HIPERTENSI

edited by :
ESTI DYAH UTAMI, M.Sc., Apt.
1. Menjelaskan patofisiologi
penyakit hipertensi
2. Menjelaskan data laboratoriun
dan klinik yg berhubungan dgn
penyakit hipertensi
3. Menjelaskan terapi farmakologi
dan non farmakologi penyakit
hipertensi
4. Memberikan alternatif terapi
penyakit hipertensi
Tujuan
Instruksional
khusus :
CARDIOVASCULAR SYSTEM

5/9/2014
Cardiovascular System Function
Functional components of the cardiovascular
system:
HEART
BLOOD VESSELS
BLOOD
General functions these provide
Transportation
Everything transported by the blood
Regulation
Of the cardiovascular system
Intrinsic v extrinsic
Protection
Against blood loss
Production/Synthesis
Location of Heart in Thorax
Chapter 18, Cardiovascular System 6
External Heart: Anterior View
Figure 18.4b
7
Review Anatomi
Jantung berada dalam rongga
thoraks di area mediastinum
(ruang antar paru)
Terdiri dari sisi apeks
(intercostalis 5) dan basal
(costalis 2)
Terdiri dr 3 lapisan :
perikardium, miokardium dan
endokardium
Functional Anatomy of the Heart
Chambers
4 chambers
2 Atria
2 Ventricles
2 systems
Pulmonary
Systemic
What is the cardiovascular system?


The heart is a double pump

Heart arteries arterioles

Veins venules capillaries
10
Sistem Sirkulasi
11
Pathway of Blood Through the
Heart and Lungs
Right atrium tricuspid valve right
ventricle
Right ventricle pulmonary semilunar valve
pulmonary arteries lungs
Lungs pulmonary veins left atrium
Left atrium bicuspid valve left ventricle
Left ventricle aortic semilunar valve
aorta
Aorta systemic circulation
12
Pathway of Blood Through the Heart and Lungs
The double pump
Larry M. Frolich, Ph.D.,Human Anatomy
Artery/Vein differences
Arteries (aa.) Veins (vv.)
Direction
of flow
Blood Away from
Heart
Blood to Heart
Pressure Higher Lower
Walls THICKER: Tunica
media thicker than
tunica externa
THINNER: Tunica
externa thicker
than tunica media
Lumen Smaller Larger
Valves No valves Valves (see next)
Arteri Vena
Dindingnya elastis dan tebal Dindingnya tipis dan kurang elastis
Tekanan darahnya kuat/cepat Tekanan darahnya lemah
Darah kaya akan O2 kecuali arteri
pulmonalis
Darah kaya akan CO2 kecuali vena
pulmonalis
Letaknya agak dalam Letaknya dekat dengan permukaan kulit
Denyut jantung terasa Denyut jantung tidak terasa

Perbedaan Arteri dan Vena
Tidak memilki katup Memilki katup
Arah aliran menuju keluar jantung Aliran darah menuju jantung
17
Pengontrolan Curah Jantung
Curah jantung (cardiac output): jumlah darah yg dipompa
oleh tiap ventrikel dlm waktu 1 menit
Pd org dewasa (istirahat) 5 L/menit; meningkat sesuai dg
kebutuhan
Curah jantung = Isi sekuncup x denyut jantung per menit

Isi sekuncup (stroke volume): volume darah yang dipompa
ventrikel tiap denyut.
Setiap berdenyut, ventrikel memompa 2/3 vol ventrikel;
jml darah yg dipompa: fraksi ejeksi
sisa darah yg masih ada di ventrikel setelah sistol
berakhir: volume akhir sistol (ESV = end systolic volume)
jumlah darah yg dpt ditampung ventrikel sampai diastol
berakhir: volume akhir diastol (ESD = end diastolic
volume)
18

19
Pengontrolan Kerja
Jantung
BLOOD PRESSURE


Blood flow is generally equal to cardiac output

Blood flow affected by pressure and resistance

Blood pressure: the force that is exerted by blood against
blood vessel walls

Resistance depends on size of blood vessel and thickness
(viscosity) of blood
Blood pressure is highest in large arteries
will rise and fall as heart pumps

highest with ventricular systole
lowest with ventricular diastole
pulse pressure is the difference between
the two

Resistance is highest in capillaries
More cells constriction of blood
vessel walls
Control of blood pressure

Regulation of cardiac output
contraction strength
heart rate
venous return
skeletal muscles
breathing rate
Long term regulation of blood flow (hormones)

If blood pressure is too low:

ADH (antidiuretic hormone) promotes water
retention

Angiotensin II- in response to renin
signal (renin) produced by kidney- why?
drop in blood pressure
stimulation by sympathetic nervous
system
sodium levels too low
What happens?
vasoconstriction (by angiotensin II)
what will that do to blood pressure?
ADH is secreted
aldosterone is secreted

EPO (erythropoietin) secreted by kidneys
if blood volume is too low

ANP secreted if blood pressure is too
HIGH
HIPERTENSI
APA ITU HIPERTENSI?
hipertensi
adalah kondisi medis
di mana terjadi
peningkatan tekanan
darah secara kronis
(dalam jangka waktu
lama)
Yaitu penderita yang
mempunyai tekanan
darah yang melebihi
140/90 mmHg saat
istirahat.
Hipertensi dapat didefinisikan sebagai tekanan
darah persisten dimana tekanan sistoliknya
diatas 140 mmHg dan tekanan diastoliknya diatas
90 mmHg.( Smith Tom, 1995 )
Hipertensi adalah tekanan darah tinggi atau
istilah kedokteran menjelaskan hipertensi adalah
suatu keadaan dimana terjadi gangguan pada
mekanisme pengaturan tekanan darah
(Mansjoer,2000 : 144)
Pengertian
Hipertensi sebenarnya bukanlah suatu penyakit,
melainkan merupakan suatu kelainan suatu gejala dari
gangguan pada mekanisme regulasi Tekanan Darah.
TD = Sistol/Diastol (mmHg)
Sistol : tekanan pada dinding arteliole sewaktu jantung
menguncup
Diastol : bila keadaan jantung mengendur kembali.
31
HTN
The Truth is
It is only a marker of the bigger problem
HTN is a multi-organ systemic disease
What we record as B.P.
The Problem is
HTN is asymptomatic in 85% of cases
TEKANAN
DARAH
tekanan yang
dialami darah pada
pembuluh arteri
darah ketika darah
di pompa oleh
jantung ke seluruh
anggota tubuh
manusia
MENGUKUR TEKANAN DARAH
Sphygmomanometer
PENYEBAB HIPERTENSI
1. Tidak diketahui,
90-95 % kasus
hipertensi tidak
diketahui
penyebabnya
( Primary
Hypertension)
2. Secondary Hypertension
(5 to 10%)
Kidney
Abnormalities
Narrowing of certain
arteries
Rare tumors
Adrenal gland
abnormalities
Pregnancy


PATOGENIS
Mekanisme berbagai Vascular Growth Promotors dalam menimbulkan hipertensi

Epidemiologi
Hipertensi diperkirakan menjadi penyebab
kematian sekitar 7,1 juta orang di seluruh
dunia, yaitu sekitar 13% dari total kematian.
Mengapa Tekanan Darah Bisa Tinggi?
1. Controllable Risk
Factors
Increased salt
intake
Obesity
Alcohol
Stress
Lack of
exercise

2. Uncontrollable Risk
Factors
Heredity
Age
Men between age 35
and 50
Women after
menopause
Race
1 out of every 3
African Americans
Higher incidence in
non-Hispanic blacks
and Mexican
Americans

Regulasi Tekanan Darah
Ginjal memegang peranan penting pada pengaturan tingginya TD, yang
berlangsung melalui suatu sistem khusus, yaitu RENIN-ANGIOTENSIN
(RAS). Bila volume darah yang mengalir melalui ginjal berkurang dan TD di
glomeruli ginjal menurun, misalnya karena penyempitan arteri setempat,
maka ginjal dapat membentuk dan melepaskan enzim proteolitis renin.
Dalam plasma, renin ini menghidrolisa protein Angiotensinogen (yang
terbentuk dalam hati) menjadi angiotensin I (AT I ). Zat ini diubah oleh
enzim ACE ( Angiotensin Converting Enzim ) yang disintesa antara lain di
paru-paru, menjadi zat aktif angiotensin II (AT II). AT II ini antara lain
berdaya vasokontriktif kuat dan menstimulasi sekresi hormon aldosteron
oleh anak ginjal dengan sifat retensi garam dan air. Akibatnya ialah
volume darah dan TD naik lagi menjadi normal.
Tekanan Darah
Tekanan darah banyak bergantung pada :
Curah jantung, yang merupakan cerminan fungsi
jantung
Resistensi vaskular perifer (TPR), ditentukan oleh
diameter pembuluh darah perifer.
Tonus dan elastisitas arteri, menggambarkan kondisi
dinding pembuluh darah perifer.
Volum darah dalam arteri, menunjukkan jumlahnya
darah intravaskular.
Viskositas darah, menunjukkan kondisi cairan
intravaskular.

B. Etiologi/Penyebab
Hipertensi essensial ( hipertensi primer )
: tidak diketahui penyebabnya
Hipertensi sekunder : di sebabkan oleh
penyakit lain

Hipertensi essensial (hipertensi
primer )
Genetik : Respon nerologi terhadap stress
atau kelainan eksresi
Obesitas : terkait dengan level insulin yang
tinggi
Hilangnya Elastisitas jaringan dan
arterisklerosis pada orang tua serta
pelebaran pembuluh darah.
Kebiasaan hidup : Konsumsi garam yang
tinggi, makan berlebihan, stress, merokok,
minum alkohol.
Hipertensi sekunder
a. Ginjal : Glomerulonefritis, Pielonefritis, Nekrosis
tubular akut, Tumor
b. Vascular :
Aterosklerosis, Hiperplasia, Trombosis, Aneurisma,
Emboli kolestrol, Vaskulitis
c. Kelainan endokrin :
DM, Hipertiroidisme, Hipotiroidisme
d. Saraf : Stroke, Ensepalitis
e. Obat obatan : Kortikosteroid






Table 1. Classification and Management of Blood Pressure for Adults Aged 18 Years or Older



HTN Classification
?Prehypertension
NOT a DISEASE category
Should encourage Lifestyle modification as this
group has an increased risk of becoming
hypertensive
NOT candidates for drug therapy (unless
compelling indications ie DM etc goal
<130/80)

5/9/2014
KLASIFIKASI TEKANAN DARAH
How HTN is diagnosed
Based on the average of
2+ seated BP
measurements at the
MDs office
Must be averaged
Must be seated BP
measurements
Must be in the MDs
office

Laboratory Tests
Routine Tests
Electrocardiogram
Urinalysis
Blood glucose, and hematocrit
Serum potassium, creatinine, or the corresponding estimated GFR,
and calcium
Lipid profile, after 9- to 12-hour fast, that includes high-density and
low-density lipoprotein cholesterol, and triglycerides
Optional tests
Measurement of urinary albumin excretion or albumin/creatinine ratio
More extensive testing for identifiable causes is not generally indicated
unless BP control is not achieved
Signs and Symptoms
Known as the Silent killer
If BP is very high, you may experience:
-fatigue
-decreased activity tolerance
-dizziness
-palpitations
-angina
-dyspnea
Sign and Symptoms
Essential HTN is usually
- asymptomatic
- undetected for many years
- headache, BP elevated systolic
beyond 200 mmHg or BP rising
rapidly (can occur in malignant
HTN)
Symptomatic associated with malignant HTN
Headache
Blurred vision
Chest pain
Breathlessness
Nausea, vomiting
Anxiety, confusion, coma
Seizures
Komplikasi
Stroke
Gagal jantung
Gagal Ginjal
Gangguan pada Mata

Consequences of Malignant HTN
End Organ Complications
Aorta Aortic disection
Brain Hipertensive encepahlopathy
Cerebral Infarction or Haemmorharge
Heart Cardiac failure
Myocardial ischemic or infarction
Kidney Renal failure
Haematuria
Gastrointestinal Anorexia,nausea,vomiting,abdominal
pain
Placenta Eclampsia
Other Micro-angiopathic haemolytic anemia
Consequences of hypertension
Cardiac disease
Left ventricular failure
Angina
Myocardial infarction

Cerebrovascular disease
Transient ischemic attacks
Stroke
Multi-infarct dementia
Hypertensive encephalopathy

Consequences of hypertension
Vascular disease
Aortic aneurysm
Occlusive peripheral vascular disease
Arterial dissection

Others
Progressive renal failure
Hypertensive retinopathy
Isolated Systolic hypertension increase the risk
of :
stroke and coronary heart disease by about
40%
cardiovascular death by about 50%
heart failure by about 50%

Complications Related to HTN
Heart Failure
Enlarged Left Side of the Heart
Coronary Artery Disease
Cerebrovascular disease (Brain)
Peripheral Vascular Disease
Kidney Failure
Retinal Damage (Eyes)

"The Goal is to Get to Goal!
HTN
-PLUS-
Proteinuria > 1 gr/day
< 140/90 mmHg < 130/80 mmHg
Measurements & goals should
be provided to the patient
verbally and in writing at each
office visit
58
Causes of Resistant HTN
Improper BP measurement
Excess sodium intake
Inadequate diuretic therapy
Medication
Inadequate doses
Drug actions and interactions:
NSAIDs, illicit drugs, sympathomimetics, OCP
OTC drugs & herbal supplements
Excess alcohol intake
Identifiable causes of HTN
JNC 7 Express. JAMA. 2003 Sep 10; 290(10):1314
59
Drug-Induced HTN: Prescription
Medications
Steroids
Estrogens
NSAIDS
Phenylpropanolamines
Cyclosporine/tacrolimus
Erythropoietin
Sibutramine
Methylphenidate
Ergotamine
Ketamine
Desflurane
Carbamazepine
Bromocryptine
Metoclopramide
Antidepressants
Venlafaxine
Buspirone
Clonidine
60
COX-2 Inhibitors & NSAIDs
Inhibition of cyclooxygenase, inhibits
prostaglandin synthesis that normally maintains
afferent arteriole vasodilatation
Afferent vasoconstriction decreases renal
perfusion increased BP
Increasing salt & water retention
Increasing renin release
COX-1 is thought to be primary enzyme
responsible for renal vasodilatory
prostaglandins
61
COX-2 Inhibitors & NSAIDs
Case reports of severe increases in BP exists in
patients after one dose or more typically after
4 weeks for regular usage
Consider scheduled acetaminophen as an
alternative to NSAIDs in patients with difficult
to manage HTN

Drugs Aging. 2004; 21:479-84; JAMA. 2001; 286:954-59
62
Drug-Induced HTN: Street Drugs &
Herbal Products
Cocaine
Ma huang herbal ecstasy
Nicotine
Anabolic steroids
Narcotic withdrawal
Methylphenidate
Phencyclidine
Ketamine
Ergot-containing herbal products
St Johns wort


63
Substances Associated with HTN
Food Substances
Sodium Chloride
Ethanol
Licorice
Tyramine-containing
foods (with MAOI)
Chemicals
Lead
Mercury
Thallium & other
heavy metals
Lithium salts
64
65
Resistant Hypertension
Resistant HT Usually Stage 2 HTN
May present in young individuals
May have secondary causes
Reasons Not taking medication (liers)
Improper BP measurement
Excessive Na intake, Inadequate diuretic Rx
Full doses of drugs not employed
Drug interactions NSAIDs, SMA, OCP, OTC
Herbal remedies, Excessive alcohol use
Rationale Identify the above & correct
Secondary causes to be searched for






Figure. Algorithm for Treatment of Hypertension






Table 3. Lifestyle Modifications to Manage Hypertension*



5/9/2014
Pivotal role in glomerular hypertension in the
initiation and progression of structural injury
Kaplans, N, M, Clinical Hypertension, 2006
5/9/2014
Hypertension with renovascular
disease
Kaplans, N, M, Clinical Hypertension, 2006

PENATALAKSANAAN
A. penatalaksanaan nonfarmakologi
atau perubahan gaya hidup
Penurunan berat badan
penurunan asupan garam
menghindari faktor resiko
(merokok, minum alkohol,
hiperlipidemia dan stres)
B. penatalaksanaan farmakologi
atau dengan obat
Diuretik
Golongan penghambat
simpatetik
Penyekat Beta (-blocker)
Vasodilator
Penghambat ACE
Antagonis kalsium

Aims:
1. To relieve or forestall symptoms
2. To prevent complications
3. To prolong life

Antihypertensive Class Therapy:
1. Diuretics
2. Sympatoplegics (central, ganglial, peripheral)
3. Direct vasodilators
4. CCB
5. ACEI
6. ARBs

ANTIHYPERTENSIVE THERAPY
5/9/2014
McNeil, J, J & Krum, H, Avery Drugs Treatment, 2000
5/9/2014
Algorithm for treatment of hypertension
Chobanian, A, V, et al, JNC VII, 2003
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