fkumj fis sistem kardiovaskuler 2009

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06/17/22 FISIOLOGI SISTEM KARDIOVASKULER Dr. dr. H. Busjra M. Nur MSc. Departemen Fisiologi FKUI - FKK UMJ

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Page 1: Fkumj Fis Sistem Kardiovaskuler 2009

05/03/23

FISIOLOGI SISTEM KARDIOVASKULER

Dr. dr. H. Busjra M. Nur MSc.

Departemen Fisiologi FKUI - FKK UMJ

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T.D. : JANTUNG PEMBULUH DARAH

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FUNGSI: JALAN PENGANGKUT : Nutrien 02, CO2 Sisa metabolisme Panas Hormon

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PEMBULUH DARAH: t.d.

- Distributing system ---- nadi,- Collecting system ---- vena- Capillary system ---- antara keduanya • William Harvey: susunan tertutup• Rangkaian : - seri - paralel

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JANTUNG : t.d.:

Atrium: kiri - kanan ---- septum atrium Ventrikel : kiri - kanan ---- septum ventrikel

Dinding Atrium : tipis Dinding Ventrikel : tebal.

Kiri lebih tebal

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KATUP- KATUP :

- Atrio-ventrikular: - trikuspid - mitral- Semilunar: - aorta - pulmonal

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KATUP-KATUP• Merupakan selaput tipis -- pasif• mencegah darah kembali • keempat katup saling berdekatan• semua melekat pada anulus fibrosus

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05/03/23 Katup-katup dengan anulus fibrosus

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• HISTOLOGI: - serat otot lurik - intercalated disc– syncitium (sinsitium) • 2 JENIS OTOT - miokardium : kontraksi - susunan hantar khusus fungsi = saraf

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Susunan Hantar Khusus

1. Simpul SA di dinding atrium kanan2. Simpul AV di bag. Bawah septum atrium3. Berkas His. Menembus anulus fibrosus Right Bundle Branch (RBB) dan Left Bundle Branch (LBB) LBB : fasikulus anterior fasikulus posterior

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Internodal pathways

• Berkas yang hubungkan SA – AV - anterior (Bachman) - midle (Wenckebach) - posterior (Thoree)• > mudah hantarkan impuls daripada mikardium atrium

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Sel / serat Purkinye• Ujung susunan hantar khusus di

ventrikel (subendokardium)

• Sel > besar dari pada sel miokardium• pucat, lurik tidak jelas• menyerap > banyak glikogen

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Sifat-sifat Faali Otot Jantung 1. Otomasi / ’Rhythmicity’ - membentuk impuls sendiri - normal: simpul SA (70-80) - patologis : simpul AV (40-60) berkas His (20-40) 2. Hukum gagal atau tuntas

-- sinsitium3. Fenomena tangga

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SIFAT - SIFAT FAALI :

4. Tidak ada kontraksi tetanus sifat biolistrik

5. Panjang awal awal kuat kontraksi hukum Starling

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KELISTRIKAN JANTUNG(Elektrofisiologi)

• Pembangkitan (pencetusan)• Penjalaran• Perangsangan

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Pencetusan Impuls di SA

• Terjadi secara otomatis (self induced action potential)

• Dimulai dengan prepotensial (depolarisasi lambat), Potensial membran istirahat tidak tetap (Pacemaker potential)

• Setelah mencapai ambang letup potensial aksi

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Pencetusan impuls di SA

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Potensial Aksi Jantung

• Autorhythmicity – pacemaker cells• Potensial Aksi teratur• Dipengaruhi elektrolit, SSP, hormon dan

obat-obat

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Potensial aksi

ventrikel

SA node

Atrium

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Jalan Impuls • Dihasilkan di SA Miokardium atrium (internodal pathways)

Simpul AV (perlambatan) Berkas Hiss Serat Purkinye Miokardium ventrikel

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Potensial Aksi Pada Otot Jantung

• Mempunyai lima fase, masing-masing:– Fase 0 (upstroke, fast depolarization)– Fase 1 (early repolarization)– Fase 2 (plateau)– Fase 3 (fast repolarization)– Fase 4 (resting membrane potential)

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Potensial aksi

ventrikel

SA node

Atrium

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Di miokardium

• Listrik dari SA : mencetuskan : depolarisasi potensial aksi (di atrium dan ventrikel) dihantarkan ke seluruh tubuh disadap di kulit EKG.

• Potensial aksi di miokardium atrium dan ventrikel kontraksi mekanik

peristiwa listrik mendahului peristiwa mekanik

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Otot lurik >< otot jantung

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Gangguan Irama Jantung

• Gangguan pembentukan impuls• Gangguan penghantaran impuls• Gangguan pembentukan dan penghantaran impuls

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Gangguan Pembentukan Impuls

• Otomatisitas normal– Kecepatan abnormal: Takikardi dan Bradikardi– Irama abnormal : Impuls premature

• Otomatisitas abnormal• Trigger activity

– Early after depolarization (EAD)– Delayed after depolarization (DAD)

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Gangguan Konduksi Impuls

• Perlambatan dan hambatan konduksi– Blok SA– Blok AV– Blok percabangan berkas His

• Mekanisme reentry

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ION-ION ESENSIAL UNTUK JANTUNG

• K+ - intrasel = 30 X ekstrasel

- penting pada potensial membran istirahat

• Ca++

• Na+

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Effects of Potassium ions• on Pacemaker cells:

– Determines the resting membrane potential– Increased [K+]o reduce transmembrane potential

increase firing frequency with lower amplitude of action potential

– 2-3 fold increase of [K+]o ectopic foci & arrhythmia

– Decreased [K+]o hyper-polarization decrease firing frequency of action potential

• on Myocardial cells:– Trans-membrane potential varies inversely with [K+]o

– Increased [K+]o decrease myocardial contractility the heart become flaccid and dilates.

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Effects of Calcium ions• on Pacemaker cells:

– [Ca++]o is essential in forming the action potential of pacemaker cells

– Decrease [Ca++]o decrease in firing rate and alter characteristics of pacemaker action potential

• on Myocardial cells:– Increased [Ca++]o prolong plateau phase of

action potential increase of [Ca++] in cytosol enhance contractility

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Effects of Sodium ions• on Pacemaker cells:

– [Na+]o influence the slope of pacemaker potential

– Decreased [Na+]o reduce firing frequency of action potential decrease heart rate

• on Myocardial cells:– [Na+]o determines the amplitude of action potential– Relatively little effect on resting membrane potential

because of low gNa– Decreased [Na+]o low voltage ECG low

contractility

Page 42: Fkumj Fis Sistem Kardiovaskuler 2009

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JANTUNG SEBAGAI POMPA

• Sistole-diastole pada atrium-ventrikel• Terbuka-tertutup katup-katup• Ada “pressure gradient” Darah mengalir

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Systemic circulation

Pulmonary circulation

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Sistole Atrium

• Tidak begitu penting untuk pengisian ventrikel

• Tanpa sistol atrium darah tetap mengalir dari atrium ke ventrikel

• Mungkin penting bila denyut jantung meningkat tinggi

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Sistole Ventrikel

fase kerja ventrikel :

A . Selama sistole

1. Fase kontraksi isometrik (isovolumetrik)

2. Fase ejeksi maksimal3. Fase ejeksi lambat

Page 48: Fkumj Fis Sistem Kardiovaskuler 2009

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B. Selama diastole

4. Fase protodiastole5. Fase relaksasi isometrik6. Fase pengisian cepat7. Fase pengisian lambat

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The Wiggers diagram

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Bunyi Jantung

• Auskultasi Lub - Dub I – II

• BJ. I : 3 Faktor : - Otot : kontraksi ventrikel - Katup : mitral + trikuspid menutup - Pembuluh : getaran aorta + a. pulmonalis

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.

• BJ. II : - Penutupan katup semilunaris aorta + pulmon. - Awal diastole ventrikel - Penutupan katup semilunaris aorta sedikit lebih dahulu - Dapat “splitting” terutama saat inspirasi

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.• B J. III - Bila arus darah atrium ke ventrikel sangat besar saat pengisian cepat - Biasa pada anak & dewasa saat olah raga

• B J. IV - Bila darah dariatrium ke ventrikel sangat banyak pada sistole atrium - Patologis

Page 56: Fkumj Fis Sistem Kardiovaskuler 2009

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Tempat auskultasi jantung

• Sela iga II parasternal kanan• Sela iga II parasternal kiri• Sela iga IV parasternal kanan• Sela iga IV parasternal kiri • Apeks jantung, sela iga V garis medio-

klavikuler kiri

Page 57: Fkumj Fis Sistem Kardiovaskuler 2009

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Tempat auskultasi

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Bising jantung

• Akibat arus turbulensi melalui celah sempit

• Bising sistolik: antara BJ. I – II• Bising diastolik: antara BJ II – BJ I

berikutnya

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.• STENOSIS (SEMPIT) - Semilunaris ( AS, PS) – bising sistolik - Atrioventrikuler ( MS,TS) – bising diastolik

• INSUFISIENSI (BOCOR) - Semilunaris (AI,PI) – bising diastolik - Atrioventrikuler (MI,TI) – bising sistolik

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CURAH JANTUNG

• Jumlah darah yang dipompakan tiap ventrikel per menit

• = isi sekuncup X frekuensi : bila denyut jantung + isi

sekuncup• Curah jantung kiri = kanan

Page 62: Fkumj Fis Sistem Kardiovaskuler 2009

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CURAH JANTUNG :

• Marah/cemas (50% - 100%) • Makan (30%)• Olah raga ( sampai 700% )• Suhu tubuh • Hamil tua• Epinefrin

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Cardiac Output

Stroke Volume

Heart Rate

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Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

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Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

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End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

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Ventr. E-D pressure (Preload)

End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

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Filling time

Ventr. E-D pressure (Preload)

End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

Page 69: Fkumj Fis Sistem Kardiovaskuler 2009

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Venous Return

Filling time

Ventr. E-D pressure (Preload)

End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

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Blood Volume

Passive movement of

fluid from intestine to

plasma Water &

salt retention

Venous Return

Filling time

Ventr. E-D pressure (Preload)

End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

Page 71: Fkumj Fis Sistem Kardiovaskuler 2009

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Respiratory Pump

Blood Volume

Passive movement of

fluid from intestine to

plasma Water &

salt retention

Venous Return

Filling time

Ventr. E-D pressure (Preload)

End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

Page 72: Fkumj Fis Sistem Kardiovaskuler 2009

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Skeletal Muscle Pump

Respiratory Pump

Blood Volume

Passive movement of

fluid from intestine to

plasma Water &

salt retention

Venous Return

Filling time

Ventr. E-D pressure (Preload)

End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

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Sympathetic Vasoconstricto

r Activity

Skeletal Muscle Pump

Respiratory Pump

Blood Volume

Passive movement of

fluid from intestine to

plasma Water &

salt retention

Venous Return

Filling time

Ventr. E-D pressure (Preload)

End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

Page 74: Fkumj Fis Sistem Kardiovaskuler 2009

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Sympathetic Vasoconstricto

r Activity

Pressure exerted by contraction of

the heart

Skeletal Muscle Pump

Respiratory Pump

Blood Volume

Passive movement of

fluid from intestine to

plasma Water &

salt retention

Venous Return

Filling time

Ventr. E-D pressure (Preload)

End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

Page 75: Fkumj Fis Sistem Kardiovaskuler 2009

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Sympathetic Vasoconstricto

r Activity

Negative pressure in the heart

Pressure exerted by contraction of

the heart

Skeletal Muscle Pump

Respiratory Pump

Blood Volume

Passive movement of

fluid from intestine to

plasma Water &

salt retention

Venous Return

Filling time

Ventr. E-D pressure (Preload)

End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

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Venous Valves

Sympathetic Vasoconstricto

r Activity

Negative pressure in the heart

Pressure exerted by contraction of

the heart

Skeletal Muscle Pump

Respiratory Pump

Blood Volume

Passive movement of

fluid from intestine to

plasma Water &

salt retention

Venous Return

Filling time

Ventr. E-D pressure (Preload)

End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

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Venous Valves

Sympathetic Vasoconstricto

r Activity

Negative pressure in the heart

Pressure exerted by contraction of

the heart

Skeletal Muscle Pump

Respiratory Pump

Blood Volume

Passive movement of

fluid from intestine to

plasma Water &

salt retention

Venous Return

Filling time

Ventr. E-D pressure (Preload)

End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

Short term regulation

Long term regulation

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Volume residu (residual volume)

• Volume darah yang tertinggal dalam ventrikel setelah sistole.

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Daya Cadangan Jantung (reserve capacity)

• Curah jantung maksimal – curah jantung istirahat• > pada orang terlatih

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Indeks Jantung

• Curah jantung / Luas Permukaan Badan (korelasi terbaik dengan LPB)

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PENGATURAN KERJA JANTUNG

• Faktor intrinsik : Hukum Frank-Starling

• Faktor ekstrinsik: saraf kimia

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Regulation of heart contractility

Intrinsic Regulation

Extrinsic Regulation

Change in muscle length

heterometric regulation Frank

Starling Law

No change in muscle length

homometric regulation

End Diastolic Volume

Autonomic regulationHormonesChemical

substances

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PENGATURAN INTRINSIK• Pengaturan intrinsik berlangsung melalui mekanisme otoregulasi:

– heterometrik– homeometrik

• Prinsip dasar pengaturan intrinsik adalah:

– mengatur panjang otot jantung– pengaturan kontraktilitas

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FrankStarling Curve

10 20 30 40 50 60 70 80

0

30

60

90

120

150

180

210

240

270

300Pr

essu

re (m

mHg

)

Diastolic volume (mL)

Systolic intraventricular pressure

Diastolic intraventricular pressure

Optimal length

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OTTO FRANK (1895) Jt kodokSTARLING (1914) Jt mamalia

• Heterometrik regulation

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Pengaturan heterometrik

• Preload merupakan tekanan akhir diastolik (EDP) yang pada keadaan normal berkisar 4-5 mmHg.

• Faktor-faktor yang mempengaruhi preload:– Tekanan pengisian (Filling pressure)– Waktu pengisian (Filling time)– Distensibiltas ventrikel (Ventricle disten

sibility)

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Pengaturan heterometrik• Faktor-faktor yang mempengaruhi

tekanan pengisian– Tonus vena perifer– Volume darah– Latihan fisik– Pernafasan– Curah jantung– Perubahan posisi

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Pengaturan heterometrik

• Tekanan darah arteri merupakan parameter kinerja afterload yang paling baik

• Peningkatan afterload menyebabkan perubahan curah jantung

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Pengaturan oleh Saraf

• Saraf Autonom SA Node

• Simpatis Kronotropik + ( frekuensi ) Inotropik +

• Parasimpatis Frekuensi

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Parasympathetic stimulation

permeability

to K ion K efflux

Hyperpolarization

heart rateChronotropic negative

Atrium MyocardiumSA node AV node

influx of Ca

Contractility

INOTROPIC NEGATIVE ??

AV delay

impulse conductionDromotropic negative

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Sympathetic stimulation

influx of Ca

ContractilityInotropic positive

inactivation of K

channels K efflux

Hypopolarization

heart rateChronotropic positive

Atrium Ventricle Myocardium

SA node AV node

AV delay

impulse conductionDromotropic positive

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Venous Valves

Sympathetic Vasoconstricto

r Activity

Negative pressure in the heart

Pressure exerted by contraction of

the heart

Skeletal Muscle Pump

Respiratory Pump

Blood Volume

Passive movement of

fluid from intestine to

plasma Water &

salt retention

Venous Return

Filling time

Ventr. E-D pressure (Preload)

End Diastolic Volume

Sympathetic stimulation

Parasympathetic stimulation

Cardiac Output

Stroke Volume

Heart Rate

Afterload

Ventricular contractility

Short term regulation

Long term regulation

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Pengaturan oleh baroreseptor• Baroreseptor terdapat pada - dinding sinus karotis, lengkung aorta - dinding atria, muara v. cavae,v. pulmonal• Baroreseptor merupakan reseptor regang

yang diaktifkan oleh peregangan pada daerah dimana reseptor tersebut berlokasi

• Dua jenis baroreseptor: 1) baroreseptor perifer 2) baroreseptor kardiopulmoner

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Baroreceptor reflex

Increased Blood Pressure

Decrease heart rate

&Blood pressure

Carotid/aortic baroreceptor

s

Ascending fibers of n. IX and n.X

Cardio-inhibitor center

Descending fibers of Vagal nerve

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Baroreceptor reflex

Decreased Blood Pressure

Increase heart rate

&Blood pressure

Carotid/aortic baroreceptor

s

Ascending fibers of n. IX and n.X

Cardio-accelerator center

Sympathetic nerve

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Volume darah ,Aliran darah balik, Pengisian atria

Aktifasi reseptor venoatrial

Aktifasi simpatis nodus SA

Frekwensi jantung

Aktifasi simpatis ginjal

Sekresi renin

Sekresi angiotensin II,aldosteron

Konsentrasi garam , air

Pituitari posterior

Sekresi ADH

Reabsorbsi air padatubulus

Ekskresi air

V o l u m e d a r a h k e m b a l i n o r m a l

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Vagal Escape (Lolos vagus)

1. Lab: Rangsang Vagus(lama) Cardiac arrest Darah terus masuk ventrikel Ventrikel teregang rangsang mekanik SA node escape beat

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Vagal escape

2. Rangsang vagus (lama)

Pace maker tidak berfungsi Diambil alih bagian jantung lain Escape beat

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Refleks Jantung

• Tidak spesifik : rasa sakit• Spesifik: A. Baroreseptor: - sinus karotikus - arkus aorta - atrium - ventrikel

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B. Kemoreseptor - glomus karotikum - glomus aortikum 02 , CO2 , dll

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Kemoreseptor• O2 : (ringan) : denyut : (berat) : denyut • CO2 : kronotropik ( - ) dromotropik ( - )• Epinefrin/Norepinefrin : • Asetilkolin : • Tiroksin : takikardia aritmia : fibrilasi bradikardia

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• Refleks Sinus Karotikus Rs : tekanan darah dlm sinus karotikus

TD tonus parasimpatis tonus simpatis TD tonus simpatis tonus parasimpatis

• Refleks Okulo-Kardia: RS: tekan bola mata Vagus d.j.

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• Refleks Bainbridge Infus cepat d.j.

• Refleks Goltz Rangsang isi abdomen d.j. / Stop

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TES KESANGGUPAN KARDIOVASKULER

• Cold pressor test: tangan direndam air es nyeri simpatis tekanan darah • Harvard steps test: naik turun bangku : d.j. terlatih: kemampuan

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