HIPERTENSI :

PATOFISIOLOGI DAN
TATALAKSANA

Dyah Siswanti

Divisi Kardiologi , FK Universitas Riau /

RS Arifin Ahmad Pekanbaru
 Pendahuluan

BP = CO x PVR

HR x SV
 Definisi
• Hipertensi adalah sindroma kardiovaskular
yang progresif yang timbul dari etiologi
yang kompleks dan saling berhubungan

• Progresivitas sangat dipengaruhi oleh

gangguan jantung dan pembuluh darah baik
struktural maupun fungsional dan akan
menimbulkan kerusakan pada jantung,
ginjal, otak dan saraf, pembuluh darah dan
organ2 lain yang akan mengakibatkan
kematian dini
 Pathophysiology of Hypertension

Excess sodium Stress Genetic Obesity

Reduced nephron
intake

Renal sodium Decreased Sympathetic RAA Cell Hyper-

retention filtration overactivity excess Alteration insulin

Fluid Venous
Volume constriction

Preload Contractility Functional Structural

constriction hypertrophy

Blood pressure = cardiac output x peripheral resistance

Hypertension = increased CO and/or increased PR Kaplan 2005
 Hypertension Control Rates (%)
Around the World
<140/90 mm Hg <160/95 mm Hg

United States 27
France 24
Canada 22
Italy 9
Egypt 8 Germany 23
England 6 Finland 21
Korea 5 Spain 20
China 3 Australia 19
Poland 2 Scotland 18
India 9
Zaire 3
 Classification of Blood Pressure for
Adults Aged 18 Years or Older
JNC V

Category Systolic mmHg Diastolic

mmHg

Normal < 130 < 85

High normal 130 – 139 85 – 89
Hypertension
Stage I ( mild ) 140 – 159 90 – 99
Stage 2 ( moderate) 160 – 179 100 – 109
Stage 3 ( severe) 180 – 209 110 – 119
Stage 4 very severe) > 210 > 120
 Classification of Blood Pressure for
Adults Aged 18 Years or Older
JNC VI

Category Systolic mmHg Diastolic mmHg

Optimal < 120 and < 80

Normal < 130 and < 85
High normal 130 – 139 or 85 – 89

Hypertension

Stage I 140 – 159 or 90 – 99

Stage II 160 – 179 or 100 – 109
Stage III > 180 or > 110
Classification of Blood Pressure for
Adults Aged 18 Years or Older
JNC VII
 Hypertension classification of
WHO - ISHWG

Category Systolic Diastolic

Optimal <120 <80

Normal <130 <85
High normal 130 -139 85 -89

Stage 1 ( mild) 140 – 159 90 - 99

Subgroup : borderline 140 -149 90-94
Stage 2 ( Moderate) 160-179 100-109
Stage 3 ( severe >180 >110

ISH >140 <90

Subgroup : borderline 140-149 < 90
Effects of hypertension on target organ

• Increase risk of fatal stroke

• Increase risk of coronary heart disease
• Increase risk of vascular disease ( renal,
peripheral vasculatr etc )
 Target Organ Damage in Hypertension
Organ System Manifestations

Heart -Left ventricular hypertrophy

-Heart failure
-Myocardial ischemia and infarction

Cerebrovascular Stroke

Aorta and peripheral vascular -Aortic aneurysm and/or dissection

-Arteriosclerosis

Kidney -Nephrosclerosis
-Renal failure

Retina -Arterial narrowing

-Hemorrhages, exudates,
papilledema
 Normal heart (cross section)

Concentric hypertrophy of the left

ventricle; there is myocardial
thickening without dilatation of the
ventricular lumen. There is
increased ratio of wall thickness to
cavity radius. This change is
associated with pressure overload
as in HTN, and aortic stenosis.
Group BP Goal (mm Hg)
General DM* CKD**
JNC 8: <60 yr: <140/90 < 140/90 < 140/90

>60 yr: <150/90

ESH/ESC: < 140/90 < 140/85 < 140/90

Elderly 140-150/90 (SBP < 130 if proteinuria)

(<80 yr: SBP<140)

ASH/ISH < 140/90 < 140/90 < 140/90

>80 yr: <150/90 (Consider < 130/80 if proteinuria)

 Treatment of hypertension
LIFESTYLE MODIFICATION

• Healthy eating plan ( DASH eating plan )

• Doing enough physical activity
• Maintane helthy weight
• Quit smoking
• Manage stress and learning to cope with
stress
 Drugs

There are six main drug classes used

worldwide :
diuretics
beta-blockers
ACE inhibitors
calcium antagonists
alpha blockers
angiotensin II antagonists
● Thank you !!
 Development of Antihypertensive Drugs
Reserpin (1949)
1950
HCT (1958)
Diuretics 1960
Verapamil (1963)
Furosemide (1964)
Propanolol (1965)
Beta blockers
1970
Nifedipin (1975)
CCBs
Prazosin (1977)
α1-blockers 1980 Captopril (1981)

ACE-inhibitors 1990 Losartan (1995)

Valsartan
AT1-antagonists 2000 ?
 Treatment of hypertension
Medication

• Thiazide like diuretic

• ACE inhibitor ( ACE-I )
• Angiotensin Receptor blocker ( ARB )
• Beta blocker
• Calcium chanel Blocker
• Alpha receptor blocker
 Type of medication
thiazide diuretics

• Inhibit sodium and chloride contrasport

across luminal membrane of the early
segment of distal convoluted tubule
• In chronic use, peripheral resistance
decrease
 Type of medication
ACE Inhibitor

• Influence RAAS
• Inhibits ACE so angiotensin I cannot
change to Angiotensin II
• Angiotensin II have vasoconstriction effect,
Na retention and aldosteron stimulation
 Angiotensinogen

Renin Tissue renin

Cathepsin G
Angiotensin I
Bradykinin Elastase
Tissue ACE
ACE TPA
Chymase
Peptide Cathepsin G

Angiotensin II
ARBs

AT2R
AT1R
 ARB ACE-I

Ang Ι Ι
Ang Ι Ι ↓ Bradykinin ↑

• Vasoconstriction NO
AT 2 AT 1 AT 1 AT 2
• Renal sodium reabsoption PGI2
• Aldosteron secretion

• Vasodilatation • Sympathetic activation

• Antiproliferation • Cell growth and proliferation

• Apoptosis
 Type of medication
central alpha agonist / alpha blocker

• Decline symphatetic activity reflected in

lower levels of norepinephrine
• Reduction of the ability of the baroreceptor
reflex to compensate for decrease BP
• Decrease CO and PR
• Decrease plasma renin
• Maintenance of renal blood flow
 Type of medication
beta blockers

• Reduction in CO
• Decrease of renin release
• Decrease in central symphatetic nervous
outflow
• Differences due to non selective or
selective beta 1 or 2 blockers, with or
without ISA and with activity in alpha
blocking
 Type of medication
Calcium chanel blocker
• Inhibits Ca transport into myocardium ang
vascular smooth muscle vasodilators
• Decrease myocardium contractility,
decrease HR by slowing down nervous
impulse conduction
• Differences due to dihydrophyridines or
non dihydrophyridines