fkumj fis sistem kardiovaskuler 2009
TRANSCRIPT
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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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• 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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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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