ESSENTIAL HYPERTENSION

Lecture plan
• Definition
• Etiology
• Clinical presentation
• Diagnosis
• Management
• Sustained high blood pressure is known
as hypertension. Blood pressure 140/90,
at least two readings on separate
occasion is considered hypertension.
ETIOLOGY

• Primary (Essential) hypertension In about

95% of cases no cause of hypertension
can be identified, and this form of
hypertension is called primary or essential
hypertension. The onset of essential
hypertension is usually between ages 25
and 55 years; it is uncommon before age
20.
 Secondary hypertension

• In about 5% of cases, cause of

hypertension can be discovered. This
form is called secondary hypertension.
Most of the patients are young and cause
of hypertension is usually renal failure,
renal artery stenosis, or coarctation of
aorta.
• Secondary hypertension is more likely and
investigations should be performed to rule out
secondary causes in the following patients:
• Onset of hypertension below age 20 or after 50
years.
• Patients with clinical or biochemical features
of specific disorder.
• Patients who have previously controlled
hypertension but now become refractory to
treatment.
• Accelerated hypertension.
 Precipitating factors

• Genetic factors: children of hypertensive

patients are more prone to develop hypertension.
• Obesity, lack of exercise
• Heavy alcohol intake
• Excessive salt intake
• Cigarette smoking
• Polycythemia
• NSAIDs increase blood pressure about 5mmHg
• Low potassium intake
• Sympathetic over activity
• Insulin resistance
• Symptomatic or secondary hypertension
is not an independent disease, and is
accompanied by another disease.
• There are several causes of secondary
hypertension.
Renal disease

• Renal vascular disease

• Parenchymal renal disease, particularly
glomerulonephritis
• Polycystic kidney disease
Endocrine disease
• Pheochromocytoma
• Cushing`s syndrome
• Primary hyperaldosteronism Conn`s )
• Hyperparathyroidsm
• Thyrotoxicosis
• Congenital adrenal hyperplasia
Drugs

• Oral contraceptives containing estrogens

• Anabolic steroids
• Corticosteroids
• NSAI drugs
• Sympathomimetic agents
Others

• Alcohol
• Coarctation of aorta
• Pregnancy(pre- eclampsia)
 Renal vascular disease
• Results from fibromascular dysplasia in
young people due to atheroma of renal
artery in elderly.
• Renal vascular disease should be suspected
• If the onset hypertension below age 20 and
after 50 years
• If there are epigasric or renal artery bruit
• If there is abrupt deterioration of renal
functionafter administration of ACE
inhibitors(in case of bilateral renal artery
stenosis).
• If there is atherosclerotic disease of aorta or
peripheral arteries.
• Renal causes of hypertension are often
associated with sodium and water
retention with high plasma concentration of
renin.
• Renin causes production of potent
vasoconstrictor agent angiotensin II that
stimulates aldosterone secretion.
• Salt and water retention produces
hypertension.
 Clinical features
• Mostly asymptomatic discovered on
routir3g examination or when a
complication occurs.
• Suboccipital pulsating headache,
characteristically occurring early in the
morning and subsiding during the day is
characteristic, but any type of headache
may occur.
• Accelerated hypertension is associated
with somnolence, confusion, visual
disturbances, nausea and vomiting (called
hypertensive encephalopathy).
• Symptoms of secondary causes of
hypertension if present.
• For example pheocromocytoma may
present with episodic hypertension along
with anxiety, palpitation, profuse
perspiration, pallor, tremor and nausea and
vomiting.
• Symptoms of complications such as heart
failure, stroke, renal failure etc.
 Complications of hypertension
CNS
• STROKE
• Hypertensive encephalopathy
• Subarachnoid hemorrhage
• Multi-infarct dementia.
 RETINA
Retinal changes are graded as following:

• Grade 1: tortuosity of the retinal arteries with

increased reflectiveness (silver wiring).
• Grade II: Grade I plus appearance of
arteriovenous nipping produced when
thickened retinal arteries pass over the retinal
vein.
• Grade III: grade II plus flame-shaped
hemorrhages and soft “cotton wool”
exudates due to small infarcts.
• Grade IV: Grade III plus papilledema
• (blurring of the margins of the optic disc).
 HEART

• Left ventricular hypertrophy and ultimately

left ventricular failure.
• Ischemic heart disease.
• Aortic dissection
 KIDNEYS

• Long standing hypertension may cause

nephrosclerosis (hypertensive
nephropathy) that
 EXAMINATION OF HYPERTENSIVE
PATIENT
• General inspection
• Look for evidence of associated diseases
such as: round face and truncal obesity of
Cushing’s syndrome.
• Acromegaly, polycythemia and uremia.
• Pulse
• Feel radial pulse and examine for radio
femoral delay and radioardial asymmetry.
Blood pressure

• Take blood pressure, with patient lying and

standing.
• A rise in diastolic blood pressure on
standing occurs typically in essential
hypertension;
• a fall in BP on standing may suggest a
secondary cause.
• Face
• : -Inspect conjunctiva for congestion
(polycythemia).

• Auscultation of lung
• Auscultate for basal crepts (for heart
failure).
 ANTI-HYPERTENSIVE DRUGS

• DIURETICS
• Mechanism of action
• Decreasing plasma volume via renal
excretion of sodium and water, therefore
reducing cardiac output.
• Reduction of peripheral vascular
resistance.
Advantages

• They are more effective in older individuals,

obese, blacks, with CHF or chronic renal
failure.
• Relatively more effective in smokers than in
non-smokers.
• Most effective agent to reduce systolic
hypertension.
• Inexpensive, once per day dosing.
• Diuretics alone control hypertension in 50%
of cases.
Side effects
Metabolic
-Hypokalemia, hyponatremia
-Hyperglycemia, hypercholesterolemia,
• Impotence, skin rash and muscle cramp
• Ototoxicity by loop diuretics with IV dosing
• Gynaecomastia in men and breast
tenderness in woman by spironolocton
 BETA - BLOCKERS Mechanism of
action

• They are effective in hypertension

because they decrease the heart rate and
cardiac output by competitive inhibition of
the effects of I catecholamine at beta-
adrenergic receptors.
• They also inhibit rennin. Beta-blockers are
effective as single therapy in about 50% of
cases of hypertension.
 Types of beta - blockers 1

• Cardioselective beta-blockers
• They are relatively specific to the cardiac
beta-1 receptors in low doses but in high
doses they do not ; remain cardioselective
and block beta - 2 receptors that are also
located in the bronchi and vasculature.
• (Blockage of beta-2 receptor causes
bronchospasm, cold extremities).
 Non cardioselective beta-blockers
• They block both beta-1 and beta-2
receptors therefore along with decreasing
heart rate and cardiac output they also
cause bronchospasm and cold extremities.
• Propranolol (Inderal), timolol and nadolol
are non-selective beta-bockers.
• Labelalol blocks alpha and beta both types
of - receptors.
 Advantages of beta blockers

• Ideal in hypertensive patients with angina

or previous myocardial infarction.
• Favored in young and in patients with
migraine.
Side effects

• • Fatigue, and impotence

• Insomnia, depression and nasal congestion
• Adverse effects on lipid profile: increased
triglyceride and decreased HDL.
• Deterioration of CHF, bronchospasm,
hyperglycemia and peripheral vascular disease
• Abrupt withdrawal can precipitate angina.
• Heart block is also a common complication;
therefore monitor pulse for bradycardia.
•
CALCIUM CHANNEL ANTAGONISTS

• Mode of action
• They decrease blood pressure by
arteriolar vasodilatation by selectively
blocking the slow inward calcium
channels in the vascular smooth muscle
cells.
• Classes of calcium antagonists Non-
dithydropyridine agents
• Verapamil (Calan)
• Diltiazem (Dilzem)
• Verapamil has negative inotrpic effect and
reduces heart rate by depressing SA node
and AV node.
• Therefore it should not be combined with
beta - blocker, combination of both may lead
to heart block.
• Diltiazem has 50% effect on heart and 50% on
peripheral vessels causing vasodilatation, it
may be combined with beta-blocker but in
small dose and very cautiously.
• Dihydropyridines
• Amiodipine (Norvasc)
• Nifedipine (Adalat)
• Felodipine (Plendil)
• Drugs in this group are mainly vasodilator
and minimal effect on heart, therefore they
can be combined with beta blockers.
• They should not be used alone in angina
because peripheral vasodilatation causes
reflex tachycardia that may aggravate
angina.
 Advantages of calcium channel blockers

• They are particularly useful when

hypertension coexists with angina.
• They are preferable in black and old
patients.
• They are also effective in isolated systolic
hypertension.
 Side effects

• Headache, flushing, palpitations and

peripheral edema (more common with
felodipine, nifedipine and amlodipine).
• Bradycardia and constipation (more
common with verapamil and to lesser
extent with diltiazem.
• Exacerbation of heart failure due to
negative inotropic effects.
• Heart block is not an uncommon
complication of verapamil (and beta-
blockers); always monitor the pulse and
educate the patient that these drugs are
not for indefinite period.
ANGIOTENSIN - CONVERTING ENZYMES
Mode of action
• They block the conversion of angiotensin I
to angiotensin II (a vasoconstrictor)
producing arterial and venous dilation.
 Advantages
• Useful in hypertension complicated by CHF.
• Helpful in prevention of diabetic nephropathy
• Effective in decreasing left ventricular
hypertrophy.
• Relatively less side effects.
• Fosinopril (Monopril) has dual route of
excretion (liver & kidney) therefore preferred
over other ACE inhibitors in case of renal
insufficiency.
•
 Side effects

• Less effective in elderly and predominant

systolic hypertension.
• Hyperkalemia may occur especially in
patients with diabetes or renal insufficiency.
• First dose hypotension.
• Chronic dry cough due to bronchial or
laryngeal irritation more often with
captopril and enalapril.
• Skin rash, taste disturbance and
leukopenia: more often with captopril.
• Worsening of renal function if given in
patient with bilateral renal artery stenosis.
• Angioedema: an uncommon but
potentially dangerous side effect. Patient
presents with acute dyspnea.