hipertensi by. dr. rudy utantio, sp.jp

8/13/2019 Hipertensi by. Dr. Rudy Utantio, Sp.jp

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HIPERTENSI

=

TEKANAN DARAH

TINGGI

Dr.BRudy Utantio, Sp.JP

Konsultan Kardiologi


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Perjalanan penyakit kardiovaskulerSindrom

KoronerAkut

Trombosis koronerAritmia &berkurangnyasel miokardAktivitas

neurohormonal

Matimenda

dakIskemia miokard

PJKRemodeling

Aterosklerosis Pembesaran ventrikel

GJ

Kematian

Fakto r-2 risiko

DislipidemiaHTNDiabetes

Merokok, dll

Dzau V. Braunwald E. Am Heart J. 1991:121:1244-163


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PERUBAHANPOLA MAKAN

Kadar lemak tinggi, protein tinggi, garam tinggi

dan kandungan serat pangan (dietery fiber)

yang rendah menyebabkan penyakitdegeneratif yang meningkat :

- penyakit jantung

- diabetes mellitus- kanker

- osteoporosis

- hipertensi

PENDAHULUAN


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PREVALENSI HIPERTENSI

Di Dunia : 5-18%

Di Indonesia :

Hasil SKRT (1995) 83/1000 anggota RT:

* Perempuan > pria* Di luar Jawa & Bali prevalensinya >

Ungaran : 1.8%

Silungkang : 19.4 %

Lembah Balim : 0,6 %


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HIPERTENSI ~ TEKANAN DARAH TINGGI

Masih merupakan masalah kesehatanSilent Killer

Pembunuh terselubung !!!!

* Tidak ada keluhan* Tidak memberikan gejala

- stroke

- peny J Koroner

- gagal ginjal, dll

Fenomena gunung es


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COMMUNITY STUDIES :

* POORLY CONTROLLED

* THE RULE OF HALVES

Penderita Hipertensi

Tidak terdignosa= 50% Terdiagnosa = 50 %

Tidak berobat = 50 % Berobat = 50 %

Tidak teratur = 50 %

Teratur 50 %

Penderita HTN

Tidak terdiagnosa 50 % Terdiagnosa 50 %

Tidak berobat 50 % Berobat 50 %

Tidak teratur 50 %

Teratur 50 %


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25%12.5%

12.5%

50%

Tahu punya HTN

Sudah minum obat

Tidak kontrol

Tahu punya HTN

Tetap minum obat

Kontrol teratur

Tidak tahu

Tidak terdiagnosa

Tahu punya HTN

Tidak minum obat

Tidak kontrol

Source : Joffres et al. (1997) Am. J. Hypertension 10: 1097-1102

Hukum 50% kelompok penderita

hipertensi


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APAKAH TEKANAN DARAH ?

Tekanan dari jantung memompa darah

mengalir ke seluruh pembuluh darah (+ oksigen )

mempertahankan kehidupan

Jantung: Pompa bekerja non stop

Pembuluh darah: Saluran untuk aliran darah

Mengukur tekanan darah mengukur kekuatandarah pada saat menekan dinding pembuluh darah


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SPIGMOMANOMETER

TENSI METER

Tekanan darah sistolik:

* Nilai atas

* Tekanan pada saat

jantung memompa Tekanan darah diastolik:

* Nilai bawah

* Tekanan pada saat

jantung istirahat


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TERMINOLOGI

1. Hipertensi Esensial

= HT. Primer

= HT. Idiopatik

Kausa ? 95%2. Hipertensi Sekunder

Kausa 5 %

3. Penyakit Jantung Hipertensi= Hypertensive Heart Disease ( HHD )

HT + Hipertrofi Ventrikel Kiri ( L.V.H )

(+)


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4. Hypertensive Heart Failure = H.H.F

HT + Decompensatio cordis

5. Hipertensi Labil

Tekanan darah kadang-kadang

6. Krisis Hipertensi: peningkatan TD mendadak (180/120)

* HT. Gawat : kerusakan organ target yang progresif

* HT Darurat : tidak disertai kerusakan organ target

7. White Coat Hypertension

= Stress Hypertension

= Office Hypertension

= Responsive Hypertension

8. Hipertensi Sistolik

TDS 140 mmHg

9. Hipertensi Diastolik

TDD 90 mmHg


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DEFINISI HIPERTENSI

T.D. Sistolik 140 mmHg dan atau

T.D. Diastolik 90 mmHg

Perubahan tekanan darah :

TDD : Selalu sama sepanjang waktu

TDS : - Sering berubah-ubah


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B lood Pressure Class i f ication

( JNC VII 2003)

BP Classification SBP-mmHg DBP-mmHg

Normal < 120 and < 80

Prehypertension 120-139 or 80-90

Stage 1 Hypertension 140-159 or 90-99

Stage 2 Hypertension 160 or 100

Klasifikasi lain dari WHO-ISH 1999


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Classification of BP

JNC VI (1997)

Category SBP DBP

Optimal


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MENGAPA T.D TINGGI ??

PATOFISIOLOGI HIPERTENSI

MEKANISME HIPERTENSITidak dapat dijelaskan dengan satu penyebab spesifik

HT Essensial :

Akibat Interaksi Dinamis :

- faktor genetik

- faktor lingkungan- faktor lain

RUMUS TD = C.O X TAHANAN PERIFER


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CARDIAC OUTPUT = CO

= Curah Jantung= Darah yang dipompa oleh jantung

= HR x SV

TD = HR x SV x Periferal resistance

TAHANAN PERIFER* Ditentukan oleh diameter pembuluh darah

arteri


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FAKTOR LA IN :

Retensi sodium

Turunnya filtrasi ginjal

Me saraf simpatis Me aktifitas RAA

Perubahan membran sel

Hiperinsulinemia

Disfungsi endotel


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PATHOPHYSIOLOGY

(reduced

nephron number)


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Peningkatan asupan sodium

Volume cairan meningkat (retensicairan )

preload meningkat

stroke volume meningkat

cardiac output meningkat

Hipertensi


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Penurunan filtrasi ginjal

Retensi sodium di ginjal

Volume cairan meningkat

Preload meningkat

Stroke volume meningkat

Cardiac output meningkat

Hipertensi

R l f k d


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Regulasi Sistem Saraf Simpatik padaTD (Review)


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Disfungsi Endotel

Sintesis nitric oxide (NO)dari ginjal

menurun (NO = primary endogenvasodilator)

Hypertension


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Peningkatan AktivitasSistem Renin Angiotensin

Aldosteron(RAA)


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RAAS


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The Renin -Ang iotens in Sys tem

Alternate Pathway

Angiotensinogen

Renin

Angiotensin 1

Converting enzyme

Angiotensin 2

Angiotensin Receptors

Circulating( Liver )

Renin Inhibitors

Ace Inhibitors

A-II receptor blockers

Local( Tissue )

Non Renin Pathway

* t-PA* Cathepsin G

* Tonin

Non ACE Pathway* Chymase

* CAGE

* Cathepsin G

Renin mempunyai peran


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Renin mempunyai peransentral pada regulasi tekanan

darah

Juxtaglomerular cells

Glomerulus

Renin is released

into the vasculature


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Sekresi renin : 4 mekanisme

Distal tubule

Tekanan didalam

Arteriol aferen

1


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Sekresi Renin : 4 mekanisme

Stimulasi saraf simpatik padabeta1 receptor didalam JGA Distal tubule2


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Na+didalam macula densa

Distal tubule

3


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Negative feedbackoleh Ang IIDistal tubule

4

R i A i i C d


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Renin-Angiotensin Cascade

dan bradikinin

Angiotensinogen

Angiotensin I

Angiotensin II

AT1 AT2 ATn

Bradykinin

Inactivepeptides

Non-renin(e.g. tPA)

Non-ACE(e.g. chymase) ACE

Renin

Ang II & bradik in in


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Ang II& bradik in inEfek yang bertentangan :

proatherogenic >< vasculopro tect iveBradykinin

B2R

Vasodilation

NO

Prostaglandins

EDHF

tPA

Inactive peptides

Ang I

Ang II

ACE

Adapted from Ferrario CM, Strawn WB.Am J Cardiol. 2006;98:121-8.

Adapted from Murphey L et al. Eur Heart J Suppl. 2003;5(A):A37-41.

ACEI

ACEI+

- -

AT1R

Vasoconstriction

Aldosterone secretion

Fibrosis

Proliferation

Oxidative stress

Matrix formation

Inflammation


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HIPERTENSI ESSENTIAL

Hipertensi Primer

95 % dari semua HT

Etiologi tidak diketahui

Merupakan :

Complex Disease

Multifaceted DiseaseMeliputi :

- Disfungsi sistim saraf simpatis

- Gangguan transport sodium

- Hiperaktivitas sistim RAA

- Defisiensi Renal Vasodilator Subtances - Kelebihan hormon Mineralokortikoid

- Sodium Sensitivity

- Obesitas


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KAUSA HT SEKUNDER

A. Renal

* Polycystic Kidneys

* Renovascular Disease

B. Coarctatio AortaeC. Endrocrine :

* Pheochromocytoma

* Cushings Syndrome

D. Pregnancy Induced HT (Pre/Eclampsia)

E. Drugs / Substances


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Hipertens i Renovasku ler

Stenosis arteri renalis menyebakan jaringanginjal mengalami iskemia yang akanmeningkatkan produksi renin. Akibatnyaproduksi angiotensin II bertambah

(vasokonstriktor) dan meningkatkan produksialdosteron Penebalan fibromuskuler dinding arteri

Wanita muda < 40 th

Atherosclerotic plaque Faktor risiko ateroslerosis (+)

Abdominal bruit (+)


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PROSEDUR DIAGNOSIS HT

I. Anamnesis

II. Pemeriksaan Fisik dan Evaluasi KlinikIII. Pemeriksaan Laboraturium

IV. Pemeriksaan Lanjutan


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I. ANAMNESIS

Tanpa keluhan Sakit kepala bagian belakang

Berdebar, dada berat

Sukar konsentrasi

Sulit tidur Riwayat penyakit dahulu

- HT + obat ?

- Kehamilan ? DM ?

- Penyakit ginjal

Faktor resiko HT- Merokok

- Makanan asin

- Stress

- Obat Kontrasepsi


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II. Pemeriksaan Fisik dan Evaluasi Klinik

SPHYGMOMANOMETER

TIDAK APAKAH TD 140/90 YA

HT

III PEMERIKSAAN LABORATURIUM


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III. PEMERIKSAAN LABORATURIUM1. FOTO THORAX

menilai bentuk dan ukuran jantung

2. Elektrokardiografi ( EKG )menilai :

* Hipertrofi V.ki ( LVH)

* Abnormalitas Atrium ki

* Iskemia / infark miokard3. Laboratorium

* Hemoglobin dan hematokrit (DL)

* Urinalisis (dengan tes mikroalbuminuria dipst ick

dan pemeriksaan mikroskopik)

* Kreatinin serum* Asam urat serum

* Gula plasma puasa

* Profil lipid

* Elektrolit : NA, K, Cl

IV PEMERIKSAAN LANJUTAN


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Diagnosis Initial AdditionalChronic Kidney Disease

(CKD)

Urinalysis, BUN or Creatinine,

sonografy (USG)

Plasma Renin Assay ( PRA) ,

renal biopsy, IVP

Renovascular Disease Bruit, PRA and renography

before and one hour after 50 mg

captopril

Arteriogram, renal vein resins

Coarctatio Blood pressure in legs (ABI) Aortogram, carotid USG

Primary Aldosteronism Plasma Pottasium; plasma

aldosterone; renin ratio

Urinary pottasium, plasma

aldosterone after saline infusion

Cushings syndrome AM plasma cortisol after 1 mg

dexamethasone at bed time

Urinary cortisol after variable

doses of dexamethasone

Pheochromocytoma Urinary metanephirine andcatechols; plasma catechols,

basal and after 0,3 mg clonidine

IV. PEMERIKSAAN LANJUTANOVERALL GUIDES FOR EVALUATION

DIAGNOSTIC PROCEDURE

Untuk Mencari penyebab hipertensi

( HT sekunder )


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Renal Ang iog ram


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MANIFESTASI KERUSAKAN ORGAN SUBKLINIK

1. Cardiac* CAD ( Coronary Artery Dis )

* LVH ( Left Ventr. Hypertrophy )

* Left Ventr. Dysfunction

* Cardiac Failure

2. Cerebrovascular* Transient Ischaemic Attack (TIA)

* Stroke

3. Peripheral Vascular

* Intermitten Claudication

* Aneurysm* Epistaxis

4. Renal

* S. Creatinin 1,5 mg/dl

* Proteinuria : 1+

5. Retinophaty

* Papilledema / Exudates / Hemorhages


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Otot jantung bilik kiri yang sangat tebal, tetapi bagian laindari jantung tidak membesar.Keadaan ini khas pada

Penyakit Jantung Hipertensi (HHD).


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Otot jantung bilik kiri yang sangat tebal

Pada penderita HTN yang tidak berobat selama

bertahun-tahun.


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Funduskop i

Untuk mencari adanya Retinopati HT.( Keith Wagner I-IV )


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TUJUAN PENGOBATAN HTN

1. Menurunkan TD

2. Mencegah / mengurangi kerusakan

organ target3. Mengurangi morbiditas dan mortalitas

penyakit kardiovaskuler


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PENATALAKSANAAN

INDIVIDUALIZED TREATMENT

Jika modifikasi gaya hidup tidak

menurunkan tekanan darah yang

diinginkan, terapi farmakologis

harus diberikan !

PENGELOLAAN


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PENGELOLAAN

HIPERTENSII. Non FarmakologikII. Farmakologik = Obat

Terapi Non Farmakologik = Lifestyle Modifications

S Stop MerokokE Exercise TeraturH Hindari stress ---- Kelola stressA Awasi minum alkohol / konsumsisodiumT Turunkan berat badan

O.A. H : - Efek samping obat- Kwalitas hidup- Biaya


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Not at Goal Blood Pressure (100 mmHg)

2-drug combination for most (usuallythiazide-type diuretic and

ACEI, or ARB, or BB, or CCB)

Stage 1 Hypertension(SBP 140159 or DBP 9099 mmHg)

Thiazide-type diuretics for most.

May consider ACEI, ARB, BB, CCB,

or combination.

Without Compelling

Indications

Not at Goal

Blood Pressure

Optimize dosages or add additional drugs

until goal blood pressure is achieved.

Consider consultation with hypertension specialist.

Algorithm for Treatment of Hypertension

Stage 2 Hypertension(SBP >160 or DBP >100 mmHg)

2-drug combination for most

(usually thiazide-type diuretic and


LIFESTYLE CHANGES !!!

Weight reductionDietary sodium reduction

DASH eating plan

Physical activity

Moderation of alcohol consumption


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Not at Goal Blood Pressure (100 mmHg)

2-drug combination for most (usuallythiazide-type diuretic and


Stage 1 Hypertension(SBP 140159 or DBP 9099 mmHg)

Thiazide-type diuretics for most.

May consider ACEI, ARB, BB, CCB,

or combination.

Without Compelling

Indications

Not at Goal

Blood Pressure

Optimize dosages or add additional drugs

until goal blood pressure is achieved.

Consider consultation with hypertension specialist.

Algorithm for Treatment of Hypertension


2-drug combination for most

(usually thiazide-type diuretic and



2-drug combination for most (usually

thiazide-type diuretic andACEI, or ARB, or BB, or CCB)


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1999 WHO-ISH Gu idelines

Obat An t i Hipertensi L ini Pertama

Diuretics

Beta-Blockers ( BB )

ACE inhibitor ( ACEI )Calcium antagonists ( CCB )

Alpha-Blockers

Angiotensin II Receptor Blockers ( ARB )

Guidelines Subcommitee.1999.WHO-Intl Society of Hypertension.

Guidelines for Management of Hypertension. J Hypertens 1999;17:151-83.

Guidel ines fo r Ini t iat ion o f An t i -


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Guidel ines fo r Ini t iat ion o f An t i

Hypertensive Treatmen t

(Compend ium of ESC Guidel ines

07)

Thiazide diuretics

Beta-Blockers ( BB )ACE inhibitor ( ACEI )

Calcium antagonists ( CCB )

Angiotensin II Receptor Blockers ( ARB )

Choice of antihypertensive drugs

ESC Guidelines Desk Reference 2007


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JNC VINEW BP

GOALS


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Diuretics

Angiotensin

receptor blockers

(ARBs)

Calcium channel

blockers (CCBs)

Angiotensin-converting enzyme (ACE) inhibitors

b-blockers

a-blockers

for Combining BP-lowering

Drugs

Preferred combination

Less frequently used/

combination used as necessary Task Force of ESHESC. J Hypertens 2007;25:110587Copyright 2007, with permission from Lippincott Williams and Wilkins


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Adverse Effects of Commonly Used


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y

Antihypertensive Agents

Diuretics BBs CCBs ACEIs ARBs

Muscle cramps

Impotence

Gout

Glucose Intolerance

Hypokalemia

Hyperuricemia

Hypomagnesemia

Hypercalcemia

Depression

Sleep disorders

Exercise Intolerance

Dysiplidemia

Glucose Intolerance

Impotence

Edema

Flushing

Headache

Dizziness

GI disorders

Changes in heart

rate

Cough

Rash

Hyperkalemia

Angioedema

Hyperkalemia

Angioedema

( rare )


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PROGNOSIS

Tergantung :

1. Stratifikasi Risiko Kardiovaskuler :

* Rendah

* Sedang* Tinggi

* Sangat tinggi

2. Kerusakan organ target

3. Kondisi Klinik yang berhubungan

4. Respon ke pengobatan

5. Kepatuhan penderita

TIGA PEDOMAN UNTUK


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TIGA PEDOMAN UNTUK

PENDERITA TEKANAN

DARAH TINGGI

1. Periksakan tekanan darah

secara teratur2. Minum obat seperti yang

dianjurkan dokter

3. Patuhi dengan baik segalanasehat dokter


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A ti l f H t i


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Aetiology of Hypertension Primary90-95% of casesalso termed essential

of idiopathic Secondaryabout 5% of cases

Renal or renovascular disease

Endocrine disease

Phaeochomocytoma

Cusings syndrome

Conns syndrome

Acromegaly and hypothyroidism

Coarctation of the aorta

Iatrogenic

Hormonal / oral contraceptive

NSAIDs


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This left ventricle is very thickened (slightly over 2 cm inthickness), but the rest of the heart is not greatly enlarged.

This is typical for hypertensive heart disease. The

hypertension creates a greater pressure load on the heart to

induce the hypertrophy.


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The left ventricle is markedly thickened in this patientwith severe hypertension that was untreated for many

years. The myocardial fibers have undergone

hypertrophy.


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Logical Combinations

Diureticb-

blockerCCB

ACE

inhibitor

a-

blocker

Diuretic - -

b-blocker - * -

CCB - * -

ACE inhibitor - -

a-blocker -

* Verapamil + beta-blocker = absolute contra-indication


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ACE Inhibitor Side Effects

Cough (15% of patients. Is reversible)

Taste disturbance (reversible)

Angiodema

First-dose hypotension

Hyperkalaemia ( esp. in patients with type

II diabetes and renal dysfunction)


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Follow-up

For patients with BP stabilised by management, followup should normally be three monthly (interval should not

exceed 6 months), at which the following should be

assessed by a trained nurse:

* Measurement of BP and weight

* Reinforcement of non-pharmacological advice

* General health and drug side-effects

* Test urine for proteinuria (annually)

ECG


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ECG


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A Muscular Pump

L f C S


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Left Coronary System

Di ti


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Diuretics

Thiazides

Work by sodium and water excretion

Side effects include hypokalemia,

hyperuricemia and glucose intolerance Less effective in severe renal dysfunction

Potassium sparing diuretics

Aldosterone antagonists


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ACE (angiotensin converting

enzyme) Inhibitors Method of action Block the enzyme that converts angiotensin I to angiotensin II ( avasoconstrictor)

Promote vasodilatation

Lowers aldosterone secretion

Side effects

Cough Rash

Angioneurotic edema

Taste disturbance

Hyperkalemia especially with renal impairment

Especially useful HTN with CHF or DM

Contraindications Pregnancy

Bilateral renal artery stenosis

FDA-Approved Indications for ACE


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Inhibitors

Left Prevention of Myocardial

Congestive Ventricular Infarction, Stroke, and

Hypertension Heart Failure Dysfunction Cardiovascular Death

All ACE Captopril Captopril Ramipril

Inhibitors Enalapril Enalapril

Fosinopril Lisinopril

Lisinopril Ramipril

Quinapril

Ramipril

A i t i II t bl k


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Angiotensin II receptor blockers

Method of action

Block the AT1 receptor causing a fall in

peripheral resistance

Very similar to ACE inhibitors but does notcause a cough

B t Bl k


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Beta Blockers

Decrease BP by reducing cardiac output and inhibitingsympathetically mediated renin release from the kidney

Relative contraindications Asthma/COPD

Decompensated CHF

Raynauds phenomenon Peripheral vascular disease

Depression

Side effects Tiredness

Cold hands and feet Impotence and sexual dysfunction

May mask the effect of hypoglycemia in DM

B t Bl k


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Beta Blockers

Decrease BP by reducing cardiac output and inhibitingsympathetically mediated renin release from the kidney

Relative contraindications Asthma/COPD

Decompensated CHF

Raynauds phenomenon Peripheral vascular disease

Depression

Side effects Tiredness

Cold hands and feet Impotence and sexual dysfunction

May mask the effect of hypoglycemia in DM

Secondary HTN who to


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Secondary HTN who to

evaluate?Accounts for


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Most common causes of secondary

HTN

Renovascular HTN

Catecholamine excess states

Mineralocorticoid excess states

R l HTN


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Renovascular HTN

Stenosis of a renal artery increases reninproduction from the ischemic kidney which

causes increased production of angiotensin II

(vasoconstrictor) and increased production of

aldosterone

Fibromuscular thickening of the arterial wall

Women younger than 40

Atherosclerotic plaque Older people with risk factors for atherosclerosis

Listen for an abdominal bruit

Renal Angiogram


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Renal Angiogram


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Right Stent in-situ


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Right Stent in situ

Coronary Stents


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Coronary Stents

Endocrine Abnormalities


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Hypokalemia (low potassium) in theabsence of diuretic therapy may indicate a

state of mineralocorticoid excess

Excess aldosterone production (Conns)

Excess glucocorticoid production

(Cushings)

Hyperthyroidism

Cushings Syndrome


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g y

Hypercortisolism

Aetiologies Iatrogenicexcess corticosteroid administration

ACTH hypersecretion by the pituitary

Bilateral adrenal hyperplasia

Signs/symptomshypertension, central obesity,abdominal striae, buffalo hump, moon facies,hirsuitism, easy bruising, hyperglycemia,hypokalemia

Evaluationelevated free urinary cortisol, low-dose dexamethasone suppression test

Treatmentresection +/- irradiation

Primary Hyperaldosteronism


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Primary Hyperaldosteronism

Due to excess aldosterone production(Conns)

Usually due to an adrenal adenoma

Features include hypertension,hypokalemia (tetany), polyuria, elevatedurinary potassium, elevated plasma/urinealdosterone, low plasma renin

Treatment

Adrenalectomy for Conns

Spironolactone for bilateral hyperplasia

Pheochromocytoma


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Pheochromocytoma

Catecholamine secreting neoplasms of theadrenal glands (medulla) or extra-adrenal

chromaffin tissue

Headache, diaphoresis and tachycardia

Severe HTN with the induction of

anesthesia

The diagnosis depends on thedemonstration of increased excretion of

catecholamines or their major metabolites

in the urine

Hypertension Defined


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Hypertension (HTN)

is defined as

sustained abnormalelevation of the

arterial blood

pressure (Brashers,

2006, p.1).

Hypertension Defined

Physiology of Blood


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Physiology of Blood

Pressure IBlood Pressure =Cardiac Output (CO) X

Peripheral Vascular Resistance

Components of Blood Pressure

Systolic Pressure

Diastolic PressurePulse Pressure

Mean Arterial Pressure


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Guidelines


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Guidelines

The Seventh Report of the Joint National Committee onDetection, Evaluation, and Treatment of High BloodPressure (JNC VII) uses the following guidelines to

define HTN in adults: (Brashers, 2006, p.1)

Category Systo l ic Diasto l ic

Normal 100

Epidemiology I


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Epidemiology I

Epidemiology

The most common primary diagnosis in the United States, 50 millionAmerican affected.

Only 70% are aware they have HTN Of those aware of their HTN, only 50% are being treated.

Only 25% of all hypertensive patients have their BP under control

HTN is a risk factor for coronary artery disease (CAD), congestiveheart failure (CHF), stroke, and renal failure

Epidemiology II


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Epidemiology II

Epidemiology (cont) Cardiovascular risk increases two-fold for each 20mm/Hg

rise in systolic pressure or each 10mm/Hg rise in diastolicpressure

Risk factors in all populations include age, obesity,sedentary life-style, family history, smoking, alcohol, highsodium intake, low potassium or magnesium intake, and theuse of NSAIDS

Pathophysiology I


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Pathophysiology I

Primary Hypertension

Genetics

Environment

Neurohormonalmediators

Pathophysiology II


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Pathophysiology II

Contributing factors forPrimary HTN: Increased activity of:

sympathetic nervous system (SNS)

Renin-angiotensin-aldosteronesystem (RAA)

Defects in natriuretic hormonefunction

Inflammation

Obesity

Endothelial dysfunction

Insulin resistance

Pathophysiology III


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Pathophysiology III

Secondary Hypertension

Causes

Complications

Treatment

Pathophysiology IV


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Pathophysiology IV

Other forms of HTN

Complicated HTN

Malignant HTN

Hypertensive Crisis

Differential Diagnosis


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Differential Diagnosis

1. Rule out isolated incident of increased bloodpressure.

2. Rule out secondary hypertension related to:

Renal diseaseCushing's disease

Pheochromocytoma

HyperthyroidismHyperparathyroidism


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Clinical Manifestations I

Physical exam:

Abdomen

FunduscopicVascular

Cardiac

Pulmonary

Neurological

Lab tests:

Urinalysis

Blood ChemistryECG

Renal ultrasound

Echocardiogram

Vascular studies

Management


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Management

Primary goalis to reduce cardiovascularand renal morbidity and mortality.

Other keysto management are:

PreventionPatient education

Life-style modification

Medication

Management


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Management

Medications

Diuretics-Thiazides (HCTZ), Loop (Furosemide), Potassium-sparing(Spironolactone)

Beta-Blockers-Atenolol, Nadolol, Propranolol

ACEInhibitors-Benezapril, Captopril, Cilizapril

Ca+ Channel Blockers-Nifedipine, Verapamil

Alpha blockers-Prazosin, Terazosin

ARBs- Losartan, Valsartan

Vasodilators-Apresoline

Outcome


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Outcome

Follow upFrequent monitoring is necessary until BP is under

control. Once under control office visitscan be decreases, with limited laboratory

tests.

Lipids should be checked yearly.

ECG every 2-4 years, as indicated byinitial ECG

Complications


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Complications

Complications as a result of HTN include:

Stroke

Dementia

Myocardial Infarction

Congestive Heart Failure

Retinal Vasculopathy

Aortic Dissection

Renal Disease or Failure

Referral


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Referral

A patient should be referredwhen:

BP remains uncontrolledafter three concurrentmedications

Uncontrolled BP and signsand symptoms of end-organ damage


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Conclusion


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Conclusion

Use 24 hour ambulatory BP monitors toproperly evaluate HTN

Treat very aggressively

Treat other cardiovascular risk factors

Watch for secondary causes of HTN

Essential hypertensionSites of regulation of blood pressure


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Sites of regulation of blood pressure

Peripheralresistance BloodvolumeCardiacoutput

Vasoconstriction

Heart rate

contractility

Sympathetic

Parasympathetic

Baroreceptors Renal perfusion

Urinaryoutput

Na and H O

excretion

+2

Aldosterone

Angiotensin II

Renin

Peripheralresistance

Bloodvolume

Cardiacoutput

Urinaryoutput

Renal perfusion Baroreceptors

Na and H O

excretion

+2

Aldosterone

Renin

Angiotensin II

Parasympathetic

Sympathetic

Heart rate

contractility

Vasoconstriction

BP

BPSite of action of anti-hypertensive drugs

Angiotensin II Antagonists

Methyldopa

Beta-blockers

Vasodilators

Ca Channel Blockers

a-blockers

Ace inhibitors

Diurectics


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RATIONALE OF DUAL RAS BLOCKADE WITH ACE-l

& AT1 RECEPTOR BLOCKADE (INHIBITION OF

CONSECUTIVE RAS STEPS)


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1. Minimizing ESCAPE (Incomplete blockade)

occurring with single site RAS blockersSuggested mechanisms for ESCAPE:

a. Progressive clearancefrom the body of the drug at the end of

dosing interval

b. Counter-regulatory reactive risein plasma active renin thatincreases ATl & ATllproportionally to the suppression of the ATII

negative feedback on renin release (this mechanism contributes to

the flat dose response curve of BP measured at trough reported for

RAS blockers)

c. ATll generation by pathways other than Renin & ACE

(CAGE-Chymotrypsin-like Angiotensin Generating Enzyme andChymase)

2.Additional BP lowering

Modified from AZIZI M. and MENARD J; Circulation 1/6/2004 109; 2492-2499


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Figure 14-1


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BION 3202

Lecture 2. Contraction of Heart Tissue


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Ionic Current


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NCX

INa IL,Ca

NaNa

Ca

o c Cu eNa

Na Na

CaCa

Ca

Ca

CaCa

Ca

Ca

Ca

Cell membrane

NaNa

Na

NaCa

CaCa

Ca

Ca

CaCa

CaCa

CaNa Na

Sarcoplasmic

Reticulum

RyRSR ATPase

K

KK

KK

K

KK

IKr

IK1

IKS

K K

K

KK

K

K

NKP

Na

Ionic Currents: A few more


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Ionic Currents: A few more


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Figure 14-10b

Early Morning Surge Can

T i E t


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12/3/2013 126Weber MA.Am J Cardiol. 2002;89(suppl)27A33A.

ShearstressPlaque fissure

Arterial thrombosisEarly morning

hypercoagulable

state

CV EVENTS

Increased

heart rate

BP rise

Early morningBP surge

Catecholaminesurge

Trigger Events

Aliskiren : Hits the Target


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Hypokalemia (low potassium) in theabsence of diuretic therapy may indicate a

state of mineralocorticoid excess

Excess aldosterone production (Conns) Excess glucocorticoid production

(Cushings)

Hyperthyroidism

Cushings Syndrome

Hypercortisolism


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Hypercortisolism

Aetiologies Iatrogenicexcess corticosteroid administration

ACTH hypersecretion by the pituitary

Bilateral adrenal hyperplasia

Signs/symptomshypertension, central obesity,abdominal striae, buffalo hump, moon facies,hirsuitism, easy bruising, hyperglycemia,hypokalemia

Evaluationelevated free urinary cortisol, low-dose dexamethasone suppression test

Treatmentresection +/- irradiation


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Pheochromocytoma


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y

Catecholamine secreting neoplasms of theadrenal glands (medulla) or extra-adrenal

chromaffin tissue

Headache, diaphoresis and tachycardia Severe HTN with the induction of

anesthesia

The diagnosis depends on thedemonstration of increased excretion of

catecholamines or their major metabolites

in the urine

Hypertensive Crises


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yp

HTN with clinical features of Hypertensive encephalopathy

Intracranial hemorrhage

Unstable angina and acute myocardial infarction

Aortic dissection

Papilledema

Use IV agents to reduce the BP by no more than25% in the 2 hours and to no less than160/100mmHg during the next 6 hours

Extreme care must be taken not to cause renal,coronary or cerebral ischemia by dropping theBP t i kl

hipertensi by. dr. rudy utantio, sp.jp

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