Hypertension is defined as a repeatedly elevated blood
pressure exceeding 140 over 90 mmHg -- a systolic pressure above 140 or a
diastolic pressure above 90. It is a persistent elevation in blood pressure
beyond 140/90mmHg.
There are 2 types of hypertension
·
Primary or Essential hypertension
·
Secondary hypertension
Ø PRIMARY
HYPERTENSION: Essential
hypertension is high blood pressure for which there is no clearly defined
aetiology. It is high blood pressure that doesn't have a known secondary cause
i.e. idiopathic hypertension.It accounts for about 95% of all cases of
hypertension.
PATHOPHYSIOLOGY
The pathogenesis of essential hypertension is a complex
interplay between genetic predisposition, lifestyle and environmental influences, disturbances in vascular structure and neuro-humoral
control mechanisms. A familial history
of hypertension alongside changes in diet in response to urbanisation and
civilisation leads to changes in endothelial structure of the blood vessels
leading to responses from the sympathetic nervous system. All these culminate
in increase in peripheral resistance and elevation of blood pressure.
Ø
SECONDARY HYPERTENSION:Secondary
hypertension is high blood pressure that's caused by another medical condition.
It is a type of hypertension which by definition is caused by an identifiable
underlying secondary cause. It arises from disorders from the kidney, artery,
heart or endocrine system.
PATHOPHYSIOLOGY
Blood
pressure is the product of cardiac output and systemic vascular resistance. It
follows that patients with arterial hypertension may have an increase in
cardiac output, an increase in systemic vascular resistance, or both. Vascular
tone may be elevated because of increased α-adrenoceptor stimulation.
Following
any secondary disease such as chronic kidney failure, primary aldosteronism ,diabetes
mellitus etc , there is an increase in pre load and changes in peripheral
vasculature which results in an increase in peripheral resistance. This
alongside the α adrenergic stimulation
further cause increase in vascular resistance with attendant stress on the
ventricles.strain on the ventricules causes hypertrophy and eventual
ventricular failure ,while severe pressure reduces tissue perfusion and end
organ damages.
ETIOLOGY
ü Idiopathic
ü Chronic
kidney disease
ü Diabetes
mellitus
ü Age
above 35
ü Obesity
ü hyperaldosteronism
ü dysrrthmias
ü aiortic
stenosis
ü Coarctation
of aorta
CLINICAL MANIFESTATIONS
§
Headaches
§
Light headedness
§
Altered or blurred vision
§
Excessive sweat
§
Bulging eyes
§
Fatigue
DIAGNOSIS
§
u/e/cr
§
ecg
§
lipid profile
§
chest xray
§
medical history
MANAGEMENT
Medical Management
The goal of
hypertension treatment is to prevent complications by achieving and maintaining
the arterial blood pressure at 140/90 mm Hg or lower.
1. Angiotensin
Converting Enzyme Inhibitors (ACE inhibitors) inhibit the activity of the
enzyme ACE, which decreases the production of angiotensin II. As a result,
blood vessels enlarge or dilate, and blood pressure is reduced. E.g.
captopril 25-150 mg PO bid or tds
2.
Angiotensin
Ii Receptor Blockers (ARBs) block the action of angiotensin II by
preventing angiotensin II from binding to angiotensin II receptors on the
muscles surrounding blood vessels. E.g.
losartan 25 -50mg once daily
3. Calcium Channel Blockersthat relax
blood vessels and increase the supply of blood and oxygen to the heart while
also reducing the heart's workload. E.g. amilodipine 2.5- 5 mg p o once daily.
4. Diuretics (thiazide) Inhibit sodium and
chloride reabsorption in the distal tubule of the kidney, resulting in
increased urinary excretion of sodium
and chloride ions and water e.g. chlorothiazide 10ml iv daily
Loop diuretics
inhibit the Na+/K+/2Cl- co-transporter in the thick ascending loop of Henle, in
the kidneys and stop the transport of sodium chloride out of the tubule into
the interstitial tissue, causing a decrease in sodium and chloride
re-absorption. E.g. furosemide 20-80 mg po bid.
Nursing Management
1. Dietary
modification; Diet should
be modified to reflect low salt content, a diet high in fruit and vegetables
was associated with a lower systolic and diastolic BP .Similarly diet low in fats
is beneficial.
2. Exercise:
increased bearable exercise should be
encouraged, as this alongside dietary modification is highly effective in
improving lipid profile, it also aids in vasodilation through the release of
endothelial nitric oxide which in turn reduces blood pressure.
3. History
Taking: obtain
comprehensive history which must also take into cognisance end organ damage,
4. Observation: closely observe and monitor blood pressure , monitor for
angina pain ,shortness of breath
5. Health
Education: Educate
patient on need to discountenance smoking, alcohol ,further teach the clients
on the need to comply with drug regimen, educate patient on the role and importance
of diet and exercise in the management
of the condition.
6. Psychological
preparation: in view of
the debilitating effect of the condition, it is imperative that the nurse
addresses the psychological concerns of the patient.
COMPLICATIONS
- § Congestive cardiac failure
- § Aneurysm
- § Cerebrovascular accident
- § Chronic kidney failure
NURSING DIAGNOSIS
- Acute pain related to increased cerebral vascular pressure evidenced by facial grimace
- Ineffective Tissue Perfusion related to impaired circulation evidenced by cyanosis .
- Knowledge deficit related to lack of information about the disease process and self-care evidenced by patient asking questions .
