HYPERTENSIVE VASCUAR DISEASE

(HVD)

By. dr.wondifraw
 Overview

• Blood pressure measurement

• Definition of hypertension & Classification
• Epidemiology
• Mechanism & etiology
• Effects of Hypertension
• Approach to patients with hypertension
• Management of Hypertension
 BP Measurement
.
 Patient should be seated quietly for 5 minutes in a char, feet on the floor,
and arm supported at heart level.
 Appropriate-sized cuff should be used to ensure accuracy.
 At least two measurements should be made.
 New BP categories are: AHA

1) normal (<120 systolic and <80 mm

Hg diastolic)
2) elevated (120–129 systolic and <80 mm Hg diastolic),
3) stage 1 hypertension (130–139 systolic or 80–89 mm Hg
diastolic)
4. stage 2 hypertension (≥140 systolic or ≥90 mm Hg
diastolic).
 These categories should not be based on BP readings at
a single point in time but rather should be confirmed by two or
more readings (averaged) made on at least two separate occasions.
 Individuals are classified according to their highest
systolic or diastolic BP category.
 Out of office BP readings (home or ambulatory
BP monitoring) should also be obtained for comparison
with office BP readings.
 The BP category of pre-hypertension is no longer
used
 BP measurement
The guideline provides extensive guidance regarding how to
measure BP accurately.
Accurate BP measurement in office and
home settings is required to minimize errors when diagnosing
hypertension, monitoring BP longitudinally and making
therapeutic decisions about changing the intensity of drug
therapy.
 The ACC/AHA guideline provides an extensive
algorithm for accurate BP measurement that is
unlikely to be followed in ambulatory clinic
and home settings.
 Nevertheless, the following are 7 strategies
recommended by the AHA/AMA for accurate
attainment of BP:
1) no conversation
2) empty bladder
3) use correct cuff size
4) place BP cuff on bare arm
5) support arm at heart level
6) keep legs uncrossed
7) support back and feet.
 Most of the “errors” made during measurement of BP – cuff
too small, cuff applied to arm over clothing, measurement
arm hanging, full bladder, legs crossed and/or hanging -
bias readings upwards.
 Accordingly, the usual approach to measurement of BP in
clinical settings will lead to over-diagnosis and over-treatment
of patients with hypertension.
 Irrespective of measurement location – the office or at
home – the strategies for accurate measurement
of BP are similar, if not identical.
 That is, measuring BP with validated BP measurement
devices used in conjunction with a standard measurement
protocol
 White coat and masked hypertension

 White coat hypertension is defined as office BP is ≥130/80 mm

Hg but out of office (home or daytime ambulatory BP)
<130/80 mm Hg after 3 months of diet and lifestyle modification.

 Masked hypertension also represents non-concordance

between
office and out of office BP readings and is defined as office BP <
130/80 mm Hg but home or daytime ambulatory BP ≥ 130/80 mm
Hg.
This hypertension phenotype should be
considered in individuals with office BP 120–
129/< 80 mm Hg after a three month trial
of diet and lifestyle intervention.
 Emergency(TOD) Vs Urgency( no TOD)

• Hypertensive emergencies- acute, life-threatening,

and usually associated with marked increases in BP,
generally ≥ 180/120 mmHg
• Two clinical syndromes
– Malignant hypertension- is marked hypertension with
retinal hemorrhages, exudates, or papilledema, DBP is
usually >120mmHg
– Hypertensive encephalopathy
• Hypertensive urgency-severe HTN (as defined by a
DBP >120 mmHg) in asymptomatic patients

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 Epidemiology
• HTN is the most prevalent risk factor for cardiovascular
diseases (CVD).
• ~30 % at age >18 yr;> 50 % at age >60.
• As age increases SBP increases but diastolic BP tends to
decrease after age 55 resulting in wide pulse pressure &
isolated systolic HTN
• Estimated to cause 4.5% of global disease burden

• The burden of hypertension increases with age, and

among individuals aged 60, hypertension prevalence is
65.4%
• Hypertension is one of the leading causes of the global burden
of
• disease.
• Elevated blood pressure affects more than one billion
individuals and causes an estimated 9.4 million deaths per
year.
• Hypertension doubles the risk of cardiovascular diseases,
including coronary heart disease (CHD), congestive heart
failure (CHF), ischemic and hemorrhagic stroke, renal failure,
and peripheral arterial disease (PAD).
• It often is associated with additional cardiovascular disease
risk factors
• and the risk of cardiovascular disease
increases with the total burden of risk factors.
• Although antihypertensive therapy reduces
the risks of cardiovascular and renal disease,
large segments of the hypertensive population
are either untreated or inadequately treated.
PATHOGENESIS OF HTN

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 Mechanisms of HTN
Determinants of BP
 Intravascular volume
 Autonomic nervous System
 Renin -Angiotensin-Aldosterone sytem
 Vascular system(stiffness/elasticity)
 Intravascular volume
• Is based on ECF Na content
• Slow but its effect lasts long.
• ↑ECF Na → ↑ ECF volume → This leads to
↑BP initially by increasing CO but later by
increasing TPR in order to decrease tissue flow
of blood. The final effect is to increase
natriuresis to balance for gain in Na.
• If kidney fails or has low sensitivity to
pressure diuresis the BP will remain high to
decrease the Na load.
 Adrenergic system
• For minute to minute control of BP
• Stimulated by baro reflex(carotid & aortic
arch)
• Includes :adrenergic neurons(mainly NE
&dopamine) & adrenal medula(mainly
epinephrine) Receptors Sites Effects
• Receptors : ά1 Vas sm muscle Constriction
ά2 Presynaptic Decrease release of
neurons NE-Vasodilattion

β1 Cardiac muscle ↑contarction & HR

β2 Vasc sm mus vasodilatation
 Renin-angiotensin-aldosterone
• Renin from kidneys(Juxtaglomerlar & macula densa) is
released in response to↓ renal plasma flow, low Na
states.
Renin ACE(lung)
↓ ↓
Angiotensinogen(liver)→Angio.I →Angio.II

Angiotensin II :potent vasoconstrictor, trophic for adrenal

medula (zona glomerulosa),& stimulate adrenergic
nervous system
Risk factor for HTN
1.Nonreversible risk : older age, being African
American, and having a family history of hypertension.

2. Reversible : overweight,sedentary lifestyle, high-

sodium–low-potassium diet,excessive alcohol intake
and metabolic syndrome.

3.Genetic factor: Polygenic= two or greater factors plus

environmental factor, Monogenic- on study
Metabolic syndrome
•Is defined by the presence of at least three of the following:
 abdominal obesity (waist circumference >40 inches in men or
>35 inches in women) vs BMI.
 Impaired fasting blood glucose(fasting glucose ≥100 mg/dL),
 Blood pressure ≥130/85 mmHg,
 plasma triglycerides ≥150 mg/dL, or
 HDL cholesterol <40 mg/dL in men or <50 mg/dL in women.
 Aetiology of Hypertension
• Primary – 90-95% of cases – also termed “essential” of
“idiopathic”
• Secondary – about 5% of cases
– Renal or renovascular disease
– Endocrine disease
• Phaeochomocytoma
• Cushings syndrome
• Conn’s syndrome
• Acromegaly and hypothyroidism
– Coarctation of the aorta
– Iatrogenic
• Hormonal / oral contraceptive
• NSAIDs

Kieran McGlade Nov 2001 Department of General Practice QUB

 Etiology of HTN

• Based on extent of investigation HTN in about 80-95%

has no identifiable cause
Essential/Idiopathic/Primary HTN
• 5-15 % etilogy can be identifed
Secondary hypertension

Essential HTN
tends to be familial and is likely to be the consequence
of an interaction between environmental and genetic
factors
 Effects of HTN
• Target organs : brain, Heart, kidney &
peripheral vessels. They are directly related to
increased risk of atherosclerosis or direct
effect of the elevated BP.
• Genetic , racial factors, presence of other CVD
risk factors & control of the HTN influence
development of Target organ damage(TOD).
 Clinical presentation:
• Most patients are asymptomatic : diagnosed
on routine evaluation or when they come for
other illnesses
• Others come with symptoms or signs of TOD
• Few will come sxs directly related to elevated
BP
Headache
Epistaxis, hematuria
 Effects of Hypertension.
1. Heart→HHD
• Heart disease is the most common cause of death in
hypertensive patients.
• Is the result of structural and functional adaptations
leading to left ventricular hypertrophy(LVH), diastolic
dysfunction, CHF, atherosclerotic coronary artery
and microvascular disease, and cardiac arrhythmias.
 This left ventricle is very thickened (slightly over 2 cm in
thickness), but the rest of the heart is not greatly enlarged.
This is typical for hypertensive heart disease. The
hypertension creates a greater pressure load on the heart
to induce the hypertrophy.

Kieran McGlade Nov 2001 Department of General Practice QUB

 The left ventricle is markedly thickened in this patient
with severe hypertension that was untreated for many
years. The myocardial fibers have undergone
hypertrophy.

Kieran McGlade Nov 2001 Department of General Practice QUB

 Effects of...

. 2 Brain
-Both types of stroke
-Hypertensive Encephalopathy
-Cognitive impairment/dementia
 Effects ...
3 Kidney leads to glomerulosclerosis & tubular
ischemia & atrophy.
• Primary renal disease is the most common
etiology of secondary hypertension.
Conversely, hypertension is a risk factor for
renal injury and ESRD
 Effects….Renal
• Renal risk appears to be more closely related
to systolic than to diastolic blood pressure,
and black men are at greater risk than white
men for developing ESRD at every level of
blood pressure.
• Clinically albuminuria is early marker of renal
injury
 Effects...
4.Peripheral arteries
-increased risk of atherosclerosis:
intermittent claudication or
gangrene.
Untreated hypertension can result in:
 Arteriosclerosis --Kidney damage
 Heart Attack --Stroke
 Enlarged heart --Blindness
 Patient Evaluation
History, Exam, appropriate lab tests are done with objectives of:

1. Defining the Blood pressure levels

2. Assess lifestyle and identify other CV risk factors or concomitant CV

disorders that affects prognosis and guides treatment

3. Assess the presence or absence of target organ damage

4. Identifying secondary forms of hypertension.

 Clinical evaluation

• History/Examination
– Demography
– Heart attack, Angina, CHF
– TIA, stroke
– PVD
– Retinopathy
– BMI
– Signs and symptoms of secondary hypertension
 Laboratory Tests
 Routine Tests
• Blood glucose
• Lipid profile
• serum potassium, hematocrit
• Urinalysis
• Serum creatinine
• Electrocardiogram

 Optional tests
• Measurement of urinary albumin excretion or albumin/creatinine ratio
 More extensive testing to identify secondary forms is not generally
recommended unless indicated
 Patient profile

• Determine Stage of HTN

• For the stage of HTN determine the presence and/or absence
of associated risk factors
• Determine presence or absence of TOD/associated clinical
condition
• Based on the findings decide on the nature of treatment of
the HTN and other risk factors and plan the follow up
• Set goal of the treatment
 Who should be treated?

• Those with BP levels known to cause risk

• Levels of BP known to expose to risks are
different in different conditions
• Stratification of patients and their risk profile
need definition
 Goals of Therapy

 Uncomplicated hypertension BP <130/80 mmHg

 Hypertension with risks other than diabetes <130/80
 Hypertension with diabetes BP <125/75 mmHg
 Hypertension with chronic kidney disease, CVD, CAD, PVD BP <130/80
 Control other risk factors
 BMI, quitting smoking, cholesterol, moderation on alcohol
consumption, and exercise
 Achieve SBP goal especially in persons >50 years of age.
 Treatment
• A. Non pharmacologic
Indicated for all hypertensive
Include: -Therapeutic life style change
-Modification of diet
-Exercise
 Physical activity

• Increase gradually to 30 minutes brisk walking

or cycling Salt - < 6 gm (1 teaspoon) a day
DIET
• Fruits and vegetables
Fatty Food
 Smoking cessation

• Counseling on cessation of smoking

 Life style management

• If found effective in controlling HTN, life style

intervention should be re-enforced
• If life style is in-effective drug (s) should be
added
• Drug choices made
• Other risk factors managed
 B. Pharmacoogic trea....
• Indicated for those failed to achieve goal BP
after 2-3 months of TLC .
• At beginning in those with hypertensive crisis
OR in those with TOD & BP not in target.
 Pharmacologic….
• Include
A.Diuretics
thiazides,aldactone,loop diuretis

B. Adrenergic blockers
ά blockers:prazocin,phentolamine
β blockers : atenolol,propranalol,carvidilol,
bisoprolol,metoprolol
 Pharmacologic...

C.ACEI: captopril,enalapril,lisinopril
D.Angiotensin recepto
blockers(ARB):Irbesartan,losartan

E.Vasodilator:Nitrates,hydralysine
F.Calcium channel blockers
Dihydropyridens:
nifedipine,amlodipine,nicardipine
Nondihydropyridenes: verapamil,diltazim
 Initial drug choice

• In the absence of compelling evidences

– Least expensive of the following
• Thiazide
• Calcium channel blockers
• Beta-blockers
• ACEI/ARBs
 Algorithm for Treatment of Hypertension
Lifestyle Modifications

Not at Goal Blood Pressure (<140/90 mmHg)

(<130/80 mmHg for those with diabetes or chronic kidney disease)

Initial Drug Choices

Without Compelling With Compelling

Indications Indications

Stage 1 Hypertension Stage 2 Hypertension Drug(s) for the compelling

(SBP 140–159 or DBP 90–99 mmHg) (SBP >160 or DBP >100 mmHg) indications
Thiazide-type diuretics for most. 2-drug combination for most (usually Other antihypertensive drugs
May consider ACEI, ARB, BB, CCB, thiazide-type diuretic and (diuretics, ACEI, ARB, BB, CCB)
or combination. ACEI, or ARB, or BB, or CCB) as needed.

Not at Goal
Blood Pressure

Optimize dosages or add additional drugs

until goal blood pressure is achieved.
Consider consultation with hypertension specialist.
 Followup and Monitoring
 Patients should return for followup and adjustment of medications
until the BP goal is reached.

 More frequent visits for stage 2 HTN or with complicating comorbid

conditions.

 Serum potassium and creatinine monitored 1–2 times per year.

 Followup and Monitoring
(continued)

 After BP at goal and stable, follow up visits at 3- to 6-month intervals.

 Co morbidities, such as heart failure, associated diseases, such as

diabetes, and the need for laboratory tests influence the frequency of
visits.
Management of hypertensive crisis
• The initial aim of treatment in is to rapidly lower the
diastolic pressure to about 100 to 105 mmHg by
parenteral agents; within two to six hours, with the
maximum initial fall in BP not exceeding 25 percent of
the presenting value .
• Once the BP is controlled, switch to oral therapy, with
the diastolic pressure being gradually reduced to 85 to
90 mmHg over two to three months.
• In hypertensive urgency oral agents are used to reduce
BP over 24 hour then to target level over two to three
months.
 Pearls
• For resistant HTN – sit down and take a good
history
– How much water,pop, coffee,milk,juice,tea,ice –
anything liquid do you drink daily.
– Food preferences and salt intake
– Drugs/Alcohol
– Compliance
 OK Now what?
• 2/3 of patients with hypertension will need at
least two medicines for BP control
 Treatment
Benefits
• 35 to 40 percent mean reductions in stroke
incidence
• 20 to 25 percent in myocardial infarction
• 50 percent in heart failure

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THANK YOU