HYPERTENSION

HYPERTENSION
 Hypertension

Hypertension affects approximately 1
billion individuals worldwide

 As the population ages, the prevalence

of hypertension will increase

 Recent data from the Framingham Heart

Study suggest that individuals who are
normotensive at 55 years of age have a
90% lifetime risk for developing
hypertension.
Hypertension
 Hypertension
 The cardiovascular risk remains high
among the majority of hypertensive
persons, whether treated or not

 The numbers of patients with end-stage

renal disease and heart failure—two
conditions in which hypertension plays a
major causative role—continue to rise

 Stroke and coronary heart disease are

the two of the major complications of
hypertension
 DOCUMENTATION OF
HYPERTENSION
For most patients who are in no immediate danger
from markedly elevated pressure, the following
guidelines are offered:

 Multiple readings should be obtained under

varying conditions and at various times for
at least 4 to 6 weeks
 For a rapid diagnosis, a set of readings
obtained by an automatic monitor over a
single 24-hour period will be adequate
 SYMPTOMS OF HYPERTENSION
 Uncomplicated hypertension is almost always
asymptomatic, a person may be unaware of the
consequent progressive cardiovascular damage
for as long as 10 to 20 years

 Symptoms often attributed to hypertension--

headache, tinnitus, dizziness, and fainting--may
be observed just as commonly in the
normotensive population
 Even headache, long considered a
frequent symptom of hypertension, is
poorly related to the level of blood
pressure as noted in 10 to 20 percent
of those with diastolic blood pressure
levels from below 90 to above 120
mm Hg.
 Hypertension
Important Point:
Only if blood pressure is measured
frequently and people are made
aware that hypertension may be
harmful even if asymptomatic will the
majority of people with unrecognized
or inadequately treated hypertension
be managed effectively
  Patient Evaluation
Evaluation of patients with documented
hypertension has 3 objectives:
1. to assess lifestyle and identify other
cardiovascular risk factors or concomitant
disorders that may affect prognosis and guide
treatment
2. to reveal identifiable causes of high BP
3. to assess the presence or absence of target-
organ damage and CVD

The data needed are acquired through

medical history, physical examination,
routine laboratory tests, and other
diagnostic procedures.
 The Physical

Examination
Appropriate measurement of BP, with verification in
the contralateral arm
 Examination of the optic fundi
 Body mass index calculated as weight in kilograms
divided by the square of height in meters
(measurement of waist circumference also may be
useful)
 Auscultation for carotid, abdominal, and femoral bruits
palpation of the thyroid gland
 Thorough examination of the heart and lungs
 Examination of the abdomen for enlarged kidneys,
masses, and abnormal aortic pulsation
 Palpation of the lower extremities for edema and
pulses
 Neurological assessment
Diagnosis of Hypertension

For the individual patient, hypertension
should be diagnosed when the most
readings are at a level known to be
associated with a significantly higher
cardiovascular risk without treatment.


The recommendations of the Seventh
Joint National Committee (JNC-7)are
shown in Table
 Laboratory Tests
 Hematocrit

 Urine analysis

 Blood biochemical profile (including

plasma glucose, potassium,
creatinine, and total and high-density
lipoprotein cholesterol)

 Electrocardiogram
Types of Hypertension
Primary, essential, or idiopathic
 Primary (essential) hypertension is the term
applied to the 95% of cases in which no cause for
hypertension can be identified
 The onset is usually between ages 25 and 55 years;
it is uncommon before age 20 years

Identifiable (secondary) 
 Hypertension may arise from an identifiable cause,
in which case it is called secondary hypertension
 The secondary form should be suspected in
children or young adults and in older persons in
whom onset of hypertension is new or in whom
hypertension suddenly worsens
 Pathogenesis of primary
(essential) hypertension
 The pathogenesis of primary (essential)
hypertension is multifactorial

Genetic factors
 They play an important role
 Children have higher blood pressure when one
parent is hypertensive (and more so when both
parents are hypertensive)

Environmental factors
 Increased salt intake and obesity have long been
incriminated
 These factors alone are probably not sufficient to
raise blood pressure to abnormal levels but are
synergistic with a genetic predisposition
Other factors:
 Sympathetic nervous system hyperactivity
 Abnormal cardiovascular development
 Renin-angiotensin system activity
 Defect in natriuresis
 Intracellular sodium and calcium

Exacerbating factors (including obesity, alcohol,

cigarette smoking, and polycythemia)
Renal  Hypertension
 Renal parenchymal disease            
• Acute glomerulonephritis            
• Chronic nephritis            
• Polycystic disease            
• Diabetic nephropathy            
• Hydronephrosis        

 Renovascular            
• Renal artery stenosis            
• Intrarenal vasculitis        

 Renin-producing tumors        

 Primary sodium retention (Liddle

syndrome, Gordon syndrome)
 Endocrine
• Acromegaly        
• Hypothyroidism        
• Hyperthyroidism        
• Hypercalcemia (hyperparathyroidism)  
• Adrenal
Cortical                
Cushing syndrome                
Primary aldosteronism                
Congenital adrenal hyperplasia  

Medullary : Pheochromocytoma               

• Apparent mineralocorticoid excese (licorice)                   

• Extraadrenal chromaffin tumors        
• Carcinoid        
• Exogenous hormones
 Coarctation of the aorta    
 Pregnancy-induced hypertension    
 Neurological disorders        
 Hypoglycemia        
 Burns        
 Psychogenic hyperventilation        
 Pancreatitis        
 Alcohol withdrawal        
 Acute stress, including surgery        
 Sickle cell crisis        
 Postresuscitation        
 Postoperative    
 Increased intravascular volume    
 Alcohol and drug use
COMPONENTS OF CARDIOVASCULAR
RISK STRATIFICATION IN PATIENTS
WITH HYPERTENSION
 Major Risk Factors
• Smoking
• Dyslipidemia
• Diabetes mellitus
Age >60 yr
• Sex (men and postmenopausal women)
• Family history of cardiovascular disease:
• Women >65 yr or men >55 yr

 Target Organ Damage/Clinical

Cardiovascular Disease
• Heart diseases
    Left ventricular hypertrophy
    Angina or prior myocardial infarction
    Prior coronary revascularization
    Heart failure
• Stroke or transient ischemic attack
• Nephropathy
• Peripheral arterial disease
• Retinopathy
 Target Organ Damage or
Complications of Hypertension

.
 Retinopathy
 FUNDUSCOPIC EXAMINATION
Vascular changes in the fundus reflect both hypertensive
retinopathy and arteriosclerotic retinopathy

Grade 1: The two processes first induce narrowing of the

arteriolar lumen
Grade 2: Sclerosis of the adventitia and/or thickening of the
arteriolar wall, visible as arteriovenous nicking
Grade 3: Progressive hypertension induces rupture of small
vessels, seen as hemorrhage and exudate and
Grade 4: Eventually papilledema.

The grade 3 and 4 changes are clearly indicative of an

accelerated-malignant form of hypertension, whereas the
lesser changes have been correlated with other evidence
of target organ damage
Hypertensive Retinopathy Grade 1
Hypertensive Retinopathy Grade 2
Hypertensive Retinopathy Grade 3
Hypertensive Retinopathy Grade 4
 CARDIAC INVOLVEMENT
 Hypertension places increased tension on the left
ventricular myocardium that is manifested as
stiffness and hypertrophy

 It accelerates the development of atherosclerosis

within the coronary vessels

 The combination of increased demand and

lessened supply increases the likelihood of
myocardial ischemia

 Leads to a higher incidence of myocardial

infarction, sudden death, arrhythmias, and
congestive failure in hypertension
Consequences of systolic and diastolic
dysfunction related to hypertension
 Systolic dysfunction and congestive heart failure caused
by impaired ventricular contraction may occur late in
the evolution of hypertensive heart disease

 Diastolic dysfunction is the most common manifestation

of the effect of hypertension on cardiac function and can
also lead to congestive heart failure from increased
filling pressures

 Treatment with all antihypertensive drugs has been

shown to cause LVH regression. With regression, left
ventricular function usually improves and cardiovascular
morbidity decreases
Hypertension
 RENAL INVOLVMENT
 Renal dysfunction too subtle to be recognized may
be responsible for the development of most cases
of essential hypertension

 Increased renal retention of salt and water may be

a mechanism initiating primary hypertension, but
the retention is so small that it escapes detection

 Structural damage and functional derangements

reflecting intraglomerular hypertension often
reflected by microalbuminuria can be found in
most hypertensive persons.

 As hypertension-induced nephrosclerosis proceeds,

the plasma creatinine level begins to rise, and
eventually, renal insufficiency with uremia may
develop, thus making hypertension a leading
cause of end-stage renal disease (ESRD)
CEREBRAL INVOLVEMENT
 Hypertension may accelerate cognitive
decline with age

 Hypertension, particularly systolic, is a

major risk factor for both ischemic stroke
and intracerebral hemorrhage
 Risk Stratification and Treatment
BLOOD PRESSURE RISK GROUP A (NO RISK GROUP B (AT RISK GROUP C
RISK FACTORS: NO LEAST 1 RISK (TOD/CCD AND/OR
STAGES (mm Hg TOD/CCD) FACTOR, NOT DIABETES, WITH OR
INCLUDING WITHOUT OTHER
DIABETES: NO
RISK FACTORS)
TOD/CCD)

High normal Life style modification Life style modification Drug therapy

(130-139/85-89)

Stage 1 Life style modification Life style modification Drug therapy

(up to 12 mo) (up to 6 mo)
(140-159/90-99)

Stages 2 and 3 Drug therapy Drug therapy Drug therapy

(>160/>100)
 Hypertension Therapy
Goals of Therapy

The optimal goal of anti hypertensive

treatment in most patients with combined
systolic and diastolic hypertension who are
not at high risk is a blood pressure of less
than 140/90 mm Hg

The greatest benefit is derived from lowering

the diastolic pressure to 80-85mm Hg
 In
elderly with isolated systolic hypertension,
the goal should be systolic blood pressure of
140-145 mmHg

 Caution
is advised if, diastolic pressures fall
below 65mmHg

 In
such an event, less than ideal reductions in
systolic levels need to be balanced against
the potential for harm if diastolic levels fall
below that level.
 Patients with Diabetes Mellitus, in whom a blood
pressure of less than 130/85mmHg reduces incidence
of cardiovascular events

 Itis noted that the lower the systolic blood pressure

down to 110mmHg, the lower was the risk of both
micro- and macrovascular complications related to
diabetes

 Patients with progressive chronic renal disease

excreating more than 1-2 gm of protein per day,
reducing the blood pressure to 125/75mmHg may
slow rate of loss of renal function
 Once good control of blood pressure in a
patient has been achieved, it may be
possible to reduce or withdraw drug
therapy

 One fourth of patients who have initially

mild hypertension and who achieve good
control with therapy will remain
normotensive for at least 1 year after
their therapy is stopped

 However,such patients need to remain

under observation
 Hypertension Therapy
 Lifestyle Modifications
 Adoption of healthy lifestyles by all individuals is
critical for the prevention of high BP and an
indispensable part of the management of those
with hypertension.

 Lifestyle modifications decrease BP, enhance

antihypertensive drug efficacy, and decrease
cardiovascular risk. For example, a 1600-mg
sodium Dietary Approaches to Stop Hypertension
eating plan has effects similar to single drug
therapy.

 Combinations of 2 or more lifestyle modifications

can achieve even better results.
Hypertension Therapy
 Pharmacologic
Treatment
 Desire to control a patient's hypertension
rapidly and completely often leads to undue
fatigue, weakness, and postural dizziness,
which many patients find intolerable,
particularly when they felt well before therapy
was begun

 Although hypokalemia and other electrolyte

abnormalities may be responsible for some of
these symptoms, the other explanation is as
follows
 Hypertensive Therapy
Mean cerebral blood flow autoregulation curves from
normotensive, severely hypertensive, and effectively treated
hypertensive patients are shown.
 Acutely lowering the pressure from 160/110 mm
Hg (mean=127) to 140/85 mm Hg (mean=102)
may induce cerebral hypoperfusion, although
hypotension has not been produced

 This provides an explanation for what many

patients experience at the start of
antihypertensive therapy, i.e., manifestations of
cerebral hypoperfusion, even though blood
pressure levels do not seem inordinately low

 Thus, the approach to antihypertensive therapy

should be gradual in order to avoid symptoms
related to overly aggressive blood pressure
reduction

 Fortunately, if therapy is continued for a period,

the curve of cerebral autoregulation shifts back
toward normal, allowing patients to tolerate
greater reductions in blood pressure without
experiencing symptoms
CHOICE OF INITIAL DRUG
 Thiazide-type diuretics have been the basis of
antihypertensive therapy in most outcome trials

 Thiazide-type diuretics should be used as initial

therapy for most patients with hypertension, either
alone or in combination with 1 of the other classes
(ACE inhibitors, ARBs, beta-blockers, CCBs)

 The presence of compelling indications can dictate use

of other antihypertensive drugs as initial therapy

 If a drug is not tolerated or is contraindicated, then 1 of

the other classes proven to reduce cardiovascular
events should be used instead
Algorithm for Treatment of
Hypertension
CLASS OF COMPELLING POSSIBLE COMPELLING POSSIBLE
DRUG INDICATIONS INDICATIONS CONTRAINDICATION CONTRAINDICATIONS

Diuretics Heart failure Diabetes Gout Dyslipidemia

Elderly patients
Systolic
hypertension
Beta blockers Angina Heart failure Asthma and COPD Dyslipidemia
After myocardial Pregnancy Heart block Athletes and physically active
infarction Diabetes patients
Tachyarrhythmias Peripheral vascular disease
ACE inhibitors Heart failure Pregnancy
Left ventricular Hyperkalemia
dysfunction Bilateral renal artery stenosis
After myocardial
infarction
Diabetic
nephropathy

Calcium Angina Peripheral Heart block Congestive heart failure

antagonist Elderly patients vascular disease
Systolic
hypertension
Alpha blockers Prostatic Glucose Orthostatic hypotension
hypertrophy intolerance
Dyslipidemia
Angiotensin II ACE inhibitor cough Heart failure Pregnancy
antagonists Bilateral renal artery stenosis
Hyperkalemia
 Follow-up and Monitoring
 Once drug therapy is initiated, most patients should
return for follow-up and adjustment of medications
at approx monthly intervals until the BP goal is
reached
 More frequent visits will be necessary for patients
with stage 2 hypertension or with complicating
comorbid conditions
 Serum potassium and creatinine should be
monitored at least 1 to 2 times per year
 After BP is at goal and stable, follow-up visits can
usually be at 3- to 6-month intervals
 Other cardiovascular risk factors should be treated
to their respective goals, and tobacco avoidance
should be promoted vigorously
 Low-dose aspirin therapy should be considered only
when BP is controlled, because the risk of
hemorrhagic stroke is increased in patients with
uncontrolled hypertension
 Emergency treatment of
accelerated phase or
malignant hypertension
 Unwise to lower the BP too quickly as it may
compromise tissue perfusion

 A controlled reduction to a level of about

150/90 mmHg over a period of 24-48 hours is
ideal

 In most patients BP is controlled with bed rest

and oral drugs but the following may be
needed:
 IV or IM Labetalol
 IV Glyceryl trinitrate
 IM Hydralazine
 IV Sodium Nitroprusside
 FEATURES OF “SECONDARY"
HYPERTENSION
 Onset before age 20 or after age 50
 Level of blood pressure >180/110 mm Hg
 Organ damage
 Funduscopic findings of grade 2 or higher
 Serum creatinine >1.5 mg/100 ml
 Cardiomegaly (on radiograph) or left ventricular
hypertrophy (on electrocardiogram)
 Features indicative of secondary causes
 Unprovoked hypokalemia
 Abdominal bruit
 Variable pressures with tachycardia, sweating,
tremor
 Family history of renal disease
 Poor response to therapy that is usually effective