2.  Persistent elevation of  Systolic blood pressure ≥140 mm Hg or  Diastolic blood pressure ≥90 mm Hg or  Current use of antihypertensive medication(s)

3.  Systolic blood pressure:120–139 mm Hg Or  Diastolic blood pressure:80–89 mm Hg

4. Blood Pressure = Cardiac Output x Systemic Vascular Resistance

6.  Primary hypertension  Also called idiopathic or essential  Increased blood pressure without an identified cause  Covers 90-95% of all cases of HTN  Secondary hypertension  Increased blood pressure with a specific cause that can be identified and corrected

7.  Cirrhosis  Narrowing of the aorta  Endocrine disorders  Medications  Neurologic disorders  Pregnancy induced HTN  Renal disease  Sleep apnea

8. CategorySBP (mm Hg) DBP (mm Hg)Normal < 120 and < 80 < 80 Prehypertension 120–139 or 80–89 Stage 1 140–159 or 90–99 Stage 2 > 160 or > 100 > 100

9.  For persons over age 50, SBP is more important than DBP as a CVD risk factor  Persons who are normotensive at age 55 have a 90% lifetime risk for developing HTN

10.  Age  Alcohol  Cigarette smoking  Diabetes mellitus  Elevated serum lipids  Excess dietary sodium  Gender  Family history  Obesity  Ethnicity  Sedentary lifestyle  Socioeconomic status  Stress

11.  Referred to as the “silent killer” because patients are frequently asymptomatic until target organ disease occurs

12.  Symptoms are often secondary to target organ disease and can include  Fatigue, reduced activity tolerance  Dizziness  Palpitations, angina  Dyspnea

13.  Target organ diseases occur most frequently in the  Heart  Brain  Peripheral vasculature  Kidney  Eyes

14.  Hypertensive heart disease  Coronary artery disease  Left ventricular hypertrophy  Heart failure Fig. 33-3: Top, normal heart; Bottom, left ventricular hypertrophy

15.  Cerebrovascular disease  Stroke  Peripheral vascular disease  Nephrosclerosis  Retinal damage

16.  History and physical examination  BP measurement in both arms  Use arm with higher reading for subsequent measurements  BP highest in early morning, lowest at night

17.  Use auscultatory method with a properly calibrated instrument  Patient should be seated quietly for 5 min in a chair, feet on the floor, and arm supported at heart level  Appropriate-sized cuff is necessary to ensure accurate reading  At least two measurements should be obtained

18. The correct technique for blood pressure measurements includes a) Always taking the blood pressure in both arms b) Releasing the pressure in the cuff at a rate of 1 mm Hg per second c) Inflating the cuff 5 mm Hg higher than the expected systolic pressure d) Taking additional readings if the first two readings differ more than 10 mm Hg

19.  Urinalysis, creatinine clearance  Serum electrolytes, glucose  BUN and serum creatinine  Serum lipid profile  ECG  Echocardiogram

20.  “ White coat” phenomenon may precipitate the need for ambulatory blood pressure monitoring (ABPM)  Uses a noninvasive, fully automated system that measures BP at preset intervals over a 24- hour period

22.  Overall goals  Control blood pressure  Reduce CVD risk factors  Strategies for adherence to regimens  Empathy increases patient trust, motivation, and adherence to therapy  Consider patient’s cultural beliefs and individual attitudes in formulating treatment goals

23. Average Percent ReductionAverage Percent Reduction Stroke incidence 35%–40%Stroke incidence 35%–40% Myocardial infarction 20%–25%Myocardial infarction 20%–25% Heart failure 50%Heart failure 50%

24.  Lifestyle modifications  Weight reduction: Weight loss of 10 kg (22 lb) may decrease SBP by ~ 5 to 20 mm Hg  Dietary Approaches to Stop Hypertension (DASH) Diet Low sodium <2.4 g of sodium/day Low fat Limited starchy foods Increased vegetable and fruit intake

25.  Lifestyle modifications  Moderation of alcohol consumption: Men: no more than 2 drinks/day Women: no more than 1 drink/day  Physical activity: Regular physical (aerobic) activity, at least 30 minutes, most days of the week  Avoidance of tobacco products  Stress management

26.  Drug therapy:  Primary actions of drugs to treat hypertension Reduce SVR Reduce volume of circulating blood  Classifications of drugs used to treat HTN Diuretics Adrenergic inhibitors Direct vasodilators Angiotensin inhibitors Calcium channel blockers

27.  Diuretics  Inhibit NaCl reabsorption in the tubules  Increases excretion of Na and Cl  Potassium-sparing diuretics reduce excretion of K+  Types: Thiazide diuretics: hydrochlorothiazide (HydroDiuril), metolazone (Zaroxolyn) Loop Diuretics: bumetanide (Bumex) furosemide (Lasix), torsemide (Demadex) Potassium-sparing diuretics: triamterene (Dyrenium) Aldosterone Receptor Blockers: spironolactone (Aldactone)

28.  What will you monitor in patients taking diuretics?  I & O  Daily Weight  Electrolyte abnormalities Potassium Sodium  BP Orthostatic hypotension  Ototoxicity (Lasix)  Dizziness, vertigo

29.  Adrenergic inhibitors  Central-Acting α-1 Adrenergic Antagonists Reduce sympathetic outflow from CNS Reduces peripheral sympathetic tone, produces vasodilation, decreases SVR and BP Types: Clonidine (Catapress) Methyldopa (Aldomet)

30.  Adrenergic inhibitors  α-1 Adrenergic Blockers Block α-1 adrenergic effects, producing peripheral vasodilation (decreases SVR and BP) Types: Doxazosin (Cardura), Prozosin (Minipress), Terazosin (Hytrin)  β -Adrenergic Blockers Decrease CO and reduce vasoconstrictor tone Types: Atenolol (Tenormin), metoprolol (Lopressor), propranolol (Inderal)

31.  What will you monitor in patients taking Adrenergic-Blockers?  Dry mouth Central-Acting α-1 Adrenergic Antagonists  BP Orthostatic hypotension  Retention of salt and water α-1 adrenergic blockers  Bronchospasm β -Adrenergic Blockers  Bradycardia β -Adrenergic Blockers

32.  Direct vasodilators  Reduce SVR and BP by arterial vasodilation  Types:  Hydralazine (Apresoline), nitroglycerin (Tridil), sodium nitroprusside (Nipride)  What will you monitor for?  BP  Tachycardia  Flushing  Palpitations  Dizziness  Angina  Headache

33.  Angiotensin inhibitors  Angiotensin-Converting Enzyme (ACE) Inhibitors  Reduce conversion of Angiotensin I to angiotensin II, prevent vasoconstriction  Types: captopril (Capoten), enalapril (vasotec), lisinopril (Prinivil)  Angiotensin II Receptor Blockers  Prevent action of angiotensin II and produce vasodilation and increased salt and water excretion  Types: irbesartan (Avapro), valsartan (Diovan)

34.  What will you monitor?  Angiotensin-Converting Enzyme (ACE) Inhibitors  BP  Dizziness  Loss of taste  Hyperkalemia  ARF  Angiotensin II Receptor Blockers  Hyperkalemia  Decreased RF

35.  Calcium channel blockers  Block movement of extracellular calcium into cells, causing vasodilation and decreased HR, contractility, and SVR  Types:  Amlodipine (Norvasc), diltiazem (Cardizem), nifedipine (Procardia), verapamil (Calan)  What will you monitor?  BP  Bradycardia  Headache, dizziness, peripheral edema, flushing

36.  Drug therapy and patient teaching  Identify, report, and minimize side effects Orthostatic hypotension Sexual dysfunction Dry mouth Frequent urination

37.  Nursing Assessment  Subjective data Past health history CV, renal, thyroid disease, DM, obesity Medications Prescription and OTC Functional health patterns Family history Diet Activity level Stress  Objective data Target organ damage Peripheral pulses, abnormal heart sounds, BP >140/90

38.  Nursing Diagnoses  Ineffective health maintenance r/t lack of knowledge  Anxiety r/t management regimen or lifestyle changes  Sexual dysfunction r/t medication side effects  Ineffective therapeutic regimen management r/t lack of knowledge, side effects of medications, return of blood pressure to normal while on medications  Ineffective tissue perfusion r/t complications of HTN (cerebral, CV, renal, retinal)

39.  Collaborative problems  Potential complications:  Adverse effects from antihypertensive therapy (hypokalemia)  Hypertensive crisis  Stroke  Coronary artery disease (CAD)  Myocardial infarction

40.  Severe, abrupt increase in DBP  defined as DBP >140 mm Hg  Rate of increase in BP is more important than the absolute value  Often occurs in patients with a history of HTN who have failed to comply with medications or who have been undermedicated

41.  Hypertensive Emergency  Develops within hours to days  BP > 180/120 mm Hg  Acute target organ damage  May precipitate: Hypertensive encephalopathy, cerebral hemorrhage Acute renal failure Myocardial infarction Heart failure with pulmonary edema  Hyptertensive Urgency  Develops within days to weeks  No clinical evidence of target organ damage

42.  Hypertensive Emergency  Hypertensive encephalopathy Sudden rise in BP associated with HA, N/V, seizures, confusion, coma May also have blurred vision and transient blindness Due to increased cerebral capillary permeability leading to cerebral edema and disruption in cerebral function  Renal insufficiency  CV decompensation Unstable angina MI Pulmonary edema

43.  Hospitalization  IV drug therapy Sodium nitroprusside (Nipride) – MOST EFFECTIVE Titrated to mean arterial pressure MAP = (SBP + 2 DBP) 3

44.  Nursing Interventions  Monitor BP and HR every 3-5 minutes  Titrate med based on MAP  DO NOT DECREASE BP TO QUICKLY – may cause stroke, MI  Continual ECG monitoring  Hourly UO  Strict BP  Neurologic checks LOC, pupil checks, movement and strength of extremities  CV and Respiratory assessment pulmonary edema, HF, angina

45.  Hypertensive Urgency  Managed with oral medications Difficult to regulate drugs Need follow-up within 24 hours  May not need hospitalization  Nursing Interventions Provide quiet environment Encourage patient to verbalize concerns Answer questions Eliminate stimuli Determine cause Education to avoid future crises

46.  Planning: Patient will  Achieve and maintain the individually determined goal BP  Understand, accept, and implement the therapeutic plan  Experience minimal or no unpleasant side effects of therapy  Be confident of ability to manage and cope with this condition

47. Nursing Implementation  Health Promotion Individual patient evaluation Risk factors Routine BP Health assessment Weight patterns Family history Blood pressure measurement Screening programs Cardiovascular risk factor modification Modifiable: HTN, DM, obesity, tobacco cessation, physical inactivity

48. Nursing Implementation Ambulatory and Home Care  Patient and family teaching includes Nutritional therapy Drug therapy Physical activity 30 minutes/day most days of week Home monitoring of BP (if appropriate) Rest 3-5 minutes prior to taking BP No smoking, exercise or caffeine 30 minutes prior Take daily and record in log Tobacco cessation (if applicable)

49. Nursing Evaluation  Patient will  Achieve and maintain goal BP as defined for the individual  Understand, accept, and implement the therapeutic plan  Experience minimal or no unpleasant side effects of therapy

50.  Isolated systolic hypertension (ISH) is the most common form of hypertension in individuals age >50  The lifetime risk of developing hypertension is approximately 90% for middle-aged (age 55 to 65) and older (age >65) normotensive men and women  Why?  Loss of elasticity, increased PVR, blunting of baroreceptors, decreased renal function, decreased renin production

51.  Older adults are more likely to have “white coat” hypertension  Often a wide gap between the first Korotkoff sound and subsequent beats called the auscultatory gap  Failure to inflate the cuff high enough may result in seriously underestimating the SBP  Assess disappearance of pulse upon inflation of cuff

52.  Older adults have varying degrees of impaired baroreceptor reflex mechanisms  Consequently, orthostatic hypotension occurs often especially in patients with ISH  Most commonly associated with volume depletion or decreased renal or hepatic function

53.  In general, treatment similar for all demographic and ethnic groups  Prevalence and severity of HTN increased in African Americans

54.  Mexican Americans are less likely to receive treatment for hypertension than whites and African Americans  Mexican Americans and Native Americans have lower rates of BP pressure control than whites and African Americans