Kuliah IPD III Hipertensi 06

8/13/2019 Kuliah IPD III Hipertensi 06

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SUBDIVISION NEPHROLOGY AND HYPERTENSION

DEPT. INTERNAL MEDICINE

FACULTY OF MEDICINE UNIVERSITY PADJADJARAN

HASAN SADIKIN GENERAL HOSPITAL

BANDUNG

RIA BANDIARA dr. Sp.PD


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Reference

Kaplans Clinical Hypertension, Norman M.K, 8thEdition, 2002

2003 World Health Organization International

Society of Hypertension Guidelines for theManagement of Hypertension

The Sixth Report of The Joint NationalCommittee on Prevention, Detection, Evaluation

and Treatment of High Blood Pressure The Seventh Report of The Joint National

Committee on Prevention, Detection, Evaluationand Treatment of High Blood Pressure


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Lecture Content

Introduction

Definition

Pathophysiology Pathogenesis

Pathophysiology of T.O.D

Measurement of blood pressure History, Physical examination

Treatment


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What is the JNC VII? Seventh Report of the Joint National

Committee on Prevention, Detection,

Evaluation, and Treatment of HighBlood Pressure

Uses evidence-based medicine and

consensus Updates approaches to hypertension

control including diagnosis, evaluation,

lifestyle modification, and drug therapy


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ObjectiveThe objective of identifying and

treating high blood pressure is to

reduce the risk of cardiovasculardisease and associated morbidity andmortality

JNC VII


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Why Control Hypertension? Heart disease and stroke are the 1stand

3rdleading causes of death in the U.S.

More than $259 billion in direct andindirect costs


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Epidemiology 2 million new cases of hypertension

diagnosed each year in the U.S.

23% of men and 25% of women overthe age of 18 in the U.S. have HTN

The prevalence of HTN among African

Americans is increased 30-50% in eachage group compared to persons ofEuropean descent


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Epidemiology cont. The prevalence of HTN increases

steadily with age; over 70% of women

and 50% of men in the U.S. over theage of 70 have HTN

Linear relationship between the degree

of HTN and the risk for CV and renaldisease


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Hypertension Hypertension is not a disease

It is an arbitrarily defined disorder towhich both environmental and geneticfactors contribute

Major risk factor for: cerebrovascular disease

myocardial infarction

heart failure peripheral vascular disease

renal failure


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Blood pressure is a continuous variable

which fluctuates widely during the day physical stress

mental stress

The definition of hypertension has beenarbitrarily set as:

That blood pressure above whichthe benefits of treatment outweighthe risks in term of morbidity andmortality


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At what blood pressure is a patienthypertensive?

BHS 140/90

JNC-VII 140/90 Opt


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Definition

Based on recommendation JNC VII, TheClassification of BP for adult 18 years :

Normal : systolic lower than 120

diastolic lower than 80

Pre-hypertension : systolic 120139

diastolic 8099

Stage-1 : systolic 140159 ordiastolic 9099

Stage-2 : systolic equal to or more than 160

or diastolic equal to or more than

100


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New (2003) WHO-ISH Definitionsand Classification of BP Levels

Category Systolic BP Diastolic BP(mm Hg) (mm Hg)

Optimal BP


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Guidelines for Measurement of BloodPressure

1. Patient conditions1.1. Posture

Initialy, particularly in patients over age 65,diabetic, or receiving antihypertensive therapy,check for postural changes by taking readingsafter 5 minutes supine, then immediately and 2minutes after they stand

For routine follow-up, sitting pressures arerecommended. The patient should sit quietly withthe back supported for 5 minutes and the armsupported at the level of the heart.


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1.2. Circumstances

No caffeine during the hour preceeding the reading

No smoking during the 15 minutes precding the

readingNo exogenous adrenergic stimulants (e.g.phenylephrine in nasal decongestants or eye dropsfor pupillary dilation)

A quiet, warm setting.Home readings taken under varying circumstancesand 24 hours ambulatory recordings may bepreferable and more accurate in predictingsubsequent cardiovascular disease.

Guidelines for Measurement of BloodPressure (continued)


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2. Equipment :

Cuff size : the bladder should encircle and covertwo - thirds of the length of the arm; if it doesnot, place the bladder over the brachial artery. If

bladder is too small, high readings may result. Manometer : Aneroid gauges should be

calibrated every 6 months against a mercurymanometer.

For infants, use ultrasound equipment (e.g. theDoppler method)



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3. Technique3.1. Number of readings

On each occasion, take at least two readings,separated by as much time as is practical. If

readings vary by more than 5 mmHg, takeadditional readings until two are close.

For diagnosis, obtain three sets of readings atleast 1 week apart.

Initially, take pressure in both arms; if the

pressures differ, use arm with the higherpressure.

If the arm pressure is elevated, take pressure inone leg, particularly in patients younger than

30.



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3.2. PerformanceInflate the bladder quickly to a pressure 20 mmHgabove the systolic pressure, as recognized bydisappearance of the radial pulse.Deflate the bladder 3 mmHg every second

Record the Korotkoff phase V (disappearance),except in children, in whom ose of phase IV(muffling) may be preferable.If the Korotkoff sounds are weak, have the patientraise the arm, open and close the hand.

4. RecordingsNote the pressure, patient position, the arm, cuffsize ; e.g. 140/90, seated, right arm, large adultcuff.



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Bladder Length

Muscular and Obese arms

Normal and lean arms

Usually supplied

Children > 5 years

Strongly

recommendedfor routine use

Centre of bladdermustbe overartery

12 cm

23 cm

35 cm

42 cm


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2.

The cuff must be level with theheart. If Arm Circumference

exceeds 33 cm, a large cuff mustbe used. Place stethoscopediaphragm over brachial artery

1.

The patient shouldbe relaxed and the

arm must besupported. Ensureno tight clothing

constricts the arm

3.

The column of mercurymust be vertical. Inflate

to acclude the pulse.

Deflate at 2 to 3mm/sec. Measure

systolic (first sound) anddiastolic

(disappearance) tonearest 2 mmHg.


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Control of blood pressure Blood pressure is controlled by an

integrated system

Prime contributors to blood pressure

are: Cardiac output

Stroke volume

Heart rate

Peripheral vascular resistance

Each of these factors can bemanipulated by drug therapy


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Pathophysiology

BP=TPR X CO (blood pressure is the

product of total peripheral resistanceand cardiac output)


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Autoregulation

BLOOD PRESSURE = CARDIAC OUTPUT X PERIPHERAL RESISTANCE

Hypertension = Increased CO and/or Increased PR

Preload Contractility FunctionalConstriction

StructuralHypertrophy

FluidVolume

VolumeRedistribution

Sympathetic

nervous

overactivity

Renal

Sodium

retention

Descreased

filtration

surface

Renin-

angiotensin

excess

Cell

membrane

alteration

Hyperinsuli

nemia

Genetic

alteration

Obesity Endothelium

derived

factors

StressGenetic

alterationExcess

sodium

intake


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preloadcapacitance

veins

venules

Peripheralresistance

arterioles

Angiotensin/

aldosterone

Blood pressure

Renin release

Bloodvolume

heart

Cardiac output

Sympathetic

system


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Sympathetic Nervous System

Sympathetic system activation produces

vasoconstriction

reflex tachycardia

increased cardiac output

In this way blood pressure is increased

The actions of the sympathetic systemare rapid and account for second tosecond blood pressure control


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The renin-angiotensin-aldosterone system

The RAAS is pivotal in long-term BPcontrol

The RAAS is responsible for:

maintenance of sodium balance

control of blood volume

control of blood pressure


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The RAAS is stimulated by:

fall in BP

fall in circulating volume

sodium depletion

Any of the above stimulate renin

release from the juxtaglomerularapparatus

Renin converts angiotensinogen to

angiotensin IAngiotensin I is converted to

angiotensin II by angiotensin converting

enzyme (ACE)


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Angiotensin II is a potent

vasoconstrictor

anti-natriuretic peptide

stimulator of aldosterone release from theadrenal glands

Aldosterone is also a potentantinatriuretic and antidiuretic peptide

Angiotensin II is also a potent

hypertrophic agent which stimulatesmyocyte and smooth musclehypertrophy in the arterioles


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Myocyte and smooth musclehypertrophy:

are both poor prognostic indicators inpatients with hypertension

partially explain why hypertension and the

risks of hypertension persist in somepatients despite treatment

Both the sympathetic and RAAS are keytargets in the treatment of hypertension


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ANGIOTENSINOGEN Macula densa signal

Renal arteriolar pressure

Renal nerve activity

Adrenalcortex

Kidney Intestine CNS Peripheral nervoussystem

Vascularsmoothmuscle

Heart

Contractility

Adrenergicfacilitation

Sympatheticdischarge

VasoconstrictionVasopressin

releaseThirst saltappetite

Sodium and waterreabsorption

Aldosterone

Distalnephron

reabsorption

Maintain or increase

ECFV

Total peripheral

resistance

Cardiacoutput

ANGIOTENSIN II ANGIOTENSIN III

ANGIOTENSIN I

ANGTIOTENSINASE A

Renin

Convertingenzyme


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Angiotensinogen

Renin

Angiotensin I

ACE vasoconstriction

Angiotensin II Inc. PVRaldosterone (inc. reabsorp of Na)

Inc. blood volume


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Pre

hypertension

Established hypertension

10-30 years

CO

30-50 years

Complicated hypertension

40-60 years

(T. O. D)


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HEREDITY - ENVIRONMENT

PRE - HYPERTENSION

Normotension EARLY HYPERTENSION

ESTABLISHED HYPERTENSION

UNCOMPLICATED COMPLICATED

Accelerated -malignant

course

CARDIACHypertrophy

FailureInfarction

LARGEVESSEL

AneurysmDissection

CEREBRALIschemia

ThrombosisHemorrhage

RENALNephro-sclerosisFailure

Age

0 - 30

20 - 40

30 - 50


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Causes of Hypertension

Essential or Primary

Underlying pathophysiologic alteration

of unknown cause;

95% of cases of HTN

Secondary-Resulting from a specific cause

such as renal or endocrine disorders;5% of cases


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Primary Hypertension

Is usually of gradual onset

Usually develops between the ages of

30 and 50

Tends to remain asymptomatic for 10 to20 years

Triggers include obesity, psychologicalstress, high-sodium intake, and alcoholintake over 1 ounce per day


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Aetiology of essentialhypertension

The aetiology of hypertension is

polyfactorial

polygenic


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Likely causes:

Increased reactivity of resistancevessels and resultant increase inperipheral resistance

as a result of an hereditary defect of thesmooth muscle lining arterioles

A sodium homeostatic effect

In essential hypertension the kidneys are

unable to excrete appropriate amounts ofsodium for any given BP. As a resultsodium and fluid are retained and the BPincreases


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Other factors

Age

Genetics and family history

Environment

Weight

Alcohol intake

Race


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Age

BP tends to rise with age, possibly as a

result of decreased arterial compliance. Hypertension in the elderly should be

treated as aggressively as in the young.

They have more to lose Studies such as EWPHE, Primary Care

Study,MRC Hypertension in the OlderAdult, SHEP, SYSTEUR and STOP-1 and 2

have proven that treating both diastolicand systolic hypertension in the elderlysignificantly reduces stoke and MI.


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Genetics

A history of hypertension tends to run infamilies

The closest correlation exists between sibs

rather parent and child It is also possible that environmental

factors common to members of the familyalso have a role in the development of

hypertension


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Environment

Mental and physical stress both increaseblood pressure

However removing stress does nornecessarily return blood pressure to normal

values True stress responders who have very high

BP when they attend their doctor but lownormal pressures otherwise tend to be

highly resistant to treatment


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Sodium Intake The SALT study and more recently the DASH

study have confirmed a strong relationshipbetween hypertension, stroke and salt intake

Reducing salt intake in hypertensive individualsdoes lower blood pressure

However reducing salt intake in normotensivesappears to have no effect

Reducing salt intake to 60-80mmol/day does lowerBP

However there are real difficulties in achieving thislevel of salt restriction (fast food)


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Alcohol

The most common cause oh hypertension

in the young ScotAffects 1% of the population

Small amounts of alcohol tend to decrease

BP Large amounts of alcohol tend to increase

BP

If alcohol consumption is reduced BP will

fall over several days to weeks.

Average fall is small 5/3 mmHg

i h


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Weight

Obese patients have a higher BP

Up to 30% of hypertension is attributablein part or wholly to obesity

If a patient loses weight BP will fall

In untreated patients a weight loss of 9Kghas been reported to produce a fall in BPof 19/18 mmHg

In treated patients a fall in BP of 30/21

mmHg has been reported Weight reduction is the most important

non-pharmacological measure available


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TYPE II

DIABETES

MELLITUS

Peripheral

Insulin

Resistance

Increased

Pancreatic

Insulin Secretion

Obesity + Androgen

Increased

Abdominal

Fat

DYSLIPIDEMIA

Lipolysis Release ofFree Fatty

Acids

Decreased

Hepatic Insulin

Extraction

Hyperinsulinemia

Increased

Sympathetic

Nervous

Activity

SodiumRetention

VascularHypertrophy

Attenuated

Vasodilation

HYPERTENSION


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Race

Caucasians have a lower BP than blackpopulations living in the same environment

Black populations living in rural Africa have alower BP than those living in towns

Reasons are not clear

Possibly black populations are more susceptible tostress when living in towns

Respond in different ways to changes in diet

Black populations are genetically selected to be

salt retainers and so are more sensitive to anincrease in dietary salt intake

S d H t i


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Secondary Hypertension 5-10% of all hypertension has an identifiable

cause Removal of the cause does not guarantee

that the hypertension or risk will return tonormal

Sustained hypertension produces end-organdamage to blood vessels, heart and kidney

This type of damage tends to increase BP

further and so a vicious self-propagating cycleis established


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Causes for Secondary Hypertension

Renal disease 20% of resistant hypertensive patients

chronic pyelonephritis

renal artery stenosis

polycystic kidneys

Drug Induced

NSAIDs

Oral contraceptive

Corticosteroids

Pregnancy


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Pregnancy

pre-eclampsia

Endocrine

Conns Syndrome

Cushings disease

Phaeochromocytoma

Hypo and hyperthyroidism

Acromegaly

Vascular

Coarctation of the aorta

Sleep Apnoea


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The risks of hypertension

A sustained increase in BP increases theload on the heart and blood vessels

This has two effects

Myocardial hypertrophy Smooth muscle hypertrophy in the

resistance vessels

Hypertrophy of this type increases thestrength of the heart and vasculature

However it also reduces compliance


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The effects of reduced compliance are:

A reduction in the ability of the heart to to

respond to increased or variable loads a decrease in the ability of the resistance

vessels to relax

For the same level of BP andirrespective of age the presence of leftventricular hypertrophy increases 5 yearmortality by

33% in men

21% in women

Atheromatous disease


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Atheromatous disease

Sustained hypertension is associated withaccelerated atheromatous disease of the

blood vessels Peripheral vascular disease

Coronary artery disease

Cerebrovascular disease Renal artery disease

The Heart

MI Heart failure

Angina


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The kidney

Hypertension produces an increase in renal

vascular resistance and a reduction in renalblood flow

R l di


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Renal disease

RBF + afferent glomerular arteriolar resistance

efferent glomerular arteriolar constriction

glomerular hydrostatic pressure

glomerular hyperfiltration

Glomerusclerosis and impairtment of renal function


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Clinical manifestations

None in the early stages, other thanhigh BP reading, if taken

eventually report symptoms, such aspersistent headaches, fatigue, dizziness,palpitations, flushing, blurred vision or

epitaxis


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may also see signs of target organdamage

retinal changes, such as hemorrhages,exudates, arteriolar narrowing, cotton woolspots (small infarctions), and if severe,papilledema (swelling of the optic disc)

angina, MI

LV Hypertrophy, heart failure BUN & Cr, nocturia

stroke & TIA (cerebral infarcts) with such

signs as altered vision, speech, hemiplegia,


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Evaluation: Objectives

1. To identify known causes of highblood pressure

2. To assess the presence or absence oftarget organ damage and CV disease,and the response to therapy

3. To identify other CV risk factors orconcomitant disorders that may defineprognosis and guide treatment


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Evaluation: History

Known duration and levels of elevated BP

History or symptoms of CHD, heart failure,cerebrovascular disease, PVD, renal disease,DM, dyslipidemia, gout, sexual dysfunction, orother comorbid conditions

FH of HTN, premature CHD, stroke, DM,dyslipidemia, or renal disease

Symptoms suggesting causes of HTN

l


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Evaluation: History cont.

History of recent weight changes,physical activity level, tobacco use

Dietary assessment including intake ofsodium, alcohol, saturated fat, andcaffeine

History of all prescribed and meds,herbals, and illicit drugs

Results and adverse effects of previousantihypertensive therapy

Psychosocial and environmental factors

E l ti


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Evaluation:Initial Physical Exam

Two or more BP measurements 2minutes apart with pt either seated or

supine and after standing for at least 2minutes

Verification in the contralateral arm

Measurement of height, weight, andwaist circumference

E l ti


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Evaluation:Physical Exam cont.

Funduscopic exam for hypertensiveretinopathy (arteriolar narrowing, arteriolarconstrictions, AV crossing changes,

hemorrhages and exudates, disc edema) Neck exam for bruits, distended veins, or

enlarged thyroid

Heart exam for rate and rhythm, size,precordial heave, clicks, murmurs, and extraheart sounds

E l ti


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Evaluation:Physical Exam cont.

Lung exam for rales and evidence ofbronchospasm

Abdominal exam for bruits, enlargedkidneys, masses, and aortic pulsation

Extremity exam for decreased

peripheral pulses and edema Neurological exam

E al ation


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Evaluation:Diagnostic Tests

Used to determine the presence of targetorgan damage and other risk factors UA: hematuria, proteinuria, and microalbuminuria

looking for signs of renal dysfunction evidence of DM or renal disease

Lipid panel: as a screen for other risk factors foratherosclerotic disease

EKG: assess for LVH and evidence of priorischemia

Overall Guide to Workup for


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pSecondary Causes of Hypertension

Chronic renal disease

Renovascular disease

Coarctation

Primary Aldosteronism

Cushings syndrome

Pheochromocytoma

Initial AdditionalDiagnosis

Urinalysis, serum

Creatinine, renal

Sonography

Plasma renin before and 1

hour after captopril

Blood pressure in legs

Plasma potassium, plasmarenin and aldosterone (ratio)

AM plasma cortisol after 1mg dexamethasone atbedtime

Spot urine for metanephrine

Isotopic renogram, renal biopsy

Aortagram, isotopic renogram 1 hourafter captopril

Aortogram

Urinary potassium, plasma or urinaryaldosterone after saline load; adrenalcomputed tomography (CT) and

scintiscans

Urinary cortisol after variable doses ofdexamethasone; adrenal CT andscintiscans

Urinary catechols; plasma catechols,basal and after 0.3 mg clonidine;

adrenal CT and scintiscans

Diagnostic Procedure

Which Factors


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Which FactorsInfluence Prognosis? (1)

Decisions should not be made on BP

alone, but also on presence of otherrisk factors, target organ damage,and concomitant diseases, as well ason other aspects of patients personal,medical, social, economic, ethnic, andcultural characteristics

261999 WHO-ISH HYPERTENSION PRACTICE GUIDELINES FOR PRIMARY CARE PHYSICIANS

Which Factors


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Risk factors of CVD

I. Used for risk stratification

II. Other factors adversely influencingprognosis

Target organ damage (TOD)

Associated clinical conditions (ACC)


h h fl ( )


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Which Factors Influence Prognosis? (3)

I. Used for risk stratification Levels of systolic and diastolic blood

pressure (Grades 1-3)

Men >55 years Women >65 years Smoking Total cholesterol >6.5 mmol/L (250

mg/dl) Diabetes Family history of premature

cardiovascular disease

Risk factors for CVD

h h fl ? ( )


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II. Other factors adversely influencingprognosis Reduced HDL cholesterol Raised LDL cholesterol Microalbuminuria in diabetes Impared glucose tolerance Obesity Sedentary lifestyle

Raised fibrinogen High risk socioeconomic group High risk ethnic group High risk geographic region

Risk factors for CVD

Whi h F I fl P i ? (5)


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Target organ damage (TOD)

Left ventricular hypertrophy(electrocardiogram, echocardiogram, orradiogram)

Proteinuria and/or slight elevation of plasmacreatinine concentration 106-177 mmol/L (1.2-2.0 mg/dl)

Ultrasound or radiological evidence of

atherosclerotic plaque (carotid, iliac, andfemoral arteries, aorta)

Generalised or focal narrowing of the retinalarteries

Whi h F t I fl P i ? (6)


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Cerebrovascular disease Ischaemic stroke

Cerebral haemorrhage

Transient ischaemic attack (TIA)

Heart disease Myocardial infarction

Angina pectoris

Coronary revascularisation

Congestive heart failure

Whi h F t I fl P i ? (7)


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Renal disease

Diabetic nephropathy

Renal failure, plasma creatinine

concentration >177 mmol/L (>2.0 mg/dl)Vascular disease

Dissecting aneurysm

Symptomatic arterial disease

Advanced hypertensive retinopathy Haemorrhages or exudates

Papilloedema

Which Factors


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Low risk =


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Stratifying Risk - Quantifying Prognosis


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Management

The most essential element in reducingthe morbidity and mortality associated

with hypertension is long termcompliance/adherence

achieved through life style modification

alone or in combination withpharmacologic therapy (stepped care)


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Lifestyle modification

weight reduction

sodium restriction

dietary fat modification exercise

alcohol restriction

caffeine restriction relaxation techniques

potassium supplementation

Lifestyle Modification to Manage


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Lifestyle Modification to ManageHypertension

Modification Recommendation

Approximate Systolic BP

Reduction, Range

Weight reduction Maintain normal body weight

(BMI, 18.5-24.9)

5-20 mm Hg/10-Kg

weight loss

Adopt DASH eating

Plan

Consume a diet rich in fruits, vegetables, and

low-fat dairy products with a reduced

content of saturated and total fat

8-14 mm Hg

Dietary sodium

reduction

Reduce dietary sodium intake to no more

than 100 mEg/L (2.4 g sodium or 6 g

sodium chloride)

2-8 mm Hg

Physical activity Engage in regular aerobic physical activity

such as brisk walking (at least 30 minutes

per day, most days of the week)

4-9 mm Hg

Moderation of alcohol

consumption

Limit consumption to no more than 2 drnks

per day (1 oz or 30mL ethanol (eg. 24 oz

beer, 10 oz wine, or 3 oz 80-proof

whiskey) in most men and no more than

1 drink per day in women and

lighter-weight persons

2-4 mm Hg

Figure. Algorithm for Treatment of Hypertension

Lifestyle Modification


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Lifestyle Modification

Not at Goal BP

(


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Stratifying Risk - Quantifying Prognosis


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Management Strategy (1)

Is patient at:

Very High Risk

High Risk

Medium Risk

Low Risk


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Stratify Risk

Very HighHigh

Begin drug

treatmentBegin drug

treatment



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Stratify risk

Medium

Monitor BP & otherrisk factors for 3-6 months

SBP >140

or DBP >90

Begin drug

treatment

SBP 95

Begin drug

treatment

SBP


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Principles of Drug Treatment (1)

Use a low dose of one drug toinitiate therapy

If good response and tolerability butinadequate control increase the doseof the first drug

If little response or poor tolerabilitychange to another drug class


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It is often preferable to add a smalldose of a second drug rather than

increase the dose of the first drug

Use long-acting drugs providing 24-

hour efficacy on a once daily basis.Improves adherence to therapy andminimizes BP variability.


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More evidence of beneficial CVD

effects with older drugs (e.g.,

diuretics and beta-blockers)

Evidence of benefit with newer

drugs (e.g., ACE inhibitors andcalcium antagonists) is

accumulating.


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There are six main drug classesused worldwide :

diureticsbeta-blockersACE inhibitors

calcium antagonistsalpha blockersangiotensin II antagonists


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All 6 classes are suitable for the initiationand maintenance of BP lowering therapy,

but the choice of drugs will be influenced bycost and by many factors for special groupsof patients.

In some parts of the world, reserpine andmethyldopa are also used frequently.

Indications


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Compelling Possible

Heart failure Diabetes

Elderly patients

Systolic hypertension

D

iure

tics

Contraindications

Compelling Possible

Gout Dyslipidaemia

Sexually active

males

Indications


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Compelling Possible

Angina Heart failure

After myocardial infarct Pregnancy

Tachyarrhythmias Diabetes

Contraindications

Compelling Possible

Asthma and Dyslipidaemia

Chronic obstructive Athletes and

Pulmonary disease Physically activeHeart block (AV 2,3) Patients

Peripheral

vascular disease

Beta-Blockers

Indications


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Indications

Compelling PossibleAngina Peripheral

Elderly patients Vascular disease

Systolic hypertension

Calci

um

An

tago

nists

Contraindications

Compelling PossibleHeart block (AV 2,3) Heart failure*

* verapimil or diltiazem

Indications


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Compelling Possible

Heart failure

Left ventricular dysfunct

After myocardial infarct

Diabetic nephropathy

Contraindications

Compelling Possible

Pregnancy

Bilateral renal

artery stenosis

HyperkalaemiaACEInh

ibito

rs

Indications


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Indications

Compelling PossibleProstatic Hypertrophy Glucose intolerance

Dyslipidaemia

Contraindications

Compelling Possible

Orthostatichypotension

Alpha-Blocke

rs

Indications


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Compelling Possible

ACE-I cough Heart failure

Contraindications

Compelling Possible

Pregnancy

Bilateral renal

artery stenosis

Hyperkalaemia

Angiote

nsin

II

An

tago

nists

C bi ti Th (1)


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Combination Therapy (1)

In most patients, appropriatecombination therapy produces BP

reductions that are twice as great asthose obtained with monotherapy,

for example, 12-22 mm Hg systolicBP and 7-14 mm Hg diastolic BP forpatients with initial BP of >160/95mm Hg

C bi ti Th (2)


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Combination Therapy (2)

Effective drug combinations to treathypertension are:

diuretic and beta-blocker

diuretic and ACE inhibitor (orAngiotensin II antagonist)

calcium antagonist (dihydropyridine)

and beta-blocker calcium antagonist and ACE inhibitor

alpha-blocker and beta-blocker

Causes of Resistant Hypertension


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Improper blood pressure measurement

Volume overload and pseudotolerance

Excess sodium intake

Volume retention from kidney disease

Inadequate diuretic therapy

Drug-induced or other causes

Nonadherence

Inadequate doses

Inappropriate combinations

Nonsteroidal anti-inflammatory drugs; cyclooxygenase 2 inhibitorsCocaine, amphetamines, other illicitdrugs

Sympathomimetics (decongestants, anorectics)

Oral contraceptives

Adrenal steroids

Cyclosporine and taerolimus

Erythropoictin

Licorice (including some chewing tobbaco)Selected over-the-counter dictary supplement and medicines (eg. Ephedra, ma haung,

bitter orange)

Associated conditions

Obesity

Excess alcohol intake

Identifiable causes of hypertension

Causes of inadequate responsiveness totherapy


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Pseudoresistance

White-coathypertension or officeelevations

Pseudohypertension inolder patient

Use of regular cuff onvery obese arm

Nonadherence to therapy

Volume overload

Excess salt intake

Progressive renal

damage(nephrosclerosis)

Fluid retention from

reduction of bloodpressure

Inadequate diuretictherapy

therapy



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Drug-related causes

Doses too low Wrong type of diuretic

Inappropriate combinations

Rapid inactivation (e.g. hydralazine)

Drug actions and interactions Sympathomimetics - Adrenal steroids

Nasal decongestants - Oral contraceptives

Appetite suppressants - Cyclosporine, tacrolimus

Caffeine - Erythropoietin Licorice (as may be found in chewing tobacco)

Cocaine and other illicit drugs

Antidepressants

Nonsteroidal anti - inflammatory drugs

therapy



100/100

Associated conditions Smoking Increasing obesity Sleep apnea Insulin resistance/hyperinsulinemia Ethanol intake of more than 1 oz (30 mL) per dayAnxiety-induced hyperventilation or panic attacks Chronic pain

Intense vasocondtriction (arteritis) Organic brain syndrome (e.g. memory deficit)

Identifiable causes of hypertension

therapy

Documents

Kuliah IPD III Hipertensi 06