Hypertension

Hypertension 150 150 Tony Guo

Hypertension

 

  • Hypertension, or high blood pressure (BP), is one of the most important modifiable risk factors that can lead to the development of cardiovascular disease (CVD). 
  • As BP increases, so does the risk of
    • MI, Heart failure, Stroke and Renal disease 
  • Affects 1 in 3 adults in United States
  • High priority health concern identified in Healthy People 2020
  • 83% of people > age 20 with hypertension are aware they have high BP
    • 76% are being treated
    • 48% of those aware do not currently have their BP well controlled

 

  • Blood pressure (BP) is the force exerted by the blood against the walls of the blood vessel.
  • BP is primarily a function of cardiac output (CO) and systemic vascular resistance (SVR)
  • Systemic vascular resistance (SVR) is the force opposing the movement of blood within the blood vessels

 

Factors affecting BP

Blood pressure = Cardiac output X Systemic vascular resistance

 

  • Cardiac output
    • Cardiac
      • Heart rate
      • Contractility
      • Conductivity
    • Renal fluid volume control
      • Renin-angiotensin-aldosterone system
      • Natriuretic peptides
  • Systemic vascular resistance
    • Sympathetic nervous system
      • α1– and α2-Adrenergic receptors (vasoconstriction)
      • β2-Adrenergic receptors (vasodilation)
    • Local regulation
      • Vasodilators
  • Prostaglandins
  • Nitric oxide
  • Vasoconstrictors
  • Endothelin
  • Neurohormonal
    • Vasoconstrictors
      • Angiotensin
      • Norepinephrine

 

  • Cultural and ethnic health disparities
  • African Americans
    • Have the highest prevalence of hypertension in the world
    • Develop hypertension at a younger age than whites
    • Have a higher incidence of hypertension among women than among men
    • Demonstrate more nocturnal non-dipping BP than whites
    • Hypertension is more aggressive and results in more severe end-organ damage.
    • Have a higher death rate resulting from hypertension than whites
    • Produce less renin and do not respond well to renin-inhibiting drugs
    • Calcium channel blockers and diuretics provide better BP control, especially with monotherapy.
    • Have a higher risk of angioedema with angiotensin-converting enzyme inhibitors than whites
  • Mexican Americans
    • Are less likely to receive treatment for hypertension than whites and African Americans
    • Have lower rates of BP control than whites and African Americans
    • Have lower levels of awareness of hypertension and its treatment than whites and African Americans
  • Gender differences
    • Men
      • Before early middle age, hypertension is more common in men than in women.
    • Women
      • Hypertension is two to three times more common in women who take oral contraceptives than in women who do not.
      • A history of preeclampsia may be an early sign of risk for cardiovascular disease.
      • After age 64, hypertension is more common in women than in men. Part of the rise in BP in women is attributed to menopause related factors such as estrogen withdrawal, overproduction of pituitary hormones, and weight gain.
      • It is more difficult to control hypertension in older women (ages 70-79) than in women ages 50-69, despite having similar rates of treatment.

 

  • Sympathetic nervous systems (SNS)
    • Activation increases HR and cardiac contractility
    • Vasoconstriction and renin release
    • Increases CO and SVR
  • Baroreceptors
    • Sensitive to stretching
    • Send impulses to sympathetic vasomotor center
  • Vascular endothelium
    • Essential to regulation of vasodilating and vasoconstricting substances 
  • Renal system
    • Control sodium excretion and ECF volume
    • RAAS system
    • Prostaglandins
  • Endocrine system
    • Epinephrine and norepinephrine from adrenal medulla
    • Aldosterone from adrenal cortex
    • ADH from posterior pituitary

 

Classification of hypertension

  • Normal
    • SBP (mmHg) <120 
    • DBP (mmHg) <80
  • Prehypertension
    • SBP (mmHg) 120-139 
    • DBP (mmHg) 80-89
  • Hypertension, stage 1
    • SBP (mmHg) 140-159  
    • DBP (mmHg) 90-99
  • Hypertension, stage 2
    • SBP (mmHg)  ≥160 
    • DBP (mmHg) ≥100

Causes of secondary hypertension

  • Cirrhosis
  • Coarctation or congenital narrowing of the aorta
  • Drug-related: estrogen replacement therapy, oral contraceptives, corticosteroids, nonsteroidal anti-inflammatory drugs (e.g., cyclooxygenase-2 inhibitors), sympathetic stimulants (e.g., cocaine, monoamine oxidase)
  • Endocrine disorders (e.g., pheochromocytoma, Cushing syndrome,thyroid disease)
  • Neurologic disorders (e.g., brain tumors, quadriplegia, traumatic brain injury)
  • Pregnancy-induced hypertension
  • Renal disease (e.g., renal artery stenosis, glomerulonephritis)
  • Sleep apnea 

 

Etiology of hypertension

  • Primary hypertension 
    • Also called essential or idiopathic hypertension
    • Elevated BP without an identified cause 
    • 90% to 95% of all cases
    • Exact cause unknown but several contributing factors
  • Secondary hypertension
    • Elevated BP with a specific cause
    • 5% to 10% of adult cases
    • Clinical findings relate to underlying cause 
    • Treatment aimed at removing or treating cause

 

Risk factors for primary hypertension

  • Age
    • SBP rises progressively with increasing age, although DBP may decrease with age.
    • After age 50, SBP >140 mm Hg is a more important cardiovascular risk factor than DBP
  • Alcohol
    • Excessive alcohol intake is strongly associated with hypertension.
    • Moderate intake of alcohol has cardioprotective properties; males with hypertension should limit their daily intake of alcohol to 2 drinks per day, and 1 drink per day for females with hypertension.
  • Tobacco use
    • Smoking tobacco greatly increased risk of cardiovascular disease.
    • People with hypertension who smoke tobacco are at even greater risk for cardiovascular disease.
  • Diabetes mellitus
    • Hypertension is more common in patients with diabetes.
    • When hypertension and diabetes coexist, complications (e.g., target organ disease) are more severe.
  • Elevated serum lipids
    • Increased levels of cholesterol and triglycerides are primary risk factors in atherosclerosis.
    • Hyperlipidemia is more common in people with hypertension.
  • Excess dietary sodium
    • High sodium intake can
    • Contribute to hypertension in salt-sensitive patients.
    • Decrease the effectiveness of certain antihypertensive medications.
  • Gender
    • Hypertension is more prevalent in men in young adulthood and early middle age.
    • After age 64, hypertension is more prevalent in women.
  • Family history
    • History of a close blood relative (e.g., parents, sibling) with hypertension is associated with an increased risk for developing hypertension.
  • Obesity
    • Weight gain is associated with increased frequency of hypertension.
    • Risk increases with central abdominal obesity.
  • Ethnicity
    • Incidence of hypertension is 2 times higher in African Americans than in whites.
  • Sedentary lifestyle
    • Regular physical activity can help control weight and reduce cardiovascular risk.
    • Physical activity may decrease BP.
  • Socioeconomic status
    • Hypertension is more prevalent in lower socioeconomic groups and among the less educated.
  • Stress
    • People exposed to repeated stress may develop hypertension more frequently than others.
    • People who develop hypertension may respond differently to stress than those who do not develop hypertension.

 

Link among salt intake, blood pressure, and changes in the heart

  • High dietary salt intake
    • Ventricular hypertrophy
      • BP (afterload)
      • Intravascular volume (preload)
      • Direct effects on protein synthesis of myocardial cells
    • Ventricular fibrosis
      • Increased aldosterone synthesis in myocardium
      • Increased angiotensin receptors in myocardial cells
        • Increased concentration of TGF-β1

 

Clinical manifestation

  • “Silent killer”
  • Symptoms of severe hypertension
    • Fatigue
    • Dizziness
    • Palpitations
    • Angina
    • Dyspnea

Complications

  • Target organ diseases occur most frequently in 
    • Heart
      • Hypertensive heart disease
        • Coronary Artery disease
          • Hypertension disrupts the coronary artery endothelium
          • This results in a stiff arterial wall with a narrowed lumen, and accounts for a high rate of CAD, angina, and MI.
        • Left ventricular hypertrophy
          • Increased contractility increases myocardial work and O2 demand
        • Heart failure
          • Occurs when the heart’s compensatory mechanisms are overwhelmed and the heart can no longer pump enough blood to meet the body’s demands
    • Brain
    • Cerebrovascular disease
      • When BP exceeds the body’s ability to autoregulate, the cerebral vessels suddenly dilate, capillary permeability increases, and cerebral edema develops. 
      • This produces a rise in intracranial pressure. If left untreated, patients can die quickly from brain damage
    • Peripheral vascular disease
      • Hypertension speeds up the process of atherosclerosis in the peripheral blood vessels. 
      • This leads to the development of peripheral vascular disease, aortic aneurysm, and aortic dissection
    • Kidney
      • Nephrosclerosis
        • Results from ischemia caused by the narrowing of the renal blood vessels. 
        • This leads to atrophy of the tubules, destruction of the glomeruli, and eventual death of nephrons. 
        • Initially intact nephrons can compensate, but these changes may eventually lead to renal failure
        • Laboratory indications of renal disease are albuminuria, proteinuria, microscopic hematuria, and elevated serum creatinine and blood urea nitrogen (BUN) levels.
    • Eyes
      • Retinal damage
        • Damage to the retinal vessels provides an indication of related vessel damage in the heart, brain, and kidneys. 
        •  Manifestations of severe retinal damage include blurring of vision, retinal hemorrhage, and loss of vision.

    Diagnostic studies

    • Diagnostic assessment
      • History and physical examination, including an ophthalmic examination
      • Routine urinalysis
      • Basic metabolic panel (serum glucose, sodium, potassium, chloride, carbon dioxide, BUN, and creatinine)
      • Complete blood count
      • Serum lipid proile (total lipids, triglycerides, HDL and LDL cholesterol, total-to-HDL cholesterol ratio)
      • Serum uric acid, calcium, and magnesium
      • 12-lead electrocardiogram (ECG)
      • Optional:
        • 24-hr urinary creatinine clearance
        • Echocardiography
        • Liver function studies
        • Serum thyroid-stimulating hormone (TSH)
    • Management
      • Periodic monitoring of BP
      • Home BP monitoring
      • Ambulatory BP monitoring
      • Every 3-6 months by a HCP once goal BP is achieved and stabilized
      • Nutritional therapy
      • Restrict salt and sodium
      • Restrict cholesterol and saturated fats
      • Maintain adequate intake of potassium, calcium, and magnesium
      • Weight management
      • Regular, moderate physical activity
      • Tobacco cessation 
      • Moderation of alcohol intake
      • Stress management techniques 
      • Antihypertensive drugs
      • Patient and caregiver teaching

    Lifestyle modifications

    • Weight reduction
      • Weight loss of 22 lb (10 kg ) may decrease SBP by approx. 5 to 20 mm Hg
      • Calorie restriction and physical activity
    • DASH eating plan
      • Fruits, vegetables, fat-free or low-fat milk, whole grains, fish, poultry, beans, seeds, and nuts
    • Dietary sodium reduction
      • < 2300 mg/day for healthy adults
      • < 1500 mg/day for 
        • African Americans
        • Middle-aged and older 
        • Those with hypertension, diabetes, or chronic kidney disease
    • Moderation of alcohol intake
    • Physical activity
      • Moderate-intensity aerobic activity, at least 30 minutes, most days of the week
      • Vigorous-intensity aerobic activity at least 20 minutes, 3 days a week
      • Muscle-strengthening activities at least 2 times a week
      • Flexibility and balance exercises 2 times a week
    • Avoidance of tobacco products
      • Nicotine causes vasoconstriction and elevated BP
      • Smoking cessation reduces risk factors within 1 year
    • Psychosocial risk factors
      • Low socioeconomic status, social isolation and lack of support, stress, negative emotions
      • Activate SNS and stress hormones
    • Drug therapy and patient teaching
      • Follow-up care
      • Identify, report, and minimize side effects
        • Orthostatic hypotension
        • Sexual dysfunction
        • Dry mouth
        • Frequent urination
      • Time of day to take drug
      • Diuretics promote sodium and water excretion, reduce plasma volume, and reduce the vascular response to catecholamines.
      • Adrenergic-inhibiting agents act by diminishing the SNS effects that increase BP. Adrenergic inhibitors include drugs that act centrally on the vasomotor center and peripherally to inhibit norepinephrine release or to block the adrenergic receptors on blood vessels.
      • Direct vasodilators decrease the BP by relaxing vascular smooth muscle and reducing SVR.
      • Calcium channel blockers increase sodium excretion and cause arteriolar vasodilation by preventing the movement of extracellular calcium into cells.
      • Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II and reduce angiotensin II (A-II)–mediated vasoconstriction and sodium and water retention.
      • A-II receptor blockers (ARBs) prevent angiotensin II from binding to its receptors in the walls of the blood vessels.

    Hypertension medication

    Drug Examples Mechanism of Actions Nursing considerations
    Diuretics
    Thiazide and Related Diuretics Chlorothiazide (Diuril)

    Chlorthalidone

    Hydrochlorothiazide

    Indapamide

    Metolazone (Zaroxolyn)

    Inhibit NaCl reabsorption in the distal convoluted tubule. Increase excretion of Na+ and Cl. Initial decrease in ECF. Sustained decrease in SVR. Lower BP moderately in 2-4 wk. Monitor for orthostatic hypotension, hypokalemia, and alkalosis. 

    Thiazides may potentiate cardiotoxicity of digoxin by producing hypokalemia. 

    Dietary sodium restriction reduces the risk of hypokalemia. NSAIDs can decrease diuretic and antihypertensive effect of thiazide diuretics and potentially cause renal impairment. 

    Advise patient to supplement with potassium-rich foods.

    Loop Diuretics Bumetanide (Bumex)

    Furosemide (Lasix)

    Torsemide (Demadex)

    Inhibit NaCl reabsorption in the ascending limb of the loop of Henle. Increase excretion of Na+ and Cl. More potent diuretic effect than thiazides, but shorter duration of action. Less effective for hypertension.  Monitor for orthostatic hypotension and electrolyte abnormalities. 

    Loop diuretics remain effective despite renal insufficiency. Diuretic effect of drug increases at higher doses.

    Potassium-Sparing Diuretics Amiloride (Midamor)

    Triamterene (Dyrenium)

    Reduce K+ and Na+ exchange in the distal and collecting tubules. Reduce excretion of K+, H+, Ca++, and Mg++. Monitor for orthostatic hypotension and hyperkalemia. 

    Contraindicated in patients with renal failure. Use with caution in patients on ACE inhibitors or angiotensin II blockers. 

    Avoid potassium supplements.

    Aldosterone Receptor Blockers Spironolactone (Aldactone)

    Eplerenone (Inspra)

    Inhibit the Na+-retaining and K+-excreting effects of aldosterone in the distal and collecting tubules. Monitor for orthostatic hypotension and hyperkalemia. 

    Do not combine with potassium-sparing diuretics or potassium supplements. Use with caution in patients on ACE inhibitors or angiotensin II blockers. These drugs are also classified as potassium-sparing diuretics.

    Adrenergic Inhibitors
    Central-Acting α-Adrenergic Agonist Clonidine (Catapres)

    Clonidine patch (Catapres-TTS)

    Reduce sympathetic outflow from CNS.

    Reduce peripheral sympathetic tone, produces vasodilation, and decreases SVR and BP.

    Sudden discontinuation may cause withdrawal syndrome, including rebound hypertension, tachycardia, headache, tremors, apprehension, sweating.

    Chewing gum or hard candy may relieve dry mouth. 

    Alcohol and sedatives increase sedation. Transdermal patch may be related to fewer side effects and better adherence.

    Guanabenz

    Guanfacine (Tenex)

    Same as clonidine, but not available in transdermal formulation.
    Methyldopa Instruct patient about daytime sedation and avoidance of hazardous activities. 

    Taking a single daily dose at bedtime minimizes sedative effect.

    Peripheral-Acting α-Adrenergic Agonist Reserpine Depletes central and peripheral stores of norepinephrine. Results in peripheral vasodilation (decreases SVR and BP). Must be given twice daily. Contraindicated in patients with history of depression. Monitor mood and mental status regularly. 

    Advise patient to avoid barbiturates, alcohol, opioids.

    α1-Adrenergic Blockers Doxazosin (Cardura)

    Prazosin (Minipress)

    Terazosin

    Block 1-adrenergic effects, producing peripheral vasodilation (decreases SVR and BP). Beneficial effects on lipid profile. Reduced resistance to the outflow of urine in benign prostatic hyperplasia. Taking drug at bedtime reduces risks associated with orthostatic hypotension.
    Phentolamine (Regitine)  Blocks 1-adrenergic receptors, resulting in peripheral vasodilation (decreases SVR and BP). Used in short-term management of pheochromocytoma. Also used locally to prevent necrosis of skin and subcutaneous tissue after extravasation of adrenergic drug. 

    No oral formulation.

    β-Adrenergic Blockers Cardioselective Blockers 

    Acebutolol (Sectral)

    Atenolol (Tenormin)

    Betaxolol

    Bisoprolol (Zebeta)

    Esmolol (Brevibloc)

    Metoprolol (Lopressor)

    Nebivolol (Bystolic)

    Cardioselective agents block -β1– adrenergic receptors. Reduce BP by blocking –adrenergic effects. Decrease CO and reduce sympathetic vasoconstrictor tone. Decrease renin secretion by kidneys. Monitor pulse and BP regularly. Use with caution in patients with diabetes because drug may depress the tachycardia associated with hypoglycemia and may adversely affect glucose metabolism.

    Drug of choice for patients with a history of an MI or heart failure. Less effective BP reduction in African American patients. Esmolol is for IV use only. 

    Cardioselective agents lose cardioselectivity at higher doses.

    Non-cardioselective Blockers

    Nadolol (Corgard)

    Pindolol

    Propranolol (Inderal)

    Nonselective agents block -β1– and -β2-adrenergic receptors. Reduce BP by blocking -β1– and -β2-adrenergic effects. Same as cardioselective, except nonselective agents may cause bronchospasm, especially in patients with a history of asthma.
    Mixed α and β-Blockers Carvedilol (Coreg)

    Labetalol

    α1-, -β1-, and -β2-adrenergic blocking properties producing peripheral vasodilation and decreased heart rate. Reduce CO, SVR, and BP. Same as –blockers. IV form available for hypertensive crisis in hospitalized patients. Patients must be kept supine during IV administration. 

    Assess patient tolerance of upright position (severe orthostatic hypotension) before allowing upright activities (e.g., commode).

    Direct Vasodilators Fenoldopam (Corlopam) Activates dopamine receptors, resulting in systemic and renal vasodilation. IV use only for hypertensive crisis in hospitalized patients. 

    Use cautiously in patients with glaucoma. Patient should remain flat for 1 hr after administration.

    Hydralazine Reduces SVR and BP by direct arterial vasodilation. IV use for hypertensive crisis in hospitalized patients. Twice-daily oral dosage. Not used as monotherapy because of side effects. 

    Contraindicated in patients with coronary artery disease.

    Minoxidil Reduces SVR and BP by direct arterial vasodilation. Reserved for treatment of severe hypertension associated with renal failure and resistant to other therapy. Once- or twice-daily dosage.
    Nitroglycerin Relaxes arterial and venous smooth muscle, reducing preload and SVR. At low dose, venous dilation predominates; at higher dose, arterial dilation is present. IV use for hypertensive crisis in hospitalized patients with myocardial ischemia. 

    Given by continuous IV infusion with pump or control device.

    Sodium nitroprusside Direct arterial vasodilation reduces SVR and BP. IV use for hypertensive crisis in hospitalized patients. Given by continuous IV infusion with pump or control device. 

    Arterial monitoring of BP recommended. Wrap IV solutions with an opaque material to protect from light. Stable for 24 hr. 

    Metabolized to cyanide, then thiocyanate. Monitor thiocyanate levels with prolonged use (>3 days) or doses ≥4 mcg/kg/min.

    Angiotensin Inhibitors
    Angiotensin-Converting Enzyme Inhibitors Benazepril (Lotensin)

    Captopril

    Enalapril (Vasotec)

    Fosinopril

    Lisinopril (Zestril)

    Moexipril (Univasc)

    Perindopril (Aceon)

    Quinapril (Accupril)

    Ramipril (Altace)

    Trandolapril (Mavik)

    Inhibit ACE, reduce conversion of angiotensin I to angiotensin II (A-II). Inhibit A-II–mediated vasoconstriction. Aspirin and NSAIDs may reduce drug effectiveness. Addition of diuretic enhances drug effect. 

    Should not be used with potassium-sparing diuretics. Can cause increase in serum creatinine. Inhibit breakdown of bradykinin, which may cause a dry, hacking cough that can occur at any point during treatment, even years later. Captopril may be given orally for hypertensive crisis.

    Angiotensin II Receptor Blockers Azilsartan (Edarbi)

    Candesartan (Atacand)

    Eprosartan (Teveten)

    Irbesartan (Avapro)

    Losartan (Cozaar)

    Olmesartan (Benicar)

    Telmisartan (Micardis)

    Valsartan (Diovan)

    Prevent action of A-II and produce vasodilation and increased Na+ and water excretion. Full effect on BP may not be seen for 3-6 wk. Do not affect bradykinin levels, therefore acceptable alternative to ACE inhibitors in people who develop dry cough. 

    In patients with kidney disease, ACE inhibitors and ARBs should not be used together due to adverse renal effects.

    Renin Inhibitors Aliskiren (Tekturna) Directly inhibits renin, thus reducing conversion of angiotensinogen to angiotensin I.  May cause angioedema of the face, extremities, lips, tongue, glottis, and/or larynx.

    Not to be used in pregnancy.

    Calcium Channel Blockers
    Non-Dihydropyridines Diltiazem extended release (Cardizem LA)

    Verapamil intermediate release (Calan)

    Verapamil long-acting (Covera-HS)

    Verapamil timed-release (Verelan PM)

    Inhibit movement of Ca++ across cell membrane, resulting in vasodilation

    Cardioselective resulting in decrease in heart rate and slowing of AV conduction.

    Use with caution in patients with heart failure. Serum concentrations and toxicity of certain calcium channel blockers may be increased by grapefruit juice; avoid concurrent use. 

    Used for supraventricular tachydysrhythmias. 

    Avoid in patients with second- or third-degree AV block or left ventricular systolic dysfunction.

    Dihydropyridines Amlodipine (Norvasc)

    Clevidipine (Cleviprex)

    Felodipine

    Isradipine

    Nicardipine sustained release

    Nifedipine long acting (Procardia XL)

    Nisoldipine (Sular)

    Cause vascular smooth muscle relaxation resulting in decreased SVR and arterial BP. More potent peripheral vasodilators. Clevidipine is for IV use only. Use of sublingual short-acting nifedipine in hypertensive emergencies is unsafe and not effective. 

    Serious adverse events (e.g., stroke, acute MI) have been reported. IV nicardipine available for hypertensive crisis in hospitalized patients. Change peripheral IV infusion sites every 12 hr.

    Resistant hypertension

    • Failure to reach goal BP in patients taking full doses of an appropriate 3-drug therapy regimen that includes a diuretic. Reasons include
      • Improper BP measurement
      • Drug-induced
        • Nonadherence (e.g., due to drug side effects, finances)
        • Illegal drugs (e.g., cocaine, amphetamines)
        • Inadequate drug dosages
        • Inappropriate combinations of drug therapy
        • Nonsteroidal anti-inflammatory drugs
        • Sympathomimetics (e.g., decongestants, diet pills)
        • Oral contraceptives
        • Corticosteroids
        • Cyclosporine and tacrolimus (Prograf)
        • Erythropoietin
        • Licorice
        • Some chewing tobacco
        • Selected over-the-counter dietary or herbal supplements and drugs (e.g., ma huang, bitter orange)
      • Associated conditions
        • Increasing obesity
        • Excess alcohol intake
      • Identifiable causes of secondary hypertension

    Nursing management

    • Nursing Assessment
      • Subjective Data
        • Important Health Information
          • Past health history: Known duration and past workup of high BP; cardiovascular, cerebrovascular, renal, or thyroid disease; diabetes mellitus; pituitary disorders; obesity; dyslipidemia; menopause or hormone replacement status
          • Medications: Use of any prescription or over-the-counter, illicit, or herbal drugs or products; previous use of antihypertensive drug therapy
        • Functional Health Patterns
          • Health perception–health management: Family history of hypertension or cardiovascular disease; tobacco use, alcohol use; sedentary lifestyle; health literacy; readiness for change 
          • Nutritional-metabolic: Usual salt and fat intake; weight gain or loss
          • Elimination: Nocturia
          • Activity-exercise: Fatigue; dyspnea on exertion, palpitations, exertional chest pain; intermittent claudication, muscle cramps; usual pattern and type of exercise
          • Cognitive-perceptual: Dizziness; blurred vision; paresthesias
          • Sexual-reproductive: Erectile dysfunction, decreased libido
          • Coping–stress tolerance: Stressful life events
      • Objective Data
        • Cardiovascular
          • SBP consistently >140 mm Hg or DBP >90 mm Hg for patients <60 yr old or >150 mm Hg or DBP >90 mm Hg for patients >60 years old.
          • Orthostatic changes in BP and HR; bilateral BPs significantly different; abnormal heart sounds; laterally displaced apical pulse; diminished or absent peripheral pulses; carotid, renal, or femoral bruits; peripheral edema
        • Gastrointestinal
          • Obesity (BMI ≥30 kg/m2); abnormal waist-hip ratio
        • Neurologic
          • Mental status changes
      • Possible Diagnostic Findings
        • Abnormal serum electrolytes (especially potassium) 
        • Increased BUN, creatinine, glucose, cholesterol, and triglyceride levels 
        • Proteinuria, albuminuria, microscopic hematuria
        • Evidence of ischemic heart disease and left ventricular hypertrophy on ECG
        • Evidence of structural heart disease and left ventricular hypertrophy on echocardiogram; evidence of arteriovenous nicking, retinal hemorrhages, and papilledema on funduscopic examination
      • BP Measurement
        • Take in both arms initially
        • Proper size and placement of cuff
        • Can use forearm if needed
          • Document site 
        • Assess for orthostatic hypotension
          • BP and HR supine, sitting, and standing
          • Measure within 1 to 2 minutes of position change
          • Positive if decrease of 20 mm Hg or more in SBP, decrease 10 mm Hg or more in DBP, or increased 20 beats/minute or more in heart rate
    • Nursing diagnoses
      • Ineffective health management related to lack of knowledge of pathology, complications, and management of hypertension
      • Anxiety related to complexity of management regimen
      • Sexual dysfunction related to side effects of antihypertensive medication
      • Risk for decreased cardiac tissue perfusion
      • Risk for ineffective cerebral tissue perfusion
      • Risk for ineffective renal perfusion
      • Potential complication: stroke, MI
    • Planning
      • Patient will
        • Achieve and maintain the goal BP
        • Follow the therapeutic plan
          • Including appointments with the HCP
        • Experience minimal side effects of therapy
        • Manage and cope with this condition.
    • Nursing implementation
      • Health Promotion
        • Primary prevention via lifestyle modification
        • Individual patient evaluation and education
        • Screening programs
        • Cardiovascular risk factor modification
      • Ambulatory Care
        • Evaluate therapeutic effectiveness
        • Detect and report adverse effects
        • Assess and enhance compliance
        • Patient and caregiver teaching
      • Home BP monitoring
        • Patient teaching is critical for accuracy
          • Proper equipment
          • Proper procedure
          • Frequency
          • Accurate recording and reporting
          • Target BP
      • Reasons for poor adherence to treatment plan are complex
        • Inadequate teaching
        • Low health literacy
        • Unpleasant side effects of drugs
        • Return to normal BP while on drugs
        • High cost of drugs
        • Lack of insurance
      • Measures to enhance compliance
        • Individualize plan
        • Active patient participation
        • Select affordable drugs
        • Involve caregivers
        • Combination drugs
        • Patient teaching
    • Nursing evaluation
      • Patient will: 
        • Achieve and maintain goal BP 
        • Understand, accept, and implement treatment plan 
        • Report minimal side effects of therapy
    • Hypertension in older persons
    • BP goal for people > 60 is < 150/90
    • Preferred antihypertensive drugs
      • Thiazide diuretic
      • Calcium channel blockers
      • ACE inhibitors or ARBs
    • Caution use of NSAIDS
    • Hypertensive crisis
      • SBP >180 mmHg and/or DBP >110 mmHg
        • Hypertensive urgency 
          • Develops over hours to days
          • May not require hospitalization
        • Hypertensive emergency 
          • Very severe problems can result if prompt treatment is not obtained
      • Rate of rise more important than absolute value
      • Causes of hypertensive crisis
        • Exacerbation of chronic hypertension
        • Renovascular hypertension
        • Preeclampsia, eclampsia
        • Pheochromocytoma
        • Drugs (cocaine, amphetamines)
        • Monoamine oxidase inhibitors taken with tyramine-containing foods
        • Rebound hypertension (from abrupt withdrawal of some antihypertensive drugs such as clonidine [Catapres] or –blockers)
        • Head injury
        • Acute aortic dissection
      • Clinical manifestation
        • Hypertensive encephalopathy
          • Headache, nausea/vomiting, seizures, confusion, coma
        • Renal insufficiency
        • Cardiac decompensation
          • MI, HF, pulmonary edema
        • Aortic dissection
      • Nursing and interprofessional management
        • Hospitalization
          • IV drug therapy: titrated to MAP
          • Monitor cardiac and renal function
          • Neurologic checks
          • Determine cause
          • Education to avoid future crisis

    Role of Nursing Personnel

    • Registered Nurse (RN)
      • Develop and conduct hypertension screening programs.
      • Assess patients for hypertension risk factors and develop risk modification plans.

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