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
Patho: endothelial dysfunction
-prolonged vasoconstriction or reduced vasodilation
-vasodilation can be altered by O free radicals which impair NO availability
-elevated endothelin leads to vasoconstriction
Clinical manifestations of HTN
“silent killer” –> asymptomatic til severe and target organ disease occurs
Symptoms of severe HTN
-fatigue
-dizziness
-palpitations
-angina
-dyspnea
Complications: heart and brain
Heart
-CAD and atherosclerosis
-Left ventricular hypertrophy
-HF
Brain/ cerebrovascular disease
-TIA/strike; atherosclerosis
-Hypertensive encephalopathy; changes in autoregulation leading to cerebral edema
Complications: PVD, Kidney, Eyes
PVD
-atherosclerosis leads to PVD, aortic aneurysm, aortic dissection
-intermittent claudication
Kidney
-nephrosclerosis leads to CKD
-nocturia is early sign
Eyes
-retinal damage –> blurry or loss of vision
-retinal hemorrhage
**damaged retinal vessels indicate damage to vessels in heart, brain, and kidneys
Diagnostic studies
BP obviously
Labs
-identify or rule out 2ndary htn
-evaluate target organ disease
-determine CV risk
-establish baselines before treatment
Renal func, U/A, BMP, CBC, serum lipid profile, uric acid, ECG, ophthalamic exam
possible echo, LFTs, TSH
Diagnostic studies: Ambulatory blood pressure monitoring
-avoids “white coat” htn
-tests BP at regular intervals over 12-24 hr period
-keep arm still and at side during measurements
Can be used in cases of
-antihypertensive drug resistance
-hypotensive symptoms w/ medication
-SNS dysfunction
-episodic htn
-diurnal variablility; nondippers; reverse dippers
Interprofessional care: lifestyle mods in general
Overall
-get to goal BP
-reduce CV risk factors and target organ disease
Lifestyle mods
-manage BP
-control cholesterol
-reduce blood sugar
-get active
-eat better
-lose weight
-stop smoking
Lifestyle mods: weight and eating
Weight reduction
-weight loss of 1 kg decreases SBP by 1
-calorie restriction and physical activity
DASH eating
-fruits, veggies, fat free/low fat milk products, whole grains, fish, poultry, beans, seeds, nuts
Sodium reduction
-less than 2300 mg/day for healthy adults
-less than 1500 mg/day for black, mid age, old ppl, those w/ htn, diabetes, CKD
Salty six: bread/rlls, lunch meat, sandwiches, pizza, soup, poultry
**lowers risk for hypokalemia
Life mods: alcohol and physical activity
alc
-men: 2/day; women 1/day
activity
-moderate-intenity aerobics for 150 mins a week
-combo of moderate and vigorous activities is good too
-muscle training 2 times/week
-flexibility/balance 2x/week in old ppl
**all this stuff can lower SBP by 4-9
Lifestyle mods: tobacco and other risks
tobacco
-nicotine = vasoconstriction and elevated BP
-smoking cessation reduces risk factors within 1 yr
other risks
-socioeconomic status, resources to meet daily needs, emotional and social support, stress, educational preparation, access to health care and housing, exposure to crime, depression
-all these can activate SNS and stress hormones
Drug therapy goals
If over 65 with SBP over 130 and living in ambulatory setting, goal is SBP <130
If over 65 with SBP over 130 and in a care facility or with comorbidities, goal is based on specific situation
If over 18 with HTN, CVD, or other risks, goal is 130/80
Everyone else’s goal is less than 130/80
actions of antihypertensive drugs
- decrease circulating blood volume
- reduce SVR
Drugs:
Adrenergic inhibitors
ACE inhibitors
A-II receptor blockers
Adrenergic inhibitors
-decrease SNS stimulation
-work centrally on vasomotor center and peripherally to inhibit NE release or block adrenergic receptors on blood vessels
ACE inhibitors
-prevent the converstion of AI to AII
-reduces vasoconstriction and Na/H2O retension
AII receptor blockers
-prevent AII from binding to receptors in blood vessel walls
Drugs
Ca channel blockers
Direct vasodilators
Diuretics
CCB
-increase Na excretion and cause arteriolar vasodilation by preventing the movement of extracellular Ca into cells
Direct vasodilators
-relax vascular smooth muscle and reduce SVR
Diuretics
-reduce plasma volume by increased Na/H2O excretion and reduce vascular response to catecholamines
Drugs for patient with stage 1 htn
nonpharmacologic treatment along with one of the first line drugs
(a thiazide diuretic, a CCB, or an ACE inhibitor/ARB)
Drugs for patients with stage 2 hten
nonpharmacologic therapy along with 2 antihypertensives from two dif classifications
-if drug not tolerated, use one from dif classification
-monthly follow ups until goal is reached, then every 3-6 mnths
-stage 2 htn or comorbidities require more frequent appointments
Drug therapy side effects
-important to report them
Common
-orthostatic htn
-sex probs - ED/ low libido
-dry mouth - use gum or candy
-frequent voiding - take diuretic in morning
Resistant htn:
definition
causes
treatment
-failure to reach goal BP with drug regimen and therapy –> higher risk of strok or MI
Causes
-improper BP measurement
-volume overload
-drug induced or other causes
-co-conditions
-2ndary htn
Treatment
-determine cause
-overactive renal nerve requires renal nerva ablation
Assessment: subjective
history
Drugs
History
-htn, CVD, cerebrovascular issues, renal or thyroid issues
-DM, pituitary issues, obesity, dyslipidemia
-menopause or HT
Drugs
Assesment: func health patterns
health perception
-fam history, alc/nic, sedentary, literacy
nutritional
-salt/fat, weight
elimination
-nocturia
activity
-fatigue, dyspnea on exertion, palpitations, pain
cognitive
-dizziness, blurred vision, paresthesias
sexual
-ED and low libido
Coping
-stress
Assessment objective data
CV
-BP, orthostatic changes, heart sounds, pulses, edema
GI
-body measurements and BMI
Neuro
-mental status changes
Diagnostic studies
Nursing diagnoses and goals
diagnoses
-altered blood pressure
-ineffective tissue perfusion
-impaired sexual func
-potential complications: stroke and MI
Goals
-achieve and maintain goal BP
-minimal side effects
-manage and cope with condition
Primary prevention
Individual patient evaluation and education
Primary
-lifestyle modification - DASH and decreased Na+
-education regarding dangers of htn
Individual patient evaluation
-screening programs
-identify risks
-BP measurements
-drugs and other treatments
Protocol for BP measurement
-no smoking, exercise, or caffeine 30 mins before
-rest 5 mins - no talking
-correct cuff size and placement
-arm at heart level
-use auscultatory method
-deflate 2-3 mm hg/s
-take both arms, note dif, use higher one from now on
-use forearm and rradial artery or doppler if upper arm is inaccessible
-clean cuff bt patients
How to assess for ortho hypo
-Supine for 5 mins, then take BP and HR
-help them stand
-measure BP/HR after 1 min
-measure BP/HR again after 3 mins
Normal: SBP decreases less than 10; DBP and HR slightly increase
Abnormal: SBP decreases 20 or more; DBP decreases 10 or more; HR increases 20 or more; lightheaded or dizzy
Acute care of htn
BP, Vs, volume status, drug effects –> look at trends
If persistent high BP, evaluate for htn and check in with HCP
Maybe dietitian or PT
Screening programs
-give patient written BP report and explain need for further evaluation
Focus efforts on
1. contoling BP in htn ptnts
2. identigying risk gps
3. screening ppl with limited access
4. connecting ppl to HCP and/or insurance
Ambulatory care
-help ptnt reduce BP
-evaluate therapeutic effectiveness
-detect and report adverse effects
-assess and enhance adherence
-patient and caregiver teaching
Home BP monitoring
Patient teaching is essential
-need proper equipment and procedure, frequency, accuracy, reporting
-once in morning and once at night
Patient adherence
-major problem
Reasons
-inadequate teaching
-low health literacy
-unpleasant drug side effects
-return to normal BP
-high cost of drugs
-lack of insurance
Measures to enhance comliance
-individualize plan
-active patient participation
-select affordable drugs
-involve caregivers
-combo drugs
-patient teaching
Age related physical changes that contribute to htn
loss of elasticity in arteries
increased collagen and stiffness in myocardium
increased PVR
decreased adrenergic receptor sensitivity
blunted baroreceptor reflexes
decreased renal function
decreased renin response to Na/H2O depletion
Other age things
-90% greater risk over 55
-altered drug processing
-wide auscultatory gap
-assess for otho hypo, AKI, and postprandial hypotension
Start with diuretic usually
Be careful with NSAIDs –> kidney issues and hyperkalemia when used with heart drugs
Hypertensive emergency
SBP > 180 and/or DBP > 120
-target organ damage
-requires hospitalization
-prompt treatment needed
-encephalopathy, intracranial or subarachnoid hamorrhage, HF, MI, renal failure, dissecting, aortic aneurysm, or retinopathy
Untreated = 79% mortality in one year
Hypertensive urgency
SBP > 180 and/or DBP > 120
-no evidence of target organ disease
-hospitalization usually not needed
-a/w chronic stable disorders (angina, HF, prior MI or CVA)
Hypertensive crisis in general
-turbulent blood flow causes shearing of blood vessels leading to further vasoconstriction
-coke, amphetamines, PCP, LSD can all cause heart issues leading to stroke, MI, or encephalopathy
HTN crisis manifestations
HTN encephalopathy
-headache, nausea/vomiting, seizures, confusion, coma; retinal changes
Renal insufficiency
Cardiac decompensation
-MI, HF, pulmonary edema, chest pain, dyspnea
Aortic dissection
-chest and back pain, reduced/absent peripheral pulses
Hospitalization for htn
-treatment related to BP and evidenc of target organ disease
-IV drugs: slow titration
-goal is to decrease MAP to 110 to 115
-use vasodilators, adrenergic inhibitors, CCBs
-drugs work fast for monitor HR and BP every 2-3 mins
EXCEPTIONS
-Aortic dissection –> decrease MAP as fast as possible
-ischemic stroke –> reduce to allow thrombolytic agents
-poststroke patients –> no drugs
Hypertensive urgency outpatient care
oral meds: captopril, labetalol, clonidine, amlodipine
-requires follow-up in 24 hrs
