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Manual of
Hypertension
M. Mohsen Ibrahim,
MD
MANUAL
OF
HYPERTENSION
M. MOHSEN IBRAHIM,
MD
Professor of Cardiology - Cairo University
President of the Egyptian Hypertension Society
Principal Investigator of the Egyptian
National Hypertension Project.
PREFACE
Hypertension is a major public health problem
in many parts of the world. It has been identified as the most
common, most potent and most universal contributor to cardiovascular
mortality. The disease carries special importance for a number
of reasons.
First: It has been
found that hypertension is the commonest cause of doctors’ consultations
in many western countries. In most parts of the world its prevalence
varies between 10-30% of population and it increases with old
age.
Second: Hypertension if left uncontrolled
without treatment can lead to disastrous sequelae.
High blood pressure damages the heart, the kidneys, the brain
and the aorta producing heart failure, renal failure, strokes
and aortic dissection. It is a major risk factor for coronary
artery disease and premature atherosclerosis.
Third: High blood pressure can be treated.
Control of hypertension can prevent most of the previous complications.
Available antihypertensive medications can control even severe
cases.
Fourth: The identification
and management of hypertension is misunderstood and has been
surrounded by a number of false beliefs shared by both the public
and medical profession. Hypertension is not nervousness and
should not be equated with headache or dizziness. It is in the
majority of cases a silent disease without symptoms. It should
be treated with specific antihypertensive therapy and not by
tranquilizers. It can be present in quiet, relaxed, emotionally
stable persons. Antihypertensive medications should be continued
for the rest of patient’s life. Since the etiology of essential
hypertension is not known, therapy is directed to the symptomatic
level of mere lowering of blood pressure. Discontinuation of
therapy should lead to recurrence of hypertension and rise of
blood pressure. There is no cure from established essential
hypertension except in the unfortunate patients who develop
cerebral stroke or myocardial infarction.
Systolic hypertension is equally
important as diastolic hypertension. Furthermore, cardiac and
cerebral complications are related more to the level of systolic
than the diastolic blood pressure.
The aim of this manual is to provide the medical
student and the practitioner with a short practical review of
hypertension. It addresses the everyday clinical problems and
is written in a simple language that suits the beginner. The
book is not intended to be a detailed textbook. Stress has been
made all through the book on the practical issues avoiding theoretical
and controversial issues. This manual is based upon both the
author’s personal experience in the management of hypertensive
patients over the past 30 years and the review of the current
world literature in the field of hypertension.
M. Mohsen
Ibrahim, MD
Professor of Cardiology - Cairo University
President
of the Egyptian Hypertension Society
Cairo, August 2001
TABLE OF CONTENTS
Chapter
1: Hypertension - An Overview
Chapter
2: Hypertension: Definition, Classification and
Pathophysiologic Mechanisms
Chapter
3: Measurement of Blood Pressure
Chapter
4: Clinical Evaluation of
Hypertensive Patients
Chapter
5: Laboratory Evaluation of
Hypertensive Patients
Chapter
6: Antihypertensive Drugs
Chapter
7: Inititation and Monitoring
of Antihypertensive Therapy
Chapter
8: Non-Pharmacologic Therapy:
Lifestyle Modification
Chapter
9: Hypertension in Special Groups
Chapter
10: Renal Artery Stenosis
Chapter
11: Primary Aldosteronism
Chapter
12: Hypertensive Emergencies
Chapter
13: Resistant Hypertension
Chapter
14: Patient Education
Chapter
15: Epidemiology of Hypertension
in Egypt
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CHAPTER
1
HYPERTENSION –AN OVERVIEW
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Hypertension-An
Overview
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The diagnosis of hypertension is established
by simple measurement of arterial pressure. Headache, dizziness,
faintness mentioned by many anxious patients are not symptoms
of diagnostic significance since they are equally present
in both normotensive and hypertensive subjects. Diagnosis
of hypertension should not be made simply by the patient’s
feelings. The only way to identify hypertension is to have
blood pressure checked. The Joint National Committee (JNC)
on Detection, Evaluation and Treatment of High Blood Pressure
in the USA have put the following classification of blood
pressure in adults aged 18 years or older based on the average
of two or more readings on two or more occasions.
|
| Category |
Systolic
(mmHg) |
Diastolic
(mmHg) |
| Normal |
<
130 |
>
85 |
| High Normal |
130-139 |
85-89 |
| Hypertension |
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|
| Stage
I |
140-159 |
90-99 |
| Stage
II |
160-179 |
100-109 |
| Stage
III |
≤ 180 |
≥
110 |
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Isolated systolic hypertension, when diastolic blood pressure is < 90 mmHg.
|
| Normal |
<
140 |
| Borderline Isolated Systolic Hypertension |
140-159 |
| Isolated Systolic Hypertension |
≥ 160
Hypertension-An
Overview |
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Risk of cardiovascular complications related to hypertension increases
continuously with increasing levels of both systolic and
diastolic pressure. Data from clinical trials have indicated
that mild hypertension requires medical attention.
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ETIOLOGY OF HYPERTENSION
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The exact cause of elevation of arterial blood
pressure remains obscure in about 95% of hypertensive patients.
In this large group, hypertension can be defined as essential
or primary. In the remaining 5% of patients, hypertension
can be related or is secondary to a well-defined disease
and is called secondary hypertension.
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Causes of Secondary Hypertension
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1.
Renal Disease
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Constitutes
the commonest group of known diseases that can lead to elevation
of arterial pressure and these include renal parenchymal
and renal vascular (renal arteries) diseases.
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· Renal Parenchymal diseases, e.g., congenital
atrophic, hypoplastic or polycystic
kidney, collagen autoimmune disorders, hydronephrosis,
pyelonephritis, obstructive uropathies,
tumors and end stage renal failure.
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· Renovascular hypertension, e.g., narrowing or
stenosis of one or both renal
arteries due to congenital defect in vessel wall, e.g.,
fibromuscular dysplasia
of the renal arteries seen in young females or secondary
to atherosclerosis which is a disease of old age.
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2. Endocrine Disorders
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· Primary
Aldosteronism: Excessive production
of the mineralocorticoid aldosterone secondary
to suprarenal cortical hyperplasia or tumor produces hypertension
with potassium loss in urine and hypokalemia.
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· Cushing’s Syndrome: Glucocorticoid excess is associated with hypertension, special
type of obesity, skin changes, osteoporosis and
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metabolic disturbances. · Pheochromocytoma
due to chromaffin tissue tumors
producing excessive production of catecholamines,
noradrenaline and adrenaline is
characterized by symptomatic hypertension with headaches,
sweating, palpitations, pallor, tremors and hypermetabolism.
3. Coarctation
of the Aorta
A congenital anomaly producing
narrowing of the thoracic aorta before or after the origin
of left subclavian artery and
characterized by hypertension in the upper limbs with weak
and delayed arterial pulsation in the lower limbs. Murmurs
over the back and precordium are present.
4.
Toxemia of Pregnancy
In pre-eclampsia, rise in blood
pressure is associated with edema and proteinuria.
Eclampsia is accompanied by convulsions.
5.
Drugs
Oral contraceptives, non-steroidal
anti–inflammatory drugs, sympathomimetics,
corticosteroids and some psychoactive drugs. Drugs can produce
transient elevation of arterial pressure and can sometimes
make hypertension resistant to therapy.Etiology
of Essential HypertensionThere is now enough evidence that essential
hypertension can be attributed to the interaction of genetic
and environmental factors. Hypertension, especially before
the age of 60 is a genetically determined disease and it
runs in families due mostly to genes but with some effects
from the shared family environment. The specific genes that
mediate the increased vascular resistance characterizing
essential hypertensives remain to be identified. The following
may complicate genetic studies of
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hypertension in humans:
1.
The likelihood that essential hypertension has multiple genetic
causes.
2.
Difficulty in controlling the numerous environmental factors
that affect blood pressure.
Genetic abnormalities were hypothesized to involve genes
for renin
(a proteolytic enzyme), Kallikrein (a vasodilator peptide),
and angiotensin converting enzyme. Genetic abnormalities
increase the susceptibility of the individual and prepare
the scene for the development of hypertension when there
are unfavorable environmental conditions either related
to dietary intake (Na, K, Cl, Ca, alcohol, saturated or
unsaturated fat, and total calories), physical inactivity,
or psychological factors (e.g., stressful, demanding, or
uncontrolled job conditions). Epidemiological studies have
provided evidence of a relationship between dietary sodium
intake and blood pressure. However, individuals vary in
salt sensitivity. Salt sensitive subjects increase their
blood pressure with dietary excess salt intake. Blacks,
elderly, non-insulin dependant diabetics are salt sensitive.COMPLICATIONS OF HYPERTENSIONReduction of arterial pressure is a prerequisite
for prevention of hypertensive complications. We treat hypertension
not because of symptoms but in order to prevent its serious
consequences.
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Cardiac Complications: Left ventricular hypertrophy (LVH),
coronary artery disease and abnormalities of the cardiac
function are the commonest cardiac complications. LVH is
associated with decreased life span. Left ventricular failure
complicates uncontrolled hypertension. Shortness of breath
is a common symptom of hypertension. High blood pressure
accelerates the atherosclerosis process, predisposes to
vascular damage and is a major risk factor for coronary
artery disease, angina pectoris and myocardial infarction.Renal Complications: Progressive loss of renal glomerular
population secondary to renal arteriosclerosis and glomerular
hypertension leads to renal failure and azotemia.Cerebral Complications: Cerebral hemorrhage is directly linked
to high blood pressure and can be a fatal event. Cerebral
vascular thrombosis and brain infarction are secondary to
atherosclerotic process accelerated by hypertension.Aortic Dissection: Dissection of the media of the thoracic
aorta resulting in aneurysmal formation, fatal rupture or
occlusion of subclavian, innominate, carotid or coronary
arteries.Malignant Hypertension: Severe untreated hypertension can
progress to the malignant phase with widespread severe vascular
injury producing spasm, edema and necrosis of small arteries
leading to damage of vital organs, specially the kidneys.
The condition, if not aggressively treated, can lead to
death from renal failure, cerebral hemorrhage or pulmonary
edema. Papilledema in optic fundi is diagnostic of the malignant
Hypertension-An Overview
phase.MANAGEMENT OF HYPERTENSION Establish
the presence of hypertension Accurate Blood Pressure MeasurementPrecautions
and details of measuring arterial pressure are present in
chapter 3 of this manual. Sources of potential errors include
improper equipment and inaccurate readings. Special attention
should be paid to factors that may alter blood pressure
and produce transient pressor effect such as anxiety, mental
stress, recent smoking or eating, talking, xertion, cold,
caffeine consumption, bladder distension, and medication.
Blood pressure readings are higher in the morning than in
the evening. Diurnal variations should be considered in
the follow-up of patients.Repeat Blood Pressure Measurement
A single casual office arterial pressure reading is not
enough to establish the presence of hypertension. Repeated
measurements are necessary and persistent elevation is a
requisite for diagnosis (see paragraph on definition of
hypertension). Persons whose resting values of diastolic
blood pressure remain persistently above 90 mmHg, after
repeated measurements are at increased risk of cardiovascular
mortality and morbidity. In practice, when the initial diastolic
blood pressure averages 90–104 mmHg, measurements should
be repeated on at least two further occasions during the
following four weeks. With repeated measurements both systolic
and diastolic pressures often fall substantially. It is
therefore necessary to identify those patients with sustained
high or increasing blood pressure. EvaluationThe objectives of clinical and laboratory evaluation
are to assess target organ damage, identify other associated
risk factors and rule out secondary forms of hypertension.
A complete history and physical examination are essential. HistorySymptoms suggestive of ischemic heart disease, cardiac failure or transient
cerebral ischemic episodes. Previous measurements of blood
pressure, maximum and minimum readings and details of previous
and present antihypertensive therapy. Family history of
hypertension, diabetes, hyperlipidemia, ischemic heart or
strokes. Smoking and alcohol consumption, weight gain since
early adult life, ingestion of prohyperten-
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ive substances or drugs notably oral contraceptives and non-steroidal
anti-inflammatory drugs. Other drugs with potential pressor
effect include nasal decongestants and other cold remedies,
appetite suppressants, cyclosporins, tricyclic antidepressants
and monoamine oxidase inhibitors. Physical
ExaminationMeasurement of weight and height, evaluation
of heart size, evidence of cardiac failure, arterial disease
in the carotid, renal, and peripheral arteries. Abdominal
examination for renal masses. Optic fundi examination. InvestigationsUrine analysis, blood examination for glucose,
potassium, urea, creatinine, uric acid, cholesterol, and
standard electrocardiogram are done for all patients. In
selected cases further investigations should be carried
out to exclude potentially curable causes of hypertension. Electrocardiogram
and EchocardiogramRoutine ECG is advised in all hypertensive patients to detect
signs of cardiac involvement, which might be an indication
to initiate drug treatment at milder grades of hypertension
and can influence the choice of therapy. ECG will help to
diagnose left ventricular hypertrophy, follow its response
to therapy, and detect signs of associated myocardial infarction,
ischemia or electrolyte disorders. P wave alterations, increased
QRS voltage and repolarization abnormalities of left ventricular
hypertrophy were found to be associated with increasingly
severe hypertension. ECG has a low sensitivity of detection
of hypertensive left ventricular hypertrophy. Echocardiography
is more sensitive than ECG for detection of left ventricular
hypertrophy. It is indicated in patients with resistant
hypertension, when there is lack of any signs of cardiac
hypertrophy in a patient
with severe uncontrollable hypertension that may
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oint to office hypertension as the
cause of resistance. The presence of signs or symptoms of
cardiac dysfunction or significant atherosclerotic disease
in major vessels are other indications of echocardiography.
In patients with mild hypertension signs of echocardiographic
left ventricular hypertrophy are an indication of early
active drug therapy. Optic
Fundus ExaminationChanges in retinal arteries may be an indication
of widespread vascular disease. The earliest vascular changes
in hypertensive patients are deposition of hyaline material
under the endothelium in the smallest vessels, hyperplasia
and reduplication of the elastic lamina in small arteries.
Early fundus changes include arterial wall thickening, increased
tortiousity, increased light reflex, and obliteration of
veins at site of arterio-venous crossing. In accelerated
hypertension hemorrhages and cotton wool exudates are present.Assessment
of Renal DiseaseSimple urine analysis, measurements of
blood urea and plasma creatinine are mostly normal even
in patients with long standing and ill controlled hypertension.
Abnormal renal function as judged by these crude indices,
raises the possibility that renal disease is primary and
hypertension secondary rather than vice versa. Other
Laboratory TestsSerum potassium is reduced in patients with primary aldosteronism and mineralocorticoid
hypertension, in those who are on diuretic therapy specially
chlorthalidone or after chronic laxative intake. Periodic
estimation of serum potassium is recommended in patients
receiving potassium supplements, potassium sparing diuretics,
on digitalis or in the presence of cardiac rhythm disturbances.
Hyperlipidemia is a major risk factor for premature coronary
artery disease. Estimation of serum cholesterol is recommended especially in high-risk groups, e.g., males,
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smokers, diabetics and in patients with coronary artery disease.
Detailed plasma lipid profiling is recommended if serum
cholesterol is elevated. Measurement of blood sugar level
is advised in all patients specially before prescribing
diuretic therapy. High levels of serum uric acid (Hyperuricemia)
can be primarily due to genetically determined metabolic
defect or can be the result of renal failure or diuretic
therapy. There is an inverse relation between serum uric
acid and renal blood flow. TreatmentThe goal is to lower the blood pressure to normotensive
levels, to lower the diastolic to below 90 mmHg, and systolic
blood pressure below 140 mmHg. Non-pharmacological
InterventionSeveral non-pharmacological interventions have been shown to lower blood
pressure in patients with mild hypertension. Weight reduction
in overweight subjects, cessation of heavy alcohol consumption,
regular exercise in sedentary patients, and in some patients
sodium restriction and dietary changes are effective in
lowering blood pressure. Some of these measures may take
months to become fully effective. If non-pharmacological
methods are successful in maintaining diastolic BP levels
< 90 mmHg they should be continued, if not, drug therapy
should be considered. Initial BP readings that are markedly
elevated (i.e., DBP > 110 mmHg) or associated with evidence
of target organ damage require earlier drug therapy.The United States JNC report on Detection, Evaluation
Treatment of High Blood Pressure recommends the following
follow–up program for hypertensive patients based upon the
initial BP measurement.
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Follow-Up Based Upon Initial DBP
| Range
(mmHg) |
Recommended
Follow-up |
| <
85 |
Recheck within 2 years |
| 85-89 |
Recheck within 1 year |
| 90-104 |
Confirm within 2 months |
| 105-114 |
Evaluate or refer to source of care within 2
weeks |
| >
115 |
Evaluate or refer immediately to source of care |
| <
140 |
Recheck within 2 years |
| 140-199 |
Confirm within 2 months |
| >
200 |
Evaluate or refer to a source of care within 2 weeks |
Systolic When Diastolic BP is < 90 mmHgIn mild hypertensives, observation over a 3 to 12 months period interval
may be elected prior to initiating drug therapy since pressures
may return to normal during that time. Individuals with
such temporary elevations of pressure are at increased risk
of later developing persistent hypertension and should be
informed of this and observed at approximately 6 months
intervals. In a few patients in whom therapeutic decisions
may be difficult because of marked liability in BP, a 24-hour
ambulatory monitoring may be of value. However the exact
role of this technique has not been established.Drug
Treatment
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If non-pharmacological methods are successful in maintaining diastolic
BP < 90 mmHg they should be continued, if not, drug therapy should
be considered. Initial BP readings that are markedly elevated
(i.e. DBP > 115 mmHg) or associated with evidence of
target organ damage may require immediate drug therapy.
Factors favoring earlier drug intervention include systolic
blood pressure levels of 160 or greater, presence of clinical,
electrocardiographic, echocardiographic or radiological
evidence of left ventricular hypertrophy or clinical, electrocardiographic
or angiographic evidence of ischemic heart disease. A history
of cerebrovascular disease or signs of renal disease or
presence of strong family history of stroke, heart disease
or sudden death are indicators to begin treatment. Presence
of other risk factors as diabetes mellitus, hypercholesterolemia,
and cigarette smoking favors early drug treatment. Selection of Drug TreatmentAbout one-half of patients with mild hypertension will respond to a moderate
dose of one of several antihypertensive drugs by achieving
a DBP reduction of 10 mmHg or more or by lowering the diastolic
pressure to the desired goal, i.e. < 90 mmHg. Initial
drug therapy includes either a diuretic or b-blocker or calcium antagonist or angiotensin
converting enzyme (ACE) inhibitor or angiotensin receptor
blocker. If after a one to two months interval, the response
to the initial choice of therapy is inadequate, the patient
is not experiencing side effects, and adherence to therapy
is adequate, three options of subsequent therapy should
be considered:1. Increase the dose of the first drug if it is below the maximum
recommended.2. Add an agent from another class; or,3. Discontinue the initial choice, and substitute a drug from
another class.
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The following table
shows the different classes of antihypertensive drugs
1.
Diuretics:
a. Thiazides.
b. Loop diuretics.
c. Potassium sparing.
2. α and β adrenergic receptor blockers:
a. β
adrenergic receptor blockers: Atenolol, Propranolol
b. α adrenergic receptor blockers: Prazosin.
c. Combined alpha and β-blockers: Labetalol, Carvedilol.
3. Sympatholytics:
a. Central adrenergic inhibitors (a2 –
agonists): Clonidin, Guanfacine, Methyldopa.
b. Peripheral adrenergic inhibitors: Guanethidine
c. Imidazoline receptor agonists.
4. Direct vasodilators:
Hydralazine, Minoxidil, Sodium nitroprusside,
Diazoxide.
5. Calcium antagonists: Verapamil, Nifedipine, Diltiazem,
Amlodipine, Lacidipine.
6. Converting enzyme inhibitors:
Captopril, Enalapril, Lisinopril, Ramipril, Perindopril, Quanapril, Fusinopril.
7. Angiotensin
receptor blockers:
Losartan, Valsartan, Candesartan.When additional drugs are added and the combination
succeeds, a later attempt should be made to reduce the dose
and, if possible, to eliminate the initial drug. For patients
with mild hypertension who have satisfactorily controlled
their BP through treatment for at least 1 year, antihypertensive
drugs may be reduced in a stepwise fashion. Regular follow-up
must be maintained because BP can rise again to hypertensive
levels. Prediction
of Response to Drug TherapyIn spite of many advances in the pathophysiology of hypertension
and the definition of different pressor mechanisms, drug
Hypertension-An
Overview
therapy is still on empirical basis in the vast majority of patients. However, the following
factors might influence the choice of antihypertensive therapy:
1.
Age: Elderly hypertensives respond better
to diuretics and calcium antagonists. Sympatholytics
and β-adrenergic
receptor blockers are usually more effective in the young
hypertensives.
2.
Sex: Women seem to respond better than men to Methyldopa.
3.
Race: Blacks respond better to diuretics or calcium antagonists
than to β-adrenergic
receptor blockers or ACE inhibitors.
4.
Obesity: Obese subjects have usually a volume dependent form of hypertension
which responds better to diuretic therapy.
5.
Heart Rate: Patients with tachycardia and hyperkinetic circulation respond
better to β-adrenergic
receptor blockers and sympatholytics.
6.
Renal Parenchymal Disease:
The type of hypertension in these patients is usually volume
dependent that responds to diuretic therapy.
7.
Postural Hypertension: Patients
with primary postural rise in BP might respond better to
central adrenergic inhibitors.
8.
Steroid Dependent Hypertension:
Patients with primary aldosteronism
and oral contraceptive hypertension have volume dependent
hypertension that responds to diuretic therapy.
9.
Biochemical Profile:
Hypertensives with high plasma
catecholamines are good candidates
for central adrenergic inhibitors. High renin
hypertensives respond well to sympatholytics
and ACE inhibitors.
10.
Hemodynamic Profile:
Hyperkinetic hypertensives with
high or normal cardiac output are candidates for β-blockade therapy. Patients with significant elevation of
total systemic resistance are given vasodilators or ACE
inhibitors. |
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