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Shock dan Gagal Jantung(Heart Emergencies)

DEPARTEMEN FISIOLOGIFK UNIMAL

2010

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

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

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

OO22

CARDIOGENICCARDIOGENIC

HYPOVOLEMIKHYPOVOLEMIK

OO22

OO22

OBSTRUCTIVEOBSTRUCTIVE

SEPTICSEPTIC

EFEK SHOCK PADA TINGKATAN SELEFEK SHOCK PADA TINGKATAN SEL

HYPOXIAHYPOXIA

LOW-FLOW,LOW-FLOW,POOR PERFUSIONPOOR PERFUSION

ANAEROBIC METABOLISM

ACIDOSIS

DECREASED CELLULAR ENERGY EFFICIENCY

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.

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

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

PATOFISIOLOGI DARI RESPON TUBUH TERHADAP SHOCK

Respon Neuroendokrin

Respon Hemodinamik

Respon Metabolik

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

RESPON HEMODINAMIKMekanisme untuk memperbaiki Mekanisme untuk memperbaiki keseimbangan kardiovaskularkeseimbangan kardiovaskular

Redistribusi aliran darah

Peningkatan “cardiac output”

Memperbaiki volume intravaskular

STIMULASI NEUROENDOKRIN

HYPOTENSION

BLOOD FLOW PROTECTEDHeartBrain

Adrenal/pituitary gland

BLOOD FLOW DECREASEDSkin

MuscleSplanchnic circulation

RESPON HEMODiNAMiKREDISTRIBUSI ALIRAN DARAH

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

Memperbaiki volume darahTranscapillary refill phase

1. Decreased capillary pressure caused by hypotension2. Sympathetic increase in precapillary arteriolar constriction

Decrease capillary hydrostatic pressure promotes passage of fluid from interstitium to intravascular space

Plasma protein restitution phaseIncreased plasma osmolarity due to mainly hepatic release of

glucose, pyruvate, amino acids, etc.

Increased interstitial osmolarity

Increased interstitial volume and pressure

Transcapillary movement of albumin into intravascular space

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

RESPON METABOLIK

Hyperglikemia

Mobilisasi lemak

Katabolisme/pemecahan ProteinPeningkatan sintesis ureaPeningkatan asam amino aromatik

Peningkatan osmolalitas ekstrasel

RESPON METABOLIK

Breakdown of skeletal muscle

into a.a.

Conversion of a.a. to glucose

Release of:CatecholaminesCortisolGlucagonGrowth hormone

Impaired peripheral

glucose uptake

HYPERGLYCEMIA

Glycogen breakdown

METABOLIC RESPONS

Decreased blood volume

Decreased CO

Cellular hypoperfusion and hypoxia

Anaerobic glycolysisPyruvate converted to lactic acid

METABOLIC ACIDOSIS

Release of:CatecholaminesCortisolGlucagon

LIPOLYSIS

INCREASE IN PLASMA FREE FATTY ACIDS

METABOLIC RESPONS

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

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

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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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 32SHK 32®

• 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

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

Pediatric ConsiderationsPediatric Considerations

• BP not good indication of hypoperfusion• Capillary refill, extremity temperature better

signs of poor systemic perfusion • Epinephrine preferable to norepinephrine due to

more chronotropic benefit• Fluid boluses of 20 mL/kg titrated to BP or total 60

mL/kg, before inotropes or vasopressors• Neonates – consider congenital

obstructive left heart syndrome as cause of obstructive shock

• Oliguria– <2 yrs old, urine volume <2 mL/kg/hr– Older children, urine volume

<1 mL/kg/hr

• BP not good indication of hypoperfusion• Capillary refill, extremity temperature better

signs of poor systemic perfusion • Epinephrine preferable to norepinephrine due to

more chronotropic benefit• Fluid boluses of 20 mL/kg titrated to BP or total 60

mL/kg, before inotropes or vasopressors• Neonates – consider congenital

obstructive left heart syndrome as cause of obstructive shock

• Oliguria– <2 yrs old, urine volume <2 mL/kg/hr– Older children, urine volume

<1 mL/kg/hr ®

How Much Fluid To Give?• Some measure of intravascular filling

– Pressure (CVP or PAOP) • Some assessment of risk of pulmonary

oedema and capillary leak– Pulmonary gas exchange (PaO2:FiO2)– Requirement for positive pressure (PEEP)– Chest X-ray

• Some assessment of response to treatment– Changes in acid base balance, lactate– Measurement of cardiac output

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)• Some clinical assessment of tissue perfusion

– “warm and well perfused” or “cold and shut down”

• 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

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

TREATMENT CONCEPT OF SHOCKTREATMENT CONCEPT OF SHOCK

ENHANCING PERFUSION / OXYGEN DELIVERYENHANCING PERFUSION / OXYGEN DELIVERY

Oxygen delivery/DOOxygen delivery/DO22 == HR X SVHR X SV X X Hb X S0Hb X S02 2 X 1.34 + Hb X paOX 1.34 + Hb X paO22

Cardiac Cardiac outputoutput

Arterial OArterial O22 contentcontent

FluidsFluids TransfuseTransfuse Partially Partially dependent on dependent on

FIOFIO22 and and pulmonary pulmonary

statusstatus

InotropesInotropes

DO2 = CO x CaO2

SUMMARY Shock is an altered state of tissue perfusion severe

enough to induce derangements in normal cellular function

Neuroendocrine, hemodynamic and metabolic changes work together to restore perfusion

Shock has many causes and often may be diagnosed using simple clinical indicators

Treatment of shock is primarily focused on restoring tissue perfusion and oxygen delivery while eliminating the cause

TENSION PNEUMOTHORAXTENSION PNEUMOTHORAX

PRINSIP RESUSITASIPRINSIP RESUSITASI

Mempertahankan ventilasiMempertahankan ventilasi

Meningkatkan perfusiMeningkatkan perfusi

Terapi penyebabTerapi penyebab

MAINTAIN VENTILATIONMAINTAIN VENTILATIONIncreased oxygen Increased oxygen

demanddemand

HyperventilationHyperventilation

Respiratory failureRespiratory failureRespiratory acidosis, lethargy-coma, hypoxiaRespiratory acidosis, lethargy-coma, hypoxia

Especially in:Especially in:

SepsisSepsisHypovolemiaHypovolemia

TraumaTrauma

Respiratory fatigueDiversi blood flow from

vital organ

Organ injury

Hypovolemia (blood loss)Hypovolemia (blood loss)

Decreased CO Decreased CO

Decreased oxygen delivery, increased Decreased oxygen delivery, increased oxygen requirementoxygen requirement

Metabolic acidosis, hypoxemia Metabolic acidosis, hypoxemia tachypneatachypnea

TREATMENT:TREATMENT:Primary resuscitationPrimary resuscitation

OxygenOxygenMechanical ventilation if neededMechanical ventilation if needed

TREATMENT OF RESPIRATORY FAILURETREATMENT OF RESPIRATORY FAILURE

GAGAL JANTUNG

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

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).

Klasifikasi gagal jantung berdasarkan NYHA (New York Heart Association)/Perkumpulan Jantung New York.

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

Terminologi

• Gagal jantung kiri

• Gagal jantung kanan

• Gagal jantung kongestif

• Gagal jantung akut

• Gagal jantung kronik

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.

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.

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.

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.

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.

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.

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.

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

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

Chest x ray film in patient with acute pulmonary oedema

BENTUK LAIN GAGAL JANTUNG SECARA TEORITIS DAPAT BERUPA :

1. FORWARD FAILURE BACKWARD FAILURE

2. HIGH OUTPUT LOW OUTPUT

3. SISTOLIK DIASTOLIK

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.

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.

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.

TREATMENT OPTION : GENERAL ADVICE AND GENERAL MEASURE

GENERAL ADVICE :

a. COUNSELLING: TERANGKAN KELUHAN DAN GEJALA GAGAL JANTUNG KEPADA PENDERITA DAN KELUARGA. MONITOR BERAT BADAN.

b. SOCIAL ACTIVITY & EMPLOYMENT: JANGAN DISISIHKAN, USAHAKAN DAPAT MENERUSKAN KERJA SEHARI-HARI.

c. TRAVEL: PERJALANAN JAUH PROBLEM: DEHIDRASI, EDEMA TUNGKAI, RESIKO VENOUS THROMBOSIS, EFEK PEROBAHAN DIET.

d. CONTRACEPTION: NYHA III-IV RESIKO KEMATIAN IBU , HINDARI KEHAMILAN, HORMONE REPLECEMENT THERAPY (HRT) MENGURANGI RESIKO P.J. KORONER

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.

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

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

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.

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

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.

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.

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.

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.

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.

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

• Tindakan khusus

Pompa Balon Intra-aorta dan Peralatan mekanis

Left ventricular assist device

• 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

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)

THANK’S