Pathophysiology of Hypertension

and
Hypertension Management

dr.YUDI FADILAH SPPD, KKV

RS MUHAMMADIYAH-FK MUHAMMADIYAH
 SAP
Pokok Bahasan : Hipertensi
Sub Bahasan : pengertian, penyebab, tanda dan gejala , diagnosis,
terapi
Tujuan : mampu memahami dan mengerti tentang hipertensi
Tujuan khusus : menjelaskan, menyebutkan penyebab, tanda gejala,
diagnosis dan terapi
Waktu :
Metode : ceramah dan tanya jawab
Media: power point , bahan kuliah.
 HIPERTENSI
DEFINISI
PATOGENESIS
KLASIFIKASI
JENIS HIPERTENSI
FAKTOR RISIKO
PENGUKURAN TEKANAN DARAH
PENGOBATAN
 EPIDEMIOLOGI

Di Indonesia
Prevalensi hipertensi sebesar 31,7%
Belum terjangkau oleh pelayanan kesehatan
(pedesaan)
Berobat kalau ada keluhan
Tidak makan obat teratur

4
 Hipertensi

Bila tekanan sistolik >= 140 mmHg, dan atau

tekanan diastolik >= 90 mmHg,
atau sedang mendapat obat anti hipertensi.
Patogenesis Hipertensi
Secara hemodinamik, tekanan darah arteri (TD)
merupakan resultan dari cardiac output (CO) dan
resistensi perifer
Heart Rate + Stroke volume

Cardiac output + Peripheral resistance

Blood Pressure
Patogenesis  Hemodinamik Tekanan Darah

Tekanan Darah

Cardiac Output Resistensi perifer

Heart rate Stroke volume Resistensi Viskositas

Pembuluh darah Darah

Kontraktilitas Pre-load
miokard

Kapasitas
Volume darah
vena
8
Hipertensi
 Regulation of BP
o Baroreceptor reflex – changes in arterial pressure – medulla
(brain stem)
◦ Location : left and right carotid sinuses, aortic arch

o Renin – angiotensin system (RAS)

◦ Long – term adjustment of arterial pressure

◦ Kidney - compensation
◦
Endogenous vasoconstrictor – angiotensin I

o Aldosterone release (adrenal cortex)

◦ Stimulates sodium retention and potassium excretion
by the kidney
◦ Increases fluid retention and indirectly arterial
pressure
Primary HTN

o No medical cause

o Risk factors :
o Sedentary lifestyle
o Obesity ( body mass index
greater than 25)
o Salt ( sodium) sensitivity
o Alcohol, smoking
o Family history
Secondary HTN
Common Uncommon
◦ Intrinsic renal disease ◦ Pheochromocytoma

◦ Renovascular disease ◦ Glucocorticoid excess

◦ Mineralocorticoid excess ◦ Coarctation of Aorta

◦ Sleep Breathing disorder ◦ Hyper/hypothyroidism

 Pathophysiology of HTN

oInability of the kidneys to excrete sodium

oAn overactive renin – angiotensin system, vasoconstriction and

retention of sodium and water
– hypertension
oAn overactive sympathetic nervous system
The ANS
o Increased production of catecholamines
(epinephrine and norepinephrine) results in
SNS overactivity.

o This results in an increased heart rate,

increased peripheral vascular resistance
due to systemic vasoconstriction, and
hypertension.
o Additionally, an overactive SNS effects insulin
resistance, vascular remodeling, has
procoagulant effects, which can lead to
neospasm and narrowing of the blood vessels
The
RAAS
 Endothelial
Dysfunction
• Oxidative stress upsets balance
between endothelin and Nitric
oxide

• leads to changes in the

endothelium and sets up a “vicious
cycle” that contributes to the
maintenance of high blood
pressure

• Alterations in endothelial function

are a reliable indicator of target
organ damage and atherosclerotic
disease, as well as prognosis
Genetics
o Caused by single gene mutations which leads to several forms of high blood
pressure

o Ten genes have been identified which cause these monogenic forms
of hypertension.

o HTN has been linked with several chromosomal regions, including regions
linked to familial combined hyperlipidemia, was found.
Risk factors
o Non Modifiable: o Modifiable:

o Age o Weight

o Sex o Physical fitness

o Race o Smoking and alcohol

o Family history o Diet

o Stress

o diabetes

o Certain chromic conditios (e.g. kidney disease,

sleep apnea)
 Complications

o Changes in the vessel wall leading to vessel trauma and arteriosclerosis

throughout the vasculature

o Complications arise due to the “target organ” dysfunction and ultimately

failure.

o Damage to the blood vessels can be seen on fundoscopy.

Target Organs
o CVS (Heart and Blood
Vessels)

o The kidneys

o Nervous system

o The Eyes
Effects On CVS
o Ventricular hypertrophy, dysfunction and failure

o Arrhithymias

o Coronary artery disease, Acute MI

o Arterial aneurysm, dissection, and rupture

Effects on The Kidneys

oGlomerular sclerosis leading to impaired

kidney function and finally end stage
kidney disease

o Ischemic kidney disease especially when

renal artery stenosis is the cause of HTN
Nervous System
o Stroke

ointracerebral and subaracnoid hemorrhage

o Cerebral atrophy and dementia

The Eyes

oRetinopathy, retinal hemorrhages and impaired

vision

o Vitreous hemorrhage, retinal detachment

oNeuropathy of the nerves leading to extraoccular

muscle paralysis and dysfunction
 SIGNS AND SYMPTOMS

oNo symptoms – many people unaware they have

hypertension until accidentally found

o Non–specific symptoms – mild symptoms

Headache, Morning headache, Tinnitus,
Dizziness, Confusion, Fatigue, Shortness of
breath, Changes in vision – blindness, Nausea
BP Classification Systolic Blood Pressure Diastolic Blood Pressure
ESH 2003
Optimal <120 <80
Normal 120-129 80-84
High Normal 130-139 85-89
Grade 1 HT (mild) 140-159 90-99
Grade 2 HT (moderate) 160-179 100-109
Grade 3 (severe) >180 >110
Isolated systolic HT >140 <90

JNC VII
Normal <120 and <80
Prehypertension 120-139 or 80-89
Stage 1 HT 140-159 or 90-99
Stage 2 HT >160 or >100
White coat hypertension

more commonly known as white coat

syndrome, is a phenomenon in which
patients exhibit elevated blood
pressure in a clinical setting but not
in other settings.
Saraf
Jantung
Ginjal
Mata
Pembuluh Darah
 Bagaimana mengukur tekanan darah
yang benar ?
 Alat pengukur tekanan darah yang mana yang paling
baik dipakai ?
 Sfigmomanometer ada 3 jenis: air raksa, aneroid,
dan digital.
Yang paling ideal air raksa.
• Syarat : Penggunaannya harus benar.
Bagaimanakah posisi terbaik saat
pengukuran tekanan darah ?
Pemeriksaan TD sebaiknya dilakukan dalam posisi duduk dg
siku lengan menekuk di atas meja dg posisi telapak tangan
menghadap ke atas dan posisi lengan sebaiknya setinggi
jantung

PENGUKURAN TD YG TIDAK AKURAT AKAN MENIMBULKAN KESALAHAN

DIAGNOSIS DAN TERAPI HIPERTENSI !!
Bagaiamana prosedur pemeriksaan TD yg baik ?

1. Pasanglah manset pd lengan atas, dg batas bawah

manset 2-3 cm dari lipat siku & perhatikan posisi
manset ( lebar manset sebaiknya 2/3 dari panjang
lengan atas).
2. Letakkan stetoskop tepat di atas arteri brakialis.
3. Rabalah pulsasi arteri pada pergelangan tangan (arteri
radialis).
4. Pompalah manset hingga tekanan manset mencapai
30 mmHg setelah pulsasi arteri radialis menghilang.
5. Bukalah katup manset dan tekanan manset dibiarkan
menurun perlahan dg kecepatan 2-3 mmHg/detik.
6. Bila bunyi pertama terdengar, ingatlah dan
catatlah sbg tekanan sistolik.
7. Bunyi terakhir yg masih terdengar dicatat sbg
tekanan diastolik.
8. Turunkan tekanan manset sampai 0 mmHg,
kemudian lepaskan manset.
9. Pengukuran TD sebaiknya dilakukan 2 kali, utk
mendapatkan nilai tekanan darah rerata.
 Pemeriksaan Penunjang
The diagnostic test include:
Electrolytes (sodium, potassium)
Glucose
Lipid profile : Cholesterol, HDL, LDL, Trigliseride
Creatinine (renal function), Testing of urine samples for proteinuria

Electrocardiogram (EKG/ECG)
May show (left ventricular hypertrophy) or the previous silent cardiac
disease even a myocardial infarction).
Chest X-ray - again for signs of cardiac enlargement or evidence of
cardiac failure.
Echocardiography (HHD)
 RSMP
1. Pengobatan non farmakologik( modifikasi gaya hidup )

2. Pengobatan farmakologik (obat-obatan)

R eduction of weight, intake chol,salt
S top smoking
M odification of life
P harmacologic treatment
 Treatment of HTN
o Antihypertensive drugs – act by lowering blood pressure

o Aim of treatment - <140/ 90

o Reduction of blood pressure by 5-6 mm/Hg decreases the risk of stroke by

40%, coronary heart disease by 15- 20%, heart failure and mortality from
vascular disease
 Treatment Options: Antihypertensives
ACE Inhibitors; ARBs
Beta blockers
Calcium cannel blockers; Centrally acting alpha-agonists
Diuretics ; Direct Vasodilators