Hypertension, its causes, types and management

HYPERTENTION
BY: M ABUBAKAR
MPHIL PHARMACY PRACTICE
QUAID E AZAM UNIVERSITY ISLAMABD

Hypertension
 Definition
Persistent elevation of arterial blood pressure is called
as hypertension.
High blood pressure is said to be present if it is often
at or above 140/90 mmHg.
• Blood pressure = CO X TPR
• Cardiac output = stroke vol X heart rate
 Types of BP:
• Systolic BP ( contraction).
• Diastolic BP ( relaxation).
 Normal BP
• Systolic BP = 120 mmHg
• Diastolic BP =80 mmHg

Blood Pressure SBP DBP
Classification mmHg mmHg
• Normal <120 and <80
• Prehypertensi
on
120–139 or 80–89
• Stage 1
Hypertension
140–159 or 90–99
• Stage 2
Hypertension
≥160 or ≥110
Classification of BP according to JNC
7 Its the Seventh Report of
the Joint National Committee (USA) on Prevention,
Detection, Evaluation, and Treatment of High Blood
Pressure .

Epidemiology
• Overall, approximately 20% of the world’s adults are
estimated to have hypertension, when hypertension is
defined as BP in excess of 140/90 mm Hg.
• The prevalence dramatically increases in patients older
than 60 years.
• In many countries, 50% of individuals in this age group
have hypertension.
• Worldwide, approximately 1 billion people have
hypertension, contributing to more than 7.1 million
deaths per year.
• National health surveys in various countries have shown
a high prevalence of poor control of hypertension.

 Age Distribution for Hypertension :
A progressive rise in BP with increasing age is observed. Age-related
hypertension appears to be predominantly systolic rather than
diastolic.
 Cardiovascular disease risk :
According to the JNC in individuals older than 50 years :
• SBP of greater than 140 mm Hg is a more important cardiovascular
disease risk factor than DBP.
• Beginning at a BP of 115/75 mm Hg, the cardiovascular disease
risk doubles for each increment of 20/10 mm Hg.
 Prevalence of Hypertension by Race :
• Black individuals have a higher prevalence and incidence of
hypertension than white persons .
• The prevalence of hypertension has been reported to be increased
by 50% in blacks.

 To understand ethnic influence, an understanding of the renin-
angiotensin system (RAS) is essential.
 Renin secretion is suppressed when the kidney detects that the
amount of sodium excretion is increased; thus, this is a clue to the
excess sodium in the circulation.
• Black people tend to develop hypertension at an earlier age and
have lower renin activity.
• Genetics of Hypertension :
• There are rare forms of hypertension due to genetic mutations.
• These involve mutations in the epithelial sodium channel (ENaC) in
the distal renal tubule (Liddle syndrome). involves abnormal kidney
function, with excess reabsorption of sodium and loss of potassium
from the renal tubule, and is treated with a combination of low
sodium diet and potassium-sparing diuretic drugs (e.g., amiloride)
• The inheritance of the mutation almost always results in the
development of hypertension.

Age
Gro
ups
(y)
All Races White Black
Me
n
(%)
Wo
men
(%)
Tota
l (%)
Me
n
(%)
Wo
men
(%)
Tota
l (%)
Me
n
(%)
Wo
men
(%)
Tota
l (%)
18-24 2.6 4.6 0.7 2.5 4.6 0.5 2.6 4.1 1.4
25-34 5.4 8.4 2.4 4.9 8.1 1.6 8.2 10.6 6.2
35-44 13.0 16.0 10.2 11.3 14.3 8.5 25.9 29.5 22.9
45-54 27.6 30.0 25.2 25.8 29.1 22.6 46.9 44.3 48.8
55-64 43.7 44.2 43.2 42.1 43.0 41.4 60.0 58.0 63.0
65-74 59.6 55.8 62.7 58.6 54.9 61.7 71.0 65.2 75.6
75+ 70.3 60.5 76.2 69.7 59.0 76.1 75.5 71.3 77.9
Total 23.4 23.5 23.3 23.2 23.4 23.1 28.1 27.9 28.2
National Estimates of Hypertension
National High Blood Pressure Education Program
The prevalence according to age group, sex, and race is shown in Table :

HTN in Pakistan
• The National Health Survey of Pakistan
estimated that hypertension affects 18% of
adults and 33% of adults above 45 years old.
• In another report, it was shown that 18% of
people in Pakistan suffer from hypertension
with every third person over the age of 40
increasingly effected to HTN.
• It was also mentioned that only 50% of the
people with hypertension were diagnosed and
that only half of those diagnosed were ever
treated.
• Thus, only 12.5% of hypertension cases were
adequately controlled.

MECHANISM
• The renin-angiotensin system (RAS) or the renin-
angiotensin-aldosterone system (RAAS) is a
hormone system that regulates blood pressure and water
(fluid) balance.
• When blood volume is low, juxtaglomerular cells in the
kidneys activate their prorenin and secrete renin directly
into circulation.
• Plasma renin then carries out the conversion of
angiotensinogen released by the liver to angiotensin I.
• It is subsequently converted to angiotensin II by the
enzyme angiotensin-converting enzyme found in the
lungs.

• Angiotensin II is a potent vaso-active peptide that
causes blood vessels to constrict, resulting in
increased blood pressure.
• Angiotensin II also stimulates the secretion of the
hormone aldosterone from the adrenal cortex.
• Aldosterone causes the tubules of the kidneys to
increase the reabsorption of sodium and water into
the blood.
• This increases the volume of fluid in the body, which
also increases blood pressure.
• If the renin-angiotensin-aldosterone system is
abnormally active, blood pressure will be too high.

Types of Hypertension
Primary HTN.
Secondary HTN.
• Drugs related HTN.
• Food related HTN.
• Chemicals related HTN.

Primary HTN
• It may be from an underlying pathophysiologic
mechanism of unknown cause.
• Also called essential or idopathic HTN.
• 95 % cases no cause of HTN is found.
• Uncommon before age 20.
• Onset is between ages 25 and 55 years.
• Life long persist.

Multiple factors may contribute to the development of primary
hypertension :
✓ Abnormalities involving the renin-angiotensin-aldosterone system.
✓ A pathologic disturbance in the CNS, like stress.
 Abnormalities in either the renal or tissue autoregulatory processes
for sodium excretion, plasma volume, and arteriolar constriction.
 A high sodium intake .
✓ Increased intracellular concentration of calcium, leading to altered
vascular smooth muscle function and increased peripheral vascular
resistance.
✓ A deficiency in the local synthesis of vasodilating substances in the
vascular endothelium, such as prostacyclin, bradykinin , and nitric oxide,
or an increase in production of vasoconstricting substances such as
angiotensin II.

Secondary HTN
Identifible causes revealed by :
• History
• Physical examination
• Routine lab tests.
• In 5% cases causes of HTN discovered.
• Over age 50 years.

Disease related HTN
 chronic kidney disease or renovascular disease
(2-6%) :
• Chronic glomerular nephritis.
• Polycystic kidney disease. is characterized by the presence of
multiple cysts
• chronic pyelonephritis. an inflammation of the renal
parenchyma, calyces, and pelvis.[
 Endocrine disorders (1- 2%) :
• Pheochromocytoma.
• Cushing’s syndrome.
• Hyperthyroidism.
• primary aldosteronism.

 Renovascular
HTN or muscular
disorders (1-2%) :
• coarctation of
aorta.
• Atherosclerosis.
• Renal artery
stenosis.
 Miscellenous:
• obesity
• obstructive sleep
apnea

Food related
• Sodium
• Ethanol.
 CHEMICALS
• Lead
• Mercury
• Lithium
• thallium
DRUGS
Corticosteroids.
Estrogen.
NSAID,s.
Cyclosporins.
Amphetamine.
MAOI,s.
TCA.
Cocaine.
Oral contraceptives.
Nicotine.

Diagnosis of HTN
• Take history of
patient.
• Measurement
of BP.
• Physical
examination.
• Lab findings.

PHYSICAL EXAMINATION
• Frequently, the only sign of primary hypertension on
physical examination is elevated BP.
• The diagnosis of hypertension should be based on
the average of two or more readings taken at each of
two or more clinical encounters.
• As hypertension progresses, signs of end-organ
damage begin to appear chiefly related to pathologic
changes in the :
o Eye.
o Brain.
o Heart.
o Kidneys.
o peripheral blood vessels.

• Cardiopulmonary examination may reveal :
o Abnormal heart rate or rhythm.
o Left ventricular (LV) hypertrophy.
o Third and fourth heart sounds.
• Peripheral vascular examination can detect
evidence of :
o Atherosclerosis.
o Distended veins.
• Patients with Cushing’s syndrome may have the
classic physical features of :
o Moon face
o Buffalo hump
o Hirsutism
o Abdominal striae.

• Baseline hypokalemia may suggest mineralocorticoid-
induced hypertension.
• The presence of protein, blood cells, and casts in the urine
may indicate renovascular diseases.
• Laboratory findings that should be obtained
in all patients prior to initiating drug therapy include :
o Urine analysis.
o complete blood cell count.
o serum chemistries (sodium, potassium, creatinine, fasting
glucose).
o These tests are used to assess other risk factors and to
develop baseline data for monitoring drug-induced
metabolic changes.

Tests to Evaluate the Heart.
 An electrocardiogram (ECG) :
 It records the electrical activity of the heart.
 The heart produces tiny electrical impulses which
spread through the heart muscle to make the heart
contract.
 These impulses can be detected by the ECG machine.
 The machine amplifies the electrical impulses that
occur at each heartbeat, and records them on to a
paper or computer.
 An ECG recording is painless and harmless.
 The ECG machine records electrical impulses coming
from your body, it does not put any electricity into your
body.

An exercise tolerance test (ETT) records the
electrical activity of your heart while you exercise.
How is an exercise tolerance test done?
Small electrodes are stuck on to your chest.
Wires from the electrodes are connected to the ECG machine.
You will then be asked to exercise on a treadmill or on an
exercise bike.
The exercise starts at a very easy pace, and is gradually made
more strenuous by increasing the speed and incline of the
treadmill, or by putting some resistance on the bike wheel.
While you exercise, ECG tracings are made and you will also
have your blood pressure measured from time to time.
The test lasts about 15-20 minutes.

Why is an exercise
tolerance test done?
The ETT helps to diagnose and
assess the severity of ischaemic
heart disease (sometimes called
coronary heart disease or coronary
artery disease).
This disease is due to narrowing of
the coronary arteries. It can cause
angina (chest pains) and other
problems. So, if you develop chest
pains you may be advised to have
an ETT to help to clarify the cause.

Investigations
 For Pheochromocytoma:
• Plasma norepinephrine.
• Urinary metanephrine
levels Plasma. (PCC) is a
neuroendocrine tumor of
the medulla of the
adrenal glands
 primary aldosteronism:
• urinary aldosterone levels
for Plasma renin activity.
 For renovascular disease
• Captopril stimulation test.
• Renal vein renins . Renal

A Doppler ultrasound is a noninvasive test that can be used to
estimate your blood flow through blood vessels by bouncing high-
frequency sound waves (ultrasound) off circulating red blood cells. A
regular ultrasound uses sound waves to produce images, but can't
show blood flow.
A Doppler ultrasound may help diagnose many conditions, including:
o Blood clots
o Poorly functioning valves in your leg veins, which can cause blood or
other fluids to pool in your legs (venous insufficiency)
o Heart valve defects and congenital heart disease
o A blocked artery (arterial occlusion)
o Decreased blood circulation into your legs (peripheral artery
disease)
o Narrowing of an artery.

• A Doppler ultrasound can estimate how fast blood flows by
measuring the rate of change in its pitch (frequency).
• A Doppler ultrasound test may also help your doctor check for
injuries to your arteries or to monitor certain treatments to your
veins and arteries.

CLINICAL PRESENTATIONS
• Patients with uncomplicated primary hypertension are
usually asymptomatic.
• Patients with secondary hypertension may complain of
symptoms suggestive of the underlying disorder.
 Patients with pheochromocytoma may
have a history of :
o headaches
o Sweating
o Tachycardia
o Palpitations
o Orthostatic hypertension.

 In primary aldosteronism :
Hypokalemic symptoms of muscle cramps and weakness.
 Patients with hypertension secondary to
Cushing’s syndrome may complain of :
o weight gain.
o Polyuria.
o Edema.
o Menstrual irregularities.
o Acne.
o Muscular weakness.
 Symptoms of complications such as :
o heart failure.
o Stroke.
o renal failure.

Complications of HTN
Central nervous
system
• Stroke.
• Hypertensive
encephalopathy.
• Subarachnoid
hemorrhage.
• Multi infarct dementia.
Heart :
• Ventricular hypertrophy.
• Ischemic heart disease.
• Heart failure.
Kidneys:
• Nephropathy.
• Proteinuria.
• Renal failure.
Eyes related
problems :
• Retina grade 1 to 4.
• Sometimes blindness.

Symptoms of Malignant Hypertension
In rare cases (fewer than 1% of all patients with
hypertension), the blood pressure rises quickly resulting in
malignant or accelerated hypertension.
 This is a life-threatening condition and must be treated
immediately.
 People with uncontrolled hypertension or a history of
heart failure are at increased risk for this crisis.
People should call a doctor immediately if these symptoms
occur:
o Drowsiness
o Confusion
o Headache
o Nausea
o Loss of vision
o Respiratory distress (difficulty breathing)

DESIRED OUTCOME
• The overall goal of treating hypertension is to reduce
morbidity and mortality by the possible means.
 Goal BP values are <140/90 for most patients,
but <130/80 for patients with :
o Diabetes mellitus.
o Significant chronic kidney disease.
o Coronary artery disease .
o Myocardial infarction
o Angina.

Patients with LV dysfunction have
a :
o BP goal of <120/80 mm Hg.
o SBP is a better predictor of CV risk than DBP and
must be used as the primary clinical marker of
disease control in hypertension.

Treatment
 NONPHARMACOLOGIC THERAPY
• All patients with prehypertension and hypertension should
be prescribed lifestyle modifications, including :
• Weight reduction if overweight.
• Adoption of the Dietary Approaches (eating plan) to Stop
Hypertension.
• Dietary sodium restriction .
• Regular aerobic physical activity.
• Moderate alcohol consumption (two or fewer drinks per day)
• Smoking cessation.

• Lifestyle modifications alone is appropriate therapy for
patients with prehypertension. Patients diagnosed with stage
1 or 2 hypertension should be placed on lifestyle
modifications and drug therapy concurrently.

Pharmacological therapy
• Initial drug selection depends on the degree of BP
elevation and the presence of compelling indications
for selected drugs.
• Most patients with stage 1 hypertension should be
treated initially with :
• Thiazide diuretics, angiotensin-converting enzyme
(ACE) inhibitors, angiotensin II receptor blockers
(ARB), or calcium channel blockers (CCB).
• Combination therapy is recommended for patients
with stage 2 disease, with one of the agents being a
thiazide-type diuretic unless contraindications exist.

• Diuretics, ACE inhibitors, ARBs, and CCBs are primary
agents acceptable as first-line options based on outcome data
demonstrating CV risk reduction benefits .
β-Blockers may be used either to treat a specific compelling
indication or as combination therapy with a primary
antihypertensive agent for patients without a compelling
indication.
α1-Blockers, direct renin inhibitors, central α2-agonists,
peripheral adrenergic antagonists, and direct arterial
vasodilators are alternatives that may be used in select
patients after primary agents .

Preclampsia or Eclampsia
• Hypertension occurs in approximately 8–10% of pregnancies.
• High BP in pregnancy may usually be due to pre-existing HTN or
pre-eclampsia.
• Two blood pressure measurements in six hours an apart of greater
than 140/90 mm Hg is considered diagnostic of hypertension in
pregnancy.
• Pre-eclampsia is characterised by increased blood pressure and the
presence of protein in the urine. proteinuria (≥300 mg/24 hours),
can lead to life-threatening complications for both the mother and
fetus.
• It occurs in about 5% of pregnancies and is responsible for
approximately 16% of all maternal deaths globally.
• Usually there are no symptoms in pre-eclampsia and it is detected
by routine screening.

When symptoms of pre-eclampsia occur the most
common are :
• Headache
• Visual disturbance .
• Vomiting.
• Epigastric pain
• Edema.
Eclampsia can occasionally progress to life-threatening
which is a hypertensive emergency and has several
serious complications including :
• vision loss
• cerebral edema
• seizures or convulsions
• renal failure
• pulmonary edema
• intravascular coagulation (a blood clotting disorder)

 TREATMENT :
• Methyl dopa is safe in pregnancy.
• Beta blockers are effective and safe in 3rd trimester of
pregnancy.
• Modified release preparations of nifidipine are also
used in HTN in pregnancy.
• IV labetolol or hydralazine can be used to control
hypertensive crisis.
• Mg sulphate is drug of choice to prevent seizures in
preclampsia.
• ACE inhibitors and ARB,s are contraindicated
because they cross placenta.

HTN with liver disease
• All hypertensive drugs can be used except methyldopa.
HTN with gout
All hypertensive drugs can be used.
But all diuretics can increase serum uric acid level.
So diuretics should be avoided if possible.

White coat HTN also known as white coat
syndrome :
It is a phenomenon in which patients exhibit elevated blood pressure in
a clinical sitting but not in other sittings.
It is believed that this is due to the anxiety some people experience
during a clinic visit.
In general, individuals with white coat hypertension have lower
morbidity than patients with sustained hypertension.
White coat" hypertension do not require even very small doses of
antihypertensive therapy as it may result in hypotension, but must still
be careful as patients may show signs of vascular changes and may
eventually develop hypertension.
The term "masked hypertension" can be used to
describe the contrasting phenomenon, where blood pressure is
elevated during daily living, but not in an office sitting.

Measurement of BP
• Arterial pressure is most commonly measured via a
sphygmomanometer which historically used the height of a column
of mercury to reflect the circulating pressure.
• Systolic and diastolic arterial blood pressures are not static but
undergo natural variations from one heartbeat to another and
throughout the day (in a circadian rhythm).
• They also change in response to :
o Stress.
o Nutritional factors.
o Drugs.
o Disease.
o Exercise.

Hypertensive urgencies
• Severe HTN without or with minimal symptoms
and controlled slowly in 24 hours.
• It is ideally managed by adjusting maintenance
therapy by adding a new antihypertensive and/or
increasing the dose of a present medication.
• Acute administration of a short-acting oral drug
(captopril, clonidine, or labetalol) followed by
careful observation for several hours to ensure a
gradual BP reduction is an option.

Hypertensive emergencies :
• Hypertensive emergency is severe HTN with
symptomatic end organ damage require
immediate BP reduction to limit new or
progressing target-organ damage.
• The goal is not to lower BP to normal; instead,
the initial target is a reduction in mean arterial
pressure of up to 25% within minutes to hours.
• If BP is then stable, it can be reduced toward
160/100– 110 mm Hg within the next 2 to 6
hours.

• If BP reduction is well tolerated, additional gradual
decrease toward the goal BP can be attempted after 24 to
48 hours.
• Nitroprusside is the agent of choice :for minute-
to-minute control in most cases. It is usually given as a continuous IV
infusion at a rate of 0.25 to 10 mcg/kg/min.
• Its onset of hypotensive action is immediate and disappears within 1
to 2 minutes of discontinuation.
• When the infusion must be continued longer than 72 hours, serum
thiocyanate levels should be measured, and the infusion should be
discontinued if the level exceeds 12 mg/dL.
• The risk of thiocyanate toxicity is increased in patients with
impaired kidney function.

Refractory HTN
The more common cause of treatment failure in
HTN :
• Non compliance i.e patient is not taking drug regularly.
• Inadequate therapy.
• Failure to recognize secondary causes of HTN e.g renal
artery stenosis & pheochromocytoma.
• Use of antagonistic drugs e.g NSAIDS
o Steroids
o cocaine
• Increase alcohol intake.

EVALUATION OF
THERAPEUTIC OUTCOMES
• Clinic-based BP monitoring is the standard for managing
hypertension.
• BP response should be evaluated 2 to 4 weeks after initiating or
making changes in therapy.
• More frequent evaluations are required in patients with a
history of :
 Poor control.
 Non adherence
 Progressive target-organ damage
 Symptoms of adverse drug effects.
• These techniques are currently recommended only for select
situations such as suspected white coat hypertension.

 Monitoring for adverse drug effects should typically occur 2
to 4 weeks after starting a new agent or dose increases,
and then every 6 to 12 months in stable patients.
 Additional monitoring may be needed for other
concomitant diseases.
 Patients taking aldosterone antagonists should have
potassium concentration and kidney function assessed .
 Patients should be questioned periodically about changes
in:
o their general health perception.
o energy level.
o physical functioning.
o overall satisfaction with treatment.
.

Hypertension, its causes, types and management

Hypertension, its causes, types and management

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