Tutorial a5

7/29/2019 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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12

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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13

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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15

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
http://localhost/var/www/apps/conversion/tmp/scratch_1/intro%20Heart%20Circulation.flv


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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
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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.

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