PELATIHAN RESUSITASIPEDIATRIK TAHAP LANJUTS Y O K

KOMISI RESUSITASI PEDIATRIKUKK PEDIATRI GAWAT DARURAT IDAIAPRC

DEFINISI SYOKSINDROM KLINIS AKIBAT KEGAGALAN SISTEM SIRKULASI UNTUK MENCUKUPI :NUTRISI PASOKAN METABOLISMEOKSIGENUTILISASIJARINGAN TUBUHFASE: KOMPENSASI DEKOMPENSASI IREVERSIBEL DEFISIENSI O2 SELULER

Etiologi SyokTypePrimary InsultCommon CausesHypovolemicDecreased circulatingDehydration, hemorrhage, blood volcapilarry leaksDistributiveVasodilation -> venousSepsis, anaphylaxis, pooling -> decreased preloaddrug intoxication, spinal cord injuryObstructiveObstruction of cardiacCardiac tamponade, tension filling/out flowpneumothoracx, pulmonary embolusCardiogenicDecreased contractilityCongenital heart disease, myocarditis, dysritmiaDissociativeO2 not released fromCO poisoning, hemoglobinmethemoglobinemia

FUNGSI SISTEM SIRKULASIJANTUNGCURAH JANTUNGMETABOLISME PEMB. DARAHALIRAN DARAH ADEKUATJARINGANVOL. DARAHO2 DELIVERYMETABOLIT ELIMINASIDI ORGAN PEMBUANGANDO2 = CO x CaO2CaO2 = (1,34 x Hb x sat O2) + (0,003 x PaO2)

Pengaturan curah jantung dan tekanan darah

PreloadContractilityAfterload

Heart rateStroke volume

Cardiac outputSystemic vascular resistance

Blood pressure

Distribution of CO & VO2 in a Healthy Resting Normal Subject% TotalAVDO2% TotalOrganCOvol %VO2GI tract and liver244.125Skeletal muscle218.030Kidney191.3 7Brain136.320Skin 91.0 2Heart 411.411Other organs103.0 5Adapted from Wade OL, Bishop JM: Cardiac output and regional blood flow, Oxford, Blackwell, 1962

Extracel. FluidLow Output Cardiac FailureIntra vasc. Vol. due to VolumePericardial TamponadeOncotic PressureConstrictive PericarditisCapillary Permeability CARDIAC OUTPUT

Activation receptor of ventricular & arterial Non-osmotic Stimulation ofActivation of theVasopressin Sympathetic Nervous Renin-Angiotensin-Stimulation System Aldosterone System

RENAL WATER PERIPHERAL & RENAL RENAL SODIUM RETENTION ARTERIAL VASC. RESISTANCE RETENTION MAINTENANCE OF EFFECTIVE ARTERIAL BLOOD VOLUME

FRANK STARLING`S LAW SYMPATHOMIMETIC AMINESXANTHINESGLUCAGONCARDIAC GLYCOSIDES

HYPOXEMIAACIDOSISHYPOGLYCEMIAENDOTOXEMIADRUG TOXICITYVOLUME INFUSIONSTROKE VOLUME423150510CENTRAL VENOUS PRESSURE (Toor)ADBCPOSITIVEINOTROPYNEGATIVEINOTROPY

Oxyhemoglobin saturationH+2,3-DPGCO2PiH+2,3-DPGCO2PiPaO2The Oxygen-hemoglobin Dissociation Curve

Shock

Hypotension

Preload Cellular hypoxia

Intravasculer volume Myocardial contractility Anaerobic metabolism

Membrane permeability

Metabolic by-products:- lactic acid- myocardial depressant factor- endogeneous catecholamines- adenine nucleotides

STADIUM SYOK

KOMPENSASIDEKOMPENSASIIREVERSIBEL (PRETERMINAL)PERJALANAN KLINIS BERSIFAT PROGRESIF

FASE I: KOMPENSASIKOMPENSASI TEMPORER SIMPATIS, SVR, TEKANAN NADIDISTRIBUSI SELEKTIF ALIRAN DARAH RETENSI NA & AIRKLINIS : * TAKHIKARDIA * GADUH GELISAH * KULIT PUCAT DINGIN * PENGISIAN KAPILER >>

FASE 2: DEKOMPENSASIKOMPENSASI MULAI GAGALHIPOPERFUSI HIPOKSIA JAR. METAB. ANAEROBIK GGN. METAB. SELULERPELEPASAN MEDIATOR : * VASODILATASI * PERMEABILITAS * DEPRESI MIOKARD * GGN KOAGULASI KLINIS : TAKHIKARDIA TEKANAN DARAH TAKIPNU PERFUSI PERIFER ASIDOSIS (+)OLIGURI (+) TINGKAT KESADARAN

FASE 3: IREVERSIBELKOMPENSASI GAGALCADANGAN ENERGI TUBUH KERUSAKAN/KEMATIAN SELDISFUNGSI ORGAN MULTIPELKLINIS : * T.D TAK TERUKUR* NADI TAK TERABA * TINGKAT KESADARAN * ANURIA (+) * GAGAL MULTI ORGAN DAN KEMATIAN

Manifestasi Klinis SyokClinical SignsCompensatedUncompensated Irreversible

Blood loss (%)Up to 2525 - 40> 40

Heart rate Tachycardia + Tachycardia ++ Tachy/bradycardiaSystolic BPN N or falling PlummetingPulse volumeN/ + ++Capillary refill N/ + ++SkinCool, pale Cold, mottled Cold, deathly paleRespiratory rateTachypnoea + Tachypnoea ++Sighing rsp.Mental state Mild agitationLethargic Reacts only to painUncooperativeor unresponsive

GANGGUAN PERFUSI PERIFERCORE > PERIFER TEMP. ~ > 2O CCAPILLARY REFILL >> : * NAIL BED PRESS * BLANCHING SKIN TESTPRODUKSI URIN (N) BAYI = 2 ml/kg/jam ANAK= 1 ml/kg/jam

TATALAKSANA RESUSITASI SYOKRESUSITASI AWALOKSIGEN 100% + VENTILATORY SUPPORTPASANG AKSES VASKULER (90 DETIK)FLUID CHALLENGE (20 ml/kg BB)SECEPATNYA < 10 MENITDPT DIULANGI 2-3 KALIKRISTALOID/KOLOIDPEMANTAUAN AWALRESPON THD FLUID CHALLENGEPANTAU PROD. URIN (KATETER)STAT. LAB/PENUNJANG

MonitoringState of consiousness-Glasgow Coma ScaleRespiratory rate and characterCardiovascular parametersSkin and core temperature differencePulse rate and volumeBlood pressureCapillary perfusion timeCentral venous pressure - should be monitored in a patient where there has been poor response to fluid therapy or with established shock. Urinary output - urine bag, or preferably catheter; output should be 1-2 ml/kg body weightPulse oximetry

RESUSITASI LANJUTBILA FLUID CHALLENGE NON RESPONSIVEINTUBASI & VENT. MEKANIKPASANG CVP & LOADING HATI-HATIKOREKSI EFEK INOTROPIK NEGATIF Hb < 5 g/dl PRC 10 ml/kg BB (Ht 40-50 vol %)OBAT INOTROPIK

PEMANTAUAN LANJUTCARI PENYEBAB SYOK (CXR, KONSULTASI)EVALUASI FUNGSI SIST. ORGAN LAIN : ATN/PRE RENAL FAILUREARDSCARDIAC FUNCTIONGGN. KOAGULASI/DICORGAN-ORGAN LAIN

CHILD IN SHOCK(1) OXYGEN (2) CRYSTALLOID 20 ml/kg)IMPROVEMENT NO IMPROVEMENT NO IMPROVEMENT (3) CRYSTALLOID - INCREASE MABP (20 ml/kg)- NORMALIZATION HR - IMPROVED PERFUSION - URINE OUTPUT > 1 ml/kg/hrURINARY CATHETER

ESTABLISH CVPESTABLISH ETIOLOGY,OBSERVATIONCVP < 5 Torr CVP > 5 TorrCRYSTALLOID INFUSION NO IMPROVEMENT UNTIL CVP - 5 Torr IMPROVEMENT ABG, HT, NaK, GLUC Ca, SWAN GANZ CATHETERESTABLISH ETIOLOGY CO, RAP, PAP, POAPCONFIRM SOURCE OF FLUID LOSSCENTRAL VENOUS PRESSURESTROKE VOLUME1. CORRECT ACIDOSIS

2. Co. GLUCOSE

3. INTROPIC SUPPORT

Stadium syok septik dan manifestasi klinisStadiumTanda KlinisGang fisiologisBiokimiawi

Warm Shock perfusi perifer (N) Smv O2hipokarbia(Hiperdinamik)kulit hangat kering VO2hopoxiaHR nadi bounding COkadar laktat suhu / (tak stabil) SVRhiperglikemiaRR , gg. kesadaran

Cold Shocksianosis CO hipoxia(Hipodinamik)kulit dingin lembab SVR asidosis metabnadi kecil, lemah CVPkoagulopatiHR , Oliguria Smv O2 hipoglikemishallow breathing pe kesadaran

MOSFbergantung sistem Komasesuai yang terkenaARDS, CHF, RFjenisGI bleeding/DIC organ failure

TATALAKSANA SYOK SEPTIKAB BROAD SPECTRUM SESUAI KULTURRESUSITASI CAIRAN : KOLOID/KRISTALOIDOBAT INOTROPIK : DOBUTAMIN + DOPAMIN ISOPRENALIN/ADRENALIN SVR VASODILATASI PERIFERKOREKSI : - HIPO/HIPERGLIKEMI - ASAM BASA - ELEKTROLIT

TATALAKSANA SYOK ANAFILAKTIKSTOP ALERGEN PENYEBAB + ADRENALIN (IM)AIR WAY & RESPIRATION ADEKUATWHEEZING NEBULASI ADRENALIN/SALBUTAMOLOBSTRUKSI INTUBASI/SURGICAL AIRWAYSIRKULASI & HEMODINAMIKVASOPRESOR : ADRENALIN (10 mg/kg BB)FLUID LOADING : KRISTALOID (20 ml/kg BB/IV-IO)RE ASSESSMENT ABC RESUSITASIWHEEZING (+) NEBULASI SALBUTAMOL BILA PERLU (+) HIDROKORTISON (IV) (+) AMINOPILIN/SALBUTAMOL DRIPSYOK BERLANJUT : KOLOID + INOTROPIK

TATALAKSANA SYOK KARDIOGENIKOKSIGENASI ADEKUATKOREKSI GGN ASAM BASA & ELEKTROLITKURANGI RASA SAKIT & ANSIETAS ATASI DISRITMIA JANTUNGKELEBIHAN PRELOAD: DIURETIKAKONTRAKTILITAS:FLUID CHALLENGE SESUAI CVP/POAP OBAT INOTROPIK (+) BEBAN AFTERLOAD (SVR ) : VASODILATORKOREKSI PENYEBAB PRIMER

Key points in managementRemember BP and pulse are unreliable indicators in early septic shockLook for minor degrees of mental impairment (anxiety, restlessness)Do not delay treatment, try to prevent the onset of hypotension, metabolic acidosis, and hypoxiaGive adequate fluids early in treatment, especially colloidsDo not use inotropic agents until the patient has received adequate fluid therapyMonitor blood glucose, gases, and pH, and treat appropriately

SEQUENCE OF THERAPEUTIC MANEUVERS (VIPPS)PriorityMnemonicTherapyPurpose 1VVentilateAdequate O2&CO2 exchange2IInfuseVascular Access Blood, fluid & electrolite balance3PPumpRestoration cardiac performance4PPharmacologicImproved perfusion by vasoactive agents5SSpecific/Medical & surgical Surgicalmanagement of primary causes