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NORMAL REGULATION
HYPERTENSION
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
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
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.
• 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)