SEMINAR ON HYPERTENSION, FOR NURSING STUDENTS

1. VIVEKANANDA COLLEGE OF NURSING
SEMINAR ON;
PRESENTED BY- APURVA DWIVEDI [M.Sc. Nsg. 2st Yr.]

2. 0

3. BLOOD PRESSURE
• Blood flow refers to the movement of blood through a vessel, tissue, or organ,
and is usually expressed in terms of volume of blood per unit of time.
• It is initiated by the contraction of the ventricles of the heart, Ventricular
contraction ejects blood into the major arteries, resulting in flow from regions of
higher pressure to regions of lower pressure, as blood encounters smaller
arteries and arterioles, then capillaries, then the venules and veins of the
venous system.
• This section discusses a number of critical variables that contribute to blood flow
throughout the body.

4. Conti.
• It also discusses the factors that impede or slow blood flow, a
phenomenon known as resistance.
• As noted earlier, hydrostatic pressure is the force exerted by a fluid due to
gravitational pull, usually against the wall of the container in which it is
located.
• One form of hydrostatic pressure is blood pressure, the force exerted by
blood upon the walls of the blood vessels or the chambers of the heart.

5. Conti.
• Blood pressure may be measured in capillaries and veins, as well
as the vessels of the pulmonary circulation; however, the term
blood pressure without any specific descriptors typically refers to
systemic arterial blood pressure—that is, the pressure of blood
flowing in the arteries of the systemic circulation.
• In clinical practice, this pressure is measured in mm hg and is
usually obtained using the brachial artery of the arm.

7. Introduction
• Hypertension (high BP) is a disease of vascular regulation in which the
mechanisms that control arterial pressure within the normal range are
altered.
• Predominant mechanisms of control are the central nervous system
(CNS), the renal pressor system (Renin-Angiotensin-Aldosterone System),
and extra- cellular fluid volume.
• Why these mechanisms fail is not known.
• The basic explanation is that BP is elevated when there is increased
cardiac output plus increased peripheral vascular resistance.

8. Conti.
• Hypertension is sometimes called “The Silent Killer” because people
who have it are often symptom free.
• In a national survey (1991 to 1994), 32% of people who had
pressures exceeding 140/90 mm hg were unaware of their elevated
blood pressure (burt et al., 1995a).
• Once identified, elevated blood pressure should be monitored at
regular intervals because hypertension is a lifelong condition.

9. Definition
Blood Pressure
• According to the American heart association blood pressure is the force
of blood push against the arterial wall
• Systolic blood pressure-highest arterial pressure(heart contract and
empty the blood)
• Diastolic blood pressure(heart relaxed and fill the blood)-lowest pressure.

10. Hypertension
Hypertension is defined as a systolic blood pressure (SBP) of
140 mm hg or more, or a diastolic blood pressure (DBP) of 90
mm hg or more, or taking.

11. INCIDENCE
• About 31% of the adults in the united states have hypertension, and the prevalence
increases significantly as people get older or have other cardiovascular risk factors.
• The prevalence also varies by ethnicity, with African americans having the highest
prevalence at approximately 37% (Wong, Lopez, L’italien, et al., 2007).
• In the total U.S. Population of persons with hypertension, 90% to 95% have Primary
Hypertension, high blood pressure from an unidentified cause (Oparil, Zaman &
Calhoun, 2003).
• The remaining 5% to 10% of this group have Secondary Hypertension, high blood
pressure related to identified causes.

12. Classification Of Hypertension
Classification SBP(mmhg) DBP(mmhg)
Normal 120 80
Prehypertension 120–139 80-89
Stage 1 hypertension 140–159 90-99
Stage 2 hypertension 160 100
Stage 3 hypertension (hypertensive
emergency)
≥180 ≥110
Isolated systolic hypertension ≥140 <90

13. Risk Factor For
Hypertension

14. Modifiable Factor
Poor Socio
Economic
Factor
Lower
education
Stress
Sedentary
life style
Elevated
serum
cholesterol
Alcohol
Dietary intake
of increased
sodium
decreased
potassium
Tobacco
Smoking

15. Non Modifiable Factor
Age. : male-34%,Female-
30%
Certain Non
communicable disease
Family history
Ethnicity
Gender
Race

16. Types of hypertension

17. ON THE BASIS OF TYPES
Systolic
hypertension
Diastolic
hypertension

18. ON THE BASIS OF ETIOLOGY
Primary
hypertension
Secondary
hypertension

19. ON THE BASIS OF SEVERITY
Boaderline
hypertension
Benign
hypertension
Malignent
hypertension

20. WHITE COAT HYPERTENSION
Sometimes, a patient may have elevated blood pressure in the
doctors office, but not at any other time. This is called white coat
hypertension and may be credited to a person feeling anxious
around all the doctors in white coat. In this case a doctor may
prescribe a 24 hr. Ambulatory monitoring.

21. Sub types
Isolated systolic
hypertension
Resistant
hypertension

22. Causes
Primary hypertension
Primary (essential or idiopathic) hypertension is elevated BP without
an identified cause
When the diastolic pressure is 90 mm hg and/or the systolic pressure
is 140 mm hg or higher and other causes of hypertension are absent,
the condition is said to be primary hypertension.
Accounts for 90% to 95% of all cases of hypertension.

23. Conti.
Although the exact cause of primary hypertension is unknown,
several contributing factors, including;
Greater than ideal body weight,
diabetes mellitus, and excessive
alcohol consumption have been
identified.
Overproduction of
sodium-retaining
hormones and
vasoconstrictors,
Increased
SNS
activity,
Increased
sodium
intake,

24. Secondary Hypertension
Secondary hypertension is the term used to signify high
blood pressure from an identified cause.
These may be due to :-

25. Renal Disease
Endocrine Disorders
Like Cushing's
Syndrome
Neurological Disorders
Like Brain Tumours And
Head Injury
Sleep Apnoea
Medications Like Oral
Contraceptive Pills,
NSAID, And Cocaine
Cirrhosis Of
Liver
Food Subtracts- Sodium
Chloride, Ethanol,
Licorice.

26. Isolated Systolic Hypertension
• Isolated systolic hypertension is defined as an average
SBP≥140 mmhg with an average DBP< 90 mmhg.
• Although it is occur in younger adults, it is much more
common in older adults.

27. Pathophysiology
The Normal Blood Pressure Is Maintained By Four Mechanisms
 Sympathetic Nervous System Activities
 Activities Of Vascular Endothelium
 Activities Of Renal System
 Activities Of Endocrine System

28. Sympathetic Nervous System Activities
When the BP se the activation of SNS will occur.
The sed SNS activity ses the heart rate and cardiac contraction.
sed heart rate and cardiac contraction produce vasoconstriction in peripheral
arterioles and promotes the release of renin from kidney.

29. Activities Of Vascular
Endothelium

30. Activities Of Endocrine System
Angiotensin-II is
stimulated in the
adrenal cortex, and
secret aldosterone.
Aldosterone
stimulate the kidneys
to retain sodium and
water.
The BP and cardiac
output will get
increases.

31. Schematic Of
The
Pathophysiology Of
Hypertension
Sympathetic
activation
Cardiac
output
Peripheral
resistance
Blood
pressure
HR Stroke
volume
Aldosterone
AT II
Renin
Plasma
volume

33. Diagnostic Evaluation

34. • ECG: To determine effects of hypertension on the heart (left
ventricular hypertrophy, ischemia) or presence of underlying
heart disease

35. • Chest x-ray: may show cardiomegaly.

36. • Proteinuria, elevated serum blood urea nitrogen (BUN), and
creatinine levels: Indicate kidney disease as a cause or effect
of hypertension; first voided urine microalbumin or spot urine for
albumin-creatinine ratio are earlier indicators

37. • Serum potassium: decreased in
primary hyper-aldosteronism; elevated
in Cushing's syndrome, both causes of
secondary hypertension

38. • Urine (24-hour) for
catecholamines:
increased in
pheochromocytoma
(PCC) (hormone secreting
tumor that can occur in
the adrenal gland)

39. • Renal scan to detect renal
vascular diseases; may include
ingestion of captopril, an ACE
inhibitor, to detect its effect on
renal blood flow.

40. • Renal duplex imaging
to identify renal artery
stenosis

41. • Outpatient ambulatory
BP measurements

42. • Tests for essential
hypertension are generally
done first, unless specific
signs and symptoms of
secondary hypertension
are present.

43. Management
Lifestyle modifications
• Lose weight if body mass index is greater
than or equal to 25.
• Limit alcohol no more than 1 oz alcohol
daily for men, 0.5 oz for women.
• Get regular aerobic exercise equivalent to
30 to 45 minutes of brisk walking most
days.
• Cut sodium intake to 2.4 g or less per day.

44. Conti.
• Include recommended daily allowances of
potassium, calcium, and magnesium in diet.
This can be accomplished through following
the DASH diet (dietary approaches to stop
hypertension) rich in fruits, vegetables, low-fat
dairy products, and fibre and low in saturated
and total fat.
• Smoking cessation.
• Reduce dietary saturated fat and cholesterol.

45. Conti.
• Consider reducing coffee intake (5 cups per day has
been shown to increase bp in hypertensive men).
• If, despite lifestyle changes, BP remains at or above
140/90 mm hg (or is not at optimal level in the
presence of other cardiovascular risk factors) over 3
to 6 months, drug therapy should be initiated.
• If BP is extremely elevated or in presence of
cardiovascular risk factors, single drug therapy may
be given.

47. Drug therapy
Considerations in selecting therapy include:
 Race: blacks respond well to diuretic therapy; whites respond well to ACE
inhibitors.
 Age: some adverse effects may not be tolerated well by elderly people.
Diuretics are typically the first drug prescribed.
 Concomitant diseases and therapies—some agents also treat migraines,
benign prostatic hyperplasia, heart failure; have beneficial effects on conditions
such as renal insufficiency; or have adverse effects on such conditions as
diabetes or asthma.

48. Conti.
 Quality-of-life impact—tolerance of adverse effects.
 Economic considerations—newer agents very expensive.
 Doses per day—may be compliance problem.

49. Agents include:
• Diuretics: lower BP by promoting urinary excretion of water and sodium
to lower blood volume
• Beta-adrenergic blockers: lower BP by slowing the heart and reducing
cardiac output as well as release of renin from the kidneys
• Alpha-receptor blockers: lower BP by dilating
• Peripheral blood vessels and lowering peripheral vascular resistance.
Research has indicated these medications provide little protection
against heart failure.

50. Conti.
• Central alpha agonists: lower BP by diminishing sympathetic outflow
from the brain, thereby lowering peripheral resistance.
• Peripheral adrenergic agents: inhibit peripheral adrenergic release of
vasoconstricting catecholamines such as norepinephrine.
• Combined alpha and beta-adrenergic blockers: work through alpha
and beta receptors.

51. CONTI.
• Ace inhibitors: lower bp by blocking the enzyme that converts
angiotensin i to the potent vasoconstrictor, angiotensin ii.
• These drugs also raise the level of bradykinin, a potent
vasodilator, and lower aldosterone levels.
• Angiotensin receptor blockers: similar in action to ACE
inhibitors.

52. Conti.
• Calcium antagonists (calcium channel blockers): stop the movement
of calcium into the cells; relax smooth muscle, which causes vasodilation;
and inhibit reabsorption of sodium in the renal tubules.
• Direct vasodilators: smooth muscle relaxants that primarily dilate
arteries and arterioles.
• Direct renin inhibitors: suppress the entire renin-angiotensin-
aldosterone system.

53. Conti.
If hypertension is not controlled with the first drug within 1 to 3 months, three
options can be considered:
• If the patient has faithfully taken the drug and not developed adverse effects, the
dose of the drug may be increased.
• If the patient has had adverse effects, another class of drugs can be substituted.
• A second drug from another class could be added. If adding the second agent
lowers the pressure, the first agent can be slowly withdrawn or, if necessary,
combination therapy can be continued.

54. Conti.
• The best management of hypertension is to use the fewest drugs at the
lowest doses while encouraging the patient to maintain lifestyle changes.
• After BP has been under control for at least 1 year, a slow, progressive
decline in drug therapy can be attempted. However, most patients need to
resume medication within 1 year.
• If the desired BP is still not achieved with the addition of a second drug, a
third agent or a diuretic or both (if not already prescribed) could be added.

55. Complications
• Angina pectoris or MI due to decreased coronary perfusion
• Left ventricular hypertrophy and heart failure due to consistently
elevated aortic pressure
• Renal failure due to thickening of renal vessels and diminished
perfusion to the glomerulus
• TIAs, stroke, or cerebral haemorrhage due to cerebral ischemia
and arteriosclerosis
• Retinopathy
• Accelerated hypertension

56. Nursing Assessment
Nursing History
Query the patient about the following:
1. Family history of high BP
2. Previous episodes of high BP
3. Dietary habits and salt intake
4. Target organ disease or other disease processes that may place the patient in a high-
risk group—diabetes, CAD, kidney disease and cigarette smoking
5. Episodes of headache, weakness, muscle cramp, tingling, palpitations, sweating,
vision disturbances.

57. Conti.
6. Medication that could elevate BP:
a) Hormonal contraceptives, steroids
b) NSAIDS
c) Nasal decongestants, appetite suppressants ,tricyclic
antidepressants
Other disease processes, such as gout, migraines, asthma, heart
failure, and benign prostatic hyperplasia, which may be helped or
worsened by particular hypertension drugs.

58. Physical Examination
 Auscultate heart rate and palpate peripheral pulses; determine
respirations.
 If skilled in doing so, perform funduscopic examination of the eyes for
the purpose of noting vascular changes. Look for oedema, spasm, and
haemorrhage of the eye vessels. Refer to ophthalmologist for definitive
diagnosis.
 Examine the heart for a shift of the point of maximal impulse to the left,
which occurs in heart enlargement.

59. Conti.
 Auscultate for bruits over peripheral arteries to determine the
presence of atherosclerosis, which may be manifested as
obstructed blood flow.

60. Blood Pressure Determination
 Measure the BP of the patient under the same conditions each
time.
 Avoid taking BP readings immediately after stressful or taxing
situations. Wait 30 minutes after patient has smoked.
 Have the patient assume position of comfort and remain silent.
 Make sure feet are on the floor or otherwise supported.

61. Conti.
 Support the bared arm; avoid constriction of arm by a rolled sleeve. Use a BP
cuff of the correct size.
a. The bladder within the cuff should encircle at least 80% of the patient’s arm.
b. Many adults will require a large cuff
c. Two or more readings separated by 2 minutes should be averaged.
 Be aware that falsely elevated bps may be obtained with a cuff that is too
narrow; falsely low readings may be obtained with a cuff that is too wide.
 Auscultate and record precisely the systolic and diastolic pressures based on
korot koff sounds.

62. Conti.
 Systolic:- the pressure within the cuff indicated by the level of the mercury
column at the moment when the first clear, rhythmic pulsatile sound is heard
(Phase 1).
 First diastolic:- the pressure within the cuff indicated by the level of the
mercury column at the moment when the sound becomes muffled (Phase 4).
 Second diastolic:- the pressure within the cuff at the moment the sound
disappears (i.e., the onset of silence) (Phase 5).
• Phases 2 and 3 are less distinct sounds produced between systolic and first
diastolic and are not identified clinically or recorded.

63. Nursing Diagnoses
 Deficient knowledge regarding the relationship between the
treatment regimen and control of the disease process.
 Ineffective therapeutic regimen management related to medication
adverse effects and difficult lifestyle adjustments.

64. Nursing Intervention
Providing basic education
Explain the meaning of high BP, risk factors, and their influences on the
cardiovascular, cerebral, and renal systems.
Stress that there can never be total cure, only control, of essential
hypertension; emphasize the consequences of uncontrolled hypertension.
Stress the fact that there may be no correlation between high bp and
symptoms; the patient cannot tell by the way he or she feels whether bp is
normal or elevated.

65. Conti.
Have the patient recognize that hypertension is chronic and requires persistent therapy
and periodic evaluation. Effective treatment improves life expectancy; therefore, follow-
up health care visits are mandatory.
Present a coordinated and complementary plan of guidance.
Inform the patient of the meaning of the various diagnostic and therapeutic activities to
minimize anxiety and to obtain cooperation.
Solicit the assistance of the patient’s spouse, family, and friends—provide information
regarding the total treatment plan.
Be aware of the dietary plan developed for this particular patient.

66. Conti.
Explain the pharmacologic control of hypertension.
Explain that the drugs used for effective control of elevated BP will likely
produce adverse effects.
Warn the patient of the possibility that orthostatic hypotension may occur initially
with some drug therapy.
Instruct the patient to get up slowly to offset the feeling of dizziness.
Encourage the patient to sit or lie down immediately if feeling faint.

67. Conti.
Alert the patient to expect initial effects, such as anorexia, light
headedness, and fatigue, with many medications.
Inform the patient that the goal of treatment is to control BP, reduce
the possibility of complications, and use the minimum number of
drugs with the lowest dosage necessary to accomplish this.
Educate the patient to be aware of serious adverse effects and
report them immediately so that adjustments can be made in
individual pharmacotherapy.

68. Conti.
Note that dosages are individualized therefore, they may need to be
adjusted because it is often impossible to predict reactions.
Warn the patient on vasodilating drugs to use caution in certain
circumstances that produce vasodilation—a hot bath, hot weather, febrile
illness, consumption of alcohol—which may exacerbate bp reduction.
Warn patients that bp is often decreased when circulating blood volume is
reduced—as in dehydration, diarrhoea, haemorrhage—so BP should be
monitored closely and treatment adjusted.

69. Encouraging Self-management
1. Enlist the patient’s cooperation in redirecting lifestyle in keeping with the guidelines of therapy,
acknowledge the difficulty, and provide support and encouragement.
2. Develop a plan of instruction for medication self- management:-
a. Plan the patient’s medication schedule so that they are given at proper and convenient times;
set up a daily checklist on which the patient can record the medication taken.
b. Be sure the patient knows the generic and brand names for all medications and throws away
old medications and dosages so they will not be mixed up with current medications.
c. Instruct the patient regarding proper method of taking bp at home and at work if health care
provider so desires. Inform patient of desired range and the readings that are to be reported.
d. Determine recommended dietary plans and provide dietary education as appropriate.

70. Evaluation: Expected Outcomes
• Demonstrates increased knowledge about high BP,
medication effects, and prescribed therapeutic activities
• Takes medications, keeps follow-up appointments

71. Summary

72. Conclusion

73. THANK YOU..