tutorial a5
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TUTORIAL A5
PEMICU 1
BLOK CARDIOVASCULAR 1
FAKULTAS KEDOKTERANUNIVERSITAS SUMATERA UTARA
2013
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Lembar 1
Tn. S, laki-laki 59th
datang ke praktek seorang dokter karenakeluhan kepala pusing. Keadaan ini sudah dialami OS dalam
satu tahun terakhir. Satu bulan yang lalu, OS ke puskesmas
dan dinyatakan oleh dokter menderita hipertensi. Pasien
mendapatkan beberapa jenis obat, tetapi tidak jelas apa namaobatnya. Dan gejalanya tidak berkurang. Tidak ada riwayat
sesak nafas, dan juga diabetes disangkal.
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Lembar 2
Pemeriksaan Fisik :
1. Tanda vital
sensorium : compos mentis, BB : 67 kg, TB : 171 cm, frekuensi nadi
: 90x/menit, reguler, tekanan dan volume sama, pulsasi di keempetekstremitas sama. Frekuensi napas : 20x/menit, suhu tubuh 36,50C.Ikterus, edem, sianosis, dan pucat tidak ditemukan
2. Pemeriksaan kardiovaskularTekanan vena jugularis normal, dada terlihat simetris, perkusi dadasonor, batas jantung kiri 1 cm lateral LMCS, ICR 5-6. Padaauskultasi jantung, suara jantung I dan II normal, tidak ada murmurmaupun gallop
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3. Pemeriksaan Respirasi
Trakhea teraba di garis tengah dan pergerakan dada normal
serta simetris. Auskultasi paru terdengar vesikuler di kedualapangan paru
4. Pemeriksaan abdomen
Abdomen lemas (soepel), hepar dan limpa tidak teraba,
peristaltik baik
5. Pemeriksaan eksterimtas
Akral hangat, pulsasi arteri radialis kiri dan kanan serta arteri
dorsalis pedis kiri dan kanan sama, tidak dijumpai oedem. Tidak
dijumpai dilatasi vena di ekstremitas bawah.
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Lembar 3Pemeriksaan penunjang
1. Pemeriksaan laboratorium
Darah dan urin dalam batas normal
2. Foto ToraksJantung sedikit membesar dengan CTR 55%, paru normal, tulangnormal, kesan : kardiomegali ringan
3. EKG
Sinus ritme, rate 80x/menit, gelombang P normal, aksis QRS -30derajat (kesan left axis defiation), QRS kompleks normal, gelombang Tnormal, dan LV high voltage
Kesan : left ventricel hipertrophy
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LEARNING ISSUE1. Anatomi dan Histologi Kardiovaskuler
2. Fisiologi jantung sebagai pompa3. HIPERTENSI
a. defenisi dan klasifikasi
b. etiologi dan faktor resiko
c. patogenesis hipertensi
d. gejela klinis
e. diagnosis
f. diagnosis banding
g. komplikasi, pencegahan, prognosis
i. penatalaksanaan
4. PENYAKIT JANTUNG HIPERTENSIF
a. Mekanisme hipertensi menyebabkan penyakit jantung
b. diagnosis
c. prognosis dan indikasi rujuk
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ANATOMI JANTUNG
ORGAN BERONGGA & BEROTOT YANG MEMOMPA DARAHMELALUI SIRKULASI PULMONAL & SISTEMIK
MENERIMA DARAH VENOSA KE DLM ATRIUM KANAN MENYALURKAN KE VENTRIKEL KANAN KE PARU-PARU UNTUKOKSIGENASI
MENERIMA DARAH TEROKSIGENASI KE ATRIUM KIRIVENTRIKEL KIRI DAN MENYALURKAN KE SELURUH TUBUH
PUNCAK /APEX : LATERAL KIRI DEPAN
BASIS : POSTERIOR BENTUK : SEPERTI KERUCUT BERAT : 300 GR KAPASITAS : 300 CC BESAR /KONTRAKSI : 12,5 X 3,5 X 2,5 CM (SEBESAR TINJU )
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RUANG COR : ATRIUM KA & KI, VENTRIKELKANAN & KIRI
BATAS MYOCARDIUM ATRIUM & VENTRIKEL :SULCUS CORONARIUS
MYOCARDIUM (ATRIUM):
LUAR : TRANSVERSAL
DALAM : CIRCULAR MYOCARDIUM (VENTRIKEL) :
LUAR : LONGITUDINAL
TENGAH >>: SILINDRIS
DALAM : LOGITUDINAL
DINDING COR : EPICARDIUM
MYOCARDIUM
ENDOCARDIUM
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MEMPUNYAI 2 KATUP DIANTARA ATRIUM-VENTRIKEL :
1. VALVULA TRICUSPIDALIS (KANAN)
2. VALVULA BICUSPIDALIS/MITRALIS (KIRI)
MEMPUNYAI OTOT JANTUNG (MUSCULUS PAPILLARIS)YG TERHUBUNG DG VALVULA MELALUI CORDATENDINEA
MEMPUNYAI AURICULA CORDIS PD KEDUA ATRIUM,DIDALAMNYA TERDAPAT MUSCULUS PECTINATI
MEMPUNYAI SEKAT JANTUNG DISEBUT SEPTUM
INTERVENTRICULORUM YANG MEMISAHKAN JANTUNG
BAGIAN KIRI & KANAN
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PEMBULUH ARTERI BESAR YG KELUAR DARI VENTRIKEL :
TRUNCUS/ARTERI PULMONALIS (KANAN)
AORTA (KIRI)
KEDUA PEMBULUH TSB MEMPUNYAI KATUP DISEBUT VALVULASEMILUNARIS
PERDARAHAN PERICARDIUM :
A. PERICARDIACOPHRENICA (A THORACICA INTERNA)
A. MUSCULOPHRENICA (CAB.AKHIR A THORACICA INTERNA) CAB A BRONCHIALIS, OESOPHAGEALIS & A PHRENICA SUPERIOR
A. CORONARIA (HANYA LAMINA VISCERALIS)
VENA PERICARDIACOPHRENICA (VENA THORACICA INTERNA)
CAB VENA AZYGOS
PERSARAPAN PERICARDIUM :
N. PHRENICUS
N. VAGUS
TRUNCUS SYMPHATICUS
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I. Endocardium Inner layer of atriums & ventricles2
Homologous with tunica intima of blood
vessels
Consist of : 1, 2
1.Endothelium :
Simple squamous epithelium
Junctions : Tight/occluding junctions
Gap junctions
2. Subendocardial layer :
Loose connective tissue
Contain veins, nerves, Purkinje
cells (branches of impulse
conducting system of heart
Connected to myocardium
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II. Myocardium
Thickest tunics
cardiac muscle cells
Thinnest
Smaller cardiac
muscle cells
Speciallized muscle cells in atrium
produce atriopeptin, ANF(Atrial Natriuretic
Factor), cardiodilatin, cardionatrin
help in maintain fluid & electrolyte balance3
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Type Of Cardiac Muscle
Fiber
1. Conducting ImpluseFiber
2. Contractile
Fiber
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Conduction system of heart: 2,
3 Modification of cardiac muscle
cells
Generate a rythmic stimulus
Consist of :
1. 2 node in atrium wall:
Sinoatrial node/SA node
Atrioventricular node/AV
node
2. AV bundle branches of
AV node
3. Purkinje fibers branches
of AV bundle
1. Conducting Impulse Fiber
2 3
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Purkinje fibers : 2, 3
Branches ofAV Bundle Located at subendocardial
Distinctive appearance with ordinary
cardiac muscle : Larger & contain more cytoplasm
Less myofibril
Rich in mitochondria & glycogen
1 or 2 central nuclei
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2. Contractile Fiber
Elongated, cylindrical & branching fiber
Each fiber contains only 1 or 2 nuclei,
centrally placed Cross striations similar to skeletal muscle
(A/I/H band & M/Z line)
Sarcoplasm contain numerous largemitochondria
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III. Epicardium Homologue to tunica adventitia in
blood vessels3
Outermost layer of heart wall3
Consist of : 1, 2
1. Pericardium viceralmesothelium (simple
squamous epithelium)2. Subepicardial layerloose connective tissuewith coronary vessels,nerves & ganglia
3. Pericardium parietal:mesothelium & conn.tissue
Space between pericardiumcontain serous liquid forlubricating
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BLOOD VESSELS
Differ in size, distribution & function but have similarity in several
feature 2, 3
Wall divided into : 1, 2, 3
1. Tunica Intima :
Endothelium : simple squamous epthelium, rest on basal
lamina
Provide smooth surface of blood vessel
Secreting type I, IV & V collagen, lamin, endothelin,
nitric oxide, von Willebrand factor.
Posses membrane bound enzyme such as
angiostensin converting enzyme (ACE)
Subendothelium loose conn. tissue, few scattered
smooth muscle
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2. Tunica Media:
Equivalent to myocardium
Most variable layer in size &
structure Contain variable amount of
smooth muscle & elastic tissue
depend on blood vessel
function3. Tunica Adventitia:
Correspond to epicardium
lack mesothelial cells
Varies in thicknes Mostly composed of fibroblast,
type I collagen fiber & elastic
fiber
l d l ll
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Blood Vessel Wall Composition
LARGE ARTERIES
SMALL ARTERIES
ARTERIOLES
CAPILLARIES
VENULES &VEINS
INSIDE DIAMETER
SMALL LARGELARGE
ELASTIC TISSUE
MUSCLE
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Membrana Elastica :
Interna :
Separating T. Intima &T. Media
Composed of
perforated elastin
tissue
Function: permits
diffusion of substances
Eksterna :
Separating T. Media &T. Adventitia
More delicate than
interna
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Vasa Vasorum :
Found in large vessels
Small arteries branching to
serve nutrition to cells in t. media& t. adventitia
More prevalent in veins thanarteries coz venous blood containless oxygen & nutients than
arterial blood
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Nerve Supply Of Blood Vessel 3
A network of vasomotor nerve of sympathetic component ofautonomic nervous system supplies smooth muscle cells of
vessels release norepinephrine diffuse to smooth
muscle cells nearby impulses propagated to entire
smooth muscle via gap junction Arteries supply the skeletal muscle also receive
parasympathetic nerves vasodilatation
CLASSIFICATION OF BLOOD VESSELS
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CLASSIFICATION OF BLOOD VESSELS
ARTERIES
VEIN
CAPILLARIES
Elastic arteries / conducting arteries
Medium (muscular) arteries / distributing arteries& small arteries
Arteriole
Large vein
Medium & small veins
Venule
Continuous capillaries
Fenestrated capillaries
Sinusoidal capillaries
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Conducting System of the Heart
AV Node
Posterior Inferior Fascicle
Anterior Superior Fascicle
Septal Depolarization Fibers
Purkinjie Fibers
Inter- nodal Tracts
Bundle of HIS
Left Bundle
Branch
Right Bundle
Branch
SA Node
CARDIAC CYCLE
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CARDIAC CYCLE
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Heart Sounds
Normally heard by a stethoscope
First sound: low, slightly prolonged lub, caused by
closure of mitral and tricuspid valves, at ventricular
systole. Duration 0.15 s & fequency 25-45 Hz. Second sound; shorter, high-pitched dup, caused by
closure aortic and pulmonary valves, after end of
ventricular systole. 0.12 s & 50 Hz.
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Third sound: soft, low-pitched, at one-third diastole, period
rapid ventricular filling , due to inrush of blood. In young
individuals. 0.1 s.
Fourth sound: when atrial pressure is high and ventricle is
stiff in ventricular hypertrophy , due to ventricular filling, before
first sound.
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Murmurs or Bruits
abnormal sounds heard in various parts of the vascular
system.
Bruits heard over a large, highly vascular goiter, over
carotid artery when its lumen is narrowed & distorted byatherosclerosis.
Murmurs heard over aneurysmal dilation of large
arteries, an arteriovenous (A-V) fistula, or patent ductus
arteriosus.
ELECTRICAL
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ELECTRICALPROPERTIES
The resting membrane
potential -90 mV
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This diagram illustrates ECG waves and intervals as wellas standard time and voltage measures on the ECG paper.
1. ECG Waves and Intervals: What do they mean?
P wave: the sequentialactivation(depolarization) of the right and left atria
QRS complex: right and left ventriculardepolarization (normally the ventricles areactivated simultaneously)
ST-T wave: ventricular repolarization
U wave: origin for this wave is not clear - butprobably represents "afterrepolarizations" inthe ventricles
PR interval: time interval from onset of atrialdepolarization (P wave) to onset of ventriculardepolarization (QRS complex)
QRS duration: duration of ventricular muscledepolarization
QT interval: duration of ventriculardepolarization and repolarization
RR interval: duration of ventricular cardiaccycle (an indicator of ventricular rate)
PP interval: duration of atrial cycle (anindicator of atrial rate)
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Heart rate (state atrial and
ventricular, if different)
PR interval (from beginning of Pto beginning of QRS)
QRS duration (width of mostrepresentative QRS)
QT interval (from beginning of
QRS to end of T)
QRS axis in frontal plane
1. Measurements (usually made in frontal plane leads):
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Kwantitatif
Gel.P: panjang 0.06 stinggi : 0.20 mV
QRS: lebar : 0.06
0.10 sP-R interval: 0.12 0.20 s.
Q T interval: 0.32 0.40 s.
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Examples of QRS Axis
Axis in the left axis deviation (LAD)
range:
Lead aVR is the smallest and
isoelectric lead.
The two perpendiculars are -60 o and
+120 o.Leads II and III are mostly negative
(i.e., moving away from the + left leg)
The axis, therefore, is -60 o.
Axis in the normal range
Lead aVF is the isoelectric lead.
The two perpendiculars to aVF are
0 o and 180 o.
Lead I is positive (i.e., oriented to
the left).Therefore, the axis has to be 0 o.
Axis in the right axis deviation
(RAD) range:
Lead aVR is closest to being
isoelectric (slightly more positive
than negative)
The two perpendiculars are -60 oand +120 o.
Lead I is mostly negative; lead III
is mostly positive.
Therefore the axis is close to +120
o. Because aVR is slightly more
positive, the axis is slightly beyond
+120 o (i.e., closer to the positive
right arm for aVR
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Sokolow-Lyon Indices
electrocardiographic diagnosis ofLVH
There are two criteria with these widely used indices:
Sum of S wave in V1 and R wave in V5 or V6> or =3.5 mV (35 mm) and/or
R wave in aVL > or =1.1 mV (11 mm)
AMMSR
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Example 1: (Limb-lead Voltage Criteria; e.g., R in aVL >11 mm; note wide QRS/Tangle)
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Example 2: (ESTES Criteria: 3 points for voltage in V5, 3 points for ST-T changes
Note also the left axis deviation of -40 degrees, and left atrial enlargement)
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Cardiothoracic Ratio (CTR)
Buat garis lurus dari pertengahan thorax (mediastinum)
mulai dari atas sampai ke bawah thorax.
Tentukan titik terluar dari kontur jantung sebelah kanan
dan namakan sebagai titik A. Tentukan titik terluar dari kontur jantung sebelah kiri
dan namakan sebagai titik B.
Buat garis lurus yang menghubungkan antara titik A
dan B
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Tentukan titik terluar bayangan paru kanan dan namakan
sebagai titik C.
Buat garis lurus yang menghubungkan antara titik C
dengan garis mediastinum. Perpotongan antara titik C dengan garis mediastinum
namakan sebagai titik D
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Jika nilai perbandingan di atas nilainya 50% (lebih dari/sama dengan 50%
maka dapat dikatakan telah terjadi pembesaran jantung (Cardiomegally)
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Menilai pembesaran jantung pada radiografi thoraks sering
mengalami kesulitan karena bentuk jantung dapat berubah-
ubah tergantung pada usia, respirasi, posisi penderita waktu
eksposi, bentuk tubuh, kelainan paru dan kelainan sternum.
Membedakan jatung yang normal dengan yang agak
membesar sering sulit dan memerlukan ketelitian.
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HIPERTENSI
Hypertension is defined as an arterial pressure greater
than 140/90 mm Hg in adults on at least three
consecutive visits to the doctor's office.
Symptoms, nonspecific; headaches, fatigue, anddizziness
"the silent killer"
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Hypertension: Predisposing factors
Age > 60 years Sex (men and postmenopausal women)
Family history of cardiovascular disease
Smoking High cholesterol diet
Co-existing disorders such as diabetes,
obesity and hyperlipidaemia High intake of alcohol
Sedentary life style
9/11/2013 Kuliah Penyakit Jantung Hipertensi 45
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Hypertension Syndrome
Its More Than Just Blood PressureDecreasedArterialCompliance EndothelialDysfunction
Abnormal
GlucoseMetabolism
NeurohormonalDysfunctionRenal-Function
Changeslood-ClottingMechanismChanges
Obesity
AbnormalInsulinMetabolism
LV Hypertrophyand Dysfunction
AcceleratedAtherogenesis
AbnormalLipidMetabolism Hypertension
Kannel WB. JAMA. 1996;275:1571-1576. Weber MA et al. J Hum Hypertens. 1991;5:417-423. Dzau VJ et al. J CardiovascPharmacol. 1993;21(suppl 1):S1-S5.
Cl ifi ti d M t
http://rd.yahoo.com/M=232617.2895566.4241568.2848579/D=he/P=m1d0jod311vv1900/S=95489332:SKY/A=1435695/R=0/*http:/shop.store.yahoo.com/cgi-bin/clink?1800flowers2+shopping:dmad/M=232617.2895566.4241568.2848579/D=he/P=m1d0jod311vv1900/S=95489332:SKY/A=1435695/R=1/1045140916+http://us.rmi.yahoo.com/rmi/http://www.1800flowers.com/rmi-framed-url/http://www.1800flowers.com/cgi-bin/flowers/product.pl/VD02i79aF3SKYHEALTHYH/1153http://rd.yahoo.com/M=232617.2895566.4241568.2848579/D=he/P=m1d0jod311vv1900/S=95489332:SKY/A=1435695/R=0/*http:/shop.store.yahoo.com/cgi-bin/clink?1800flowers2+shopping:dmad/M=232617.2895566.4241568.2848579/D=he/P=m1d0jod311vv1900/S=95489332:SKY/A=1435695/R=1/1045140916+http://us.rmi.yahoo.com/rmi/http://www.1800flowers.com/rmi-framed-url/http://www.1800flowers.com/cgi-bin/flowers/product.pl/VD02i79aF3SKYHEALTHYH/1153http://rd.yahoo.com/M=232617.2895566.4241568.2848579/D=he/P=m1d0jod311vv1900/S=95489332:SKY/A=1435695/R=0/*http:/shop.store.yahoo.com/cgi-bin/clink?1800flowers2+shopping:dmad/M=232617.2895566.4241568.2848579/D=he/P=m1d0jod311vv1900/S=95489332:SKY/A=1435695/R=1/1045140916+http://us.rmi.yahoo.com/rmi/http://www.1800flowers.com/rmi-framed-url/http://www.1800flowers.com/cgi-bin/flowers/product.pl/VD02i79aF3SKYHEALTHYH/1153http://rd.yahoo.com/M=232617.2895566.4241568.2848579/D=he/P=m1d0jod311vv1900/S=95489332:SKY/A=1435695/R=0/*http:/shop.store.yahoo.com/cgi-bin/clink?1800flowers2+shopping:dmad/M=232617.2895566.4241568.2848579/D=he/P=m1d0jod311vv1900/S=95489332:SKY/A=1435695/R=1/1045140916+http://us.rmi.yahoo.com/rmi/http://www.1800flowers.com/rmi-framed-url/http://www.1800flowers.com/cgi-bin/flowers/product.pl/VD02i79aF3SKYHEALTHYH/1153 -
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Classification and Managementof BP for adults
BP
classification
SBP*
mmHg
DBP*
mmHg
Lifestyle
modification
Initial drug therapy
Without compelling
indication
With compelling
indications
Normal 100 Yes Two-drug combination for
most (usually thiazide-type
diuretic and ACEI or ARB or
BB or CCB).
*Treatment determined by highest BP category.Initial combined therapy should be used cautiously in those at risk for orthostatic hypotension.
Treat patients with chronic kidney disease or diabetes to BP goal of
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DD Hipertensi
White coat hypertension
Rasa nyeri
Akibat obat
Ensefalitis
P th h i l f H t i
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Excess
Na
intake
Reduced
Nephron
Numbers Stress
Genetic
Alterations Obesity
Endotheliu
m
derivedfactors
Renal Na
retention
Decreased
filtration
surface
Sympatheic
Over activity
RAS
Excess
Cell-membrane
alterations
Hyper
insulinemia
FluidVolume
Venous
constriction
Preload Contractibility Functionalconstriction Structuralhypertrophy
Blood pressure=
HTN
Cardiac Output Peripheral ResistanceX
and/or
Patho-physiology of Hypertension
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Renin-Angiotensin System
Angiotensinogen
Angiotensin I
Angiotensin II
Renin
ACEChymase
tPA
Catepsin
AT1-R AT2-R ?
Bradykinin
Inactive quinines
B1-R
B2-R
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Effects of angiotensin II
Peripheral
vasoconstriction
Vascular
proliferation
Adrenergicactivity
Renin
secretion
Aldosterone
secretion
Thirst
mechanism
Water and sodium retention
Efferent arteriole
vasoconstriction
AII
AT1-R
Complications of HTN
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Retinopathy
Heart diseases
Stroke or TIA
Nephropathy,Proteinuria, CrCl
Peripheral arterial Disease(atherosclerotic plaqueiliac,carotid, femoral artery,
aorta)
Sequelae of
Hypertension
Complications of HTN
Cardiac
CNS
VascularRetinal
Renal
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HIPERTENSIVE HEART
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HIPERTENSIVE HEARTDISEASE
HYPERTENSON(AFTERLOAD MENINGKAT)
Terjadi Myocardial Fibers hypertrophy,atherosclerossis of epicardiac coronary
artery, greater collagen content and
microvasculardamage
LEFT VENTRICULAR
HYPERTROPHY ANDMYOCARDIAL
ISCHEMIA
Diastolic Dysfunction Systolic Dysfunction HYPERTENSIVEHEART DISEASE
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Contoh Hypertensive Heart Disease:
1. Myocardial Infarction
2. Arrythmia dan loss of muscle
3. Heart Failure
4. Ischemia cardiomyopathy
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Development of Cardiac Lesions
due to Hypertension
LEFT VENTRICULAR
HYPERTROPHYISCHEMIA
Myocardial fibers
hypertrophy
Greater collagen
content
Heart
failureArrhythmias
Atherosclerosis of
epicardiac coronary
arteries
Microvascular
damage
Ischemic
cardiomyopathy
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Pathogenesis of LVHPressure Volume Overload
Age
Gender
Genetics
Race
Obesity
Neurohormonal Factors
Angiotensin II
Aldosterone
ACE
Myocardial
Ischemia
Impaired
contractility
Impaired
LV Filling
Ventricular
Arrhythmias
Infarctio
n
Congestive Heart Failure Sudden Death
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Clinical Presentation
absent in early hypertension
in advanced severe cases;
hypertensive retinopathy (ie, narrowed
arterioles seen on funduscopic examination),
retinal hemorrhages and exudates along with
swelling of the optic nerve head (papilledema)
left ventricular hypertrophy renal hypertension
Hypertension treatment strategy: JNC VII
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Hypertension treatment strategy: JNC VIILifestyle modifications
Not at goal blood pressure (
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Main classes of antihypertensive drugs
Diuretics
Inhibit the reabsorption of salts and water from kidney tubules into thebloodstream
Calcium-channel antagonists
Inhibit influx of calcium into cardiac and smooth muscle
Beta-blockers
Inhibit stimulation of beta-adrenergic receptors Angiotensin-converting enzyme (ACE) inhibitors
Inhibit formation of angiotensin II
Angiotensin II receptor blockers (ARBs)
Inhibit binding of angiotensin II to type 1 angiotensin II
Receptors Vasodilators
Direct renin inhibitors
Compelling Indication for
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Compelling Indication forIndividual Drug Classes
Compelling
indication
Recommended Drugs
Diuretic BB ACEI ARB CCBAldo
ANT
Heart failure
X X X X XPost-myocardial
infarctionX X X
High coronary risk X X X X
Diabetes X X X X XChronic renal
diseaseX X
Recurrent stroke
preventionX X
Chobanian AV, JNC VII, Hypertension. 2003
JNC 7
2009 Reappraisal of 2007 European Guidelines:
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Diuretics
ACE inhibitors
Calcium channel
blockers
Angiotensin
receptor blockers
-blockers
1-blockers
2009 Reappraisal of 2007 European Guidelines:
recommended combinations
2007 Guidelines for the management of hypertension J Hypertens. 2007;25:11051187.J Hypertens. 2009;27:2121-2158.
Preferred combinations
Other possible combinations
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Life style modifications
Lose weight, if overweight
Limit alcohol intake
Increase physical activity
Reduce salt intake
Stop smoking
Limit intake of foods rich in fats andcholesterol
9/11/2013 Kuliah Penyakit Jantung Hipertensi 63
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Indikasi Rujuk : 3a
Seorang dokter umum mampu membuat
diagnosis klinik berdasarkan pemeriksaan fisik dan
pemeriksaanpemeriksaan tambahan yang diminta oleh
dokter (misalnya : pemeriksaan laboratorium sederhana
atauX-ray). Dokter dapat memutuskan dan memberi terapipendahuluan, serta merujuk ke spesialis yang relevan
(bukan kasus gawat darurat).
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Kesimpulan
Tuan S usia 59 tahun mengalami penyakit jantung
hipertensif akibat hipertensi kronis yang dialaminya.