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TINJAUAN FARMAKOLOGI
OBAT-OBAT
PENANGANAN GAGAL
JANTUNG
PENDAHULUAN
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PENDAHULUAN
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GAGAL JANTUNG
• Kondisi klinik yang kompleks dimana jantung tidak
mampu lagi memompa darah ke seluruh tubuh secara
memadai untuk memenuhi kebutuhan oksigen dan
nutrisi jaringan tubuh
• Gagal jantung ------> curah jantung tidak memadai!!!
GAGAL JANTUNG
GANGGUAN GANGGUAN
SISTOLIK: DIASTOLIK:
Ketidakmampuan Ketidakmampuan
ventrikel berkontraksi ventrikel untuk
secara memadai dan mengisi/berelaksasi
memompa darah secara memadai
keluar
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AKTIVASI NEUROHORMONAL :
RENIN-ANGIOTENSIN-
ALDOSTERON
1. Renin
• Dilepaskan ketika tekanan/volume darah arteri
ginjal menurun akibat CO menurun
• Berfungsi mengubah angiotensinogen dari hati
menjadi angiotensin I
AKTIVASI NEUROHORMONAL :
RENIN-ANGIOTENSIN-
ALDOSTERON
3. Angiotensin II
• merupakan vasokonstriktor kuat
• menstimulasi produksi dan pelepasan aldosteron dari kelenjar
adrenal di ginjal
• menstimulasi sekresi hormon Antidiuretik dari pituitari à
meningkatkan rasa haus dan retensi air
4. Aldosteron
• meningkatkan reabsorbsi Na+ dan air pada tubulus distal dan
collecting duct dengan meningkatkan sekresi dan ekskresi K+
melalui ginjal
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AKIBATNYA …………
• Pelepasan RAA dan ADH meningkatkan volume cairan
darah à meningkatkan aliran balik masuk dalam jantung
dan vasokonstriksi
• Secara sementara à berakibat peningkatan curah
jantung dan perfusi organ vital
• secara kronik à menyebabkan kongesti pulmonar,
edema, gangguan kontraktilitas dan peningkatan
penggunaan energi jantung
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AKIBATNYA …………
• Peningkatan kekuatan kontraksi dan irama jantung
melalui stimulasi β1 reseptor, serta vasokonstriksi
melalui stimulasi α1 reseptor di vaskular
• Secara sementara à meningkatkan volume sekuncup
dan curah jantung
• Secara kronik à meningkatkan penggunaan energi
jantung dan remodeling ventrikel (hipertropi)
REMODELING VENTRIKEL
• Akibat peningkatan aktivasi neurohormonal maka terjadi
peningkatan aliran balik (venous return) à preload
• Peningkatan preload menyebabkan stretching pada
ventrikel à dilatasi ventrikel
• Selain itu, vasokonstriksi juga terjadi akibat peningkatan
pelepasan neurohormonalà afterload
• Akibatnya dapat terjadi perubahan struktur ventrikel
sebagai mekanisme kompensasi à hipertropi ventrikel
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AKIBATNYA …..
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ACE INHIBITOR
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DIURETIK
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DIURETIK
BETA BLOCKER
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BETA BLOKER
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e193
AHA guidelines 2013
JACC Vol. 62, No. 16, 2013 Yancy et al.
October 15, 2013:e147–239 2013 ACCF/AHA Heart Failure Guideline: Full Text
Figure 3. Stages in the development of HF and recommended therapy by stage. ACEI indicates angiotensin-converting enzyme inhibitor;
AF, atrial fibrillation; ARB, angiotensin-receptor blocker; CAD, coronary artery disease; CRT, cardiac resynchronization therapy; DM, diabetes
mellitus; EF, ejection fraction; GDMT, guideline-directed medical therapy; HF, heart failure; HFpEF, heart failure with preserved ejection
fraction; HFrEF, heart failure with reduced ejection fraction; HRQOL, health-related quality of life; HTN, hypertension; ICD, implantable
cardioverter-defibrillator; LV, left ventricular; LVH, left ventricular hypertrophy; MCS, mechanical circulatory support; and MI, myocardial
infarction. Adapted from Hunt et al. (38).
HRQOL (682–688). The greatest survival benefit is seen in 8. The Hospitalized Patient
those patients who are at highest risk of death from advanced
HF (689). Cardiopulmonary exercise testing helps refine
8.1. Classification of Acute Decompensated HF
candidate selection (690–696). Data suggest acceptable
Hospitalization for HF is a growing and major public health
posttransplant outcomes in patients with reversible pulmonary
issue (703). Presently, HF is the leading cause of hospitali-
hypertension (697), hypertrophic cardiomyopathy (698),
zation among patients >65 years of age (51); the largest
KESIMPULAN
peripartum cardiomyopathy (699), restrictive cardiomyopathy
(700,701), and muscular dystrophy (702). Selected patients
with stage D HF and poor prognosis should be referred to
percentage of expenditures related to HF are directly attrib-
utable to hospital costs. Moreover, in addition to costs,
hospitalization for acutely decompensated HF represents
a cardiac transplantation center for evaluation and transplant
a sentinel prognostic event in the course of many patients with
• Farmakologi obat yang digunakan
consideration. Determination of HF prognosis is addressed in
Sections 6.1.2 and 7.4.2. The listing criteria and evaluation
HF, with a high risk for recurrent hospitalization (e.g., 50% at
6 months) and a 1-year mortality rate of approximately 30%
dalam penanganan gagal jantung
and management of patients undergoing cardiac trans-
plantation are described in detail by the International Society
(211,704). The AHA has published a scientific statement
about this condition (705).
pada umumnya menargetkan
for Heart and Lung Transplantation (680).
There is no widely accepted nomenclature for HF syndromes
See Table 27 for a summary of recommendations from this
penghambatan aktivitas
section, Figure 3 for the stages of HF development; and
requiring hospitalization. Patients are described as having
“acute HF,” “acute HF syndromes,” or “acute(ly) decom-
Online Data Supplement 36 for additional data on
neurohormonal yang terlibat dalam
transplantation.
pensated HF”; while the third has gained greatest acceptance,
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TERIMA KASIH
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