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NURS_308_Exam_2_Hypertension: Lewis, Chapter 33, pp 709-726_With Answers

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Hypertension: Lewis, Chapter 33, pp 709-726 • Modifiable major risk factor for CVD. • “The silent killer”. • In the beginning, when no organs or involved usually pt won’t feel it (possible HA, fatigue). Don’t feel it until there are severe complications. • 65 million American adults; nearly 1 in 3 individuals. • Prevalence increases with age. (Lose collagen and elastic ability, atherosclerosis) • Heart and blood vessels under strain (↑ afterload [bc ↑ peripheral resistance, vasoconstriction], increasing cardiac workload) • Increased risk for MI, heart failure (HF), CVA (stroke), renal failure (RF). • RAAS, Hardening of Arteries, and increased vascular resistance • If someone has hypertension, they are going to have it their whole life. If may go down if they are eating right and taking treatment, but they are still hypertensive. If they stop their meds their BP will go back up. BP = Cardiac output X Systemic Vascular Resistance BP Regulation:  SNS: vasoconstriction and vasodilation.  Vascular endothelium: endothelium-derived relaxing factor causes vasodilation, endothethelin causes vasoconstriction.  Endothelium – inner layer of the blood vessels  Renal System: RAAS, natriuretic peptides.  Endocrine System: ADH, epinephrine from adrenal medulla, aldosterone from

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NURS 308 Exam 2


Hypertension: Lewis, Chapter 33, pp 709-726
• Modifiable major risk factor for CVD.
• “The silent killer”.
• In the beginning, when no organs or involved usually pt won’t feel it (possible HA,
fatigue). Don’t feel it until there are severe complications.
• 65 million American adults; nearly 1 in 3 individuals.
• Prevalence increases with age. (Lose collagen and elastic ability, atherosclerosis)
• Heart and blood vessels under strain (↑ afterload [bc ↑ peripheral resistance,
vasoconstriction], increasing cardiac workload)
• Increased risk for MI, heart failure (HF), CVA (stroke), renal failure (RF).
• RAAS, Hardening of Arteries, and increased vascular resistance
• If someone has hypertension, they are going to have it their whole life. If may go down
if they are eating right and taking treatment, but they are still hypertensive. If they stop
their meds their BP will go back up.
BP = Cardiac output X Systemic Vascular Resistance
BP Regulation:
 SNS: vasoconstriction and vasodilation.
 Vascular endothelium: endothelium-derived relaxing factor causes vasodilation,
endothethelin causes vasoconstriction.
 Endothelium – inner layer of the blood vessels
 Renal System: RAAS, natriuretic peptides.
 Endocrine System: ADH, epinephrine from adrenal medulla, aldosterone from
adrenal cortex, prostaglandins (renal medulla).
Definition:
 Sustained elevation of BP: SBP ≥ 140 mm Hg, DBP ≥ 80 mm Hg, or current use
antihypertensive medication
 Cardiovascular risk begins 115/75 (already producing damage in the blood vessels)
 Use to be 120/80, not anymore, numbers went DOWN. Discovered some people
that had that BP were experiencing difficulties R/T HTN
 Dx: 3 elevated readings over several weeks.
 The higher the BP, the greater the chance for coronary, cerebral, renal, and PVD
Classification of SBP (mm DBP (mm
HTN Hg) Hg)
Normal <120 & <80
Prehypertension 120-139 or 80-89
HTN, Stage 1 140-159 or 90-99
HTN Stage 2 ≥160 or ≥100

Blood Pressure Classification:
• Primary (Essential) Hypertension
 Elevated BP without an identified cause


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, NURS 308 Exam 2


 90% to 95% of all cases
 many risk factors
• Secondary Hypertension
 Elevated BP with a specific cause 5% to 10% in adults
• Ex: taking corticosteroids, or vasoconstrictor medications.
Secondary Hypertension Contributing factors:
 Coarctation of aorta (stenosis)
 Renal disease
 Stenosis of renal artery, renal failure. Kidneys can’t get rid of water & sodium
 Endocrine disorders: hyperaldosteronism (also relates to cirrhosis of liver; retains water &
sodium).
 Retaining more Na and water
 Pheochromocytoma
 Rare condition, a tumor, usually benign, situated in the adrenal medulla where
norepinephrine/epinephrine is secreted; cause vasoconstriction, increased
peripheral resistance & hypertension. Catecholamine’s.
 Cushing’s disease
 Increased secretion adrenal corticoid hormones. (glucocorticoids, mineral
corticoids, and sex hormones) Mainly talking about mineral.
 Pt on corticosteroid Tx tends to have higher BP
 Pheochromocytoma – rare tumor of adrenal gland tissue (adrenal medulla- secretes
catecholamines [epinephrine, norepinephrine] - Vasoconstrictors)
 Can be removed, usually not malignant
 Every time pt moves or pushes on the kidney (or if they’re scared, stress) it
secretes more catecholamines, causing more vasoconstriction. Or palpating the
abdomen.
 Neurologic disorders: brain tumors
 Release of ADH, severe vasoconstrictor
 Pre-eclampsia (during pregnancy)
 Characterized by HTN & protein in urine of pregnant woman
 Obstructive sleep disorders
 Untreated sleep apnea = heart disease & HTN because of extra effort to get
oxygen
 Medications: Corticosteroids, Estrogen, NSAID (contain lots of sodium), amphetamines
Other Hypertensions:
• Isolated systolic HTN: ISH
– At one point in time, pt may have high systolic with a normal diastolic that
manifests.
• Resistant HTN: persistent in-spite of Tx; does not respond to treatment, out of control
• ‘White coat’ HTN
– Why we take several blood pressure readings

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, NURS 308 Exam 2


– "White-coat hypertension" is a condition in which people experience high blood
pressure only when they visit the doctor's office. People who experience it have
an elevated systolic blood pressure between 140 and 180 mmHg while at the
doctor's office and a "normal" blood pressure in other situations. Most healthcare
providers agree that no treatment is required.
• HTN crisis: diastolic 120 – 130 mmHg – MEDICAL EMERGENCY
– BP needs to be brought down quickly. Could have a stroke at this point.
Primary Hypertension:
Risk Factors:
 Age
 Alcohol consumption
 Cigarette smoking
 Increases acidity, very strong vasoconstrictor
 Diabetes mellitus (atherosclerosis presents at a younger age for this population, changes in
blood vessels, early renal failure)
 ↑ serum lipids
 ↑ dietary sodium
 Hypokalemia
 Stress
 Gender (more in males)
 Family history
 Obesity
 The association b/t obesity and the development of HTN Is specifically
accounted for by the visceral adiposity.
 Ethnicity: higher in African-American males
 Sedentary lifestyle
 Socioeconomic status (deals with the consumption of fatty foods & an unbalanced diet,
increased salt consumption )
Pathophysiology:
 Heredity
 Level of HTN is strongly familial.
 In most cases results from the interaction of: genetic factors, environmental
factors, & demographic factors.
 Water and Na retention (know the mechanism)
 High sodium intake may activate a number of pressor mechanisms & cause
water retention.
 Big contributor to this is canned foods- very high in sodium.
 These patients can still use canned food, just need to rinse food off with
water first.
 Multiply amount of sodium you see on can x 2.5 = g of salt
 Stress and increased SNS activity (stress reaction)

3

, NURS 308 Exam 2


 Produces increased vasoconstriction
  HR
  Renin release (causes vasoconstriction)
Clinical Manifestations: Frequently asymptomatic (“Silent Killer”) until it becomes severe and
target organ disease has occurred:
 Fatigue, reduced activity tolerance, dyspnea
 Dizziness
 Palpitations, angina as it progresses
 Later stages start seeing HF, RF
Diagnostic Studies:
 History (diet, physical activity) and physical examination (damage in target organs)
 BP measurement in both arms
 Use arm with higher reading for subsequent measurements.
 Sometimes can’t get BP in both arms due to mastectomy, hemodialysis, fistulas,
shunts
 ↑BP in early morning, ↓ at night.
 Routine urinalysis (evaluate kidney function)
 One of the first signs of renal failure- protein in the urine
 Serum electrolytes, glucose
 CBC
 BUN and serum creat., creat. Clearance (elderly) aka renal function test
 Plasma Serum lipid profile (bc also at risk for atherosclerosis)
 ECG (because of the possibility of heart problems)
Complications:
• Effects of high blood pressure
• Hypertensive ht disease, CAD, left ventricular hypertrophy, CVD-Stroke, PVD
(speeds atherosclerosis), HF, nephrosclerosis because of ischemia or stenosis (like
a plaque in renal artery), retinal damage (little BV in the eye can break and
bleed, explains pt difficulty seeing) retinal hemorrhage/blurring/loss of vision. HTN
risk actor or atherosclerosis. HTN is leading cause of renal disease.
• Treatment
• Lifestyle modifications- try this first; exercise (will check the ht first, stress test, to
make sure pt can handle it) and Nutrition Therapy (low sodium, low cholesterol).
If these don’t work, go then to drug therapy
• Drug Therapy (Add 1 drug if liestyle changes don’t work:thiazide diuretic, CCB, ACEI)
• Even if they’re taking medications, they still need to continue exercise and diet
Lifestyle Modifications: (risk for pt being noncompliant is high bc it’s a big change)
 Dietary changes: reduce weight, decrease Na intake (DASH Diet), cholesterol and
saturated fats. Increase potassium intake (if taking a thiazide diuretic).
 Establish a goal BP.
 Limit alcohol intake

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