
high PVR (normal or high diastolic BP)
low SV (low systolic BP)
old person w/ stiff arteries will have…
high systolic BP (HTN forever)
short term BP regulation
keep BP constant for minutes-hours
neural
humoral
neural short term BP regulation has sensors in…
baroreceptors (pressure)
work via SNS and PNS
neural short term BP regulation mechanisms
sensors in carotid and aortic bodies
baro/chemo receptors
respond to low BP, pH, O2, high CO2
communicate to cardiovascular centers (SNS)
chemoreceptors up ventilation
neural responses brain stem
output to heart increases HR and contractility
output to vessels increases PVR
humoral short term BP regulation has sensors in…
JGA and elsewhere
uses RAA system
increases blood volume
humoral short term BP regulation mechanisms
low BP, blood volume, blood NA sensed by JGA
JGA releases renin, which converts angiotensin –> A1
A1 –> A2 by ACE (lung capillaries)
A2 is a vasoconstrictor –> aldosterone release from adrenal cortex
A2 –> ADH release from posterior pituitary
blood volume increased, BP restored
aldosterone
increases Na retention by kidneys
ADH
increases H2O retention by kidney
kidneys in long term BP regulation
vascular volume controls BP, and BP controls kidney filtration
some ppl with HTN respond to sodium restriction
many diuretics useful in BP regulation
kidney damage or chronic increases in Na/H2O intake (high BP)
ECF volume in long term regulation of BP
one time ECF increase = high CO and PVR –> high BP
urine output increases
diuresis returns blood volume and BP to normal
chronic high ECF causes persistent HTN with high PVR
indirect ascultation
Sphygmomanometer (bladder)
width of bladder > 40% of upper arm circumference
undersize bladder –> overestimation of BP
slower deflation = higher accuracy
automated methods of BP measurement
doller
microphone
pressure sensor
direct methods of BP measurement
arterial catheter
essential HTN
90% of cases
High BP without evidence of other disease
BP > 140/90
requires more than 1 elevated reading
stages of HTN
normal 120/80, recheck in 2 yrs
pre HTN 120-139/80-89, recheck in 1 yr
stage 1 HTN 140-159/90-99, confirm within 2mo
stage 2 HTN >160sys OR >100 dia, treat within 1mo
HTN risk factors
family history
age: SBP higher throughout life, DBP increases until 50
race: african americans have more and more severe HTN
metabolic problems: type 2 DM, obesity
lifestyle factors in HTN
Na intake
obesity
EtOH
K+ intake
Na intake
high salt and H2O intake increases blood volume and BP
salt restriction helps treat
75% of dietary salt in food processing
DASH
dietary approach to stop HTN
advocates fruits and veggies, and whole grains
obesity and HTN
distribution more important than weight
high waist/hips ratio associated with HTN
EtOH
3+ drinks/day increases SBP
K intake
low K increases SBP
mechanism unknown
HTN can be ____, ____ or ____
systolic, diastolic, or both
isolated systolic HTN
high complication risk
high shear stress (vessel damage)
elevated PP strong risk indicator for elderly
target organ damage in systolic HTN
heart increased workload –> LVH (left ventricular hypertrophy)
risk factor for atherosclerosis, HF, CHD, stroke, PAD, renal failute
diagnosis of isolated systolic HTN
requires multiple elevated readings
person should be relaxed and seated
treatment of systolic HTN
drugs
TLC (theraputic lifestyle changes)
goals relaxed for 60+ years of age & DM
drug classes for HTN
diuretics lower blood volume and PVR
beta-blockers lower HR and SV to lower BP
ACE inhibitors block A1 –> A2
A2r blockers block A2 action (receptors)
calcium channel blockers dilate arteries
antagonists of A1 receptors
how to treat HTN
under 60 treat @ 140/90
60+ no DM treat at 150/90
if DM or chronic kidney disease treat at 140/90 regardless of age
theraputic lifestyle changes
DASH
exercise
less salt
moderate EtOH
lose weight
less stress
no smoking
secondary HTN (10%) due to another disease
renal HTN
steroid hormone abnormalities
pheochromocytoma
coarctation of aorta
oral contraceptives
renal HTN
type of 2ndary HTN
any disease that lowers salt and water excretion –> high BP
renovascular HTN activated RAA system
renal artery stenosis is usual cause
may require angioplasty or open surgery
steroid hormone abnormalities
type of 2ndary HTN
primary hyperaldosteronism (Na absorbed, K excreted) or glucocorticoids
often show hypokalemia
use Aldo blockers
pheochromocytoma
2ndary HTN
tumor of adrenal medulla or sympathetic chain
makes NE and Epi
produces headache, nervousness, sweating
measure carechole metabolisms in urine (VMAs)
use alpha and beta blockers –> surgery
coarctation of the aorta
2ndary HTN
often at takeoff of subclavian arteries
activates RAA system
oral contraceptives
2ndary HTN
major cause of HTN in young women
mechanism unk, but hormone induced volume expansion
generally resolves when drugs stopped
malignant HTN
sudden BP elecation to DBP > 120 – seen in 2ndary HTN
cerebral vasospasm occurs to protect brain
cerebral edema, renal damage likely without aggressive treatment
HTN in pregnancy (6-8%)
good prenatal care mandatory
chronic HTN: high BP prior to 20 wks
preeclampsia/eclampsia
gestational HTN: high BP 1st seen in pregnancy w/o protinuria
preeclampsia/eclampsia
high BP after 20 wks
protinuria, high creatinine/liver enz, low platelet count
more common in women with chronic high BP, DM, multiple pregnancies
low placental blood flow –> toxins –> endothelial damage –> end organ damage
platelets aggregate at damages epithelium
definitive diagnosis at delivery
HELLP
hemolysis, elevated liver enzymes, and low platelets
variant of preeclampsia
classification system addresses lab abnormalities of blood vessels, liver and other organ systems (higher platelets is worse)
pediatric HTN
norms based on height and sex
most is 2ndary
primary seen in adolescents
should be treated
orthostatic hypotension
abnormal drop in HTN
occurs when blood pools in legs
cause dizziness and blackouts
cardiovascular reflexes are supposed to prevent this
causes of orthostatic hypotension
hypovolemia – diuretics
other drugs like antihypertensives
aging – poor cerebral circulation
prolonged bedrest – low plasma volume
ANS disorders
treatment of orthostatic hypotension
physical exam and history
correct cause (fluid and electrolyte imbalance) if possible
support hose
mineralocorticoids or alpha agonists
diseases of venous circulation – lower extremities
leg has superficial veins… saphenous and deep
incompetent veins can allow backflow (valves fail)
muscle pump & 1 way valves direct blood flow
varicose veins
dilated tortuous veins in legs
primary: originate in saphenous
2ndary: result from blockage of deep venous channels
etiology of varicose veins
prolonged standing and abdominal pressure (pregnancy)
diagnosis and treatment of varicose veins
physical exam
pressure stockings, surgical removal of superficial
chronic venous insufficiency
consequences of DVT and valve failure
produces tissue congestion and edema –> necrosis/ulceration
compression and surgery, skin grafting
venous thrombosis
thrombus (clot) in vein –> inflammation
can be deep or superficial
can produce a pulmonary embolism
statins may prevent
risk factors for venous thrombosis
venous stasis (bed rest, shock)
increased coagulation (dehydration, BCP/HRT)
vascular trauma (surgery/injury)
symptoms, diagnosis, treatment of venous thrombosis
pain, swelling, fever
venography, ultrasound
anticoagulants, maintain bedrest until no swelling
increase activity slowly with elastic hose
surgery
