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Chapter 32

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.

• 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.

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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 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) o

 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

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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. o o

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. o

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. o


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 awakening…take med with 24-hour duration as early in the morning as possible. Lack of Responsiveness to Therapy • Cost

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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

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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)

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