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

05/03/2023

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

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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 HeartChambers

• 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

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Sistem Sirkulasi

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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

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Pathway of Blood Through the Heart and Lungs

The double pump

Larry M. Frolich, Ph.D.,Human Anatomy

Artery/Vein differencesArteries (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

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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)

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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 arterieswill rise and fall as heart pumps

highest with ventricular systolelowest with ventricular diastolepulse pressure is the difference betweenthe two

Resistance is highest in capillaries

More cells constriction of bloodvessel walls

Control of blood pressure

Regulation of cardiac outputcontraction strengthheart ratevenous return

skeletal musclesbreathing rate

Long term regulation of blood flow (hormones)

If blood pressure is too low:

ADH (antidiuretic hormone) promotes waterretention

Angiotensin II- in response to reninsignal (renin) produced by kidney- why?drop in blood pressurestimulation by sympathetic nervous

systemsodium levels too low

What happens?vasoconstriction (by angiotensin II)what will that do to blood pressure?ADH is secretedaldosterone is secreted

EPO (erythropoietin) secreted by kidneysif blood volume is too low

ANP secreted if blood pressure is tooHIGH

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)

PengertianHipertensi 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

menguncupDiastol : bila keadaan jantung mengendur kembali.

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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 DarahGinjal 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 DarahTekanan 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, menggambar kan 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, Ensepalitise. 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)

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KLASIFIKASI TEKANAN DARAH

How HTN is diagnosed

• Based on the average of 2+ seated BP measurements at the MD’s office

• Must be averaged• Must be seated BP measurements• Must be in the MD’s 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 HTNEnd Organ ComplicationsAorta Aortic disectionBrain Hipertensive encepahlopathy Cerebral Infarction or HaemmorhargeHeart Cardiac failure Myocardial ischemic or infarctionKidney Renal failure HaematuriaGastrointestinal Anorexia,nausea,vomiting,abdominal painPlacenta EclampsiaOther 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)

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"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

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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

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Drug-Induced HTN: Prescription Medications

• Steroids• Estrogens• NSAIDS• Phenylpropanolamines• Cyclosporine/

tacrolimus• Erythropoietin• Sibutramine• Methylphenidate• Ergotamine

• Ketamine• Desflurane• Carbamazepine• Bromocryptine• Metoclopramide• Antidepressants

– Venlafaxine• Buspirone• Clonidine

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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

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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

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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 John’s wort

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Substances Associated with HTN

• Food Substances– Sodium Chloride– Ethanol– Licorice– Tyramine-containing

foods (with MAOI)

• Chemicals– Lead– Mercury– Thallium & other

heavy metals– Lithium salts

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Resistant Hypertension

Resistant HT Usually Stage 2 HTNMay present in young individualsMay have secondary causes

Reasons Not taking medication (liers)Improper BP measurementExcessive Na intake, Inadequate diuretic

RxFull doses of drugs not employedDrug interactions – NSAIDs, SMA, OCP,

OTCHerbal remedies, Excessive alcohol use

Rationale Identify the above & correctSecondary causes to be searched for

                                                                                                                                                            

                 

Figure. Algorithm for Treatment of Hypertension

                                                                                                                              

            

Table 3. Lifestyle Modifications to Manage Hypertension*

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Pivotal role in glomerular hypertension in the initiation and progression of structural injury

Kaplan’s, N, M, Clinical Hypertension, 2006

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Hypertension with renovascular disease

Kaplan’s, N, M, Clinical Hypertension, 2006

PENATALAKSANAANA. 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 (β-blocker) Vasodilator Penghambat ACE Antagonis kalsium

• Aims:1. To relieve or forestall symptoms2. To prevent complications3. To prolong life

• Antihypertensive Class Therapy:1. Diuretics2. Sympatoplegics (central, ganglial, peripheral)3. Direct vasodilators4. CCB5. ACEI6. ARBs

ANTIHYPERTENSIVE THERAPY

05/03/2023McNeil, J, J & Krum, H, Avery Drugs Treatment, 2000

05/03/2023

Algorithm for treatment of hypertension

Chobanian, A, V, et al, JNC VII, 2003

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Attention 05/03/2023

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