SYOK Dept. Anestesiologi & Terapi IntensifFK USU/RSUP H.Adam Malik Medan

Modul 6

DEFINISIIT 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 syok mengakibatkan gangguan pada perfusi jaringan yang selanjutnya berkembang menjadi gagal sirkulasi akut atau disebut juga sindroma syok

Shock CategoriesCardiogenicHypovolemicDistributiveObstructive

ShockAlways a symptom of primary causeInadequate blood flow to meet tissue oxygen demandMay be associated with hypotensionAssociated with signs of hypoperfusion: mental status change, oliguria, acidosis

Cardiogenic ShockDecreased contractilityIncreased filling pressures, decreased LV stroke work, decreased cardiac outputIncreased systemic vascular resistance compensatory

Hypovolemic ShockDecreased cardiac outputDecreased filling pressuresCompensatory increase in systemic vascular resistance

Distributive ShockNormal or increased cardiac outputLow systemic vascular resistanceLow to normal filling pressuresSepsis, anaphylaxis, neurogenic, and acute adrenal insufficiency

Obstructive ShockDecreased cardiac outputIncreased systemic vascular resistanceVariable filling pressures dependent on etiologyCardiac tamponade, tension pneumothorax, massive pulmonary embolus

O2CARDIOGENICHYPOVOLEMICO2O2OBSTRUCTIVESEPTIC

PATOFISIOLOGI DARI RESPON TUBUH TERHADAP SHOCKRespon Neuroendokrin

Respon Hemodinamik

Respon Metabolik *

HYPOVOLEMIANeuroendocrine Respons*

*Haemodynamic ResponsVenoconstrictionSympathetic n. system (SNS)Catecholamines (CA)Angiotensin II (ATII)ADHIncreased myocardial contractilitySNS, CASVR

Release of :CatecholaminesCortisolGlucagonLIPOLYSISINCREASE IN PLASMA FREE FATTY ACIDSMetabolic Respons*

RESPON METABOLIKHyperglikemia

Mobilisasi lemak

Katabolisme/pemecahan Protein Peningkatan sintesis urea Peningkatan asam amino aromatik

Penurunan sintesis reactan fase akut

Peningkatan osmolalitas ekstrasel*

RESPON METABOLIK*

METABOLIC RESPONSDecreased blood volumeDecreased COCellular hypoperfusion and hypoxiaAnaerobic glycolysisPyruvate converted to lactic acidMETABOLIC ACIDOSIS*

Mekanisme untuk memperbaiki keseimbangankardiovaskuler

Redistribusi aliran darah

Peningkatan cardiac output

Memperbaiki volume intravaskular*

STIMULASI NEUROENDOKRINHYPOTENSIONBLOOD FLOW PROTECTEDHeartBrainAdrenal/pituitary glandBLOOD FLOW DECREASEDSkinMuscleSplanchnic circulationREDISTRIBUSI ALIRAN DARAH*

CARDIAC OUTPUT = HR X SVSympathetic n. systemCatecholamine release Increase EDV via:VenoconstrictionArteriolar constrictionRenal reabsorptionIncreased contractilityPENINGKATAN CARDIAC OUTPUT *

MEMPERBAIKI VOLUME DARAHTranscapillary refill phase1. 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*

*EFEK SHOCK PADA TINGKATAN SELLOW-FLOW,POOR PERFUSION

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CELL MEMBRANE FAILURE:

DIRECT EndotoxinComplement INDIRECTFailure to maintain normal Na+, K+ or Ca2+ gradientDecreased oxidative phosphorylationEFEK SHOCK PADA TINGKATAN SEL*

Kidney Oliguric renal failure High output renal failure

Liver Liver failure

GI tractFailure of intestinal barrier (sepsis, bleeding)

Lung Capillary leak associated with or caused by sepsis and infectionEFEK SHOCK PADA TINGKATAN ORGAN*

STAGES OF SHOCK

*COMPENSATED SHOCK Body defense mechanisms attempt to preserve major organsPrecapillary sphincters close, blood is shuntedIncreased heart rate and strength of contractionsIncreased respiratory function, bronchodilation

*COMPENSATED SHOCK Will continue until problem solved or shock progresses to next stage Can be difficult to detect with subtle indicators Tachycardia Decreased skin perfusion Alterations in mental status Some medications such as propranolol can hide signs and symptoms

*UNCOMPENSATED SHOCK Physiological responsePrecapillary sphincters open, blood pressure fallsCardiac output fallsBlood surges into tissue beds, blood flow stagnatesRed cells stack up in rouleaux

*UNCOMPENSATED SHOCK Easier to detect than compensated shock Prolonged capillary refill time Marked increase in heart rate Rapid thready pulse Agitation, restlessness, confusion

Decompensation*

*IRREVERSIBLE SHOCK Compensatory mechanisms fail, cell death begins, vital organs falter Patient may be resusitated but will die later of (ARDS, renal and liver failure, sepsis)

Clinical Differentiation Shock Hemorrhagic Shock Non Hemorrhagic Shock Cardiogenic Tension pneumothorax Neurogenic Septic Anaphylactic *

Hemorrhagic Shock

Paling sering terjadi terutama pada kasus trauma

Dijelaskan secara khusus pada Modul 5 (Terapi Cairan 1) *.Syok Perdarahan

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Non Hemorrhagic Shock

Cardiogenic Shock Myocardial dysfunction Blunt cardiac trauma Cardiac tamponade Air embolism Valve rupture ECG monitoring Isoenzynme-CPK Echocardiography Tachycardia Blowing heart sound Venectasia regio colli Hypotension Pumping dysfunctionDiminished blood return to the heart*

Riwayat kejadianTrauma torak : tumpul, tajamDisfungsi miokard Kontusio, disritmia, emboli udara, infark, tamponadeEKG monitoringUltrasonografiPemasangan CVPPemeriksaan laboratoriumPerikardiosentesis.Syok Kardiogenik*

Trauma torak : tajam, tumpul Takikardia Hipotensi/syok Vena leher meninggi Suara jantung menjauh EKG low voltage Ultra sonografi PerikardiosentesisTamponade Jantung*

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Ventil mechanism/flap-valve Sesak nafas , RR > Emphysema subcutan Perkusi hypersonor Suara paru menghilang pada ipsilateral Trakhea terdorong kontralateral Tachycardia Hypotension

Tension Pneumothorax Mediastinum tergeser Venous return terganggu Pumping terganggu*

Mirip tamponade jantung Peningkatan tekanan intra pleural Pergeseran mediastinumVenous return Pre load Cardiac output Pergeseran trakhea Paru kolaps, suara napas hilang Perkusi hipersonor Dekompresi pleura JarumChest tube

Pneumothoraks tension*

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Punksi pleura untuk dugaan pneumothorax (sistim jarum + spuit + air)NEEDLE THORACOSYNTHESIS*

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Neurogenic Shock Spinal Shock Cedera tulang belakang Cedera medulla spinalis Sympathetic denervasi Vasodilatasi, gambaran hypovolemia No tachycardia, No vasokonstriksiHypotensi,Shock Perifer hangatInappropriate vasodilatationInadequate pump function*

.Neurogenik Syok

Perdarahan otak tak shock !!! Cedera tulang leher (spinal cord) Kehilangan tonus simpatisHipotensiVasodilatasiNadi Tekanan nadi lebar Pemberian volume Monitoring CVP Vasopressor/Atropin*

Septic Shock Jarang terjadi segera setelah trauma Dapat terjadi pada kasus trauma yang terlantar Luka tembus abdomen, perforasi Shock septik pada periode awal : Tachycardia Perifer hangat Sistolik bisa normal Pulse pressure lebarInadequate pump functionInappropriate vasodilatation*

.Septik Syok

Jarang pada awal trauma Fase awalKulit hangatTekanan nadi lebar Bila tak febris, sulit dibedakan dgn syok hipovolemik Kontaminasi perforasi usus (trauma abdomen)*

SYOK ANAFILAKSIS

MENDADAK, TAK DAPAT DIRAMALKAN KEMATIAN DALAM WAKTU SINGKAT

SYOK (HIPOVOLEMIK) GAGAL NAFAS AKUTAnaphylactic Shock*

Reaksi Anafilaktik1. Adrenalin (1 ampul = 1 mg ) iv im sc - sl - transtracheal - etBerat : 0.50 - 1 ampulSedang : 0.25 0.50 ampulRingan : tanpa shock - tidak perlu2. Baringkan penderita, kedua tungkai angkat keatas (Shock Position)Jaga jalan nafas tetap bebasO2 masker 10 lpm, bila ada.Siap Ambu Bag, siap beri nafas buatan , siap RJPOLIHAT : gerak dada, ada nafas ?DENGAR : suara nafas, tensi. Ada nafas ? Shock ?RABA : hawa nafas, perfusi perifer. Ada nafas ? Shock?Pasang Infus : RL/ PZ grojok 500-1000 cc3. 5-10 menit kemudiank/p ulangi AdrenalinBeri Oradexon iv 1-2 ccatau Dexamethason 100-200mg imAvil/ Delladryl 1 cc im, hati-2 tensi turun lagi4. Bila ada wheezing beri aminofilin iv pelan 5-10 cc ( 1Ampul )Hati-hati bila tensi < 100 mmHg, K/P pemberian dg titrasi.

Laki-laki 50 th KP Fisik baik Tensi/Nadi baikRiwayat alergi (-) sesak (-) asthma (-) disuntik streptomycine - Penicillin Shock : nadi kecil cepat perfusi dingin pucat basah, sesak hebat, pasien gelisahKASUSTime Saving is Life Saving*

Initial Assesment Airway , Breathing ok?

Circulation HR within normal limit Pulse pressure WNL Warm, Pink, DryNO SHOCK*

Initial Assesment Airway , Breathing ok?

Circulation Tachycardia Cutaneous vasoconstriction Pulse pressure Calmy SHOCK*

PRINSIP RESUSITASIMempertahankan ventilasi

Meningkatkan perfusi

Terapi penyebab*

MAINTAIN VENTILATIONIncreased oxygen demandRespiratory fatigueDiversi blood flow from vital organOrgan injury*

TREATMENT:Primary resuscitationOxygenationMechanical ventilation if neededTREATMENT OF RESPIRATORY FAILURE*

TREATMENT CONCEPT OF SHOCK

ENHANCING PERFUSION / OXYGEN DELIVERYOxygen delivery/DO2 = HR X SV X Hb X S02 X 1.34 + Hb X paO2Cardiac outputArterial O2 contentDO2 = CO x CaO2*

THERAPEUTIC GOALS IN SHOCKIncrease O2 deliveryOptimize O2 content of bloodImprove cardiac output and blood pressureMatch systemic O2 needs with O2 deliveryReverse/prevent organ hypoperfusion

Cardiac Output x SVRPipe = VascularPump =HeartVolume =BloodHypovolemic ShockCardiogenic ShockDistributive ShockInotropes (Dob,Dop,Adr,Amr)Vasopressor ( NE,PE,Adr,Dop)FluidsObstructive ShockRelease tamponade,etcBlood Pressure

Cardiogenic Shock ManagementTreat arrhythmias Diastolic dysfunction may require increased filling pressures Vasodilators if not hypotensiveInotrope administration

Cont..Vasopressor agent needed if hypotension present to raise aortic diastolic pressure Consultation for mechanical assist devicePreload and afterload reduction to improve hypoxemia if blood pressure adequate

Hypovolemic Shock Management Volume resuscitation crystalloid, colloidInitial crystalloid choicesLactated Ringers solutionNormal saline (high chloride may produce hyperchloremic acidosis)Match fluid given to fluid lostBlood, crystalloid, colloid

Distributive Shock ManagementRestore intravascular volumeHypotension despite volume therapyInotropes and/or vasopressorsVasopressors for MAP < 60 mm HgAdjunctive interventions dependent on etiology

Obstructive Shock TreatmentRelieve obstructionPericardiocentesis Tube thoracostomy Treat pulmonary embolusTemporary benefit from fluid or inotrope administration

Fluid TherapyCrystalloidsLactated Ringers solutionNormal salineColloidsHetastarchAlbuminGelatinsPacked red blood cellsInfuse to physiologic endpoints

ContCorrect hypotension firstDecrease heart rateCorrect hypoperfusion abnormalitiesMonitor for deterioration of oxygenation

How Much Fluid To Give?Some measure of intravascular fillingPressure (CVP or PAOP) Some assessment of risk of pulmonary oedema and capillary leakPulmonary gas exchange (PaO2:FiO2)Requirement for positive pressure (PEEP)Chest X-raySome assessment of response to treatmentChanges in acid base balance, lactateMeasurement of cardiac output

Inotropic / Vasopressor AgentsDopamineLow dose (2-3 g/kg/min) mild inotrope plus renal effectIntermediate dose (4-10 g/kg/min) inotropic effectHigh dose ( >10 g/kg/min) vasoconstrictionChronotropic effect

Cont.Dobutamine5-20 g/kg/minInotropic and variable chronotropic effectsDecrease in systemic vascular resistance

Cont..Norepinephrine0.05 g/kg/min and titrate to effectInotropic and vasopressor effectsPotent vasopressor at high doses

Cont..EpinephrineBoth and actions for inotropic and vasopressor effects0.1 g/kg/min and titrateIncreases myocardial O2 consumption

Pediatric ConsiderationsBP not good indication of hypoperfusionCapillary refill, extremity temperature better signs of poor systemic perfusion Epinephrine preferable to norepinephrine due to more chronotropic benefitFluid boluses of 20 mL/kg titrated to BP or total 60 mL/kg, before inotropes or vasopressors

Pediatric ConsiderationsNeonates consider congenital obstructive left heart syndrome as cause of obstructive shockOliguria

What Do You Need to Know When You Resuscitate a Patient in Shock?Arterial blood pressureUrine outputSystemic acidbase balance (pH, SBE, lactate)Some clinical assessment of tissue perfusionwarm and well perfused or cold and shut downSome measurement of global blood flow and tissue perfusionCardiac output or cardiac indexArterial oxygen delivery, oxygen uptake indexMixed venous saturation and PvO2*

SUMMARYShock 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*

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***Heart: myocardial hypoxia-->systolic and diastolic dysfunction (decrease cardiac output)Kidneys pre-renal renal failure occurs secondary toVasocontriction and reduced GFR, Leads to acute tubular necrosis--> Damaged tubules fail to absorb saltLungs-decreased compliance-->decreased ventilation--> V/Q mismatch-->hypoxemia and ARDS Also Release of inflammatory mediators TNF-a, nitric oxideInjury to endothelial cells allowing leakage of fluids and neutrophils into interstium

GI tractVasoconstriction of splacnich vesselsInfarction-->Ileus--> fluid imbalance and acidosis Brain: CPP=MAP-ICPMAP < 60mmHg cerebral perfusion decreases secondary to pressure below autoregulatory range

*Picture of israeli army---who have plenty of trauma experience and know a thing or two about trauma care