kegagalan fungsi jantung dan syock
DESCRIPTION
Gagal jantungTRANSCRIPT
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Kegagalan fungsi Jantung dan Syock
DEPARTEMEN FISIOLOGIFK UNIMAL
2011
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ShockShock
• Always a symptom of primary cause
• Inadequate blood flow to meet tissue oxygen demand
• May be associated with hypotension
• Associated with signs of hypoperfusion: mental status change, oliguria, acidosis
• Always a symptom of primary cause
• Inadequate blood flow to meet tissue oxygen demand
• May be associated with hypotension
• Associated with signs of hypoperfusion: mental status change, oliguria, acidosis
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DEFINISI
IT IS NOT LOW BLOOD PRESSURE !!!
IT IS HYPOPERFUSION…..
Gangguan dari perfusi jaringan yang terjadi akibat adanya ketidakseimbangan antara suplai oksigen ke sel dengan kebutuhan oksigen dari sel tersebut.
Semua jenis shock mengakibatkan gangguan pada perfusi jaringan yang selanjutnya berkembang menjadi gagal sirkulasi akut atau disebut juga sindroma shock
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Shock Categories Shock Categories
• Cardiogenic
• Hypovolemic
• Distributive
• Obstructive
• Cardiogenic
• Hypovolemic
• Distributive
• Obstructive
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Cardiogenic ShockCardiogenic Shock
• Decreased contractility
• Increased filling pressures, decreased LV stroke work, decreased cardiac output
• Increased systemic vascular resistance compensatory
• Decreased contractility
• Increased filling pressures, decreased LV stroke work, decreased cardiac output
• Increased systemic vascular resistance compensatory
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Hypovolemic ShockHypovolemic Shock
• Decreased cardiac output
• Decreased filling pressures
• Compensatory increase in systemic vascular resistance
• Decreased cardiac output
• Decreased filling pressures
• Compensatory increase in systemic vascular resistance
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Distributive ShockDistributive Shock
• Normal or increased cardiac output
• Low systemic vascular resistance
• Low to normal filling pressures
• Sepsis, anaphylaxis, neurogenic, and acute adrenal insufficiency
• Normal or increased cardiac output
• Low systemic vascular resistance
• Low to normal filling pressures
• Sepsis, anaphylaxis, neurogenic, and acute adrenal insufficiency
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Obstructive ShockObstructive Shock
• Decreased cardiac output• Increased systemic vascular
resistance• Variable filling pressures
dependent on etiology• Cardiac tamponade, tension
pneumothorax, massive pulmonary embolus
• Decreased cardiac output• Increased systemic vascular
resistance• Variable filling pressures
dependent on etiology• Cardiac tamponade, tension
pneumothorax, massive pulmonary embolus
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OO22
CARDIOGENICCARDIOGENIC
HYPOVOLEMIKHYPOVOLEMIK
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OO22
OBSTRUCTIVEOBSTRUCTIVE
SEPTICSEPTIC
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EFEK SHOCK PADA TINGKATAN SELEFEK SHOCK PADA TINGKATAN SEL
HYPOXIAHYPOXIA
LOW-FLOW,LOW-FLOW,POOR PERFUSIONPOOR PERFUSION
ANAEROBIC METABOLISM
ACIDOSIS
DECREASED CELLULAR ENERGY EFFICIENCY
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Glucose breakdown. (A) Stage one, glycolysis, is anaerobic (does not require oxygen). It yields pyruvic acid, with toxic by-products such as lactic acid, and very little energy. (B) Stage two is aerobic (requires oxygen). In a process called the Krebs or citric acidcycle, pyruvic acid is degraded into carbon dioxide and water, which produces a much higher yield of energy.
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CELL MEMBRANE FAILURE:
• DIRECT EndotoxinComplement
• INDIRECTFailure to maintain normal Na+, K+ or Ca2+ gradientDecreased oxidative phosphorylation
OSMOTIC GRADIENT
Water entry into cell
CELLULAR EDEMA
IMPAIRED INTRACELLULAR
METABOLISM
CELL
DEATH
Na+ entry into cell
EFEK SHOCK PADA TINGKATAN SELEFEK SHOCK PADA TINGKATAN SEL
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KidneyOliguric renal failureHigh output renal failure
LiverLiver failure
GI tract Failure of intestinal barrier (sepsis, bleeding)
LungCapillary leak associated with or caused by sepsis and infection
EFEK SHOCK PADA TINGKATAN ORGAN
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PATOFISIOLOGI DARI RESPON TUBUH TERHADAP SHOCK
Respon Neuroendokrin
Respon Hemodinamik
Respon Metabolik
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HYPOVOLEMIAHYPOVOLEMIA
R atriumR atriumlow-pressure stretch low-pressure stretch
receptorsreceptors
Aorta/carotidsAorta/carotidsHigh-pressure High-pressure baroreceptorsbaroreceptors
LOSS OF TONIC LOSS OF TONIC INHIBITION OF INHIBITION OF CENTRAL AND CENTRAL AND SYMPATHETIC SYMPATHETIC
NERVOUS SYSTEMSNERVOUS SYSTEMS
Renal Renal Renin releaseRenin release
Pituitary glandPituitary glandACTH, ADH and GH releaseACTH, ADH and GH release
Adrenal gland (medulla)Adrenal gland (medulla)Epinephrine/norepinephrine Epinephrine/norepinephrine
releaserelease
Adrenal cortexAdrenal cortexCortisol releaseCortisol release
Adrenal cortexAdrenal cortexAldosterone releaseAldosterone release
Angiotensin IIAngiotensin II
Decreased renal Decreased renal perfusionperfusion
FEARFEARStimulation of limbic Stimulation of limbic
area of brainarea of brain
IncreasedIncreased: : hypothalamic, hypothalamic,
adrenomedullary adrenomedullary adrenocortical activityadrenocortical activity
Neuroendocrine Respons
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RESPON HEMODINAMIKMekanisme untuk memperbaiki Mekanisme untuk memperbaiki keseimbangan kardiovaskularkeseimbangan kardiovaskular
Redistribusi aliran darah
Peningkatan “cardiac output”
Memperbaiki volume intravaskular
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STIMULASI NEUROENDOKRIN
HYPOTENSION
BLOOD FLOW PROTECTEDHeartBrain
Adrenal/pituitary gland
BLOOD FLOW DECREASEDSkin
MuscleSplanchnic circulation
RESPON HEMODiNAMiKREDISTRIBUSI ALIRAN DARAH
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CARDIAC OUTPUT = HR X SVCARDIAC OUTPUT = HR X SV
Sympathetic n. systemSympathetic n. systemCatecholamine releaseCatecholamine release
Increase EDV via:Increase EDV via:VenoconstrictionVenoconstriction
Arteriolar constrictionArteriolar constrictionRenal reabsorptionRenal reabsorption
Increased Increased contractilitycontractility
Limited to 180 beats/min Limited to 180 beats/min before decreased CO due to before decreased CO due to
decreased diastolic filling decreased diastolic filling timetime
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HAEMODYNAMIC RESPONSESVenoconstriction
Sympathetic n. system (SNS)Catecholamines (CA)Angiotensin II (ATII)
ADH
Reduced venous capacitance
Arteriolar constrictionSNS, CA, ATII, ADH
Decreased capillary P
Fluid shift from interstitium into vascular compartment
Increased distal tubular reabsorption
Aldosterone, ADH
Increased proximal tubular reabsorption
SNS, CA, ATII
Increased myocardial contractilitySNS, CA
Restoration of blood volume
Increased ventricular filling
P
Increased ventricular ejection fraction
SV
CO
BPIncreased heart rate
SNS, CA
Increased SVR due to arteriolar constructionSNS, CA, ATII, ADH
SVR
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RESPON METABOLIK
Hyperglikemia
Mobilisasi lemak
Katabolisme/pemecahan ProteinPeningkatan sintesis ureaPeningkatan asam amino aromatik
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RESPON METABOLIK
Breakdown of skeletal muscle
glikogen
Conversion of glikogen to
glucose
Release of:CatecholaminesCortisolGlucagonGrowth hormone
Impaired peripheral
glucose uptake
HYPERGLYCEMIA
Glycogen breakdown
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METABOLIC RESPONS
Decreased blood volume
Decreased CO
Cellular hypoperfusion and hypoxia
Anaerobic glycolysisPyruvate converted to lactic acid
METABOLIC ACIDOSIS
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Release of:CatecholaminesCortisolGlucagon
LIPOLYSIS
INCREASE IN PLASMA FREE FATTY ACIDS
METABOLIC RESPONS
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Cardiogenic Shock ManagementCardiogenic Shock Management
• Treat arrhythmias
• Diastolic dysfunction may require increased filling pressures
• Vasodilators if not hypotensive
• Inotrope administration• Vasopressor agent needed if hypotension present to
raise aortic diastolic pressure
• Consultation for mechanical assist device
• Preload and afterload reduction to improve hypoxemia if blood pressure adequate
• Treat arrhythmias
• Diastolic dysfunction may require increased filling pressures
• Vasodilators if not hypotensive
• Inotrope administration• Vasopressor agent needed if hypotension present to
raise aortic diastolic pressure
• Consultation for mechanical assist device
• Preload and afterload reduction to improve hypoxemia if blood pressure adequate
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Hypovolemic Shock Management
Hypovolemic Shock Management
• Volume resuscitation – crystalloid, colloid• Initial crystalloid choices
– Lactated Ringer’s solution– Normal saline (high chloride may produce
hyperchloremic acidosis)• Match fluid given to fluid lost
– Blood, crystalloid, colloid
• Volume resuscitation – crystalloid, colloid• Initial crystalloid choices
– Lactated Ringer’s solution– Normal saline (high chloride may produce
hyperchloremic acidosis)• Match fluid given to fluid lost
– Blood, crystalloid, colloid
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Distributive Shock TherapyDistributive Shock Therapy
• Restore intravascular volume
• Hypotension despite volume therapy
– Inotropes and/or vasopressors
• Vasopressors for MAP < 60 mm Hg
• Adjunctive interventions dependent on etiology
• Restore intravascular volume
• Hypotension despite volume therapy
– Inotropes and/or vasopressors
• Vasopressors for MAP < 60 mm Hg
• Adjunctive interventions dependent on etiology
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Obstructive Shock TreatmentObstructive Shock Treatment
• Relieve obstruction
– Pericardiocentesis
– Tube thoracostomy
– Treat pulmonary embolus
• Temporary benefit from fluid or inotrope administration
• Relieve obstruction
– Pericardiocentesis
– Tube thoracostomy
– Treat pulmonary embolus
• Temporary benefit from fluid or inotrope administration
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Fluid TherapyFluid Therapy• Crystalloids
– Lactated Ringer’s solution– Normal saline
• Colloids– Hetastarch– Albumin– Gelatins
• Packed red blood cells• Infuse to physiologic endpoints
• Crystalloids– Lactated Ringer’s solution– Normal saline
• Colloids– Hetastarch– Albumin– Gelatins
• Packed red blood cells• Infuse to physiologic endpoints
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Fluid TherapyFluid Therapy• Correct hypotension first
• Decrease heart rate
• Correct hypoperfusion abnormalities
• Monitor for deterioration of oxygenation
• Correct hypotension first
• Decrease heart rate
• Correct hypoperfusion abnormalities
• Monitor for deterioration of oxygenation
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Kristaloid vs koloid
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Kristaloid vs koloid
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Inotropic / Vasopressor AgentsInotropic / Vasopressor Agents
• Dopamine
– Low dose (2-3 g/kg/min) – mild inotrope plus renal effect
– Intermediate dose (4-10 g/kg/min) – inotropic effect
– High dose ( >10 g/kg/min) – vasoconstriction
• Dopamine
– Low dose (2-3 g/kg/min) – mild inotrope plus renal effect
– Intermediate dose (4-10 g/kg/min) – inotropic effect
– High dose ( >10 g/kg/min) – vasoconstriction
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• Dobutamine
– 5-20 g/kg/min
– Inotropic and variable chronotropic effects
– Decrease in systemic vascular resistance
• Dobutamine
– 5-20 g/kg/min
– Inotropic and variable chronotropic effects
– Decrease in systemic vascular resistance
SHK 33SHK 33®
• Norepinephrine
– 0.05 g/kg/min and titrate to effect
– Inotropic and vasopressor effects
– Potent vasopressor at high doses
• Norepinephrine
– 0.05 g/kg/min and titrate to effect
– Inotropic and vasopressor effects
– Potent vasopressor at high doses
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Inotropic / Vasopressor AgentsInotropic / Vasopressor Agents
• Epinephrine– Both and actions for inotropic and
vasopressor effects– 0.1 g/kg/min and titrate
– Increases myocardial O2 consumption
• Epinephrine– Both and actions for inotropic and
vasopressor effects– 0.1 g/kg/min and titrate
– Increases myocardial O2 consumption
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Therapeutic Goals in Shock Therapeutic Goals in Shock
• Increase O2 delivery
• Optimize O2 content of blood
• Improve cardiac output and blood pressure
• Match systemic O2 needs with O2 delivery
• Reverse/prevent organ hypoperfusion
• Increase O2 delivery
• Optimize O2 content of blood
• Improve cardiac output and blood pressure
• Match systemic O2 needs with O2 delivery
• Reverse/prevent organ hypoperfusion
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What Do You Need to Know When You Resuscitate a Patient in Shock?
• Arterial blood pressure• Urine output• Systemic acid–base balance (pH, SBE, lactate)• Temperature• Some measurement of global blood flow and tissue
perfusion– Cardiac output or cardiac index
• Arterial oxygen delivery, oxygen uptake index• Mixed venous saturation and PvO2
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Cardiac Output x SVR
Pipe = VascularPump =Heart
Volume =Blood
Hypovolemic Shock
Cardiogenic Shock
Distributive Shock
Inotropes (Dob,Dop,Adr,Amr)
Vasopressor ( NE,PE,Adr,Dop)
Fluids
Obstructive Shock
Release tamponade,etc
Blood Pressure
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PRINSIP RESUSITASIPRINSIP RESUSITASI
Mempertahankan ventilasiMempertahankan ventilasi
Meningkatkan perfusiMeningkatkan perfusi
Terapi penyebabTerapi penyebab
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GAGAL JANTUNG
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GAGAL JANTUNGPENDAHULUAN
GAGAL JANTUNG ( HEART FAILURE ) :
KEADAAN DIMANA JTG TIDAK MAMPU LAGI MEMOMPA DARAH DLM JML YG CUKUP DLM MEMENUHI KEBUTUHAN SIRKULASI BADAN UNTUK KEPERLUAN METABOLISME JARINGAN TUBUH PADA KEADAAN TERTENTU, SEDANGKAN TEKANAN PENGISIAN KEDALAM JANTUNG MASIH CUKUP.
GAGAL JANTUNG PROGRESIF CURAH JANTUNG (CARDIAC OUTPUT) SINDROMA GAGAL JTG
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SINDROMA GAGAL JANTUNG
HAMBATAN PADA ARAH ALIRAN (FORWARD FAILURE) DALAM SIRKILASI AKAN MENIMBULKAN BENDUNGAN PADA ARAH BERLAWANAN DENGAN ALIRAN (BACKWARD CONGESTION).
SINDROMA GAGAL JANTUNG KUMPULAN TANDA-TANDA DAN GEJALA-GEJALA MEKANISME KOMPENSASI JANTUNG DENGAN DISERTAI AKIBAT-AKIBAT SAMPINGANNYA (FORWARD FAILURE DAN BACKWARD FAILURE).
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Klasifikasi gagal jantung berdasarkan NYHA (New York Heart Association)/Perkumpulan Jantung New York.
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Class Gejala pada PasienClass I (ringan) Tidak ada batasan dalam aktivitas fisik, Aktifitas
yang biasa, tidak menimbulkan kelelahan, dada berdebar-debar serta dyspneu (nafas pendek)
Class II (ringan) Batasan ringan dalam aktivitas fisik. Aktivitas yang biasa menimbulkan kelelahan, dada berdebar-debar serta dyspneu (nafas pendek)
Class III (sedang) Batasan sedang dalam aktivitas fisik. Nyaman kalau beristirahat. Beraktivitas sedikit saja sudah menimbulkan kelelahan, dada berdebar-debar serta dyspneu (nafas pendek)
Class IV (berat) Sudah tidak dapat beraktifitas dengan normal lagi tanpa ketidaknyamanan. Tanda-tanda gangguan pada system kardiovaskular muncul dengan kuat. Apabila pasien beraktifitas, ketidaknyaman akan langsung muncul
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Terminologi
• Gagal jantung kiri
• Gagal jantung kanan
• Gagal jantung kongestif
• Gagal jantung akut
• Gagal jantung kronik
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PENYEBAB GAGAL JANTUNG KIRI :
ISKEMIA/INFARK MIOKARD, HIPERTENSI, MIOKARDITIS, KARDIOMIOPATI, STENOSIS/REGURGITASI AORTA, REGURGITASI MITRAL, KEBUTUHAN CURAH JANTUNG MENINGKAT (HIGH OUTPUT STATE : ANEMIA, TIROTOKSIKOSIS).
PENYEBAB GAGAL JANTUNG KANAN :
PENYAKIT PARU OBSTRUKTIF MENAHUN ( COR PULMONALE), TROMBOSIS/EMBOLI PARU, PERIKARDITIS KONSTRIKTIF, STENOSIS MITRAL + TEKANAN PULMONAL, STENOSIS PULMONER, REGURGITASI TRIKUSPID.
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GAGAL JANTUNG KIRI :
GANGGUAN PEMOMPAAN DARAH OLEH VENTRIKEL KIRI CURAH JANTUNG TEKANAN & VOLUME AKHIR DIASTOLIK DALAM
VENTRIKEL KIRI BEBAN & TEKANAN ATRIUM KIRI HAMBATAN MASUK DARI VENA PULMONALIS BENDUNGAN PARU EDEMA PARU : KLINIS HAMBATAN BAGI VENTRIKEL KANAN BEBAN VENTRIKEL KANAN : KOMPENSASI HIPERTROFI & DILATASI : SAMPAI BATAS TERTENTU GAGAL JANTUNG KANAN.
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KLINIS :
KELUHAN BADAN LEMAH, CEPAT LELAH, KERINGAT DINGIN, PALPITASI, BATUK, DYSPNOE D’EFFORT, ORTOPNOE, PAROXYSMAL NOCTURNAL DYSPNOE, NOCTURIA.
TANDA-TANDA TAKHIKARDIA, PULSUS ALTERNANS, GALLOP (B.J. III), RONKI BASAH PARU DI BAGIAN BASAL.
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GAGAL JANTUNG KANAN :
GANGGUAN PEMOMPAAN DARAH OLEH VENTRIKEL ISI SEKUNCUP TEKANAN DAN VOLUME AKHIR DIASTOLIK DALAM VENTRIKEL KANAN BEBAN TEKANAN ATRIUM KANAN BEBAN TEKANAN ATRIUM KANAN HAMBATAN MASUK DARI VENA KAVA SUPERIOR & INFERIOR BENDUNGAN VENA-VENA SISTEMIK TERSEBUT (BENDUNGAN VENA JUGULARIS DAN DALAM HEPAR) : TEKANAN VENA JUGULARIS , HEPATOMEGALI BILA BERLANJUT BENDUNGAN LEBIH BERAT : ASITES DAN EDEMA TUNGKAI.
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KLINIS :
TANDA-TANDA :
BERAT BADAN >>, BENDUNGAN VENA JUGULARIS, HEPATOMEGALI HEPATO JUGULAR REFLUX +, ASITES DAN EDEMA TUNGKAI.
GAGAL JANTUNG KONGESTIF :
GAGAL JANTUNG KIRI + GAGAL JANTUNG KANAN BERSAMAAN.
KLINIS :KELUHAN TERUTAMA KELUHAN GASTROINTESTINAL: KEMBUNG, ANOREKSIA, NAUSEA.
MERUPAKAN KUMPULAN GEJALA DAN TANDA-TANDA GAGAL JANTUNG KIRI DAN KANAN.
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Gagal jantung Akut• Gagal jantung akut didefinisikan sebagai serangan cepat dari
gejala atau tanda akibat fungsi jantung yang abnormal.• Dapat terjadi dengan atau tanpa adanya sakit jantung sebelumnya. • Disfungsi jantung bisa berupa disfungsi sistolik atau disfungsi
diastolik, keadaan irama jantung yang abnormal atau ketidakseimbangan dari pre-load atau after-load, seringkali memerlukan pengobatan segera.
• Gagal jantung akut dapat berupa serangan baru tanpa ada kelainan jantung sebelumnya atau dekompensasi akut dari gagal jantung kronis.
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Gagal jantung kronik
• Gagal jantung kronik didefinisikan sebagai sindrom klinik yang komplek yang disertai keluhan gagal jantung berupa sesak, fatik, baik dalam keadaan istirahat atau latihan, edema dan tanda objektif adanya disfungsi jantung dalam keadaan istirahat.
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Gagal jantung yang berat : Kasus emergensi - perlu penanganan efektif - perlu pemeriksaan untuk mengetahui penyebab, memperbaiki status hemodinamik, mengatasi bendungan paru, memperbaiki oksigenasi jaringan - Pemeriksaan klinis dan radiologis severity dan prognosis - Klasifikasi Killip : menilai severity GJA dan GJK
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Killip classification
Class Clinical features Hospital mortality (%)
Class I No signs of left ventricular dysfunction 6
Class II S3 gallop with or without mild to 30
moderate pulmonary congestion
Class III Acute severe pulmonary oedema 40
Class IV Shock syndrome 80 - 90
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BENTUK LAIN GAGAL JANTUNG SECARA TEORITIS DAPAT BERUPA :
1. FORWARD FAILURE BACKWARD FAILURE
2. HIGH OUTPUT LOW OUTPUT
3. SISTOLIK DIASTOLIK
.
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FORWARD FAILURE (LOW OUTPUT THEORY) : MANIFESTASI KLINIS AKIBAT KEKURANGAN ALIRAN DARAH KE SISTEM ARTERIAL.
BACKWARD FAILURE (CONGESTIVE THEORY) : MANIFESTASI KLINIS AKIBAT HAMBATAN PENGOSONGAN VENA BENDUNGAN SISTEM VENA SISTEMIK & PARU
HIGH OUTPUT : GAGAL JANTUNG DENGAN SIRKULASI HIPERDINAMIS.
LOW OUTPUT : GAGAL JANTUNG DENGAN CURAH JANTUNG MENURUN.
SISTOLIK DISFUNGSI : KETIDAK MAMPUAN JANTUNG MEMOMPA DARAH.
DIASTOLIK DISFUNGSI : KETIDAK MAMPUAN PENGISIAN JANTUNG.
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KRITERIA DIAGNOSIS GAGAL JANTUNG
KRITERIA UTAMA KRITERIA TAMBAHAN
- PAROXYSMAL NOCTURNAL
DYSPNOE
- KARDIOMEGALI
- GALLOP
- PENINGKATAN TEKANAN VENA
JUGULARIS
- HEPATO JUGULAR REFLUX
- RONKI BASAH BASAL
- EDEMA PERGELANGAN
KAKI
- BATUK MALAM HARI
- DYSPNOE D’EFFORT
- HEPATOMEGALI
- EFUSI PLEURA
- TAKIKARDIA
DIAGNOSA DITEGAKAN ATAS DASAR ADANYA 2 KRITERIA UTAMA ATAU 1 KRITERIA UTAMA DISERTAI 2 KRITERIA TAMBAHAN.
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MANAGEMENT OF CHRONIC HEART FAILURE
PRINSIP-PRINSIP PENATALAKSANAAN :1. PASTIKAN PENDERITA MEMANG GAGAL JANTUNG.2. TENTUKAN KELAINAN YANG DIDAPAT : EDEMA PARU/PERIFER, SESAK NAFAS.3. TEGAKAN ETIOLOGI GAGAL JANTUNG.4. TELITI PENYAKIT PENYERTA YANG BERHUBUNGAN DENGAN GAGAL JANTUNG.5. NILAI BERATNYA GEJALA.6. TAKSIR PROGNOSA.7. ANTISIPASI KOMPLIKASI.8. NASEHATI PENDERITA DAN KELUARGA.9. PILIH PENGOBATAN YANG TEPAT.10. MONITOR PERKEMBANGANNYA DAN DITANGGULANGI SECUKUPNYA.
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GENERAL MEASURESS :
a. DIET : KURANGI KEGEMUKAN, BATASI ASUPAN GARAM.
b. SMOKING : DILARANG.
c. ALCOHOL : ALCOHOLIC CARDIOMYOPATHY DILARANG. LAINNYA : Lk. 40 g/HARI, Pr. 30 g/HARI
d. EXERCISE : LOW LEVEL ENDURANCE MUSCLE ACTIVITY WALKING : 3-5 x/MGG, 20-30 MENIT
e. REST : HANYA PADA GAGAL JANTUNG AKUT.
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PHARMACOLOGICAL THERAPY
DIURETICS :
SIMPTOMATIK DAN RETENSI CAIRAN (EDEMA PARU/ PERIFER)
INITIAL DIURETIC TX :
- LOOP DIURETIC ATAU THIAZIDE, SELALU
DIKOMBINASI DENGAN ACE INHIBITOR
- GFR < 30 ML/MIN JANGAN THIAZIDE
RESPONS TIDAK CUKUP :
- KOMBINASI LOOP + THIAZIDE
- NAIKKAN DOSIS DIURETIKA
- GAGAL JANTUNG BERAT TAMBAHKAN SPIRONOLACTONE
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POTASSIUM-SPARING DIURATIKA (PSD) : SPIRONOLACTONE, AMILORIDE, TRIAMTERENE HANYA AMAN PADA DOSIS RENDAH.
TANPA ACE INHIBITOR, LOOP DIURETIC/THIAZIDE HARUS DIKOMBINASI DENGAN PSD.
PSD : AWAL PEMBERIAN PERIKSA KREATININ & K+
SESUDAH 5-7 HARI, BILA STABIL TIAP 3-6 BULAN.
ANGOTENSIN-CONVERTING ENZIM (ACE) INHIBITORS:
PADA SEMUA TINGKAT GAGAL JANTUNG, TERUTAMA DISFUNGSI SITOLIK, +/- VOLUME OVERLOAD FIRST-LINE THERAPY
PADA GAGAL JANTUNG ASIMTOMATIK + ACE INHIBITOR SIMPTOMATIK/HOSPI TALISASI
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GAGAL JANTUNG SIMPTOMATIK ACE INHIBITOR : MEMPERBAIKI KELUHAN/GEJALA, KAPASITAS LATIHAN , REINFARCTION & UNSTABLE ANGINA , HOSPITALISASI , MORTALITAS .
EFEK SAMPING : HIPOTENSI, RENAL INSUFFICIENCY (TRT. GAGAL JANTUNG BERAT, ORTU, RENAL DYSFUNCTION, HIPONATREMIA), SINKOPE, HIPERKALEMIA DAN BATUK KERING (15 – 20 %).
PEMBERIAN : “START LOW AND GO SLOW” MAX. TARGET DOSE.
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DRUG INITIATING DOSE MAINTENANCE TARGET
#CAPTOPRIL
#ENALAPRIL
#LISINOPRIL
#PERINDOPRIL
#RAMIPRIL
6.25 mg tid
2.5 mg od
2.5 mg od
2 mg od
1.25 - 2.5 mg od
5 – 10 mg bid
10 mg bid
5 – 20 mg od
4 mg od
2.5 – 5 mg bid
50 mg tid
20 mg bid
5 mg bid
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VASODILATOR AGENTS :
KOMBINASI HYDRALAZINE-ISOSORBIDE DINITRATE: SEBAGAI ALTERNATIF BILA ACE INHIBITOR KONTRAINDIKASI ATAU TIDAK DAPAT DITOLERANSI DOSIS HARIAN HYDRALAZINE DITINGKATKAN SAMPAI 300 mg, NITRATE 160 mg.
KOMBINASI DENGAN CARDIAC GLYCOSIDE DAN DIURETIC DAPAT MENGURANGI MORTALITAS DAN MENINGKATKAN EXERCISE PERFORMANCE.
NITRATE TOLERANCE, TERUTAMA DOSIS FREKUEN (4 – 6 JAM), DAPAT DIKURANGI DENGAN INTERVAL 8 – 12 JAM ATAU KOMBINASI DENGAN ACE INHIBITOR, +/- HYDRALAZINE.
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DIGOXIN :
- ORAL DAILY DOSE 0,25 – 0,375 mg (ELDERLY 0,0625 – 0,125).
- BEGIN TX WITH 0,25 mg bid FOR 2 DAYS.
- NO LOADING DOSE IN CHRONIC CONDITION.
BETA-ADRENOCEPTOR ANTAGONIST:
FAVOURABLE EFFECT :
- REDUCTION CARDIAC SYMPATHETIC TONE
- REDUCTION IN HEART RATE
- LONGER DIASTOLIC PERIOD
- POSSIBLY THE UPREGULATION OF THE BETA-ADRENERGIC RECEPTOR SYSTEM.
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BETA-1 SELECTIVE BLOCKING AGENTS :
1. METOPROLOL : BENEFICIAL EFFECT IN DILATED CARDIOMYOPATHY. 2. BISPROLOL (CIBIS STUDY) IN DILATED CARDIOMYOPATHY AND ISCHEMIC. TERUTAMA BILA SYMPATHETIC TONE : TACHYCARDIA, PUCAT. SEBAIKNYA UNDER SPECIALIST MEDICAL CARE.
VASODILATING BETA BLOCKER :CARVEDILOL (NON SELECTIVE BETA BLOCKING + ALFA BLOCKING) FAVOURABLE EFFECT ON MORBIDITY AND SURVIVAL IN ISCHEMIC AND NON ISCHEMIC ORIGIN.
DOPAMINERGIC AGENTS :IBOPAMINE : KURANG BERMANFAAT.
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POSITIVE INOTROPIC AGENTS :
KECUALI CARDIAC GLYCOSIDE, PREPARAT INI HANYA DENGAN PEMAKAIAN PARENTERAL PADA END STAGE HEART FAILURE YANG MENUNGGU TRANSPLANTASI.
BETA AGONIST : DOBUTAMINE, DOPEXAMINE.
ACUTE HEMODYNAMIC IMPROVEMENT IS SHORTLASTING TOLERANCE.
INTERMITTENT DOBUTAMINE ADMINISTRATION HIGH MORTALITY RATE.
C AMP : PHOSPHODIESTERASE INHIBITOR.
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ANTI COAGULANT :
ASPIRIN : FOR CORONARY ARTERY DISEASE.
POSSIBLE INTERACTION WITH ACE
INHIBITOR.
AMIODARONE (CLASS III) NO NEGATIVE INOTROPIC EFFECT, EFFECTIVE AGAINST SUPRA AND VERTRICULAR ARRHYTHMIA.
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DRUGS TO AVOID OR BEWARE :
a. NON STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAID)
b. CLASS I ANTI ARRHYTHMICS
c. CALCIUM ANTAGONIST (VERAPAMIL, DILTIAZEM, 1st GENERATION DIHYDROPYRIDINE).
d. TRICYCLIC ANTI DEPRESSANTS
e. CORTICOSTEROID
f. LITHIUM
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• Tindakan khusus
Pompa Balon Intra-aorta dan Peralatan mekanis
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Left ventricular assist device
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• Transplantasi jantung
Transplantasi jantung dapat meningkatkan survival rate dan kualitas hidup Kebutuhan akan transplantasi organ telah meningkat, tetapi jumlah operasi transplantasi tetap stabil karena terbatasnya organ Dengan adanya transplantasi jantung, mortalitas < 10%, survival rate 1,5,10 tahun : 92%, 75%, 60% lebih baik dibandingkan dengan obat-obatan (angka mortalitas 1 tahun 30% - 50% pada gagal jantung
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Survival jangka panjang transplantasi manusia dipengaruhi oleh kecepatan terjadinya aterosklerosis pada graft, yang terjadi diawal tiga bulan setelah operasi Obat anti- rejeksi yang sering dipakai : cyclosporin dan obat imunosupresant lainnya Dari Eurotransplant database (1990-5) : 25% pasien meninggal saat menunggu donor, hanya 60% yang menerima transplantasi dalam jangka 2 tahun (rata-rata 12 bulan)
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THANK’S