Hypertension, HTN, High blood pressure Nursing and medical students

1. HYPERTENSION
BY:- Baljinder singh
Assistant Professor
PIMS, PNP

2. DEFINITION
High blood pressure, is generally
defined as a persistent elevation of
systolic blood pressure above 140
mm of Hg diastolic pressure above
90 mm Hg.

3. INCIDENCE
 Hypertension is the most common public
health problem in the United States.
Arterial hypertension affects nearly 60
million clients in the United States.
 Prevalence of hypertension increases
with advancing age, and blacks are
affected more than whites are.

4. INCIDENCE
The public is more knowledgeable
about high blood pressure, more
likely to visit a physician for
hypertension, and more likely to
follow medical advice. These
practices have contributed to a 50 per
cent decrease in the mortality

5. Classification of Hypertension
Hypertension may be classified
according to type (systolic and
diastolic), cause, and degree of
severity.

6. Systolic and diastolic hypertension
Systolic hypertension is systolic
pressure greater than 140 mm Hg. Clients
over age 65 frequently have systolic
pressure over 140 mm hg and diastolic
pressure over 90 mm Hg.
 For these clients, hypertension is defined
as systolic pressure over 160 mm Hg
and/or diastolic pressure over 95 mm hg.

7. CONTINUE…
 Diastolic hypertension is diastolic
pressure greater than 90 mm Hg.

8. Primary and Secondary
Hypertension
Primary hypertension, also known as essential
or idiopathic hypertension, constitutes more than
90-95 per cent of all cases of hypertension.
 The etiology of primary hypertension is
multifactorial; a number of interacting
homeostatic forces are involved.
Characteristics include either a gradual onset or
prolonged course (benign hypertension) or an
abrupt onset and a short dramatic course that
proves rapidly fatal without swift intervention
(malignant or accelerated hypertension)

9. Primary and Secondary
Hypertension
Secondary hypertension results from an
identifiable cause.
A variety of specific disease states or problems
are responsible. 5-10 per cent of the
hypertensive population has secondary
hypertension.

10. Borderline Hypertension
Borderline or labile hypertension is defined
as intermittent elevation of blood pressure
interspersed with normal readings.
Clients with borderline hypertension still
carry an increased risk of developing
cardiovascular disease.

11. Benign Hypertension
Benign hypertension is a term used to
describe uncomplicated hypertension,
usually of long duration and mild to
moderate severity.
 Benign hypertension may be primary or
secondary.

12. Malignant Hypertension
Malignant hypertension is a syndrome of
markedly elevated BP (diastolic BP over
140 mm Hg) associated with papilledema.
 Accelerated hypertension is a syndrome
of markedly elevated BP with retinal
hemorrhage and exudates.
 Accelerated hypertension presumably
develops into malignant hypertension if not
well managed.

13. ETIOLOGY

14. Etiology
Primary hypertension has no single or specific
cause but it is multifactorial. It develops in
response to increased cardiac output or to a rise
in peripheral resistance.
 Factors that affect these two forces include:-
 Genetic propensity
to a hightened neurologic response to stress or
for a defect in renal excretion or cellular transport of
sodium

15. Etiology
Obesity associated with high levels of
insulin (hyperinsulinemia) that lead to
raised blood pressure
Environmental stress
Loss of elastic tissue and arteriosclerosis
of aorta and other large arteries.

16. CAUSES OF SECONDARY
HYPERTENSION
Renal
 Renal parenchymal disease
-Acute glomerulonephritis
-Chronic nephritis
-Polycystic disease
 Connective tissue disease
 Diabetic nephropathy
 Hydronephrosis
 Renovascular
-Rennin-producing tumors

17. CAUSES OF SECONDARY
HYPERTENSION
 Endocrine
-Acromegaly
- Hypothyroidism
- Hyperthyroidism
- Hypercalcemia
 Adrenal
-Cortical:-
-Cushing’s syndrome
-Primary aldosteronism
-Congenital adrenal hyperplasia
-Medullary: pheochromocytoma
-Extra-adrenal chromaffin tumors

18. CAUSES OF SECONDARY
HYPERTENSION
 Exogenous hormones:-
Estrogen
Glucocorticoids
Mineralocorticoids
Sympathomimetics
Tyramine-containing foods and
monoamine oxidase inhibitors

19. CAUSES OF SECONDARY
HYPERTENSION
 Coarctation of the aorta
 Pregnancy-induced hypertension
 Neurologic disorders
 Increased intracranial pressure
 Brain tumor
 Encephalitis
 Respiratory acidosis
 Sleep apnea
 Quadriplegia
 Lead poisoning
 Guillain-Barre syndrome

20. CAUSES OF SECONDARY
HYPERTENSION
Acute stress, including surgery
Psychogenic hyperventilation
Hypoglycemia
Burns
Pancreatitis
Alcohol withdrawal
Postresuscitation
Postoperative
Increased intravascular volume
Alcohol, drugs, and so on

21. Risk Factors
Primary Prevention:- Prevention of
hypertension involves the identification of
nonmodifiable risk factors and the identification
and management of modifiable risk factors.
Risk factors serve to determine a client’s risk for
this chronic illness.
The relative risk for hypertension depends on
the number and severity of modifiable risk
factors.

22. Nonmodifiable Risk Factors
Family History. The genetic predisposition that
makes certain families more susceptible to
hypertension seems to be associated with
elevated intracellular sodium levels and lowered
potassium to sodium ratios.
 This is found more often in blacks. Clients with
parents who have hypertension have a greater
risk of developing hypertension at a younger
age.

23. Nonmodifiable Risk Factors
Age. The incidence of hypertension
increases with age; 50-60 per cent of
clients over 50 years of age have a blood
pressure over 140/90 mm Hg.
However, epidemiologic studies have
shown a poorer prognosis in clients whose
hypertension began at a young age.

24. Nonmodifiable Risk Factors
Gender. Men experience hypertension at
higher rates and at an earlier age than do
women until after age 60 years.
Men also have greater risk of
cardiovascular morbidity and mortality.
 After age 50, hypertension is more
prevalent in women. The reasons are not
clear.

25. Nonmodifiable Risk Factors
Ethnic Group. Hypertension is the most
serious health problem for blacks in the
United States.
Hypertension is more prevalent in blacks,
and at any given blood pressure, with
whites. The reason has been attributed to
heredity, greater salt intake, and greater
environmental stress

26. Modifiable Risk Factors
Stress. Stress has been shown to cause
increased peripheral vascular resistance
and cardiac output and to stimulate
sympathetic nervous system activity.
 Stress may be associated with
occupational factors, socioeconomic
levels, and personality characteristics.

27. Modifiable Risk Factors

28. Modifiable Risk Factors
Obesity. Obesity, in particular that located
in the upper body with increased amounts
of intra-abdominal fat, is an important
cause of hypertension; the combination
may be related to hyperinsulinemia
secondary to insulin resistance.

29. Modifiable Risk Factors
Nutrients. Sodium is an important
etiologic factor in essential hypertension. A
high salt diet may induce excessive
release of natriuretic hormone, which may
indirectly increase blood pressure
 Sodium loading has also been shown
experimentally to stimulate vasopressor
mechanisms within the central nervous
system.

30. Modifiable Risk Factors
Also Calcium intake may be lower among
hypertensive than among normotensive
clients.
The impact of caffeine is controversial. It
raises blood pressure acutely but does not
have sustained effects.

31. Secondary Prevention
Because the beginnings of adult
hypertension often lie in childhood and
adolescence, children over the age of 3
years need yearly blood pressure
determinations.
Asymptomatic youngsters who, on three
separate occasions, have an elevated
blood pressure reading require a careful
work up and follow up program.

32. Secondary Prevention
Obese teenagers have an 80 per cent
chance of becoming obese adults. In that
obesity in children is a major cause of
hypertension; these statistics dramatically
demonstrate the need for attention to this
issue.

33. Tertiary prevention
Once diagnosed, hypertension requires ongoing
management despite the absence of symptoms.
The many sequelae of unmanaged hypertension
(i.e., stroke and myocardial infarction) could be
prevented or their severity reduced if
hypertension were well managed.
Because of the cost of antihypertensive, side
effects, and lack of symptoms, unfortunately
many clients do not manage the disorder well.

34. PATHOPHYSIOLOGY
Primary (Essential )hypertension
- Atrial BP is a product of c.o.p. and t.p.r.
- COP is determined by stroke volume and
HR.
- Control of PVR is maintained by
autonomic nervous system and
circulating hormones.

35. PATHOPHYSIOLOGY
Therefore any factor producing an
alteration in PVR HR or stroke volume
affect systemic atrial BP.
Four control system play a major role.
- atrial baroreceptor system
- regulation of body fluid volume
- renin angiotensin system
- vascular autoregulation

36. Atrial baroreceptor
Found in:- carotid sinus, aorta, wall of left.
ventrical.
Monitor the level of atrial pressure and
counteract rises through vagally mediated
cardiac slowing and vasodilation.

37. Fluid volume
An abnormality in the transport of Na in the renal
tubules may cause essential hypertension.
When there is excess of Na and water total
blood volume increases increase BP.
In functional kidneys rise in pressure leads to
diuresis.
Pathologic changes alter the pressure threshold
at which kidney excrete salt and water alter
systemic BP.

38. RENIN ANGIOTENSIN SYSTEM
REDUCED
BP
DISTAL
TUBULAR
Na
Renin
Angiotensin
substrate
Angiotensin
I
Converting enzyme
Angiotensin
II

39. Angiotensin
II
Angio
III
Vasocontriction
Aldosterone
secretion
Na and fluid
retention
Increased
COPElevation
Of BP
Increased
PVR

40. Vascular auto regulation
Client may develop hypertension from
deficiencies in vasodilators such as
prostaglandin or congenital abnormalities
in resistence vessels.

41. Secondary hypertension
Mechanisms involved in secondary
hypertension include:-
Increase secretion of Catecholamines.
Increased release of renin (e.g. renal
artery stenosis)
Expansion of Na and blood volume. (e.g.
cushing’s syndrome)

42. Clinical Manifestations
The early stages of hypertension have no
clinical manifestations, other than elevations in
blood pressure.
 This unfortunate fact means that there are no
signs or symptoms to lead a person to seek
health care.
 As hypertension advances, without treatment
clients may report morning occipital headache,
fatigue, dizziness, palpitations, flushing, blurred
vision, and epistaxis.

43. PROGNOSIS
The advent of effective antihypertensive
agents has dramatically reduced the
mortality rate associated with
hypertension.
If untreated nearly one half of
hypertensive client die of heart disease;
1/3 die of stroke; and the remaining 10-
15% die of renal failure

44. PROGNOSIS
Hypertension may also be a silent factor in
many deaths attributed to stroke or heart
attacks.
When hypertension arises as a secondary
process, death usually results from the
primary disease.

45. DIAGNOSIS
The diagnosis of hypertension in the adult
is determined when the average of two
or more diastolic BP readings, on at least
two separate visits at least 2 weeks apart,
is 90 mm Hg or higher,
Or when the average of multiple systolic
BP readings over several visits is greater
than 140 mm Hg.

46. TECHNIQUE OF BP
MEASUREMENT
 Client should be seated with their arm bared,
supported, and positioned at heart level. They
should not have smoked tobacco within the
past 15 mins or ingested caffeine within the
past hour.
 Measurement should begin after 5 mins of
quiet rest. The back should be supported, and
both feet should be flat on the floor with the
legs uncrossed. The client should not speak
while BP is being monitored.

47. TECHNIQUE OF BP
MEASUREMENT
 The appropriate cuff size is used to ensure an
accurate measurement. The rubber bladder
should encircle at least two thirds of the limb
being measured.
 The bladder’s width should be one third to one
half the circumference of the limb. Several
sizes of cuffs (e. g., child, adult, and large
adult) should be available.
 If the cuff is too wide, the blood pressure
reading will be falsely high. Inaccurate cuff size
is the most common error in taking blood
pressure measurement.

48. TECHNIQUE OF BP
MEASUREMENT
 Measurements should be taken with a mercury
sphygmomanometer, a recently calibrated
aneroid manometer, or a validated electronic
device.
 Both the systolic and diastolic blood pressure
should be recorded. The disappearance of
sound (phase V) should be used for the
diastolic reading.
 Two or more readings should be averaged. If
the first two readings differ by more than 5 mm
Hg, additional readings should be obtained.

50. Categorization of severity
The 1988 joint National Committee on
Detection, Evaluation and Treatment of
High Blood Pressure has developed a
classification of diastolic and systolic blood
pressure readings.
 Clinicians can use this classification to
categorize blood pressure readings and to
diagnose hypertension in clients aged 18
years or older.

51. RANGE(MM OF Hg) CATEGORY
DBP
< 85 Normal BP
85-89 High normal BP
90-104 Mild hypretension
105-114 Moderate
>115 Severe
SBP, When DBP is <90
<140 Normal BP
140-159 Boderline isolated
systolic hypertension
Isolated systolic hyper.

52. Drugs
 Diuretics:-
 Thiazide and Related to sulfonamides
[Chlorothiazide, Methyclothiazide, Metolazone]
 Action [Promote renal excretion of sodium,
water, and potassium. }

53. Drugs
Loop Diuretics [frusemide (Laxis), Bumetadine
(bumex)]
Action [Comparable to thiazides, Act on loop of,
Henle to minimize sodium and water
reabsorption]
Potassium-Sparing Diuretics [ (Aldactone),
Triamterene (Dyrenium)]
Action [Block action of aldosterone in distal
loop, promoting excretion of sodium and water
and retention of potassium. ]

54. Drugs
 Vasodilators:-Hydralazine(apresoline)
Action : direct action on smooth muscle
walls of arterioles causing arteriolar
vasodilation.

55. Drugs
. Adrenergic inhibiting agents:-
 - Beta blockers:- propranolol, metoprolol,
nadolol, atenolol,
 - Action:- block beta receptors in the heart
and peripheral vessels to reduce peripheral
vascular resistence.
 - Alpha adrenergic inhibitors :- prazosin
hydrochloride
 - Action :- vasodilation occurs with a
decrease in peripheral vascular resistence.

56. Drugs
 - Calcium channel blocking agents:- nifedipine,
verapamil hydrochloride, Diltiazem, nicardipine.
 - Action:- block entry of calcium in to smooth muscle
cells and may interfere with the intracellular release of
Ca cause arteriolar vasodilation and decrease p.v.r.

57. Drugs
Angiotensin converting enzyme
inhibitors:- captopril, enalapril, lisinopril.
 - Action:-inhibits conversion of angio I
to II. Reduce p.v.r. without changing
cardiac output.

58. Nonpharmacologic Intervention.
Sodium Restriction
Weight reduction
Modification of Dietary Fat
Exercise
Caffeine Restriction
Restriction of Alcohol & smoking

59. Nonpharmacologic Intervention

60. Nonpharmacologic Intervention
Modification of Dietary Fat. Modification
of dietary intake of fat by decreasing the
fraction of saturated fat and increasing that
of polyunsaturated fat may decrease blood
pressure and will decrease the cholesterol
level, which is an important risk factor for
coronary artery disease.

61. Nonpharmacologic Intervention
The use of fish oil supplements to lower
cardiovascular risk has been shown to
lower blood pressure in preliminary
studies, but fish oil supplementation may
cause deficient blood clotting and
excessive bleeding in some clients.
Therefore, this therapy is not
recommended until long term results are
known

62. Nonpharmacologic Intervention
Exercise. A regular program of aerobic
(isotonic) exercise facilitates cardiovascular
conditioning, can aid the obese hypertensive
client in weight reduction, and may provide
some benefit in reducing blood pressure.
 Heavy isometric exercises such as weightlifting
may be harmful; blood pressure often rises to
very high levels because of vasovagal reflexes
that occur during an isometric contraction.

63. Nonpharmacologic Intervention
Restriction of Alcohol. The consumption of
more than 1 to 2 ounces of alcohol per day is
associated with a higher prevalence of
hypertension, poor adherence to the
antihypertensive therapy, and occasionally,
refractory hypertension.
 Alcohol intake needs to be advised to do so in
moderation (i.e., less than 1 to 2 ounces of
ethanol per day). There is 1 ounce (28 g) of
ethanol in 2 ounces of 100-proof whiskey, 8
ounces of wine, or 24 ounces of beer.

64. Nonpharmacologic Intervention
Caffeine Restriction. Although acute ingestion
of caffeine may raise blood pressure, chronic
moderate caffeine ingestion appears to have no
significant effects on blood pressure.
 Instruct clients to limit caffeine to 250 mg (the
amount in two to three cups of brewed coffee)
because it probably raises blood pressure by
activating the sympathetic nervous system. This
sympathetic response particularly affects those
not used to drinking coffee.

65. Nonpharmacologic Intervention
Relaxation Techniques. A variety of relaxation
therapies, including transcendental meditation,
yoga, biofeedback, and psychotherapy, have
been shown to reduce blood pressure in
hypertensive clients at least transiently.
 Although each has its advocates, none has
been conclusively shown to be either practical
for the majority of hypertension clients or
effective in maintaining a significant long term
effect.

66. Nonpharmacologic Intervention
Smoking Cessation. Nicotine definitely
increases heart rate and produces peripheral
vasoconstriction, which does raise arterial blood
pressure for a short time.
Smoking cessation is strongly recommended,
however, to reduce the client’s risk for cancer,
pulmonary disease, and cardiovascular disease.
Smokers appear to have a higher frequency of
malignant hypertension and subarachnoid
hemorrhage.

67. Nonpharmacologic Intervention
Potassium Supplements. The high ratio of
sodium to potassium in the modern diet has
been held responsible for the development of
hypertension.
 Potassium supplements may lower blood
pressure, they are too costly and potentially
hazardous for routine use.
 A reduction of high sodium, low potassium
processed foods with an increase of low sodium,
high potassium natural foods may be all that is
needed to achieve the potential benefits.

68. Nonpharmacologic Intervention
Calcium Supplements. The most recent
studies examining the antihypertensive effects of
calcium supplements demonstrate that this
therapy may be helpful for a small portion of the
population with hypertension.
 Clients should ensure a reasonable dietary
calcium in take rather than using potassium for
preventing or treating hypertension.

69. Nonpharmacologic Intervention
Magnesium Supplements. The
antihypertensive effect of supplemental
magnesium has been less well studies
than that of potassium or calcium.
Lower magnesium levels have been noted
in hypertensive clients, and diuretic
therapy may induce hypomagnesemia.
Supplementation may be considered.

70. The Stepped Care Approach
The goal of antihypertensive therapy is to
control blood pressure with a minimum of
side effects.
The joint National Committee on
Detection, Evaluation and Treatment of
Hypertension has recommended the
stepped-care approach to the treatment of
hypertension.

71. The Stepped Care Approach
Step 1
Implement life style modification
Step 2
Continue life style modification and make initial
pharmacological selection.
Start with lowest therapeutic dose of a long
acting drug given once daily.
- if there is inadequate BP control move to step 3

72. The Stepped Care Approach
Step 3
Increase drug dose
or
substitute another drug if no response or
side effects.
or
add second drug from a different class or
a diuretic if not already used.

73. The Stepped Care Approach
Step 4
Add second or third drug if not already
prescribed ; continue to add medication
from other classes.

74. Step-Down Therapy
Once a client with mild hypertension has
been controlled for one year or more,
medications can be titrated down slowly.
Regular follow up is essential.

75. Combination Therapy
More than 50 per cent of clients with mild
hypertension can be controlled with one
drug; the rest will require combination
therapy.
If more than one drug is necessary,
several combination therapies have
proved effective.

76. Combination Therapy
The combination of a diuretic with a beta-
adrenergic blocker or other adrenergic inhibitor
has been effective in both blacks and whites,
unlike the responses to the individual drugs.
 The combination of diuretics and ACE inhibitor
is synergistic because diuretic create high-renin
hypertension, a milieu in which ACE inhibitors
are effective.
Orthostatic clients or those with acute volume
depletion. The combination of a diuretic and
calcium channel blocker has additive effects on
blood pressure.

77. Malignant Hypertension
Malignant (accelerated) hypertension is an
emergency characterized by diastolic
pressures above 120 mm Hg, retinal
hemorrhage and exudates with
papilledema, acute renal failure, and rapid
vascular deterioration.

78. Malignant Hypertension
Malignant hypertension has a peak incidence at
age 40-50 years; its occurrence in clients below
30 or over 60 years of age should raise the
suspicion of a secondary cause of hypertension.
 Without treatment, malignant hypertension
results in a 90 per cent mortality rate within 1
year secondary to renal or congestive heart
failure, cerebrovascular accident, myocardial
infraction, or aortic dissection.

79. Malignant Hypertension
The most common cause of malignant
hypertension is untreated hypertension.
 Other causes include eclampsia,
dissecting aortic aneurysms,
pyelonephritis, sudden catecholamine
release (pheochromocytoma), drug or
toxic substance ingestion/exposure, or
food and drug interactions (monoamine
oxidase inhibitors and aged cheeses).

80. Malignant Hypertension
The presenting manifestations of malignant
hypertension include hypertensive retinopathy.
 The retinopathy is characterized by arteriolar
constriction, flame-shaped hemorrhages
resulting from damaged capillary endothelium,
and soft exudates.
 Papilledema results from obstruction of venous
outflow from the optic discs because of
intracranial hemorrhage.

81. Malignant Hypertension
Additional clinical manifestations include
hypertensive encephalopathy manifested by
restlessness, changes in level of
consciousness (confusion, somnolence,
lethargy, memory defects, coma, seizures),
blurred vision, dizziness, headache, nausea,
and vomiting.
 Assessment may also reveal renal insufficiency,
proteinuria, hematuria, urinary sediment casts,
hemolytic anemia, left ventricular failure, and
pulmonary edema.

82. Malignant Hypertension
Severe headache may be occipital or
anterior in location, is steady and
throbbing in quality, and is often worse in
the morning. Visual blurring, reduced
visual acuity, and even blindness can
occur.

83. Management
Malignant hypertension constitutes a true
medical emergency, and any delay in initiating
intervention can be catastrophic
These clients require monitoring in an intensive
care unit. Parameters requiring close scrutiny
include urinary output, blood pressure (via an
intre-arterial catheter), central venous pressure,
and pulmonary capillary wedge pressure.
Continuous electrocardiographic monitoring
helps assess for ischemic myocardial changes
and arrhythmias.

84. PARENTERAL DRUGS FOR
TREATMENT OF H. E.
 Vasodilatores
1. Nitroprusside:- 0.25-10 µg/kg/min as IV
infusion
2. Nitroglycerin:- 5-10 µg/min as IV infusion
3. Diazoxide:- 50-100 mg/IV bolus repeated, or
15-30 mg/min by IV infusion
4. Hydralazine:- 10-20 mg IV, 10-50mg IM
5. Enalaprilat:- 1.25-5 mg every 6 hr
6. Nicardipine:- 5-10 mg/hr IV

85. PARENTERAL DRUGS FOR
TREATMENT OF H. E.
 Adrenergic Inhibitors
1. Phentolamine:- 5-15 mg IV
2. Trimethaphan:- 0.5 mg/min as IV infusion
3. Esmolol:- 500 µg/kg/min for 1 min then
50-300 µg/kg/min IV for 4 min;
4. Propranolol:- 1-10 mg load; 3 ng/hr
5. Labetalol:- 30-80 mg IV bolus every 10
min

86. Management
The treatment goal is to lower blood pressure,
but as blood pressure lowers, evidence of target
organ impairment (especially of kidneys) may
appear. Consequently, restoration of blood
pressure must be done slowly and with care.
Once the client is out of immediate danger, oral
medications are administered while continuously
monitoring vital signs

87. Management
The physician typically prescribes a combination
of diuretic, beta-blocker, and hydralazine.
The nurse monitors blood pressure frequently
(every 15 minutes) and titrates the medications
to manage the blood pressure.
The clients head is raised to decrease risk of
cerebral bleeding. Anxiety is reduced, and
urinary output is also closely monitored.

88. Nursing Management
History. Note the following points when
interviewing the hypertensive client:
Family history of hypertension, diabetes mellitus,
or cardiovascular disease.
Previous documentation of high blood pressure,
including age of onset and currently prescribed
medical regimen.
History of any disease or trauma to target
organs.
Results and side effects of previous
antihypertensive therapy

89. Nursing Management
Clinical manifestation of cardiovascular
disorders, such as angina, dyspnea, or
claudication.
History of weight gain, exercise activities,
sodium intake, fat intake, and alcohol use.
Psychosocial and environmental factors (e. g.,
emotional stress, cultural food practices, and
economic status) that may influence blood
pressure control.
Presence of other cardiovascular risk factors,
including smoking, obesity, hyperlipidemia, and
exercise levels.

90. Nursing Management
History of all prescribed and over the
counter medications.
 Medications that may either raise blood
pressure or interfere with the effectiveness
of antihypertensive medications.

91. Physical Examination
 Evaluation of target organs typically includes the
following data:
 Funduscopic examination for retinal arteriolar narrowing,
hemorrhages, exudates, and papilledema;
 Examination of the neck for distended veins, carotid
bruits, and enlarged thyroid;
 Examination of the heart for increased heart rate,
arrhythmias, enlargement, precordial impulses,
murmurs, and S3 and S4 heart sounds;
 Examination of the abdomen for bruits, aortic dilation,
and enlarged kidneys;

92. Physical Examination
 Examination of extremities for diminished or absent
peripheral pulses, edema, and bilateral inequality of
pulses; and
 Neurologic evaluation for signs of cerebral thrombosis
or hemorrhage.
 Be especially alert to assessment findings suggesting
secondary hypertension. These include headache,
palpitations, and excessive perspiration leg
claudication and diminished or absent lower extremity
pulses truncal obesity with pigmented striae
(Cushing’s syndrome); and polyuria, fatigue, and
muscle cramps (hyperaldosteronism).

93. Nursing Diagnosis
Health Maintenance, Altered R/T
knowledge deficit about the disease
process, its consequences, and the
rationale for intervention and proper
administration of prescribed medications.
Nutrition, Altered: More than Body
requirements R/T high sodium, calorie,
and fat in take.

94. Nursing Diagnosis
Health Maintenance, Altered R/T lack of
exercise regimen.
Noncompliance, High Risk for R/T lack of
understanding about the seriousness of
high blood pressure, cost of therapy, side
effects of medications.

95. SUMMARY
 DEFINITION
 INCIDENCE
 ETIOLOGY
 RISK FACTORS
 PATHOPHYSIOLOGY
 C/M
 CLASSIFICATION
 PREVENTION
 STEPPED CARE
 MEDICAL MANAGEMENT
 NURSING MANAGEMENT