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Hypertension

Description
 Hypertension, or high blood pressure (BP), is defined as a persistent systolic blood
pressure (SBP) greater than or equal to 140 mm Hg, diastolic blood pressure (DBP)
greater than or equal to 90 mm Hg, or current use of antihypertensive medication.
There is a direct relationship between hypertension and cardiovascular disease
(CVD).
 Contributing factors to the development of hypertension include cardiovascular risk
factors combined with socioeconomic conditions and ethnic differences.
 Hypertension is generally an asymptomatic condition. Individuals who remain
undiagnosed and untreated for hypertension present the greatest challenge and
opportunity for health care providers.
 Is the most important modifiable risk factor for stroke.
o High blood pressure increases the risk of ischemic heart disease by 3-4 fold
o The incidence of stroke increases approximately 8 fold in persons with
definite hypertension
o It has been estimated that 40% of cases of acute MI or stroke are attributable
to hypertension

Etiology of Hypertension
 Primary (essential or idiopathic) hypertension: elevated BP without an identified
cause; accounts for 90% to 95% of all cases of hypertension.
 Secondary hypertension: elevated BP with a specific cause; accounts for 5% to 10%
of hypertension in adults.
Pathophysiology
PATHOPHYSIOLOGY OF PRIMARY HYPERTENSION
 The hemodynamic hallmark of hypertension is persistently increased SVR.
 Water and sodium retention: A high-sodium intake may activate a number of
pressor mechanisms and cause water retention.
 Altered renin-angiotensin mechanism: High plasma renin activity (PRA) results in
the increased conversion of angiotensinogen to angiotensin I causing arteriolar
constriction, vascular hypertrophy, and aldosterone secretion.
 Stress and increased SNS activity: Arterial pressure is influenced by factors such as
anger, fear, and pain. Physiologic responses to stress, which are normally protective,
may persist to a pathologic degree, resulting in prolonged increase in SNS activity.
Increased SNS stimulation produces increased vasoconstriction, increased HR, and
increased renin release.
 Insulin resistance and hyperinsulinemia: Abnormalities of glucose, insulin, and
lipoprotein metabolism are common in primary hypertension. Additional pressor
effects of insulin include vascular hypertrophy and increased renal sodium
reabsorption.
 Endothelial cell dysfunction: Some hypertensive people have a reduced vasodilator
response to nitric oxide. Nitric oxide, an endothelium-derived relaxing factor (EDRF),
helps maintain low arterial tone at rest, inhibits growth of the smooth muscle layer,
and inhibits platelet aggregation. Endothelin produces pronounced and prolonged
vasoconstriction.
Clinical Manifestations of Hypertension
 Often called the “silent killer” because it is frequently asymptomatic until it becomes
severe and target organ disease occurs.
 Target organ diseases occur in the heart (hypertensive heart disease), brain
(cerebrovascular disease), peripheral vasculature (peripheral vascular disease), kidney
(nephrosclerosis), and eyes (retinal damage).
 Hypertension is a major risk factor for coronary artery disease (CAD).
 Sustained high BP increases the cardiac workload and produces left ventricular
hypertrophy (LVH). Progressive LVH, especially in association with CAD, is
associated with the development of heart failure.
 Hypertension speeds up the process of atherosclerosis in the peripheral blood vessels,
leading to the development of peripheral vascular disease, aortic aneurysm, and aortic
dissection.
 Intermittent claudication (ischemic muscle pain precipitated by activity and relieved
with rest) is a classic symptom of peripheral vascular disease involving the arteries.
 Hypertension is one of the leading causes of end-stage renal disease, especially
among African Americans. The earliest manifestation of renal dysfunction is usually
nocturia.
 The retina provides important information about the severity and duration of
hypertension. Damage to retinal vessels provides an indication of concurrent vessel
damage in the heart, brain, and kidney. Manifestations of severe retinal damage
include blurring of vision, retinal hemorrhage, and loss of vision.
Classification of Hypertension: WHO/ISH*
Category Systolic Diastolic
Optimal
Normal
High Normal
< 120
<130
130-139
<80
<85
85-89
Grade 1 (mild hypertension)
- Subgroup: borderline
140-159
140-149
90-99
90-94
Grade 2 (moderate hypertension) 160-179 100-109
Grade 3 (severe Hypertension) ≥ 180 ≥110
Isolated Systolic Hypertension (ISH)
- Subgroup (borderline)
≥140
140-149
<90
<90
World Health Organization –ISH International Society of Hypertension


National Institutes of Health Classification

Category Systolic Diastolic
Optimal < 120 <80
Pre-hypertensive 120-139 80-89
Hypertensive ≥140 ≥90
Stage 1 140-159 90-99
Stage 2 ≥160 ≥100


Diagnostic Studies
 Basic laboratory studies are performed to (1) identify or rule out causes of secondary
hypertension, (2) evaluate target organ disease, (3) determine overall cardiovascular
risk, or (4) establish baseline levels before initiating therapy.
 Routine urinalysis, BUN, serum creatinine, and creatinine clearance levels are used to
screen for renal involvement and to provide baseline information about kidney
function.
 Measurement of serum electrolytes, especially potassium levels, is done to detect
hyperaldosteronism, a cause of secondary hypertension.
 Blood glucose levels assist in the diagnosis of diabetes mellitus.
 Lipid profile provides information about additional risk factors that predispose to
atherosclerosis and cardiovascular disease.
 ECG and echocardiography provide information about the cardiac status.

Nursing and Collaborative Management
 Treatment goals are to lower BP to less than 140 mm Hg systolic and less than 90 mm
Hg diastolic for most persons with hypertension (less than 130 mm Hg systolic and
less than 80 mm Hg diastolic for those with diabetes mellitus and chronic kidney
disease).
 Lifestyle modifications are indicated for all patients with prehypertension and
hypertension and include the following:
o Weight reduction. A weight loss of 10 kg (22 lb) may decrease SBP by
approximately 5 to 20 mm Hg.
o Dietary Approaches to Stop Hypertension (DASH) eating plan. Involves
eating several servings of fish each week, eating plenty of fruits and
vegetables, increasing fiber intake, and drinking a lot of water. The DASH diet
significantly lowers BP.
o Restriction of dietary sodium to less than 6 g of salt (NaCl) or less than 2.4 g
of sodium per day.
o This involves avoiding foods known to be high in sodium (e.g., canned soups)
and not adding salt in the preparation of foods or at meals.
o Restriction of alcohol
o Regular aerobic physical activity (e.g., brisk walking) at least 30 minutes a
day most days of the week. Moderately intense activity such as brisk walking,
jogging, and swimming can lower BP, promote relaxation, and decrease or
control body weight.
o It is strongly recommended that tobacco use be avoided.
o Stress can raise BP on a short-term basis and has been implicated in the
development of hypertension. Relaxation therapy, guided imagery, and
biofeedback may be useful in helping patients manage stress, thus decreasing
BP.

Drug Therapy
 Drug therapy is not recommended for those persons with prehypertension unless it is
required by another condition, such as diabetes mellitus or chronic kidney disease.
 The overall goals for the patient with hypertension include (1) achievement and
maintenance of the goal BP; (2) acceptance and implementation of the therapeutic
plan; (3) minimal or no unpleasant side effects of therapy; and (4) ability to manage
and cope with illness.
 Drugs currently available for treating hypertension work by (1) decreasing the volume
of circulating blood, and/or (2) reducing SVR.
o Diuretics promote sodium and water excretion, reduce plasma volume,
decrease sodium in the arteriolar walls, and reduce the vascular response to
catecholamines.
o 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.
o Direct vasodilators decrease the BP by relaxing vascular smooth muscle and
reducing SVR.
o Calcium channel blockers increase sodium excretion and cause arteriolar
vasodilation by preventing the movement of extracellular calcium into cells.
o 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.
o A-II receptor blockers (ARBs) prevent angiotensin II from binding to its
receptors in the walls of the blood vessels.
o Thiazide-type diuretics are used as initial therapy for most patients with
hypertension, either alone or in combination with one of the other classes.
o When BP is more than 20/10 mm Hg above SBP and DBP goals, a second
drug should be considered. Most patients who are hypertensive will require
two or more antihypertensive medications to achieve their BP goals.
o Side effects and adverse effects of antihypertensive drugs may be so severe or
undesirable that the patient does not comply with therapy.
 Hyperuricemia, hyperglycemia, and hypokalemia are common side
effects with both thiazide and loop diuretics.
 ACE inhibitors lead to high levels of bradykinin, which can cause
coughing. An individual who develops a cough with the use of ACE
inhibitors may be switched to an ARB.
 Hyperkalemia can be a serious side effect of the potassium-sparing
diuretics and ACE inhibitors.
 Sexual dysfunction may occur with some of the diuretics. Orthostatic
hypotension and sexual dysfunction are two undesirable effects of
adrenergic-inhibiting agents.
 Tachycardia and orthostatic hypotension are potential adverse effects
of both vasodilators and angiotensin inhibitors.
 Patient and family teaching related to drug therapy is needed to
identify and minimize side effects and to cope with therapeutic effects.
Side effects may be an initial response to a drug and may decrease with
continued use of the drug.

Hypertensive crisis
 Hypertensive crisis is a severe and abrupt elevation in BP, arbitrarily defined as a
DBP more than 140 mm Hg.
o Hypertensive crisis occurs most often in patients with a history of
hypertension who have failed to comply with their prescribed medications or
who have been undermedicated.
o Hypertensive crisis related to cocaine or crack use is becoming a more
frequent problem. Other drugs such as amphetamines, phencyclidine (PCP),
and lysergic acid diethylamide (LSD) may also precipitate hypertensive crisis
that may be complicated by drug-induced seizures, stroke, MI, or
encephalopathy.
o Hypertensive emergency develops over hours to days and is defined as BP that
is severely elevated (more than 180/120 mm Hg) with evidence of acute target
organ damage.
o Hypertensive emergencies can precipitate encephalopathy, intracranial or
subarachnoid hemorrhage, acute left ventricular failure with pulmonary
edema, MI, renal failure, dissecting aortic aneurysm, and retinopathy.
o Hypertensive emergencies require hospitalization, intravenous (IV)
administration of antihypertensive drugs, and intensive care monitoring.

Nursing Management
 The primary nursing responsibilities for long-term management of hypertension are to
assist the patient in reducing BP and complying with the treatment plan. Nursing
actions include patient and family teaching, detection and reporting of adverse
treatment effects, compliance assessment and enhancement, and evaluation of
therapeutic effectiveness.
 Patient and family teaching includes the following: (1) nutritional therapy, (2) drug
therapy, (3) physical activity, (4) home monitoring of BP (if appropriate), and (5)
tobacco cessation (if applicable).