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blood pressure
force exerted by blood against wall of vessels
helps perfuse and move blood around
systolic
pressure during ventricular contraction
diastolic
pressure during ventricular relaxation
normal BP
SBP:
<120
DBP:
60-80
elevated BP
SBP:
120-129
DBP:
<80
stage 1 HTN
SBP:
130-139
DBP:
80-89
stage 2 HTN
SBP:
greater than or equal to 140
DBP:
greater than or equal to 90
types of hypertension
primary hypertension (AKA essential HTN)
secondary hypertension
resistant hypertension
white coat hypertension
hypertensive crisis
primary hypertension (essential HTN)
develops overtime with no single known or identifiable medical cause
most common form of HTN
driven by genetics, aging, and lifestyle factors like obesity, high salt intake, and inactivity
secondary hypertension
caused by an identifiable underlying medical condition, medication, or substance - NOT from lifestyle factors
affects 5-10% of patients
appears suddenly
more severe than primary hypertension
can sometimes be cured by treating the foot cause
resistant hypertension
BP resistant to changing despite lifestyle modifications and medications
white coat hypertension
HTN during clinical readings
may bc ppl nervous seeing doctors
normal BPs at home
hypertensive crisis
hypertensive emergency
SBP over 200 or DBP over 120
preload
blood volume going into heart
amt of stretch or tension on the ventricular walls of the heart at the end of diastole, directly determined by the volume of blood in the ventricles just before contraction
cardiac output
stroke volume x HR
how much blood your heart is expelling
systemic vascular resistance
resistance the left ventricle must overcome to circulate blood
risk factors for HTN
non-modifiable
age
genetics
ethnicity
sex
modifiable
smoking
obesity
sodium
caffeine
alcohol
stress/anxiety
lack of physical activities
chronic hypertension - part 1: the calm before the storm
bloodstream flowing as usual
healthy endothelium lining
normal BP regulation
systolic 120 mmHg
diastolic 80 mmHg
chronic hypertension - part 2: the rising current
slow and silent change - asymptomatic
increased peripheral resistance results in decreased perfusion
baroreceptors send signals for vasoconstriction and increased blood volume
increased pressure causes damage to endothelial lining over time
chronic hypertension - part 3: the breaking of the banks
damage and consequences
endothelial injury
inflammation
platelet aggregation
plaque buildup
atherosclerosis
decreased perfusion to kidneys, retina, heart, brain, distal extremities (PAD)
ischemia
organ damage
chronic hypertension - part 4: the flood
the deadly finale
plaque occlusion, arterial emboli, aortic dissection or rupture
acute complications
stroke, heart attack, aneurysm rupture, limb ischemia
complications of HTN
target organ damage (TOD)
brain
eyes
peripheral arteries
kidneys
heart
and more…
DASH diet
dietary approaches to stop hypertension
lowers SBP ~11mmHg
lifestyle modifications for HTN
weight reduction
decr 5-20 mmHg per 10 kg wt loss
DASH diet
8-14 mmHg decr
physical activity
4-9 mmHg decr
sodium reduction
2-8 mmHg decr
decrease ETOH
2-4 mmHg decr
avoid tobacco
stress management
HTN assessment
history
HA
change in LOC
vision changes
nose bleeds
chest pain
medications?
CV
BP
heart sounds
pulses arterial bruits
edema
labs
renal
electrolytes
H&H
FBG
lipids
diagnostics
EKG
CXR
BUN/creatinine
arteriography
echo/ultrasound
ophthalmic exam
HTN interventions
goal for BP = <130/80
elevated (SBP 120-129)
lifestyle modifications
stage 1 (SBP 130-139)
life style modifications
medications → thiazide first, then ACE, ARBs, BB, CCB, or combo
stage 2 (SBP over 140)
lifestyle modifications
medications → two drug combo
optimize doses/meds, lifestyle changes until goal is achieved
HTN medication classes
diuretics
beta-blockers
ACEi
ARBs
CCBs
alpha-blockers
alpha-2 receptor agonists
vasodilators
diuretics
class: thiazide diuretics
ex) hydrochlorothiazide (HCTZ)
MOA: inhibits Na+ reabsorption in kidneys which promotes diuresis and reduces blood bolume
cautions: orthostatic hypotension, electrolyte imbalances, can cause nephrotoxicity
beta-blockers
ex) metoprolol
MOA: blocks beta-adrenergic stimulation that increase BP (heart and peripheral vascular system)
cautions: orthostatic hypotension, contraindicated with asthma, bradycardia
ACEis
ex) lisinopril
MOA: inhibits conversion of angiotensin I to angiotensin II → dilates arteries and veins
cautions: orthostatic hypotension, dry cough, dizziness, hyperkalemia
ARBs
angiotensin receptor blockers (ARBs)
ex) losartan
MOA: blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II
cautions: orthostatic hypotension, angioedema, hyperkalemia
HTN education and followup
routine assessment (Q3-6 months)
history
home BP logs
physical assessment
taking meds?
med SEs?
lifestyle modifications
education
pt and family teaching → med compliance
home monitoring
when to call
when to come back in
hypertensive crisis
urgency: BP > 180/120 no S/Sx TOD
emergency: BP > 180/120 and S/Sx TOD
clinical manifestations
S/Sx of TOD
retinal: papilledema. hemorrhage
neuro: HA, seizures, confusion, coma
CV: chest pain, SOB, dysrhythmias
goal of treatment
lower BP: 2-4 hours later, BP reduction of 25%
stabilize to 160/100 mmHg over next 2-6 hours
treatment
confirm reading
IV vasodilators
complications
cerebral bleed, heart failure, renal failure
too-rapid reduction in BP can lead to ischemia
orthostatic hypotension
supine to sitting to standing (AND/OR)
decrease of 20 mmHg or more in SBP
decrease in 10 mmHg or more in DBP
HR increase of 20 bpm
risks/causes
>70 years old
BP meds
hypovolemia
fever
sepsis
reduced CO
bed rest
assessment
vertigo
N/V
tachycardia
interventions
elevate HOB
BP and HR supine, sitting, upright
compression stockings
fluids
support at side of bed
patient teaching
change positions slowly
dangle before getting OOB
leg exercises
use call bell