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Hypertension

By
Elwin Shawa
MSN
Outcomes
• Define HTN
• Describe the blood pressure regulation
• Describe the classification of HTN
• Identify the types of HTN and its causes
• Describe the pathophysiology of HTN
• List the clinical manifestations of HTN
• List the complications of HTN
• Describe the diagnostic studies
Outcomes ..
• Explain the lifestyle modifications as one way
of HTN management.
• Describe the drug therapy used in HTN
• Explain the nursing management
• Define accelerated HTN
• Describe the clinical manifestations of AHTN
• Describe the management of AHTN
• Explain the nursing interventions.
Definition
• A systolic blood pressure ( SBP) >139 mmHg
and/or a diastolic (DBP) >89 mmHg.
• Based on the average of two or more properly
measured, seated BP readings.
• On each of two or more clinic visits.
• It is important medical and public health issue
Normal regulation of BP
• Short-term regulation:
– Baroreceptor reflexes.
– Chemoreceptor reflexes.
– Atrial reflexes.
– CNS-ischemic response.

• Long-term regulation:
– Role of the kidney.

• Intermediate regulation:
– Capillary fluid shift
Classification of HTN
Prehypertension
• SBP >120 mmHg and <139mmHg and/or

• DBP >80 mmHg and <89 mmHg.

• Prehypertension is not a disease category


rather a designation for individuals at high risk
of developing HTN.
Pre-HTN..
• Individuals who are pre-hypertensive are not
candidates for drug therapy but
• Should be firmly and unambiguously advised
to practice lifestyle modification
• Those with pre-HTN, who also have diabetes
or kidney disease, drug therapy is indicated if
a trial of lifestyle modification fails to reduce
their BP to 130/80 mmHg or less.
Isolated Systolic Hypertension
• ISH defined as an average SBP ≥140mmHg
coupled with an average DBP ˂90mm Hg.
• Much common in older adults because of loss
of elasticity in large arteries from
atherosclerosis.
• An SBP greater than 140 mmHg is a more
important risk factor for cardiovascular
diseases than an elevated DBP in individual
older than 50 yrs
Hypertensive Crises
• Hypertensive Urgencies: No progressive
target-organ dysfunction. (Accelerated
Hypertension)

• Hypertensive Emergencies: Progressive end-


organ dysfunction. (Malignant Hypertension)
Hypertensive Urgencies
• Severe elevated BP in the upper range of
stage II hypertension.
• Without progressive end-organ dysfunction.
• Examples: Highly elevated BP without severe
headache, shortness of breath or chest pain.
• Usually due to under-controlled HTN.
Hypertensive Emergencies
• Severely elevated BP (>180/120mmHg).
• With progressive target organ dysfunction.
• Require emergent lowering of BP.

• Examples: Severely elevated BP with:


Hypertensive encephalopathy
Acute left ventricular failure with pulmonary
edema
Acute MI or unstable angina pectoris
Dissecting aortic aneurysm
Types of Hypertension
• Primary HTN:
also known as essential HTN.
accounts for 95% cases of HTN.
no universally established cause known.
• Secondary HTN:
less common cause of HTN ( 5%).
secondary to other potentially rectifiable
causes.
Causes of Secondary HTN
• Common
– Intrinsic renal disease
– Renovascular disease
– Mineralocorticoid excess
• Uncommon
– Pheochromocytoma
– Glucocorticoid excess
– Coarctation of Aorta
– Hyper/hypothyroidism
Pathophysiology of Primary
Hypertension
• There must be an increase in either Co or SVR
• The hemodynamic hallmark of HTN is
persistently increases SVR.
• Factors known to be related to development
of primary HTN are;
– Age, alcohol, cigarette smoking, DM, elevated
serum lipids, excessive dietary sodium, gender,
Family history, obesity, sedentary lifestyle, and
stress.
Pathophysiology …
• Heredity:
– It has a very small contribution in general
population but environmental factors have a role
in contributing to development of high BP
• Water and sodium retention:
– A high sodium intake may activate a number of
pressor mechanisms and cause water retention
– Certain demographic factors such as obesity,
increasing age, diabetes, and CKD are associated
with BP salt sensitivity
Pathophysiology …
• Altered Renin-Angiotensin mechanism:
– High plasma renin activity (PRA) results in
increased conversion of angiotensinogen to
angiotensin I.
– Angiotensin II causes direct arteriolar constriction,
promotes vascular hypertrophy, and induces
aldosterone secretion.
– Thus it may contribute to development and
maintenance of hypertension.
Pathophysiology …
• Stress and increased SNS activity:
– Arterial pressure is influenced by factors such as
anger, fear, and pain.
– Physiologic response to stress may persist to a
pathologic degree, resulting in prolonged increase
in SNS activity.
– Increased SNS stimulation produces increased
vasoconstriction, HR, and renin release.
– All these may lead to elevated BP
Pathophysiology …
• Insulin resistance and hyperinsulinemia:
– Insulin resistance is a risk factor for development
of hypertension and cardiovascular disease.
– High insulin concentration in the blood stimulates
SNS activity and impairs oxide-mediated
vasodilation.
– Additional pressor effects of insulin include
vascular hypertrophy and increased renal sodium
reabsorption.
Pathophysiology …
• Endothelial cell dysfunction:
– Some hypertensive people have a reduced
vasodilator response to nitric oxide.
– Endothelin produces pronounced and prolonged
vasoconstriction.
Clinical manifestations
• Is often asymptomatic until it becomes severe
and organ disease has occurred.
• They may include:
– Fatigue
– Reduced activity tolerance
– Dizziness
– Palpitations
– Angina
– dyspnea
Clinical complications
• Hypertensive heart disease
– CAD
– Left ventricular Hypertrophy
– Heart Failure
• Cerebrovascular disease
– Stroke
– Hypertensive encephalopathy
• PAD
• Nephrosclesis
– End stage renal disease
• Retinal Damage
Diagnostic studies
• ECG to determine effects of hypertension on
the heart or presence of underlying heart
disease
• Chest X-ray may show cardiomegaly
• Proteinuria, elevated serum blood urea
nitrogen (BUN), and creatinine levels indicate
kidney disease as a cause or effect of
hypertension
Diagnostic studies …
• Serum potassium; decreased in primary
hyperaldosteronism; elevated in Cushing's
syndrome, both causes of secondary
hypertension
• Urine (24-hour) for catecholamines increased
in pheochromocytoma
• Outpatient ambulatory BP measurements
Management
Lifestyle Modifications
• Lose weight if body mass index is greater than or
equal to 25.
• Limit alcohol.
• 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.
• Smoking cessation.
• Reduce dietary saturated fat and cholesterol.
• Consider reducing coffee intake
Drug therapy
• Include the following:
– Diuretics
– Adrenergic (SNS) inhibitors
– Direct vasodilators
– Angiotensin inhibitors
– Calcium channel blockers
• They act by decreasing the volume of
circulating blood and reduce SVR
Stepped antihypertensive treatment
approach
• Step 1: Hydrochlorothiazide (HCT)25 mg each
morning, or Bendrofluazide 2.5 mg morning
• Step2: HCT 25 mg od and Amlodipine 5-10mg od
(or Nifedipine 10-20mg bd).
• Step 3: HCT 25mg od, Amlodipine 5-10mg od and
Enalapril 10-20mg od (or Captopril 12.5-50mg
tds)
• Step 4: HCT 25mg od, Amlodipine 5-10mg od and
Enalapril 10-20mg od and Atenolol 50-100mg od
(or Propranolol 40-80mg)
• Step 5: Refer to medical specialist
Nursing Assessment
• Nursing History
– Family history of high BP
– Previous episodes of high BP
– Dietary habits and salt intake
– Target organ disease or other disease processes that
may place the patient in a high-risk group e.g.
diabetes, CAD, kidney disease
– Cigarette smoking
– Episodes of headache, weakness, muscle cramp,
tingling, palpitations, sweating, vision disturbances
Nursing Assessment…
• Physical Examination
– Auscultate heart rate and palpate peripheral
pulses; determine respirations.
– Perform funduscopic examination of the eyes for
the purpose of noting vascular changes. Look for
edema, spasm, and hemorrhage of the eye
vessels.
– Examine the heart for a shift of the point of
maximal impulse to the left, which occurs in heart
enlargement.
Nursing Assessment…
– Auscultate for bruits over peripheral arteries to
determine the presence of atherosclerosis, which
may be manifested as obstructed blood flow.

– Determine mentation status by asking patient


about memory, ability to concentrate, and ability
to perform simple mathematical calculations.
Nursing Diagnosis
• Ineffective health maintenance related to lack
of knowledge of pathology, complications, and
management of hypertension
• Anxiety related to complexity of management
regimen, possible complications, and lifestyle
changes associated with HTN
• Ineffective Therapeutic Regimen Management
related to medication adverse effects and
difficult lifestyle adjustments
Nursing Diagnosis..
• Sexual dysfunction related to side effects of
antihypertensive drugs.
• Ineffective tissue perfusion related to
complications of HTN (cerebral,
cardiovascular, renal and retinal)
Nursing Interventions
• 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.
– Have the patient recognize that hypertension is
chronic and requires persistent therapy and
periodic evaluation.
Nursing Interventions…
– Explain the pharmacologic control of
hypertension.
• Encouraging Self-Management
– Enlist the patient's cooperation in redirecting
lifestyle in keeping with the guidelines of therapy,
acknowledge the difficulty, and provide support
and encouragement.
– Develop a plan of instruction for medication self-
management. Include medication schedule
Nursing Interventions…
– Instruct the patient regarding proper method of
taking BP at home and at work.
– Inform patient of desired range and the readings
that are to be reported.
– Determine recommended dietary plans and
provide dietary education as appropriate.
ACCELERATED HYPERTENSION
• Accelerated hypertension, also called malignant
hypertension.
• Occurs when the BP elevates extremely rapidly,
threatening one or more of the target organs:
brain, kidney, heart.
• Elevated diastolic pressure causes strain on
arterial wall, thickening and calcification of
arterial media (sclerosis) and narrowed blood
vessel lumen.
• Sclerosis of vessels; increased wall permeability
and deposits placed on intima and media of
vessels causing cerebral, myocardial, or renal
ischemia.
Clinical Manifestations
• Brain effects: • Kidney effects:
– Encephalopathy – Decreased blood flow,
– Stroke vasoconstriction
– Progressive headache, – BUN elevated
stupor, seizures – Plasma renin activity
• Cardiac effects: increased
– Left-sided heart failure – Urine specific gravity
lowered
– Acute MI
– Proteinuria
– Right-sided heart failure
– Renal failure
Management
• Goal is to lower BP to reduce the probability
of permanent damage to a target organ: brain,
heart, kidney.
• If diastolic BP exceeds 115 to 130 mm Hg,
clinical condition is assessed very carefully.
• Immediate hospitalization and treatment if
the following are present:
– Seizures
– Abnormal neurologic signs
– Severe occipital headache
– Pulmonary edema
Management…
• The patient is hemodynamically monitored in the
ICU.
• Antihypertensive agents are administered
parenterally. Agents include:
– Vasodilators, such as sodium nitroprusside (Nipride),
nitroglycerin (Tridil), diazoxide (Hyperstat), or
hydralazine (Apresoline).
– Adrenergic inhibitors, such as phentolamine
(Regitine), labetalol (Normodyne), and methyldopa
(Aldomet).
– The short-acting calcium antagonist nifedipine is not
presently used due to the danger of precipitating an
ischemic event.
Nursing Interventions
• Record BP frequently e.g. every 15 mins, 30
mins.
• Some drugs necessitate the taking of BP
readings every 5 minutes or more frequently
while titrating drug therapies.
• Monitor for adverse effects of medications
such as headache, tachycardia, orthostatic
hypotension.
• Measure urine output accurately.
• Observe for hypokalemia, especially if patient
is placed on diuretic therapy.
Nursing Interventions
• Observe for CNS complications.
– Note signs of confusion, irritability, lethargy, and
disorientation.
– Listen for complaints of headache, difficulty with
vision.
– Check for evidence of nausea or vomiting.
– Be alert for signs of seizure activity. Provide a safe
environment such as padded side rails. Keep bed in
lowest position.
– Reduce activity and provide quiet environment.
– Monitor ECG continuously.
– Maintain constant vigilance until BP is decreased and
stable and then begin a hypertension teaching
program.
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