Hypertension Flashcards
HTN risk factors
Age
Genetics
Diabetes and dyslipidemia
African American race
CKD
Excessive alcohol intake
avg arterial blood pressure during normal flow
90mm hg
systole hemodynamics
pressure in arteries increase
heart pumps blood into arterial system
wall of the arteries stretch
diastole
recoil elasticity of vessel
forces blood out and into the capillaries
minimum diastolic pressure
70-80 mmHg
maximum systolic pressure
110-120
BP regulation depends on
cardiac output and peripheral vascular resistance
cardiac output impact on BP
affected by sodium intake, renal function, mineralocorticoids
peripheral vascular resistance
dependent upon sympathetic nervous system, humoral factors, local vasculature autoregulation
inotrope
strength of contraction
chronotrope
beats per minute
after load
force heart exerts to overcome peripheral resistance
short term BP regulation (systems?)
neural
humoral
neural short therm BP control
baroreceptors and chemoreceptors (O2, CO2, H+) in carotids and aorta to determine response
acts on vagus n. to DECREASE HR
acts on sympathetic n. to INCREASE HR and tone
humoral BP control
RAAS promotes water retention and ADH vasoconstricts and decreases water loss
directly increases HR, contractility, vascular tone
long term BP control
kidney
regulates pressure around an individual set point
how is BP elevated?
hydrostatic pressure
widespread arteriolar vasoconstriction
normal BP
systolic less than 120
diastolic less than 80
prehypertension
120-139 systolic/ 80-89 diastolic
hypertension stage 1
systolic 140-159 or diastolic 90-99
hypertension stage 2
systolic > 160, diastolic > 100
isolated systolic HTN
BP is >140/<90
isolated diastolic HTN
<140/>90
hypertensive urgency
BP at or above 180/120 with NO end organ damage
hypertensive emergency
evidence of impending or progressive target organ dysfunction
at or above 180/120
neurological HTN damage (4)
hypertensive encephalopathy
cerebrovascular accident (stroke)
subarachnoid hemorrhage
intracranial hemorrhage
cardiac end organ damage
HTN
myocardial ischemia/infarction
acute left ventricular dysfunction
acute pulmonary edema
aortic dissection
other hypertensive emergencies
acute renal failure/insufficiency
hypertensive retinopathy
pre-eclampsia/eclampsia
microangiopathic hemolytic anemia
diagnosis of HTN
must see provider 2x
initial (if 180- dx)
then come back for several random checks and then review with provider in 3 weeks
non-dippers
failure of BP to decrease nocturnally
confers a cardiovascular disease risk
younger patients and HTN risk
diastolic BP is most closely associated with CV risk
older adults and HTN risk
older adults typically have isolated systolic HTN
adults over 60- BP remains primary determiner of CV risk
African Americans and HTN
HTN that is more responsive to sodium intake, obesity, and diet
younger pts have more severe HTN than older
vulnerable to strokes and HTN kidney disease
3-5 times as likely ot have renal complications and end stage kidney disease
HTN classifications
primary or secondary
90-95% are primary
resistant HTN
typically secondary HTN
uncontrolled BP while on meds from 3+ drug classes (and one is a thiazide diuretic)
secondary HTN etiologies
- CKD
- polycystic kidney disease
- renal artery stenosis
- coarctation of aorta
- thyroid dz
- pheochromocytoma
- primary hyperaldosteronism
- medication
renal disease and secondary HTN
CKD- mc cause
PCKD - large size of kidneys
both have lo GFR and can’t be reversed
renal artery stenosis
renovascular HTN
caused by arteriosclerosis in men and fibromuscular dysplasia in women
constant RAAS activation
when do you suspect renal artery stenosis
suspect if AKI with imitation of ACEI/ARD, refractory HTN, recurrent flash pulmonary edema, abdominal bruit
contraction of aorta
uncommon cause of secondary HTN
suspect if UE pulses and BP are higher than LE BP
medications that cause secondary HTN
ethanol
illicit drug use
estrogens
ephedra/pseudoephedrine
black licorice or licorice root
prehypertension history
asymptomatic increase in CO and intermittently elevated BP
early HTN history
persistently increased peripheral resistance
possible mechanisms causing HTN (6)
- sympathetic N.s. hyperactivity
- genetics
- reduced adult nephron mass
- sodium intake
- immunologic
- cardiac manifestations
sympathetic NS hyperactivity and HTN
over activity of sympathetic tone leads to increased vascular tone and HTN
sodium intake and HTN
increased salt intake triggers increase in BP that promotes increased natriuresis
brings BP up to basal levels
diseases that contribute to HTN (9)
- obesity
- sleep apnea
- cigarette smoking
- alcohol
- lack of exercise
- immune system activation
- polycythemia
- increased salt intake
- NSAIDs
obesity HTN
associated with increase in intravascular volume, cardiac output, activation of RAAS, increased sympathetic outflow
lowers BP modestly
cigarette smoking and HTN
raises BP by increasing plasma norepinephrine and synergistic effect of smoking and high BP on CV risk
alcohol and HTN
raises BP
increasing plasma catecholamines
can be difficult to control in alcoholics
vascular remodeling and HTN
increased after load causes increased arterial wall stiffness, increased systolic BP, widened pulse pressures
decrease coronary perfusion pressures, increased myocardial O2 consumption, hypertrophy of left vent myocytes
steps in cardiac decline due to HTN (awk. phrasing but what happens first, second and third)
- left ventricle hypertrophy
- diastolic dysfunction
- systolic dysfunction
left ventricle hypertrophy
left ventricle muscle gets thicker so that the heart can pump more strongly against the elevated pressure
increased risk of premature death and morbidity
diastolic dysfunction
incomplete passive relaxation of stiff hypertrophied left ventricle
less space to go in
cerebral auto regulation of BP
ability of vasculature to maintain constant cerebral blood flow across wide range of perfusion pressure
cerebral auto regulation and HTN
when chronic HTN present, CNS becomes accustomed to elevated perfusion pressures
therefore more prone to cerebral ischemia when BP/flow decreases
CNS auto regulation and HTN tx
pts with longstanding HTN
can be just as dangerous to lower their BP too precipitously as it is to let it stay elevated
can cause ischemia (too low) or edema (too high)
chronic HTN and the kidney
causes pathologic sclerotic changes in kidney
endothelial cell dysfunction and impaired vasodilation
alters auto regulation of blood flow to glomerulus and is instead affected by systemic arterial pressure
volume expansion is main cause
in patients with vascular disease, HTN is the result of (kidney)
activation of RAAS
secondary to tissue ischemia
volume expansion and activation of system is believed to be cause of HTN with chronic renal failure
RVHT
occurs when there is complete or partial vascular occlusion of a renal artery
RAAS Is activated by kidney with low blood flow
hyerreninemia promotes conversion of angiotensin I to angiotensin II = severe vasoconstriction and aldosterone release
CV risk factors
tobacco use diabetes mellitus obesity lack of exercise elevated LDL >55 (men) or >65 (women) GFR <60 microalbuminuria family hx
prescription drugs causing drug induced HTN
NSAIDS psych meds migraine meds high dose OCs pseudoephedrine
situations w/prescriptions drug causing drug induced HTN
b- blockers without alpha blocker first when treating cocaine induced HTN or pheo
street drugs or other causing drug induced HTN
cocaine
cocaine withdrawal
narcotic withdrawal
st. john’s wort
diagnostic HTN work up
urinalysis fasting blood glucose CBC electrolytes fasting lipids baseline EKG
HTN target
general population
<140/90
- under 60 = <150/90
HTN target
80+
<150/90
HTN target
Diabetics Mellitus
<130/80
HTN target
CKD
<130/80 `
lifestyle modifications in HTN
weight loss DASH diet reduced salt intake exercise alcohol
tx goal of essential HTN
lifestyle and if insufficient, drug tx
reduction in CV and renal morbidity and mortality
HTN tx and drug chosen
mortality benefit for HTN related to AMOUNT lowering, not drug chosen
SO look at compelling indications and try to reduce # of pills
compelling indications (def + 6)
specific classes of drugs that should be initiated where evidence based survival benefit
- heart failure
- high CAD risk
- CKD
- Post Myocardial Infarction
- Diabetes Mellitus
- Recurrent Stroke Prevention
