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

o 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.
o
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)
 Stage 2 or 3 = drug therapy and lifestyle modification
o 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
 o Restrict calories (if overweight)
o DASH Diet (Dietary Approaches to Stop Hypertension)—fish each week, lots of fruits/veggies, increase fiber
and drink water
o Limit alcohol
o <1 oz. per day (2 oz. of whiskey; 8 oz. of wine; 24 oz. of beer)
o Exercise
o 30 minutes of moderate intensity per day
o Start slow and increase gradually
o Avoid tobacco products
o Stress management
o Relaxation, guided imagery, biofeedback, etc.

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)
o 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.
o 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.
o 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.

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
o 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.
o S/E: Nausea, headache, dizziness, peripheral edema. Reflex tachycardia (with dihydropyridines). Reflex decreased
heart rate; constipation.
o 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 awakening…take 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 patient’s questions about HTN
 Eliminate excessive noise in patient’s 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)