HYPERTENSION

Chapter 32

NORMAL REGULATION

Normal BP requires both systemic and local peripheral vascular effects.

Arterial BP = cardiac output x systemic vascular resistance
Cardiac output = total blood flow through the circulatory system in one minute.
o This is the amt. of blood pumped out of the L ventricle per beat (Stroke Volume) times the heart rate for 1
minute
Systemic vascular resistance (SVR) is the force opposing the movement of blood within the vessels.
Sympathetic NS, vascular endothelium, renal system and endocrine system all contribute to BP regulation.

HYPERTENSION

HTN: >140/90 taken on three occasions over several weeks.

o Optimal: <120/80
o Normal: <130/85
o High: <139/89
o Hypertension

Stage 1: <159/99

Stage 2: <179/109

Stage 3: >180/110
African Americans at highest risk (more prevalent, younger age, more women, more severe, higher mortality, more
end-organ damage)
o African Americans produce less renin and do not respond as well to angiotensin inhibitors.
HTN risk increase with age; males more than females until age 55, then equal risk; education reduces risks.

Classification

Primary
o Essential.elevated BP without an identified cause and accounts for 90 to 95% of all HTN.

Secondary
o Elevated with a specific cause that can be identified and corrected. Accounts for 80% of HTN in children.

If under 20 or over 50 has sudden, severe HTN, a secondary cause should be suspected.

Hypokalemia

Abdominal bruit

Tachycardia, sweating, tremors R/T variable BPs

Renal disease

Other causes

Coarctation/congenital narrowing of the aorta

Renal disease such as renal artery stenosis

Endocrine disorders (hyperaldosteronism)

Neurologic disorders (brain tumor, quadriplegia, head injuries)

Sleep apnea

Medications (sympathomimetics, cocaine, MAOIs, estrogen, BC pills, NSAIDS)

Pregnancy-induced HTN
Pathophysiology

For HTN, there must be an increase in either CO or SVR. The hallmark of classic HTN is increased SVR.

Heredity

Water/Sodium retention

Altered renin-angiotensin mechanism

Stress and increased sympathetic NS activity

Insulin resistance and hyperinsulinemia

o High insulin concentration stimulates SNS activity and impairs nitric oxide-mediated vasodilation
o Pressor effects of insulin include vascular hypertrophy and increased renal sodium reabsorption

Endothelial Cell Dysfunction

o Enodthelin produces pronounced and prolonged vasoconstriction.
Risk Factors
o Age
o Alcohol

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Cigarette Smoking
Diabetes mellitus
Elevated serum lipids
Excess dietary sodium
Gender
Family history
Obesity
Ethnicity
Sedentary lifestyle
Socioeconomic status
stress

Signs/Symptoms
o Frequently asymptomatic (silent killer)
o Severe symptoms:
o Fatigue
o Reduced activity tolerance
o Dizziness
o Palpitations
o Angina
o Dyspnea
Complications
o Target Organ Diseases
o Heart (hypertensive heart disease)

Coronary artery disease (leading to MI and angina)

Left ventricular hypertrophy (from high cardiac workload leading to heart failure)

Heart failure (shortness of breath on exertion, nocturnal dyspnea, fatigue, enlarged heart)
o Brain (cerebrovascular disease)

Stroke/transischemic attacks

Hypertensive encephalopathy (cerebral edema)

o Peripheral vasculature (peripheral vascular disease)

Atherosclerosis in peripheral blood vessels

Aortic aneurysm, aortic dissection, peripheral vascular disease

Intermittent claudication (pain with activity or rest R/T lack of oxygen to tissues)
o Kidneys (nephrosclerosis)

End stage renal disease (ischemia from narrowed intrarenal vessels)

Urinalysis
o Microalbuminuria
o Proteinuria
o Elevated blood urea nitrogen/elevated Serum creatinine

Usually ratio of 10:1 or 15:1.

BUN: 5-25 mg/dl

Creatinine: 0.5 1.5 mg/dl

Microscopic hematuria

Earliest sign of renal damage is nocturia.

o Eyes (retinal damage)

Eyes are only place vessels can be directly observed.

Retinal damage can indicate damage in other target organs.

Signs/Symptoms

Blurry vision

Retinal hemorrhage

Loss of vision
Diagnostic Studies
o Hx and PE
o Urinalysis
o BUN/Serum creatinine
o Fasting blood glucose
o CBC
o Lipid profile, cholesterol, triglycerides

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ECG
Echocardiogram

Collaborative Care
o Priorities
o Assess BP carefully over several months before initiating treatment
o Treat HTN in context of overall cardiovascular risk
o Lifestyle modifications should be tried first
o Treat HTN in adults up to age 85
o Pharmacology includes five first-line drugs
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Other Collaborative Care

o Periodic/routine BP measurement

Every 3 to 6 months once BP is stabilized

o Assign risk level
o Nutritional therapy

Restrict sodium

Reduce weight

Restrict cholesterol/saturated fats

Adequate intake of potassium

Adequate intake of calcium and magnesium

o Physical activity
o Stop Smoking!
o Reduce alcohol intake
o Use antihypertensive drugs

Ambulatory BP Monitoring
o White Coat HTN
o Measure at home or in the community (fire stations/hospital auxiliaries)
o Use continuous, automated 24-hour ambulatory measurements
o Use a diary of activites that may affect BP
o Diurnal Variability
o In day-active people, BP is highest in the early morning, decreases during the day and is lowest at
night.
o If BP does not fall at night, then more target organ damage is likely.
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Risk Classifications
o Dependent upon BP measurement, target organ damage, clinical cardiovascular disease and presence of other risk
factors.
o Group A
o No risk factors, no target organ damage, no c/v disease

High normal = lifestyle modification

Stage 1 = lifestyle modification (for 12 months)

Stage 2 or 3 = drug therapy and lifestyle modification

o Group B
o At least one risk factor (not diabetes), no target organ damage, no c/v disease

High normal = lifestyle modification

Stage 1 = lifestyle modification (up to 6 months)

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Stage 2 or 3 = drug therapy and lifestyle modification

Group C
o Risk factors present, diabetes, target organ damage, evidence of c/v disease

All stages = drug therapy and lifestyle modifications

Lifestyle Modification
o Dietary changes
o Restrict sodium

<6g of salt per day

<2.3 g of sodium per day

o Maintain intake of potassium, calcium and magnesium
o Avoid caffeine

Restrict calories (if overweight)

DASH Diet (Dietary Approaches to Stop Hypertension)fish each week, lots of fruits/veggies, increase fiber
and drink water
Limit alcohol
o <1 oz. per day (2 oz. of whiskey; 8 oz. of wine; 24 oz. of beer)
Exercise
o 30 minutes of moderate intensity per day
o Start slow and increase gradually
Avoid tobacco products
Stress management
o Relaxation, guided imagery, biofeedback, etc.
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DRUG THERAPY
Goal: BP <131/85 in young adults; <140/90 in older adults
Action of drugs: Reduce SVR and decrease volume of circulating blood
Diuretics

o First line of defense

o Thiazides (Hydrodiuril)
Inhibit sodium reabsorption in the distal convoluted tubule; increase excretion of sodium; decreases ECF;
sustains a decrease in SVR
o Lowers BP moderately in 2-4 weeks
o S/E: fluid/electrolyte imbalances; CNS effects; GI effects; sexual impotence; dermatologic effects
(photosensitivity); decreased glucose tolerance
o Monitor for orthostatic hypotension, hypokalemia and alkalosis. Watch for digoxin toxicity. Avoid NSAIDS.
Eat K+-rich foods.
o Loop Diuretics (furosemide/Lasix)
o Inhibits NaCl reabsorption in ascending limb of loop of Henle; increases excretion of sodium and chloride.
o More potent than thiazides, but of shorter duration; less effective for HTN
o S/E: fluid/electrolyte imbalances (hypokalemia); ototoxicity; metabolic effects (hyperglycemia); increased
LDL and triglycerides with decreased HDL
o Monitor for orthostatic hypotension and electrolyte abnormalities. Loop diuretics remain effective despite
renal nsufficiency. Diuretic effect increases at higher doses.
o Potassium-Sparing (spironolactone/Aldactone)
o Reduce K+ and Na+ exchange in the distal tubules; Reduces excretion of K+, H+, Ca++ and Mg++; Inhibit
the Na+ retaining and K+ excreting effects of aldosterone.
o S/E: hyperkalemia, N/V, diarrhea, headache, leg cramps, dizziness, maybe gynecomastia, impotence,
decreased libido, menstrual irregularis
Adrenergic Inhibitors
o Centrally-Acting (clonidine/Catapres)
o Reduces sympathetic outflow from CNS. Reduces peripheral sympathetic tone, produces vasodilation;
decreases SVR and BP.
o S/E: dry mouth, sedation, impotence, N/V, dizziness, sleep disturbance, nightmares, restlessness and
depression. Bradycardia in pts with conduction disorders.
o Is used to treat hypertensive urgencies. Sudden discontinuation may cause withdrawal with rebound
HTN, tachycardia, headache, tremors, apprehension, sweating; Chew gum or hard candy to relieve dry
mouth; Avoid alcohol and sedatives. May be given transdermally with fewer side effects and better
compliance.
o Peripheral-Acting Adrenergic Antagonists (reserpine/Serpasil)
o Prevents peripheral release of NE, resulting in vasodilation; lowers CO and reduces SBP more than DBP.
o S/E: Orthostatic hypotension, diarrhea, cramps, bradycardia, delayed ejaculation, sodium/water retention;
sedation, inability to concentrate; depression; nasal stuffiness.
o Do not use in pts with c/v or coronary insufficiency or in older adults; tell patient to rise slowly and wear
support stockings. Hypotensive effect begins 2-3 days after meds, and lasts 7 to 10 days after stopping
meds. Do not use in patients with hx of depression. Monitor mood and mental status. Avoid alcohol and
narcotics.
o Alpha-1 Adrenergic Blocker (-azosin)
o Blocks alpha-1 effects producing peripheral vasodilation (decreases SVR and BP)
o

S/E: Hypotension dependent on volume. May produce syncope within 90 minutes of initial dose; retention of
sodium and water; cardiac arrhythmias, tachycardia, weakness, flushing; abdominal pain; N/V and
exacerbation of peptic ulcer.
o Reduced resistance to the outflow of urine in benign prostatic hyperplasia. Take drugs at bedtime
(orthostatic hypotension); beneficial effects on lipid profile.
Beta Blockers (-olol)
o Reduces BP by antagonizing beta adrenergic effects. Decreases CO and reduces sympathetic
vasoconstrictor tone. Decreases renin secretion by kidneys.
o S/E: Bronchospasm, a/v conduction block; impaired peripheral circulation; nighmares; depression;
weakness; reduced exercise capacity; may exacerbate heart failure; Sudden withdrawal may cause
rebound hypertension and cause ischemic heart disease.
o Moniotr pulse regularly; use with caution in diabetics because drug may mask signs of hypoglycemia.
Combined Alpha/Beta Blockers (labetalol/Normodyne)
o Produces peripheral vasodilation and decreased heart rate.
o S/E: dizziness, fatigue, N/V, dyspepsia, paresthesia, nasal stuffiness, impotence, edema. HEPATIC
TOXICITY.
o Keep patient supine during IV administration. Assess pt tolerance of upright position (severe postural
hypotension) before allowing upright activities.
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Direct Vasodilators (nitroglycerine/Tridil)

o Relaxes arterial and venous smooth muscle reducing preload and SVR.
o S/E: Reflex sympathetic activation (tachycardia, salt/water retention); headache, nausea, flushing, palpitation,
angina; hypotension
o Use for hypertensive crises.
Ganglionic Blockers (trimethaphan/Arfonad)
o Interrupts adrenergic control of arteries, results in vasodilation and reduces SVR and BP
o S/E: Visual disturbance, dilated pupils, dry mouth, urinary hesitancy, subjective chilliness.
o IV use for initial control of BP in dissecting aortic aneurysm.
Angiotensin Inhibitors
o Angiotensin-Converting Enzyme Inhibitors (ACE-Inhibitors) (-pril)

o First line of defense for diabetics

Inhibit angiotensin-converting enzyme; reduce conversion of angiotensin I to angiotensin II; prevent
angiotensin II mediated vasoconstriction. Inhibits angiotensin-converting enzyme when oral agents are not
appropriate.
o S/E: Hypotension, loss of taste, cough, hyperkalemia, acute renal failure, skin rash angioneurotic edema.
o ASA/NSAIDS may reduce drug effectiveness. Diuretic enhances drug effect. Do not use with K+-sparing
diuretics. Fetal morbidity or mortality.
o Antiotensin II Receptor Blockers (ARBs) (-sartan)
o Prevents action of angiotensin II and produces vasodilation and increased salt and water excretion.
o S/E: Hyperkalemia, decreased renal function.
o Full effect on BP takes 3 to 6 weeks.
Calcium Channel Blockers (-dipine)
o Blocks movement of extracellular calcium into cells, causing vasodilation and decreased SVR.
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S/E: Nausea, headache, dizziness, peripheral edema. Reflex tachycardia (with dihydropyridines). Reflex decreased
heart rate; constipation.
Use with caution in patients with heart failure. Contraindicated in patients with second- or third-degree heart block.
IV use available for HTN crisis. Avoid grapefruit!

Common side effects

Orthostatic hypotension

Sexual dysfunction (ask provider about changing med/dose or getting Viagra)

Dry mouth (chew sugarless gum or hard candy)

Frequent voiding (take diuretics earlier in the day to avoid nocturia)

Sedation (take med in the evening)

BP is lowest during the night and highest after awakeningtake med with 24-hour duration as early in the morning as
possible.
Lack of Responsiveness to Therapy

Cost

Instructions not given or misunderstood

Inadequate patient teaching
Lack of involvement in treatment plan
Side effects
Dementia
Inconvenient dosing

Dosage too low

Inappropriate combo
Rapid inactivation
Drug interactions

Increasing obesity
Alcohol >1 oz/day
Secondary HTN
Volume overload (inadequate diuretics, excess sodium intake; fluid retention; renal damage)
Pseudohypertension

Taking an Accurate BP Reading

Allow patient to rest for 5 minutes before measuring

Check BP and pulse while supine

Take it two or three times, 2 minutes apart

Use both arms (use arm with highest value from then on)

Check BP and pulse while standing

Record the average value

Check size and placement of cuff (width 40% and length 80% of upper arm circumference)
Hypertensive Crisis

A severe and abrupt elevation in BP with diastolic value above 120 to 130 mmHg
#1 cause: Non-compliance with med regimen
HTN Urgency
o Develops over days to weeks
o No evidence of target organ damage
o Allow patient to sit for 20 or 30 minutes in a quiet environment

Let patient verbalize fears

Answer patients questions about HTN

Eliminate excessive noise in patients environment

HTN Emergency

Develops over hours to days

Acute target organ damage

Hypertensive encephalopathy: headache, nausea, vomiting, seizures, confusion, stupor and coma

Treatment lowers BP, but not too fast. Decrease MAP by 10% to 20% in the first 2 hours, with further reduction
over the next 24 hours.

Tx: IV vasodilators (sodium nitroprusside is most effective med or

o IV adrenergic inhibotrs (Labetalol)or
o IV ACE inhibitors (Vasotec)