gagal jantung kronik
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GAGAL JANTUNG KRONIK
Alexandra Widita S. P.Nurrakhmanita AzizaNor Idyani
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DEFINISI
Forward Failure
•Ketidakmampuan jantung•Memompa cukup darah•Memenuhi kebutuhan metabolisme tubuh
Backward Failure
•Kemampuan jantung•Memompa cukup darah•Jika tekanan pengisian jantung tinggi lebih dari normal
*Atau keduanya
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DEFINISI
Gagal Jantung Kiri•Kelemahan ventrikel• Tekanan vena pulmonalis•Sesak napas
Gagal Jantung Kanan
•Kelainan yang melemahkan ventrikel kanan (eg. HT pulmonal)•Kongesti vena sistemik•Edema perifer, hepatomegali, distensi vena jugularis
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EPIDEMIOLOGI> 500.000 kasus baru di AS tiap
tahun2007: ± 5 juta orang terserang
gagal jantung
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FISIOLOGI
Contractility PreloadAfterload
Heart Rate X Stroke Volume
Cardiac output
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Gagal Jantung Afterload
Preload CO Total tahanan
sistem perifer Filling pressure
Mekanisme kompensasi1. Dilatasi ventrikel2. Hipertropi ventrikel3. Aktifitas neurohumoral - Saraf simpatis - Sistim renin-angiotensin4. Renal mekanisme (Retensi natrium/air) - Reabsorbi NA pada proximal tubules - Anti diuretic hormon
PATOFISIOLOGI
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Aktivitas Neurohumoral
Mempertahankan tekanan darah perfusi organ vital / koroner
dipertahankan
Tekanan darah (CO )
◦ Plasma norepineprine
◦ Plasma renin
◦ Plasma argine vasopressin
Baro receptor (Arcus Ao, Sinus caroticus)
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Pusat vasomotor (Batang Otak)
Saraf simpatis
* Vasokontstriksi (after load )
* Kontraktilitas miokard
* Frekuensi (Beban , 02 dibutuhkan )
* Vaskontriksi renal (ekskresi Natrium, Air )kongesti
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Peranan Renin Angiotensin Aldosteron Sistim
Gagal jantung
CO Angiotensinogen (Hepar)
GFR
Saraf simpatis
Renin
Angiotensin I
Angiotensin converting Angiotensin IIenzyme (ACE) (Paru-paru)
Vasokonstriksi Vasokonstriksi Aldosteron retensi
venous arterioler NA & DR
Preload Afterload Preload
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Hukum Starling
Venous return / inflowEnd diastolic volume
(Left Ventricular End Diast. Volume )
* Konstraksi miokard* CO / Stroke volume
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Gagal Jantung
CoStroke Vol.
Tensi End Sist. vol.
End Diast. vol.
(Hukum Starling)Heart RateVasokonstriksiKontraksi ventrikel
Saraf Simpatis Aliran darah renal(Perfusi)
Renin(Renin-angiotensin aldosteron)
Vasokontriksi Retensi NA
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Cardiad Output
Renin-angiotensin system Antidiuretic HormoneSympathetic nerous system
Contrac-tility
Heartrate
Vasoconstriction Circulating volume
Arteriolar Venous
Maintain blood pressure
Stroke volume
Cardiac output
Venous return to heart ( Preload)
Peripheral edema and pulmonary congestion
(+)(+)
(-)
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Gagal JantungKelelahan Miokard
Kontraksi Ventrikel
CO
Sindroma bendungan pada organ-organ (Backward Failure)
ParuLiver
Ginjal dll(Manifestasi Klinik)
Kiri KananLeft sided CHF Right sided CHFDC kiri DC kananLeft backward F. Right backward
failure
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CARDIOVASCULAR CONTINUUM
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KRITERIA FRAMINGHAM
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KLASIFIKASI
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diagnosis1. Identification of Patients
2. Identification of a Structural Abnormality
◦Complete history & P.E◦Echocardiogram◦Radionuclide ventrilography◦Chest radiography◦ECG
(1) With a syndrome of decreased exercise tolerance
(2) With a syndrome of fluid retention.(3) With no symptoms or symptoms of another cardiac ornoncardiac disorder
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3. Evaluation of Cause of Ventricular Dysfunction
a. History and Physical Examinationb. Laboratory Testing
◦ complete blood count, urinalysis, serum electrolytes (including calcium and magnesium), and blood lipids as well as tests of both renal and hepatic function
◦ chest radiograph◦ 12-lead electrocardiogram◦ BNP - 32-amino acid polypeptide that contains a 17-
amino acid ring structure common to all natriuretic peptides
◦ cardiac ventricles are the major source of plasma BNP◦ plasma BNP level greater than 100 pg per mL
supports a diagnosis of abnormal ventricular function or symptomatic HF
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European Society of Cardiology
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TERAPI
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GAGAL JANTUNG KANAN
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ETIOLOGI
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PATOFISIOLOGI
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GAGAL JANTUNG KIRIketidakmampuan jantung untuk
menghasilkan Cardiac Output (curah jantung) yang adekuat untuk perfusi jaringan.
Gagal jantung kiri
Gagal jantung sistolik
Gagal jantung diastolik
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Gagal Jantung Sistolik
ketidakmampuan jantung untuk menghasilkan curah jantung yang adekuat untuk perfusi jaringan tubuh akibat penurunan kontraktilitas otot jantung
Penyebab tersering adalah infark miokard.
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Miokard infarkMiokarditis, Kardiomiopati
Kontraktilitas jantung
Stroke volume
Hipertensi
Tahanan vaskular perifer
Resistensi pengosongan ventrikelKerja ventrikel kiri
Hipertrofi miokardium
Kontraktilitas
Volume akhir diastolik ventrikel kiri (preload )
Dilatasi jantungTekanan atrium kiri
Perfusi ginjal Aktivasi sistem Renin-angiotensin
Afterload
Vasokonstriksi sistemik
Sistem saraf simpatis teraktivasi
Perfusi ginjal Aktivasi sistem Renin-angiotensin
Preload
Tekanan kapiler dan vena paru vasokonstriksi kranialisasi
Tek. hidrostatik > tek. Onkotik vaskular
Transudasi cairan ke interstisial edema interstisial, efusi pleura/perikard
Kec. Transudasi > kec. Drainase limfatikPermeabilitas epitel alveolar
Edema alveolar
Edema paru
Hipoksemia
Kontraktilitas
Gagal jantung kongestifPenurunan perfusi ke otak dan organ lain
Retensi sodium dan air peningkatan vol.plasma & tahanan vaskular perifer
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Gagal jantung diastolikgagal jantung akibat defek
pengisian ventrikel yang diakibatkan oleh kelainan fungsi diastolik
Penyebab utama - hipertrofi miokard yang diinduksi oleh hipertensi dan iskemik miokardium dengan ventrikel remodeling
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Kemampuan ventrikel kiri untuk mengembang (compliance)
Volume akhir diastolik ventrikel kiri normal
Tekanan akhir diastolik ventrikel kiri
Tekanan yang meningkat ini direfleksikan kembali ke dalam sirkulasi pulmonal
Edema paru
Hipoksemia
Gagal jantung kongestif
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TERIMA KASIH