Hypertension Flashcards
Hypertension
modifiable risk factor to prevent CVD
As BP increases, so does risk of
-MI
-HF
-stroke
-renal disease
-retinopathy
Affects 46% of adults in US
-CVD a/w HTN leads to 23.7% of deaths in USA
National Health and Nutrition Examination Survery
83% of people over 20 yrs old with HTN are aware of it
76% are being treated
48% don’t currently have their BP well controlled
AHA and American College of Cardiology Foundation
Make HTN management goals based on age and comorbidities
Evidence-based guideline for the prevention, detection, evaluation, and management of high BP
Ethnic risks for HTN
lower risk if born outside USA, don’t speak English, haven’t lived in USA long
High risk for blacks
-dvlps at younger age
-females more than males
-nocturnal nondipping BP
-more end organ damage
-highest death rate
-less response to renin inhibiting meds –> better control with calcium channel blockers and diuretics
-increased risk of angioedema with ACE inhibitors
Hispanics
Gender difs
Hispanics less likely to receive treatment or to be aware of condition
Men: more common b4 mid age
Women: increased 2-3x with oral contraceptives
-preeclampsia = possible early sign
-more common after menopause - hard to control in older women
Blood pressure
force exerted by blood against walls of blood vessels
-involves both systemic factors and peripheral vascular effects
-importat to maintain tissue perfusion during activity and rest
-func of CO and SVR
-CO = SV*HR
What factors influence BP
nervous, CV, endothelial, renal, and endocrine funcs
SNS increases HR and contractility; vasoconstriction and renin release; increases CO and SVR
PNS decreases HR via vagus nerve and decreases CO = lower BP
SNS mechanisms
Baroreceptors
-sense decreased BP and send a message to vasomotor center in brainstem leading to efferent nerves in cardiac and vascular smooth muscle cells
NE
-released from SNS nerve endings; activate receptors in SA node, myocardium, and vascular smooth muscle
SNS receptors = a1, a2, b1, b2, and dopamine
SNS receptors
a1 in vascular smooth muscle = vasoconstriction; increased contractility (+ inotropic)
a2in presynaptic nerve terminus = inhibits release of NE
b1 in vascular smooth muscle = vasoconstriction; increased contractility, HR, conduction, and renin (+ionotropic, + chronotropic, +dromotropic)
b2 in smooth/skeletal muscle = vasodilation
dopamine in renal blood vessels = vasodilation
Sympathetic vasomotor center
activated during stress, pain and exercise to increase CO and BP in response to O2 demands
Position changes- lying to standing
-transient decrease in BP leads to SNS stimulation leads to peripheral vasoconstriction and increased venous return
-inadequate response leads to dizziness or syncope
Baroreceptor roles
Maintain BP - sensitive to touch
-increased stretch = inhibitory reflex to vasomotor center to decrease HR/contraction force and cause vasodilation
-decreased stretch = SNS stimulation leads to peripheral arteriole constriction, increased HR, and increased contractiility
-long standing HTN = baroreceptors adjust to increased BP regarding it as the new normal
Vascular endothelium
essential to regulation of substances for
-vasodilation: NO and prostacyclin
-vasoconstriction: endothelin
Smoking and diabetes reduce endothelial func and lead to increased risk of CVD
Renal system and BP
Controls sodium excretion and ECF volume
-increased Na+ leads to increased H2O leads to increased ECF leads to increased venous return and SV leads to increased CO and BP
RAAS syst - juxtaglomerular apparatus - secretes renin in response to SNS stimulation, decreased renal blood flow, and decreased serum Na+
AII is casocontricter and increases SVR and stimulates aldosterone secretion
Renal prostaglandins
PGE2 and PGI2 from renal medulla lead to systemic vasodilation
-decreased SVR and BP
ANP and BNP
oppose ADH and aldosterone leads to natriuresis and diuresis leads to decreased blood volume and BP
Endocrine effect on BP
Epinephrine and NE from adrenal medulla
-Epinephrine increases HR, contractility, CO –> also vasodilation in skeletal muscles, but vasoconstriction in skin and kidneys
Aldosterone from adrenal cortex retains water and increases CO
ADH does same
classification of HTN
Normal <120/ <80
Elevated: 120-129 / <80
Stage 1: SBP is 130-139 or DBP is 80-89
Stage 2: SBP is 140+ or DBP is 90+
Primary HTN
“essential” or “idiopathic”
-elevated BP of unknown cause
-90-95% of all cases
many contributing factors
-altered endothelium
-increased SNS activity
-increased A+ intake
-too much Na retention
-overweight
-diabetes
-alc/tobacco
Secondary HTN
-elevated BP with specific casue and sudden dvlpmnt
-5-10% of cases
Causes
-cirrhosis
-aortic probs
-drugs
-endocrine, neuro, or renal probs
-pregnancy
-sleep apnea
Pathophysiology of primary HTN
as HTN progresses from elevation to stage 1, blood volume and CO are high, leading to persistently increased SVR
SVR rises, but CO gets normal
Risk factors for primary HTN
age
alc
tobacco
diabetes
high serum lipids
high sodium
gender
fam history
obesity
ethnicity
sedentary lifestyle
socioeconomic status
stress
Patho: Primary htn genetic link
-there’s a bunch of dif genes that regulate BP thru life
-possibly endothelial genetic variants influence salt sensitivity and cause imflammation and inhibit vasodilation
Kids and sibs of ppl with HTN should get checked out
Patho: water and sodium retention HTN
-only1/3 of ppl who eat high sodium get htn
-Na+ effect on BP is mostly genetic -> blacks, mid age, and old ppl are more sensitive
-ppl who are salt sensitive have increased risk for renal issues, endothelial issues, and HF
Patho: Altered RAA mech
High plasma renin activity (PRA)
-increases angi conversion
-increased BP inhibits release of renin
-PRA should be low in HTN ppl, right? –> but its not
-maybe bc ischemic nephrons release renin?
Patho: stress and increased SNS activity
Protectice response turns pathologic
-vasoconstriction
-high HR
-renin resistance
Patho: insulin resistance
-defects in glucose, insulin, and lipoprotein metabolism are common
**probs don’t go away even if htn does
High insulin levels
-stimulate SNS activity and impair NO-mediated vasodilation
-vascular hypertrophy
-increased renal sodium absorption
-increased renal sodium absorption
