PELATIHAN RESUSITASIPEDIATRIK TAHAP LANJUTS Y O K

KOMISI RESUSITASI PEDIATRIKUKK PEDIATRI GAWAT DARURAT IDAI*APRC

DEFINISI SYOK

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

Etiologi SyokTypePrimary InsultCommon Causes

HypovolemicDecreased 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 ELIMINASI DI 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 SODIUMRETENTION 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

Stop pemberian

Le Veen HH: Surg Gynecol Obstet 1980; 150:139-149

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 Komasusai 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 & HEMODINAMIKVASO PRESOR : 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 KARDIOGENIKOKSIGENISASI 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

Pediatric Shock

Lou DeNicola, M.D.Professor, Pediatric Critical CareUniversity of Florida/Jacksonville

Linda Siegel, M.D.Assistant Professor, Pediatric Critical CareMount Sinai School of Medicine

IntroductionShock is a syndrome that results from inadequate oxygen delivery to meet metabolic demandsDO2 < VO2Untreated this leads to metabolic acidosis, organ dysfunction and death

Oxygen DeliveryOxygen delivery = Cardiac Output x Arterial Oxygen Content (DO2 = CO x CaO2)Cardiac Output = Heart Rate x Stroke Volume (CO = HR x SV) SV determined by preload, afterload and contractility Art Oxygen Content = Oxygen content of the RBC + the oxygen dissolved in plasma (CaO2 = Hb X SaO2 X 1.34 + (.003 X PaO2)

Stages of ShockCompensatedVital organ function maintained, BP remains normal.Uncompensated Microvascular perfusion becomes marginal. Organ and cellular function deteriorate. Hypotension develops.Irreversible

Compensatory Mechanisms BaroreceptorsIn aortic arch and carotid sinus, stimulated by high MAP and then excite cardioinhibitory center leading to vasodilation, decreased BP, HR and CO. Hyotension will lift the stimulation and result in vasoconstriction, increased HR, BP and CO.ChemoreceptorsRespond to cellular acidosis and results in vasoconstriction and respiratory stimulation.

Compensatory Mechanisms (cont)Renin-angiotensin systemDecreased perfusion to the kidney leads to renin secretion. Renin is eventually converted to Anigiotensin II leading to vasoconstriction and aldosterone release. Aldosterone leads to sodium and water reabsorptionHumoral responsescatecholamine release leading to increased contractility and vasoconstriction.Autotransfusion Reabsorption of interstitial fluid.

Clinical PresentationEarly diagnosis requires a high index of suspicion

Diagnosis is made through the physical examination focused on tissue perfusion

Abject hypotension is a late and premorbid sign

Hemodynamic Response to Hemorrhage25%50% % Plasma Loss

% ofControl100Vasc ResistanceCardiac OutputBlood Pressure

Initial Evaluation: Physical ExamNeurological: Fluctuating mental status, sunken fontanelSkin and extremities: Cool, pallor, mottling, cyanosis, poor cap refill, weak pulses, poor muscle tone.Cardio-pulmonary: Hyperpnea, tachycardia.Renal: Scant, concentrated urine

Initial Evaluation: Directed HistoryPast medical historyheart diseasesurgeriessteroid usemedical problemsBrief history of present illnessexposuresonset

Differential Diagnosis of Shock IHypovolemicHemorrhageSerum/Plasma lossDrugsDistributiveAnalphylacticNeurogenicSeptic

CardiogenicMyocardialDysrrhythmiaCHD-(duct dependant)ObstructivePneumo, Tamponade, DissectionDissociativeHeat, CO, CyanideEndocrine

Differential Diagnosis of Shock IIPrecise etiologic classification may be delayedImmediate treatment is essentialAbsolute or relative hypovolemia is usually presentThe size of the cardiac silhouette on plain film can be used to estimate the need for volume replacement.Differential Diagnosis of Shock IIPrecise etiologic classification may be delayedImmediate treatment is essentialAbsolute or relative hypovolemia is usually presentThe size of the cardiac silhouette on plain film can be used to estimate the need for volume replacement.

Neonate in Shock:Include in differential:Congenital adrenal hyperplasiaInborn errors of metabolismObstructive left sided cardiac lesions:Aortic stenosisHypoplastic left heart syndromeCoarctation of the aortaInterrupted aortic arch

Outcome of Pediatric ShockChang 1999

Management-GeneralGoal: increase oxygen delivery and decrease oxygen demand:Oxygen FluidTemperature controlAntibioticsCorrect metabolic abnormalities Inotropes

Management-General (cont)AirwayIf not protected or unable to be maintained, intubate.BreathingAlways give 100% oxygen to startSat monitorCirculationEstablish IV access rapidlyCR monitor and frequent BP

Management-General (cont)Laboratory studies:ABGBlood sugarElectrolytesCBCPT/PTTType and crossCultures

Management-Volume ExpansionOptimize preload NS or RLExcept for myocardial failure use 10-20cc/kg aliquots q 2-10 minutesAt 40-60cc/kg reassess and consider: ongoing losses, adrenal, intestinal ischemia, obstructive shock. Get CXR. Consider colloidFurther fluid therapy guided by response, labs, possibly CVP, CXR

Fluid in early septic shock Carcillo, et al, JAMA, 1991 Retrospective review of 34 pediatric patients with culture + septic shock, from 1982-1989. Hypovolemia determined by PCWP, u.o and hypotension.Overall, patients received 33 cc/kg at 1 hour and 95 cc/kg at 6 hours.Three groups:1: received up to 20 cc/kg in 1st 1 hour2: received 20-40 cc/kg in 1st hour3: received greater than 40 cc/kg in 1st hourNo difference in ARDS between the 3 groups

Fluid in early septic shock Carcillo, et al, JAMA, 1991Fluid in early septic shock Carcillo, et al, JAMA, 1991

Group 1(n = 14)Group 2(n = 11)Group 3(n = 9)Hypovolemic at 6 hours -Deaths6

62

20

0Not hypovolemic at 6 hours -Deaths8

29

59

1Total deaths871

Management - Cardiotonics ILack of history of fluid losses, history of heart disease, hepatomegaly, rales, cardiomegaly and failure to improve perfusion with adequate oxygenation, ventilation, heart rate, and volume expansion suggests a cardiogenic or distributive component. Prior to introduction of cardiotonics, the goals of therapy and criteria for monitoring of endpoint should be established

Management - Cardiotonics IIEpinephrine0.05-1.5 ug/kg/minincrease HR, SVR, contractilityEnd point: adequate BP; acceptable tachycardiaNorepinephrine0.05-1.0 ug/kg/minIncrease SVREnd point: adequate BPDopamine2-20 ug/kg/minLower doses, increases renal and splanchnic blood flow, & contractility. Higher doses increases HR and SVREnd Point: Improved perfusion, BP, Urine

Management - Cardiotonics IIIDobutamine1-20 ug/kg/minincreases contractility, may reduce SVR, PVREnd Point: Improved perfusion, may decrease BPProstaglandin E-10.05-0.1 ug/kg/minmaintains patency of ductus

Hypovolemic ShockMost common form of shock world-wideResults in decreased circulating blood volume, decrease in prelaod, decreased stroke volume and resultant decrease in C.O.Etiology: Hemorrhage, renal and/or GI fluid losses, capillary leak syndromes

Hypovolemic ShockClinically, history of vomiting/diarrhea or trauma/blood lossSigns of dehydration: mucous membranes, tears, skin turgorHypotension, tachycardia without signs of congestive heart failure

Hemorrhagic ShockMost common cause of shock in the United States (due to trauma)Patients present with an obvious history (but in child abuse history may be misleading)Site of blood loss obvious or concealed (liver, spleen,intracranial, GI)Hypotension, tachycardia and pallor

Hypovolemic/Hemorrhagic Shock: TherapyAlways begin with ABCsReplace circulating blood volume rapidly: start with crystalloid/colloidBlood products as soon as available for hemorrhagic shock (Type and Cross with first blood draw)Replace ongoing fluid/blood losses & treat the underlying cause

SIRS/Sepsis/Septic shockMediator release:exogenous & endogenousMaldistributionof blood flowCardiacdysfunctionImbalance of oxygensupply and demandAlterations inmetabolismOutcomes of mediator release in systemic inflammatory response syndrome (SIRS), sepsis, and septic shock Septic Shock

Septic Shock: Warm ShockEarly, compensated, hyperdynamic stateClinical signsWarm extremities with bounding pulses, tachycardia, tachypnea, confusion.Physiologic parameterswidened pulse pressure, increased cardiac ouptut and mixed venous saturation, decreased systemic vascular resistance.Biochemical evidence:Hypocarbia, elevated lactate, hyperglycemia

Septic Shock: Cold ShockLate, uncompensated stage with drop in cardiac output.Clinical signsCyanosis, cold and clammy skin, rapid, thready pulses, shallow respirations.Physiologic parametersDecreased mixed venous sats, cardiac output and CVP, increased SVR, thrombocytopenia, oliguria, myocardial dysfunction, capillary leakBiochemical abnormalitiesMetabolic acidosis, hypoxia, coagulopathy, hypoglycemia.

Cold Shock rapidly progresses to MOSF or death, if untreatedMulti-Organ System Failure: Coma, ARDS, CHF, Renal Failure, Ileus or GI hemorrhage, DICMore organ systems involved, worse the prognosisTherapy: ABCs, fluidAppropriate antibiotics, treatment of underlying causeSeptic Shock (cont)

Cardiogenic ShockEtiology:DysrhythmiasInfectionMetabolicObstructiveDrug intoxicationCongenital heart diseaseTrauma

Cardiogenic Shock (cont)Differentiation from other types of shock:HistoryPE:Enlarged liverGallop rhythmMurmurRalesCXR: Enlarged heart, pulmonary venous congestion

Cardiogenic Shock (cont)Management:Improve cardiac output::Correct dysrhymiasOptimize preloadImprove contractilityReduce afterloadMinimize cardiac work:Maintain normal temperatureSedationIntubation and mechanical ventilationCorrect anemia

Distributive ShockDue to an abnormality in vascular tone leading to peripheral pooling of blood with a relative hypovolemia.EtiologyAnaphylaxisDrug toxicityNeurologic injuryEarly sepsisManagementFluidTreat underlying cause

Obstructive ShockMechanical obstruction to ventricular outflowEtiology: CHD, massive PE, tension pneumothorax, cardiac tamponadeInadequate C.O. in the face of adequate preload and contractilityTamponade: Narrow pulse pressure and/or EMDTreat underlying cause.

Dissociative ShockInability of Hemoglobin molecule to give up the oxygen to tissuesEtiology: Carbon Monoxide poisoning, methemoglobinemia,dyshemoglobinemiasTissue perfusion is adequate, but oxygen release to tissue is abnormalEarly recognition and treatment of the cause is main therapy

Hemodynamic Variables in Different Shock States

Final ThoughtsRecognize compensated shock quickly- have a high index of suspicion, remember tachycardia is first sign. Hypotension is late and ominous.Gain access quickly- if necessary use an IO line.Administer adequate amounts of fluid rapidly. Remember ongoing losses.Correct electrloytes and glucose problems quickly.If the patient is not responding the way you think he should, broaden your differential, think about different types of shock.

Figure 1.

Factors Affecting Oxygen Delivery

Hgb

A-a gradient

DPG

Acid-Base Balance

Blockers

Competitors

Temperature

CaO2

Influenced By

Oxygenation

DO2

Drugs

Conduction System

Influenced By

HR

CVP

Venous Volume

Venous Tone

EDV

CO

Metabolic Milieu

Ions

Acid Base

Temperature

Drugs

Toxins

Ventricular Compliance

SV

Influenced By

Contractility

Afterload Blockers

TemperatureCompetitors

Drugs Autonomic Tone

ESV

Influenced By

*