kuliah ht (2)

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Dr. Dr. Suryono, Suryono, SpJP SpJP .FIHA .FIHA Bagian- Bagian- SMF Kardiologi SMF Kardiologi & Kedokteran & Kedokteran Vaskular Vaskular FK UNEJ / RSD dr. Soebandi FK UNEJ / RSD dr. Soebandi J E M B E R J E M B E R Hiperten Hiperten si si Diagnosis, Pencegahan dan Terapi

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Page 1: Kuliah  HT (2)

Dr. Dr. Suryono,Suryono,SpJPSpJP.FIHA.FIHA

Bagian-Bagian-SMF KardiologiSMF Kardiologi & Kedokteran Vaskular & Kedokteran VaskularFK UNEJ / RSD dr. SoebandiFK UNEJ / RSD dr. Soebandi

J E M B E RJ E M B E R

HipertensiHipertensi

Diagnosis, Pencegahan dan TerapiDiagnosis, Pencegahan dan Terapi

Page 2: Kuliah  HT (2)

Definisi Hipertensi (JNC VII)Definisi Hipertensi (JNC VII) Klasifikasi tekanan darah pada seseorang berumur 18 dan lebih

Page 3: Kuliah  HT (2)

Franklin, S.S., J Hypertens 1999; 17 (suppl 5): S29-S36

Hipertensi salah satu dari penyakit yang sering dijumpai di klinik

0

10

20

30

40

50

60

70

18-29 30-39 40-49 50-59 60-69 70-79 80+

SBP > 140 mm Hg DBP > 90 mm Hg

age (yrs)

pre

vale

nce

of

hyp

erte

nsi

on

(%

)

4 11

21

4454

64 65

Prevalensi dari HipertensiPrevalensi dari Hipertensi

Page 4: Kuliah  HT (2)

Hypertension Prevalence and Treatment: North America and Europe

Prevalence of Hypertension

0

5

10

15

20

25

30

35

40

45

50

55

Country

%

USCanada

Germany

ItalySwedenEnglandSpainFinland

0

10

20

30

40

50

60

70

80

90

100

Country

%

Wolf-Maier K et al. JAMA. 2003;289:2363-2369.

Patients on Therapy

Page 5: Kuliah  HT (2)

23%16%

42%19%

Hypertensive patients who are treated but uncontrolled

Hypertensive patientswho are treated and controlled

Hypertensive patients who are unaware

Patients who are awarebut remain untreated

and uncontrolled

22 % of American adults 18 to 70 years of age have hypertension20 % of Indonesian adults have hypertension

New Criteria (WHO-ISH 1999) ≥ 140 / 90 mmHg

Source : Joffres et al. (1997) Am. J. Hypertension 10: 1097-1102

Page 6: Kuliah  HT (2)

Presentasi pasien hipertensi yang terkontrol

Presentasi pasien hipertensi yang terkontrol

Adapted from G. Mancia / L. Ruilope

USA: JNC VI. Arch Intern Med 1997Canada: Joffres et al. Am J Hypertens 1997 England: Colhoun et al. J Hypertens 1998France: Chamontin et al. Am J Hypertens 1998

< 140/90 mmHg< 140/90 mmHg

Canada

16

USA

27

England6

France

24

Marques-Vidal P et al. J Hum Hypertens 1997

< 160/95 mmHg< 160/95 mmHg

Finland

20.5

Spain

20

Australia

19

Germany

22.5

> 65 years

Scotland

17.5

India

9

Page 7: Kuliah  HT (2)

Diagnosis of Hypertension

Hypertension is defined as:

- BP 140/90 mm Hg- during 1-5 visits- with an average of 2 readings per visit

Page 8: Kuliah  HT (2)

Caused of Hipertension :Caused of Hipertension :

I. Primer / essential / idiopathic

II. Sekunder :

A. Renal

B. Endocrine

C. Coartation of the aorta

D. Pregnancy induced hypertension

E. Neurological disorder

F. Drug and other abused substancen

Page 9: Kuliah  HT (2)

PATOPHYSIOLOGY

The factors affecting cardiac output: - sodium intake, renal function, & mineralocorticoids - the inotropic effects occur via extracellular fluid volume augmentation - an increase in heart rate and contractility

Peripheral vascular resistance is dependent upon the sympathetic nervous system, humoral factors, and local autoregulation

(Sharma, 2003)

Page 10: Kuliah  HT (2)

Neurohormonal control of blood pressure

Blood pressure = Cardiac output (CO) x Peripheral resistance (PR)

Hypertension = Increased CO and/or Increased PR

Preload

Fluid volume

Renal sodiumretention

Contractility

Fluid volume

Vasoconstriction

Sympatheticnervoussystem

Renin-angiotensin-aldosterone

system

Geneticfactors

Excesssodiumintake

(Adapted from Kaplan, 1994)

Page 11: Kuliah  HT (2)

Acute neurohormonal effects on blood pressure homeostasis

Acute neurohormonal effects on blood pressure homeostasis

Heart rate and cardiac output

Perfusion

Sodium and water retention

Blood pressure

RAA SNS

Page 12: Kuliah  HT (2)

Renin inhibitors

AII receptor blockers

Angiotensin II

Renin

Converting enzyme

Angiotensinreceptors

Angiotensinogen

ACE inhibitor

Angiotensin I

Liver TissueCirculating Local

Non Renin pathways - t-PA - Cathepsin G - Tonin

Non-ACE pathways - Chymase - CAGE - Cathepsin G

The Renin-Angiotensin SystemAlternate Pathway

Page 13: Kuliah  HT (2)

Effects of Angiotensin II at AT1 and AT2 Receptors

Blocked by ARB s

AT2AT1

- Vasoconstriction- Aldosterone release- Oxidative stress- Vasopressin release- SNS activation- Inhibits renin release - Renal Na+ and H2O reabsorption- Cell growth and proliferation

- Vasodilation- Antiproliferation- Apoptosis- Antidiuresis/antinatriuresis- Bradykinin production- NO release

Siragy H. Am J Cardiol. 1999;84:3S–8S.

Page 14: Kuliah  HT (2)

Diagnosa HipertensiDiagnosa Hipertensi

Page 15: Kuliah  HT (2)

Riwayat Klinik (Ax):Riwayat Klinik (Ax):

• Lama, tingkat TD

• Adanya Penyakit penyerta

• Faktor risiko

• obat-obatan

• Faktor pribadi,psikososial dan lingkungan.

Page 16: Kuliah  HT (2)

SymptomsSymptoms

• Headache

• Dizziness

• Fatigue

• Pounding of the heart

• Symptoms of complications : heart failure, chest pain, claudication, vision

Page 17: Kuliah  HT (2)

Pemeriksaan Fisik :Pemeriksaan Fisik :

• Pemeriksaan fisik & TD yang teliti• TB, BB, & BMI • Sistim kardiovaskuler • Paru • abdomen. • Fundus optikus & sistim syaraf (mengetahui

kerusakan serebro-vaskuler).

Page 18: Kuliah  HT (2)

Technique of blood pressure measurement recommended by the British Hypertension Society

Technique of blood pressure measurement recommended by the British Hypertension Society

2.The patient should be relaxed and the arm must be supported. Ensure no tight clothing constricts the arm

3.The cuff must be level with the heart. If the circumference exceeds 33cm, a large cuff must be used (2/3 of arm). Place stethoscope diaphram over brachial artery

4.The column of mercury must be vertical. Inflate to occlude the pulse (>30 mmHg). Deflate at 2-3 mm/s. measure systolic ( first sound / Korotkoff I ) & diastolic (disappearence / Korotkoff IV or V ) to nearest 2 mmHg

(From British Hypertension Society 1985)

1.Several time, rest 5 minutes before

Page 19: Kuliah  HT (2)

Recommended Technique for Measuring Blood Pressure

Standardized technique:

• Have the patient rest for 5 minutes

• Use an appropriate cuff size

• Use a mercury manometer or a recently calibrated electronic device

Page 20: Kuliah  HT (2)

• Position cuff appropriately

• Increase pressure rapidly

• Support arm with antecubital fossa or heart level

• To exclude possibility of auscultatory gap, increase cuff pressure rapidly to 30 mmHg above level of diseappearance of radial pulse

• Place stethoscope over the brachial artery

Recommended Technique for Measuring Blood Pressure (cont.)

Page 21: Kuliah  HT (2)

Recommended Technique for Measuring Blood Pressure (cont.)

• Drop pressure by 2 mmHg / beat:

- appearance of sound (phase I Korotkoff)

= systolic pressure

- disappearance of sound (phase V

Korotkoff) = diastolic pressure

• Take 2 blood pressure measurements, 1 minute apart

Page 22: Kuliah  HT (2)

Pengukuran tekanan darah ambulatory(ABPM)

Pengukuran tekanan darah ambulatory(ABPM)

Indikasi1. Adanya variasi tekanan darah yang besar 2. Office hypertension 3.Dicurigai adanya episode hipotensi4. Hipertensi yang resisten terhadap pengobatan

Page 23: Kuliah  HT (2)

Pemeriksaan penunjangPemeriksaan penunjang

• Laboratorium •EKG & Foto polos dada•Ekhokardiografi •Ultrasonografi vaskuler •Ultrasonografi renal Angiografi

Page 24: Kuliah  HT (2)

Evaluasi Klinik Hipertensi : Evaluasi Klinik Hipertensi :

Tujuan :

1. Konfirmasi hipertensi dan tingkatnya

2. Menyingkirkan & menemukan hipertensi sekunder

3. Menentukan kerusakan organ target

4. Mencari faktor risiko kardiovaskuler dan kondisi

klinik lain

Page 25: Kuliah  HT (2)

Komplikasi HipertensiKomplikasi Hipertensi

Kerusakan yang disebabkan oleh hipertensi tergantung :

• Besarnya peningkatan tekanan darah

• Lamanya kondisi tekanan darah yang tidak terdiagnosis dan tidak diobati

Kerusakan Target Organ!!Eyesretinopathy

Kidneysrenal failure

Brainstroke

Heartischaemic heart disease

left ventricular hypertrophyheart failure

Peripheral arterial disease

Page 26: Kuliah  HT (2)

Hypertension :The Disease Continuum

Hypertension :The Disease Continuum

Early Paradigm

Elevated BP Target Organ Damage

Natural History of CVD ProgressionNatural History of CVD Progression

More Recent Paradigm

Vascular Dysfunction Elevated BP Target Organ Damage

A Proposed Future Paradigm

EndothelialDysfunction

LVHRenal

DamageMI Stroke

AnginaPectoris

VascularDysfunction

Elevated BP Target OrganDamage

?

Page 27: Kuliah  HT (2)

Brown, M.J., Lancet 2000;355:653-4

Risiko Infark Miokard dan Stroke Risiko Infark Miokard dan Stroke

Systolic blood pressure (mm Hg)

5-ye

ar r

isk

(%)

0

5

10

15

0 100 200 300

StrokeStrokeMIMI

Page 28: Kuliah  HT (2)

CHFCumulativeIncidence

(%)

Years From Baseline Exam

5 10 15

20

15

10

5

0

Lenfant C, Roccella EJ. J Hypertens Suppl. 1999;17:S3-S7.Data from Levy D et al. JAMA. 1996;275:1557-1562.

Stage 2+ hypertension

Stage 1+ hypertension

Normal BP

Cumulative Incidence of CHF : Normotensives and Stage 1 and 2 Hypertensives

Cumulative Incidence of CHF : Normotensives and Stage 1 and 2 Hypertensives

Page 29: Kuliah  HT (2)

Effects of blood pressure on the risk of cardiovascular disease

Average annual incidence rate per 10.000

Source : Framingham study (after Gorlin)

100

90

80

70

60

50

40

30

20

10

0<100 120 140 180 >180

Systolic blood pressure (mmHg)

CHD

Stroke

CHF

Page 30: Kuliah  HT (2)

Khattar, R.S. et al. Circulation 1999; 100:1071-4

Assessment of the 24-hour blood pressure load isa good clinical method to identify high-risk patients

even

ts/1

00 p

t/yr

s

200+

mm Hg

< 140 140-159 160-179 180-199

1

2

3

4

5

6

7

Systolic Blood PressureSystolic Blood Pressure

Total Mortality and Continuous Ambulatory Blood Pressure

Total Mortality and Continuous Ambulatory Blood Pressure

1

2

3

4

5

Diastolic Blood PressureDiastolic Blood Pressure

mm Hg

< 80 80-89 90-99 100-109 110+

Page 31: Kuliah  HT (2)
Page 32: Kuliah  HT (2)

NON-FarmakologisNON-Farmakologis

FarmakologisFarmakologis

Page 33: Kuliah  HT (2)

Non Pharmacologic ( lifestyle modification )

Modification Approximate SBP

reduction (range)Weight reduction 5–20 mmHg/10 kg loss

Adopt DASH eating plan 8–14 mmHg

Dietary sodium reduction 2–8 mmHg

Physical activity 4–9 mmHg

Moderation of alcohol

consumption 2–4 mmHg

Page 34: Kuliah  HT (2)

DahuluDahulu :: stepped care therapystepped care therapy

KiniKini :: individualized therapyindividualized therapy

Taylored therapyTaylored therapy

Page 35: Kuliah  HT (2)

– Goal of treatment• Improved endothel function • Decreased systemic vascular resistance• Maintain cardiac output & blood suply to organ

– Life long therapy– Bad compliance failed of therapy

Therapy of Hypertension ( pharmacologic )

Page 36: Kuliah  HT (2)

Benefits of Lowering BPBenefits of Lowering BP

Average Percent Average Percent

ReductionReduction

Stroke incidence Stroke incidence 35–40% 35–40%

Myocardial infarction Myocardial infarction 20–25% 20–25%

Heart failureHeart failure 50% 50%

Page 37: Kuliah  HT (2)

Minimal BP Goal of TherapyMinimal BP Goal of Therapy

Recommendations (SBP/DBP mmHg)

Patient Type

Uncomplicated HTN

Hypertension with diabetes mellitus

Heart failure

Hypertension with renal impairment†

JNC VI

< 140/90

< 130/85 < 130/80*

< 130/85

< 125/75

(Bakris GL, et al for the National Kidney Foundation Hypertension and Diabetes Executive Committees Working Group. Am J Kidney Dis. 2000) (JNC VI. Arch Intern Med. 1997)

*National Kidney Foundation Hypertension and Diabetes Executive Committees Working Group.†Proteinuria > 1 g/24h.

Page 38: Kuliah  HT (2)

RecomendationRecomendation

Page 39: Kuliah  HT (2)
Page 40: Kuliah  HT (2)

Compelling Indications for Individual Drug Classes

Compelling Indications for Individual Drug Classes

Clinical Trial BasisInitial Therapy Options Compelling Indication

ALLHAT, HOPE, ANBP2, LIFE, CONVINCE

ACC/AHA Post-MI Guideline, BHAT, SAVE, Capricorn, EPHESUS

ACC/AHA Heart Failure Guideline, MERIT-HF, COPERNICUS, CIBIS, SOLVD, AIRE, TRACE, ValHEFT, RALES

THIAZ, BB, ACE, CCB

BB, ACEI, ALDO ANT

THIAZ, BB, ACEI, ARB, ALDO ANT

High CAD risk

Postmyocardialinfarction

Heart failure

Page 41: Kuliah  HT (2)

Compelling Indications for Individual Drug Classes

Compelling Indications for Individual Drug Classes

Recurrent stroke prevention

Chronic kidney disease

Diabetes

Clinical Trial BasisInitial Therapy Options Compelling Indication

PROGRESS

NKF Guideline, Captopril Trial, RENAAL, IDNT, REIN, AASK

NKF-ADA Guideline, UKPDS, ALLHAT

THIAZ, ACEI

ACEI, ARB

THIAZ, BB, ACE, ARB, CCB

Page 42: Kuliah  HT (2)

Possible combinations of different classes of antihypertensive agents. The most rational combinations are represented as thick lines. ACE, angiotensin-converting enzyme; AT1, angiotensin II type 1.

ACE inhibitorsACE inhibitors

DiureticsDiuretics

11-blockers-blockers

-blockers-blockersATAT11 receptor receptor

blockersblockers

CalciumCalciumantagonistsantagonists