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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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Sekresi Renin : 4 mekanisme
Na+didalam macula densa
Distal tubule
3
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Sekresi Renin : 4 mekanisme
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
ACEI, or ARB, or BB, or CCB)
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
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
ACEI, or ARB, or BB, or CCB)
Stage 2 Hypertension(SBP >160 or DBP >100 mmHg)
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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Endocrine Abnormalities
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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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
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