TUTORIAL A5

PEMICU 1 BLOK CARDIOVASCULAR 1

FAKULTAS KEDOKTERAN UNIVERSITAS SUMATERA UTARA 2013

Lembar 1
Tn. S, laki-laki 59th datang ke praktek seorang dokter karena keluhan 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 nama obatnya. Dan gejalanya tidak berkurang. Tidak ada riwayat sesak nafas, dan juga diabetes disangkal.

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 keempet ekstremitas sama. Frekuensi napas : 20x/menit, suhu tubuh 36,50C. Ikterus, edem, sianosis, dan pucat tidak ditemukan
2. Pemeriksaan kardiovaskular Tekanan vena jugularis normal, dada terlihat simetris, perkusi dada sonor, batas jantung kiri 1 cm lateral LMCS, ICR 5-6. Pada auskultasi jantung, suara jantung I dan II normal, tidak ada murmur maupun gallop

3. Pemeriksaan Respirasi Trakhea teraba di garis tengah dan pergerakan dada normal serta simetris. Auskultasi paru terdengar vesikuler di kedua lapangan 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.

Lembar 3
Pemeriksaan penunjang 1. Pemeriksaan laboratorium Darah dan urin dalam batas normal 2. Foto Toraks Jantung sedikit membesar dengan CTR 55%, paru normal, tulang normal, kesan : kardiomegali ringan 3. EKG Sinus ritme, rate 80x/menit, gelombang P normal, aksis QRS -30 derajat (kesan left axis defiation), QRS kompleks normal, gelombang T normal, dan LV high voltage Kesan : left ventricel hipertrophy

LEARNING ISSUE
1. 2. 3. Anatomi dan Histologi Kardiovaskuler Fisiologi jantung sebagai pompa 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 PENYAKIT JANTUNG HIPERTENSIF a. Mekanisme hipertensi menyebabkan penyakit jantung b. diagnosis c. prognosis dan indikasi rujuk

4.

ANATOMI JANTUNG
ORGAN BERONGGA & BEROTOT YANG MEMOMPA DARAH MELALUI SIRKULASI PULMONAL & SISTEMIK

MENERIMA DARAH VENOSA KE DLM ATRIUM KANAN MENYALURKAN KE VENTRIKEL KANAN KE PARU-PARU UNTUK OKSIGENASI
MENERIMA DARAH TEROKSIGENASI KE ATRIUM KIRI VENTRIKEL 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 )

 RUANG COR : ATRIUM KA & KI, VENTRIKEL KANAN & 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

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 CORDA TENDINEA MEMPUNYAI AURICULA CORDIS PD KEDUA ATRIUM, DIDALAMNYA TERDAPAT MUSCULUS PECTINATI MEMPUNYAI SEKAT JANTUNG DISEBUT SEPTUM INTERVENTRICULORUM YANG MEMISAHKAN JANTUNG BAGIAN KIRI & KANAN

 PEMBULUH ARTERI BESAR YG KELUAR DARI VENTRIKEL : TRUNCUS/ARTERI PULMONALIS (KANAN) AORTA (KIRI) KEDUA PEMBULUH TSB MEMPUNYAI KATUP DISEBUT VALVULA SEMILUNARIS 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

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

Speciallized muscle cells in atrium produce atriopeptin, ANF(Atrial Natriuretic Factor), cardiodilatin, cardionatrin help in maintain fluid & electrolyte balance3

Thinnest Smaller cardiac 13 muscle cells

Type Of Cardiac Muscle Fiber

1. Conducting Impluse Fiber 2. Contractile Fiber

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1. Conducting Impulse Fiber

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

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 Purkinje fibers : 2, 3
Branches of AV 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 large mitochondria

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III. Epicardium
Homologue to tunica adventitia in blood vessels3 Outermost layer of heart wall3 Consist of : 1, 2 1. Pericardium viceral mesothelium (simple squamous epithelium) 2. Subepicardial layer loose connective tissue with coronary vessels, nerves & ganglia 3. Pericardium parietal: mesothelium & conn. tissue Space between pericardium contain serous liquid for lubricating

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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 function 3. Tunica Adventitia: Correspond to epicardium lack mesothelial cells Varies in thicknes Mostly composed of fibroblast, type I collagen fiber & elastic fiber
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Blood Vessel Wall Composition

ELASTIC TISSUE
LARGE ARTERIES SMALL ARTERIES

MUSCLE

ARTERIOLES

CAPILLARIES

VENULES &VEINS
LARGE SMALL LARGE
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INSIDE DIAMETER

 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 than arteries coz venous blood contain less oxygen & nutients than arterial blood

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Nerve Supply Of Blood Vessel 3

A network of vasomotor nerve of sympathetic component of autonomic 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

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CLASSIFICATION OF BLOOD VESSELS ARTERIES

Elastic arteries / conducting arteries Medium (muscular) arteries / distributing arteries & small arteries Arteriole

VEIN
Large vein Medium & small veins Venule

CAPILLARIES
Continuous capillaries Fenestrated capillaries
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Sinusoidal capillaries

Conducting System of the Heart

Inter- nodal Tracts SA Node AV Node

Left Bundle Branch

Anterior Superior Fascicle

Bundle of HIS

Posterior Inferior Fascicle Septal Depolarization Fibers

Purkinjie Fibers

Right Bundle Branch

CARDIAC CYCLE

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.

 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.

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 by atherosclerosis. Murmurs heard over aneurysmal dilation of large arteries, an arteriovenous (A-V) fistula, or patent ductus arteriosus.

ELECTRICAL PROPERTIES

The resting membrane potential -90 mV

This diagram illustrates ECG waves and intervals as well as standard time and voltage measures on the ECG paper.
1. ECG Waves and Intervals: What do they mean? P wave: the sequential activation (depolarization) of the right and left atria QRS complex: right and left ventricular depolarization (normally the ventricles are activated simultaneously) ST-T wave: ventricular repolarization U wave: origin for this wave is not clear - but probably represents "afterrepolarizations" in the ventricles PR interval: time interval from onset of atrial depolarization (P wave) to onset of ventricular depolarization (QRS complex) QRS duration: duration of ventricular muscle depolarization QT interval: duration of ventricular depolarization and repolarization RR interval: duration of ventricular cardiac cycle (an indicator of ventricular rate) PP interval: duration of atrial cycle (an indicator of atrial rate)

1. Measurements (usually made in frontal plane leads):

Heart rate (state atrial and ventricular, if different) PR interval (from beginning of P to beginning of QRS) QRS duration (width of most representative QRS) QT interval (from beginning of QRS to end of T) QRS axis in frontal plane

Kwantitatif
Gel.P: panjang 0.06 s tinggi : 0.20 mV QRS: lebar : 0.06 0.10 s

P-R interval: 0.12 0.20 s.

Q T interval: 0.32 0.40 s.

Examples of QRS Axis

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 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 right axis deviation (RAD) range:

Lead aVR is closest to being isoelectric (slightly more positive than negative) The two perpendiculars are -60 o and +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

Sokolow-Lyon Indices
electrocardiographic diagnosis of LVH
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

Example 1: (Limb-lead Voltage Criteria; e.g., R in aVL >11 mm; note wide QRS/T angle)

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)

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

 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

Jika nilai perbandingan di atas nilainya 50% (lebih dari/sama dengan 50% maka dapat dikatakan telah terjadi pembesaran jantung (Cardiomegally)

 Menilai pembesaran jantung pada radiografi thoraks sering mengalami kesulitan karena bentuk jantung dapat berubahubah 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.

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, and dizziness "the silent killer"

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

Hypertension Syndrome

Its More Than Just Blood Pressure

Decreased Arterial Compliance

Obesity Abnormal Lipid Metabolism Accelerated Atherogenesis

Hypertension

Endothelial Dysfunction Abnormal Glucose Metabolism Neurohormonal Dysfunction RenalFunction Changes

LV Hypertrophy and Dysfunction

Abnormal Insulin Metabolism

BloodClotting Mechanism Changes

Kannel WB. JAMA. 1996;275:1571-1576. Weber MA et al. J Hum Hypertens. 1991;5:417-423. Dzau VJ et al. J Cardiovasc Pharmacol. 1993;21(suppl 1):S1-S5.

Classification and Management of BP for adults

BP classification Normal SBP* mmHg <120 DBP* mmHg and <80 Lifestyle modification Encourage Yes Yes No antihypertensive drug indicated. Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination. Two-drug combination for most (usually thiazide-type diuretic and ACEI or ARB or BB or CCB). Drug(s) for compelling indications. Drug(s) for the compelling indications. Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed. Initial drug therapy Without compelling indication With compelling indications

Prehypertension 120139 or 8089 Stage 1 Hypertension 140159 or 9099

Stage 2 Hypertension

>160

or >100

Yes

*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 <130/80 mmHg.

DD Hipertensi
White coat hypertension Rasa nyeri Akibat obat Ensefalitis

Patho-physiology of Hypertension

Excess Na intake

Reduced Nephron Numbers

Decreased filtration surface

Stress

Genetic Alterations

Obesity

Endotheliu m derived factors

Renal Na retention

Sympatheic Over activity

RAS Excess

Cell-membrane alterations

Hyper insulinemia

Fluid Volume

Venous constriction

Preload

Contractibility

Functional constriction

Structural hypertrophy

Blood pressure= Cardiac Output X Peripheral Resistance HTN and/or

Renin-Angiotensin System
Angiotensinogen Renin Angiotensin I Bradykinin

tPA Catepsin

B1-R

Chymase

ACE

B2-R

Angiotensin II

Inactive quinines

AT1-R

AT2-R

Effects of angiotensin II
Water and sodium retention
Peripheral vasoconstriction Renin secretion

Vascular proliferation

AII AT1-R

Aldosterone secretion

Adrenergic
activity Efferent arteriole vasoconstriction

Thirst mechanism

Complications of HTN
CNS

Cardiac

Stroke or TIA

Renal

Heart diseases

Sequelae of Hypertension
Nephropathy, Proteinuria, CrCl

Retinal

Vascular

Retinopathy

Peripheral arterial Disease (atherosclerotic plaque iliac,carotid, femoral artery, aorta)

HIPERTENSIVE HEART DISEASE

HYPERTENSON (AFTERLOAD MENINGKAT)
LEFT VENTRICULAR HYPERTROPHY AND MYOCARDIAL ISCHEMIA

Terjadi Myocardial Fibers hypertrophy, atherosclerossis of epicardiac coronary artery, greater collagen content and microvascular damage

Diastolic Dysfunction

Systolic Dysfunction

HYPERTENSIVE HEART DISEASE

 Contoh Hypertensive Heart Disease: 1. Myocardial Infarction 2. Arrythmia dan loss of muscle 3. Heart Failure 4. Ischemia cardiomyopathy

Development of Cardiac Lesions due to Hypertension

Myocardial fibers Greater collagen hypertrophy content Atherosclerosis of Microvascular epicardiac coronary damage arteries

LEFT VENTRICULAR HYPERTROPHY

ISCHEMIA

Heart failure

Arrhythmias

Ischemic cardiomyopathy

Pathogenesis of LVH
Pressure Volume Overload Age Neurohormonal Factors

Gender
Genetics Race Obesity

Angiotensin II
Aldosterone ACE

Myocardial Ischemia

Impaired contractility

Impaired LV Filling

Ventricular Arrhythmia s

Infarctio n

Congestive Heart Failure

Sudden Death

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

Lifestyle modifications Not at goal blood pressure (<140/90 mmHg) (<130/80 mmHg for patients with diabetes or chronic kidney disease)

Initial drug choices Without compelling indications

Stage 1 hypertension (SBP 140-159 or DBP 90-99 mmHg) Thiazide-type diuretics for most. May consider ACE-I, ARB, BB, CCB or combination Stage 2 hypertension (SBP 160 or DBP 100 mmHg) Two-drug combination for most (usually thiazide-type diuretic and ACE-I or ARB, or BB, or CCB) With compelling indications Drug(s) for the compelling indications

Other antihypertensive Drugs (diuretics, ACE-I, ARB, BB, CCB) as needed

Not at blood pressure goal Optimize dosages or add additional drugs until goal blood pressure is achieved. Consider consultation with hypertension specialist.
SBP, systolic blood pressure; DBP, diastolic blood pressure; ACE-I, angiotensinconverting enzyme inhibitor; ARB, angiotensin II receptor blocker; BB, betablocker; CCB, calcium-channel blocker
JNC VII. JAMA 2003;289:2560-2572

Main classes of antihypertensive drugs

Diuretics
Inhibit the reabsorption of salts and water from kidney tubules into the bloodstream

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 Individual Drug Classes

Recommended Drugs Compelling indication Heart failure Post-myocardial infarction High coronary risk Diabetes Chronic renal disease Recurrent stroke prevention
Diuretic BB ACEI ARB

JNC 7

CCB

Aldo ANT

X X

X X X X X

X X X

X X

X X

X X

X
Chobanian AV, JNC VII, Hypertension. 2003

2009 Reappraisal of 2007 European Guidelines: recommended combinations

Diuretics

-blockers

Angiotensin receptor blockers

1-blockers

Calcium channel blockers ACE inhibitors

Preferred combinations Other possible combinations

2007 Guidelines for the management of hypertension J Hypertens. 2007;25:11051187.J Hypertens. 2009;27:2121-2158.

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 and cholesterol
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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 atau X-ray). Dokter dapat memutuskan dan memberi terapi pendahuluan, serta merujuk ke spesialis yang relevan (bukan kasus gawat darurat).

Kesimpulan
Tuan S usia 59 tahun mengalami penyakit jantung hipertensif akibat hipertensi kronis yang dialaminya.