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Optimis Gagal Jantung - BIKO
Optimis Gagal Jantung - BIKO
Optimis Gagal Jantung - BIKO
SKDI
2019
DEFINITION
• HEART FAILURE (HF) IS A COMPLEX CLINICAL SYNDROME RESULTING FROM
STRUCTURAL AND FUNCTIONAL IMPAIRMENT OF VENTRICULAR FILLING OR
EJECTION OF BLOOD.
• ALTHOUGH THE CLINICAL SYNDROME OF HF MAY RESULT FROM
ABNORMALITIES OR DISORDERS INVOLVING ALL ASPECTS OF CARDIAC
STRUCTURE AND FUNCTION, MOST PATIENTS HAVE IMPAIRMENT OF
MYOCARDIAL FUNCTION, RANGING FROM NORMAL VENTRICULAR SIZE AND
FUNCTION TO MARKED DILATION AND REDUCED FUNCTION.
• HEART FAILURE IS PRESENT WHEN THE HEART IS UNABLE TO PUMP
BLOOD FORWARD AT A SUFFICIENT RATE TO MEET THE METABOLIC DEMANDS
OF THE BODY (FORWARD FAILURE) OR IS ABLE TO DO SO ONLY IF THE CARDIAC
FILLING PRESSURES ARE ABNORMALLY HIGH (BACKWARD FAILURE) OR BOTH.
Zipes, D.P., Libby, P., Bonow, R.O., Mann, D.L. and Tomaselli, G.F., 2018. Braunwald's Heart Disease E-Book: A Textbook of
Cardiovascular Medicine. Elsevier Health Sciences.
Lilly. 2011. Pathophysiology of heart disease 5 th Edition
• HF IS A CLINICAL SYNDROME CHARACTERIZED BY TYPICAL
SYMPTOMS(E.G. BREATHLESSNESS, ANKLE SWELLING AND
FATIGUE) THAT MAY BE ACCOMPANIED BY SIGNS (E.G. ELEVATED
JUGULAR VENOUS PRESSURE, PULMONARY CRACKLES AND
PERIPHERAL OEDEMA) CAUSED BY A STRUCTURAL AND/OR
FUNCTIONAL CARDIAC ABNORMALITY, RESULTING IN A REDUCED
CARDIAC OUTPUT AND/ OR ELEVATED INTRACARDIAC PRESSURES
AT REST OR DURING STRESS.
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HOW HEART WORKS
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Leonard S. Lilly. Pathophysiology Of Heart Disease : a Collaborative Project of
Medical Students and Faculty. Philadelphia :Lippincott Williams & Wilkins,
2016
Leonard S. Lilly. Pathophysiology Of Heart Diseas
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a Collaborative Project of Medical Students and
Faculty. Philadelphia :Lippincott Williams & Wilkin
2016
Index event may have an abrupt onset, as in the case of a
myocardial infarction (MI); it may have a gradual or insidious
onset, as in the case of hemodynamic pressure or volume
overloading, or it may be hereditary, as in the case of many of
the genetic cardiomyopathies.
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Zipes, D.P., Libby, P., Bonow, R.O., Mann, D.L. and Tomaselli, G.F., 2018. Braunwald's Heart Disease E-Book: A Textbook of
Cardiovascular Medicine. Elsevier Health Sciences.
COMPENSATORY MECHANISMS
1.The Frank–Starling
mechanism,
2.Neurohormonal alterations,
and
3.The development of
ventricular hypertrophy and
remodeling
Hukum jantung Frank-Starling adalah hubungan antara stroke volume dan volume
diastolik akhir. Hukum ini menyatakan bahwa stroke volume jantung meningkat sebagai
respons terhadap peningkatan volume darah di ventrikel, sebelum kontraksi (volume
diastolik akhir), ketika semua faktor lain tetap konstan. Ketika volume darah yang lebih
besar mengalir ke ventrikel, darah meregangkan serabut otot jantung, menyebabkan
peningkatan kekuatan kontraksi. Pentingnya fisiologis dari mekanisme ini terutama
terletak pada menjaga kesetaraan keluaran ventrikel kiri dan kanan.
Neurohormonal Alterations
Adrenergic Nervous System
Aliran simpatis ke jantung dan sirkulasi perifer meningkat, dan tonus parasimpatis berkurang.
Ada tiga konsekuensi langsung:
1. Peningkatan detak jantung,
2. Augmentasi kontraktilitas ventrikel, dan
3. Vasokonstriksi disebabkan oleh stimulasi reseptor α pada vena dan arteri sistemik.
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Zipes, D.P., Libby, P., Bonow, R.O., Mann, D.L. and Tomaselli, G.F., 2018. Braunwald's Heart Disease E-Book: A Textbook of Cardiovascular Medicine. Elsevier Health Sciences.
HOW HEART FAILURE IS DIAGNOSED
HOW HEART FAILURE IS DIAGNOSED
• MEDICAL HISTORY IS TAKEN TO REVEAL
SYMPTOMS
• PHYSICAL EXAM IS DONE
• TESTS
• CHEST X-RAY
• BLOOD TESTS
• ELECTRICAL TRACING OF HEART
(ELECTROCARDIOGRAM OR “ECG”)
• ULTRASOUND OF HEART (ECHOCARDIOGRAM OR
“ECHO”)
• X-RAY OF THE INSIDE OF BLOOD VESSELS
(ANGIOGRAM)
Common Symptoms and Physical Findings in Heart Failure
HOW HEART FAILURE IS DIAGNOSED
FRAMINGHAM CRITERIA FOR CONGESTIVE
HEART FAILURE
Ponikowski, et al.. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. European heart journal, 37(27), pp.2129-2200.
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TYPES OF HEART FAILURE
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Hunt SA et al. J Am Coll Cardiol. 2001;38:2101–2113.
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New York Heart Association/Little Brown and Company, 1964. Adapted from: Farrell MH et al. JAMA. 2002;287:890–897.
ACC/AHA Stages
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Acute Heart Failure
RAPID ONSET OF SYMPTOMS AND SIGNS SECONDARY TO ABNORMAL
CARDIAC FUNCTION
CAN PRESENT AS NEW ONSET AND WITHOUT PREVIOUSLY KNOWN
CARDIAC DYSFUNCTION OR ADHF
OFTEN LIFE THREATENING AND REQUIRES URGENT TREATMENT
Filippatos, G. and Zannad, F., 2007. An introduction to acute heart failure syndromes: definition and classification. Heart failure reviews, 12(2), pp.87-90.
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Ponikowski, P., et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure:. European heart journal, 37(27), pp.2129-2200.
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HEART FAILURE REDUCE EJECTION FRACTION
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Yancy, C.W., et al.2018. 2021 ACC expert consensus decision pathway for optimization of heart failure treatment: answers to 10 pivotal issues about heart failure with reduced ejection fraction. Journal of the
American College of Cardiology, 71(2), pp.201-230.
2021 Updated to the 2017 ACC expert consensus decision pathway for optimization of heart failure treatment: answers to 10 pivotal issues about heart failure with reduced ejection
fraction. Journal of the American College of Cardiology
THANK YOU
CASE 1
• SEORANG PEREMPUAN 65 TAHUN DATANG KE IGD DENGAN KELUHAN SESAK
NAFAS BERAT SELAMA 30 MENIT. RIWAYAT SESAK SEBELUMNYA + DIRASAKAN
SEJAK 6 BULAN YANG LALU¸ TERASA MAKIN BERAT DENGAN AKTIVITAS.
PASIEN TIDUR MENGGUNAKAN 3-4 BANTAL. RIWAYAT HIPERTENSI + SEJAK 10
TAHUN YANG LALU. PADA PEMERIKSAAN FISIK DIDAPATKAN TEKANAN DARAH
130/90 MMHG, NADI 120 KALI/ MENIT, LAJU RESPIRASI 30 KALI/ MENIT, SUHU
37OC. PADA PEMERIKSAAN TORAKS DITEMUKAN KARDIOMEGALI, GALLOP +,
WHEEZING +, RONKHI BASAH + DI BASAL KEDUA LAPANG PARU. SATURASI
OKSIGEN 86%. TELAH DILAKUKAN PEMERIKSAAN FOTO POLOS DADA DAN
TAMPAK BENDUNGAN BATWING APPEARANCE.
• APAKAH YANG MUNGKIN TERJADI PADA PASIEN TERSEBUT?
A. GAGAL JANTUNG KONGESTIF
B. ASMA EKSASERBASI
C. EMBOLI PARU
D. EDEMA PARU
E. GAGAL GINJAL AKUT
CASE 2
• SEORANG PEREMPUAN 65 TAHUN DATANG KE IGD DENGAN KELUHAN
SESAK NAFAS BERAT SELAMA 30 MENIT. RIWAYAT SESAK SEBELUMNYA +
DIRASAKAN SEJAK 6 BULAN YANG LALU¸ TERASA MAKIN BERAT DENGAN
AKTIVITAS. PASIEN TIDUR MENGGUNAKAN 3-4 BANTAL. RIWAYAT
HIPERTENSI + SEJAK 10 TAHUN YANG LALU. PADA PEMERIKSAAN FISIK
DIDAPATKAN TEKANAN DARAH 130/90 MMHG, NADI 120 KALI/ MENIT, LAJU
RESPIRASI 30 KALI/ MENIT, SUHU 37OC. PADA PEMERIKSAAN TORAKS
DITEMUKAN KARDIOMEGALI, GALLOP +, WHEEZING +, RONKHI BASAH + DI
BASAL KEDUA LAPANG PARU. SATURASI OKSIGEN 86%. TELAH DILAKUKAN
PEMERIKSAAN FOTO POLOS DADA DAN TAMPAK BENDUNGAN BATWING
APPEARANCE. OBAT APAKAH YANG TEPAT DILAKUKAN PADA PASIEN?
A. CLOPIDOGREL 300 MG TAB PO
B. ASPIRIN 160 MG TAB PO
C. DOPAMINE 2 MCG/KGBB/MNT IV
D. NITROGLISERIN 4 MG IV
E. FUROSEMIDE 1 MG/KGBB IV