kul ii - hipertensi
TRANSCRIPT
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HIPERTENSI
edited by :
ESTI DYAH UTAMI, M.Sc., Apt.
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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 :
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CARDIOVASCULAR SYSTEM
05/03/2023
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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
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Location of Heart in Thorax
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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
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Functional Anatomy of the HeartChambers
• 4 chambers– 2 Atria– 2 Ventricles
• 2 systems– Pulmonary – Systemic
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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
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The double pump
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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)
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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
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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
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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
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More cells constriction of bloodvessel walls
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Control of blood pressure
Regulation of cardiac outputcontraction strengthheart ratevenous return
skeletal musclesbreathing rate
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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
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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
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HIPERTENSI
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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.
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• 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)
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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
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TEKANAN DARAH
tekanan yang dialami darah pada pembuluh arteri darah ketika darah di pompa oleh jantung ke seluruh anggota tubuh manusia
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MENGUKUR TEKANAN DARAH
Sphygmomanometer
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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
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PATOGENIS Mekanisme berbagai Vascular Growth Promotors dalam menimbulkan hipertensi
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Epidemiologi Hipertensi diperkirakan menjadi penyebab
kematian sekitar 7,1 juta orang di seluruh dunia, yaitu sekitar 13% dari total kematian.
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Mengapa Tekanan Darah Bisa Tinggi?
1. Controllable Risk Factors
• Increased salt intake
• Obesity• Alcohol• Stress• Lack of
exercise
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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
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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.
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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.
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B. Etiologi/Penyebab
• Hipertensi essensial ( hipertensi primer ) : tidak diketahui penyebabnya
• Hipertensi sekunder : di sebabkan oleh penyakit lain
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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.
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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
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Table 1. Classification and Management of Blood Pressure for Adults Aged 18 Years or Older
HTN Classification
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?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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05/03/2023
KLASIFIKASI TEKANAN DARAH
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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
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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
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Signs and Symptoms
• Known as the Silent killer• If BP is very high, you may experience:• -fatigue• -decreased activity tolerance• -dizziness• -palpitations• -angina• -dyspnea
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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)
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Symptomatic associated with malignant HTN
• Headache• Blurred vision• Chest pain• Breathlessness• Nausea, vomiting• Anxiety, confusion, coma• Seizures
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Komplikasi
• Stroke• Gagal jantung• Gagal Ginjal• Gangguan pada Mata
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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
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Consequences of hypertension
• Cardiac disease Left ventricular failure Angina Myocardial infarction
• Cerebrovascular disease Transient ischemic attacks Stroke Multi-infarct dementia Hypertensive encephalopathy
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Consequences of hypertension
• Vascular disease Aortic aneurysm Occlusive peripheral vascular disease Arterial dissection
• Others Progressive renal failure Hypertensive retinopathy
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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%
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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
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Figure. Algorithm for Treatment of Hypertension
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Table 3. Lifestyle Modifications to Manage Hypertension*
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05/03/2023
Pivotal role in glomerular hypertension in the initiation and progression of structural injury
Kaplan’s, N, M, Clinical Hypertension, 2006
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05/03/2023
Hypertension with renovascular disease
Kaplan’s, N, M, Clinical Hypertension, 2006
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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
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• 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
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05/03/2023
Algorithm for treatment of hypertension
Chobanian, A, V, et al, JNC VII, 2003
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Thanks for Your
Attention 05/03/2023
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