Systemic Arterial Hypertension Flashcards
what is hypertension
has many diff types - portal, pulmonary and systemic arterial
high BP refers to systemic arterial HTN
hypertension is a major risk factor for ____
atherosclerotic cardiovascular disease (ASCVD)
what is ACSVD
atherosclerotic cardiovascular disease
accumulation of cholesterol plaques in arterial walls
why is HTN not usually diagnosed
many are asymptomatic
feels nothing but BP is 150-200
high BP is a major contributor to _____
coronary artery disease
congestive heart failure
cerebrovascular disease
end stage renal disease
what does high BP accelerate
accelerates atherogenesis
promotes formation and deposition of cholesterol = inc risk of CV events
what is more dangerous
inc SBP or DBP
both are dangerous
discuss elevations of SBP and DBP and its effects
normal 1 and elevated 1 = assoc c CV events
elevated SBP = strokes
elevated DBP = MI
both elevated = more CV events
hypertension occurs in association with the following atherogenic factors
dyslipedemia - high LDL and triglycerides and low HDL
glucose intolerance - pre DM to DM
hyperinsulinemia
obesity
are risk factors in HTN additive or multiplicative
multiplicative
walking time bombs
____ is twice as prevalent in hypertensives
coronary artery disease
factors that contribute to inc risk of CHD assoc c high BP
narrowing of epicardial arteries
coronary arteriolar hypertrophy
reduced myocardial vascularity
perivascular fibrosis
discuss SBP
ventricular emptying and contraction
1st korotkoff when you release BP cuff
discuss DBP
ventricular filling and relaxation
after last korotkoff sound
level below that = DBP
what is arterial pressure
product of CO and peripheral resistance
what is cardiac output
product of SV and HR
what is stroke volume
amount of blood heart pumps out
discuss determinants of arterial pressure and how it inc BP
more fluid in blood = inc BP
less fluid in blood = less BP
what warrants stopping of PT
<30% of ejection fraction will cause DV to dec
HR will compromise = tachycardia
no PT since any more inc in HR = CV events
what is MAP
average pressure in cardiac cycle against aorta
1/3 (SBP + 2DBP)
significance of MAP in PT
stroke pt: we dont want to bring MAP; maintain dapat
to protect the ischemic penumbra
discuss proper BP measurement
no smoking, coffee and exercise for 15 mins a taking
relaxed
empty bladder
no talking
proper cuff fit
what is intravascular volume
volume inside blood vessels
primary determinant of arterial pressure
sodium determines this because water follows sodium
inc volume = inc BP and
how does ANS control CV homeostasis
controls BP, volume, chemoreceptors
controls norepinephrine, epinephrine and dopamine - tonic and phasic regulation
modulates adrenergic reflexes - short term
controls adrenergic function and hormonal volume factors - long term
what are baroreceptors
stretch or pressure sensitive nerve endings in carotid sinus and aortic arch - neck
for rapid buffering of acute BP fluctuations
stretch means inc BP = ANS will bring BP down
declines to sustained inc BP and resets to higher BP
what is the RAA system
renin angiotensin aldosterone system
induces sodium reabsorption that may cause HTN
what is renin
produced in kidneys - from JG cells
induces angiotensin production
3 primary stimuli for renin secretion
dec NaCL in loop of Henle
dec pressure on renal afferent arterioles - baroreceptor detects less fluid entering
SNS stim of renin-secreting cells - nervousness, agitation
what inhibits renin
inc NaCl in loop of Henle - need more urine secretion
inc stretch refelx in renal afferent arterioles
enough angiotensin = no inc in renin
what is angiotensin II
vasconstrictor when renal arterial pressure is low or low sodium
angiotensin 1 in kidneys becomes 2 in lungs
effects of angiotensin 2
inc BP
inc calcium and constriction in vessels
stims release of vasopressin
stims aldosterone
what is aldosterone
inc sodium reabsorption and promotes water retention
effects of too much aldosterone
develops HTN
cardiac hypertrophy
cardiac fibrosis
discuss significance of vascular mechanisms
blood vessels should relax, dilate and constrict
if BP inc = vessel should dilate and vice versa
older pts = vessels become rigid and unable to adapt
discuss remodeling in blood vessels
dec lumen size and inc peripheral resistance
hypertrophic - inc cell number, size and deposition
eutrophic - no change amount; just becomes rigid
response of CV during exercise
inc SY and dec PSY
inc HR, SV, CO and venous return
CO goes to working muscles
local metabolites dilate vessels for regional flow
constrict vessels to non-working via SY
10-20 inc in SBP and no greater than 10 sa DPB
mean BP is constant or slightly elevated
dec vascular resistance
20x more O2 consumption
discuss essential HTN
no cause or from aging lang
discuss secondary HTN
has cause - another medical condition
usual causes of secondary HTN
renal parenchymal disease
renal artery stenosis
pheochromocytoma
hyperaldoteronism
coarctation of aorta
hypo-hyperthyroidism
cushing’s
steroids, HRT, PP, alcohol, nicotine
discuss renal parenchymal HTN
damaged kidneys and those with end stage renal diseases
excessive renin production
discuss renal artery stenosis
narrowing will make JG cells think that less BF to kidneys
RAA overstimulation = inc BP
discuss hyper and hypo thyroidism
hyper - inc cathecholamines = inc DBP
hypo - inc CO and dec PVR = inc SBP
discuss primary hyperaldosteronism
adrenal tumor can inc BP and low potassium
also has proximal muscle weakness
discuss pheochromocytoma
adrenal tumor cause release of catecholamines
HTN c tachycardia and sweating
fight or flight gets stimulated
discuss cushing
excess growth hormone can inc CO
pts with excess fat and inc BP
usual presentation of secondary HTN
<20 yo
diastolic HTN at > 50
target organ damage
features of secondary diseases
poor response to usual HTN tx
fam hx
discuss hypertensive emergency
> 220/140
needs to be brought down immed
has acute target organ damage
discuss hypertensive urgency
> 180/100
lower BP gradually
no target organ damage
examples of acute target organ damage
MI
heart failure
encephalopathy
stroke
aortic dissection
preeclampsia and eclampsia
discuss hypertensive cardiovascular disease
seen in chronic uncontrolled HTN
retinopathy
cardiomegaly
L ventricular hypertrophy
heart failure and cardiomyopathy
kidney failure
PVD
discuss white coat HTN
HCP induced
elevated BP in hospitals but normal at home
pathologic consequences to heart
L ventricle hypertrophy
diastolic dysfunction
CHF
arrhythmias
pathologic consequences to brain
stroke usually > 65 yo c HTN
85% - infarc
15% - hemorrhage
dementia
encephalopathy - HA and coma
pathologic consequences to kidneys
d/t RAA
primary renal disease
ESRD
glomerular injury, hypoperfusion, ischemia, sclerosis and atrophy
pathologic consequences to peripheral arteries
PAD
atherosclerotic PAD - intermittent claudication
ABI < 0.90 = stenosis in lower limb vessel
pathologic consequences to eyes
HTN retinopathy - blindness
burst BV
hemmorhage
hard exudates
papilloedema
cotton wool spot
best type of prevention in HTN
primordial prevention
lifesyle modifications for HTN
stop smoking
maintain BMI of 18.5-24.9
<2 gm of sodium and <6 gm of NaCl
healthy diet
exercise
2 drinks for male 1 for female
adequate daily intake of potassium, calcium and magnesium
what are beta blockers
olol
blocks SNS that elevates BP
what are calcium channel blockers
dipine
prevent calcium that promotes vasoconstriction
what are angiotensin converting enzyme inhibitors
pril
inhibits RAAS - no angiotensin formation
what are angiotensin receptor blockers
sartan
blocks receptors of angiotensin 2
what are alpha blockers
zosin
acts peripherally on alpha receptors
what are centrally acting drugs
dine
acts on brain to control BP
what are diuretics
promotes excretion of excess water and sodium
