SHOCK AND FLUID THERAPY IN SHOCK

Bambang Suryono S

LIFE THREAT
• Dimana saja!! • Kapan saja!! • Pada siapa saja!!

Life Threat
• • • • • Orang sehat TRAUMA/PENYAKIT MENDADAK TERANCAM JIWA PENYELAMATAN

TAHAP LIFE SUPPORT
• BASIC LIFE SUPPORT • ADVANCED LIFE SUPPORT • PROLONGED LIFE SUPPORT

FLUID THERAPY .

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which results in cellular dysfunction and is caused by inadequate systemic oxygen delivery or impairment of cellular oxygen uptake. uptake. .SHOCK • Inadequate tissue perfusion along with cellular hypoxia and oxygen debt.

• 3. A progressive stage. A nonprogressive stage (compensated) • in which the normal circulatory mechanisms eventually cause full recovery without help from outside therapy • 2. An irreversible stage . the shock become steadily worse until death. in which. without therapy.Stages of Shock • 1.

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fluid losses. . dehydration. third spacing or other fluid losses. trauma.EVALUATION OF SYMPTOMS • HISTORY • In hypovolemic shock : blood loss.

History • In adult drop Systolic BP > 40 mmHg significant hypotension .

• agitation. clammy. warm. changes in pulmonary pressure . coma. • arrhythmia. combative behavior. angina. stupor • Skin changes • *Cool.General Symptoms of Shock • CNS changes • *Confusion. low high or normal • cardiac output. diaphoresis • Cardiovascular • *Increase or decrease heart rate.

decrease O2 saturation.General symptoms of shock • Pulmonary • *Increased RR. • increased pulmonary pressures. elevation in BUN and creatinine levels. decreased tidal volume. change in urine electrolyte levels .tidal CO2. increase or decrease in • endend . • respiratory failure. • decreased FRC • RENAL • *Decreased urine output.

• arrhythmia • Haematologic : bone marrow suppression. platelet • dysfunction . cytokine release • Cardiovascular : circulatory failure. formation of micro • vascular shunts. • depression of cardiovascular function. • coagulopathy. coagulopathy . DIC.Common effects of shock on organs • Systemic : Capillary leak.

insulin • resistance. elevation of • liver enzyme levels. mitochondrial dysfunction. coagulopathy • Neuroendocrine : change in mental status. change in urine • electrolyte levels. elevation of BUN • and creatinine levels • Cellular : cell cell-to to-cell dehiscence.. • Hepatic : liver insufficiency. thyroid dysfunction • Renal : renal insufficiency. cellular • swelling. • adrenal suppression. • cellular leak .

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increase SVR • Echo :decreased :decreased rightright-sided filling. decreased PCWP. diarrhea.Hypovolemic shock • Cause : depletion of fluid in the intravascular space (hemorrhage. dehydration. vomiting. capillary leak or a combination) combination) • SIRS capillary leak • Findings : decreased CO. decreased stroke volume. increase aortic diameter .

Perdarahan • • • • • Kehilangan akut darah dari sistim sirkulasi Estimated blood volume /EBV: * Adult : 7% BW –male 70 ml/kg female 65 ml/kg *Children : 88-9% BW .

.The Role of Fluids • Optimal organ function requires the twotwoway movement of substrates and cell products between the circulatory system and the cells themselves.

Kaen MG3 • Tutofusin OPS • 3. Hydroxy – • ethylethyl -starch.Crystall stalloid : Resus esusc cita itat tion fluid (Ringer • laktat. Kaen 3B.C 2. Ringer asetat) • Maintenance fluid: • Kaen 3A. Gelatin.Classification of infus infusion ion fluids • 1.70.Dextrose/glukose/fruktose .C 3.Dextrose/glukose/fruktose solution • 2.Coll olloid : Dextran 40 . artificial blood .

Blood products : albumin. • combination • Triofusin. Aminoleban .Parenteral nutrition : carbohy arbohydrate drate. Aminofusin. SPPS. Aminofusin. FFP.Infusion Infus ion fluids • 4. • protein/amino protein/ amino acids • lipid. • cryoprecipitate . Triofusin E-1000.Parenteral 4. Lipovenous • 5.Blood 5. • Aminoleban. Triofusin .

Crystalloid • Expand the plasma volume by about 200 ml perper-liter infused diluting circulating proteins. plasma COP • Potentially harmful interstitial overhydration • Crystalloid need to be administered at volumes 3 to 55-folds greater than of (isooncotic (isooncotic) ) colloids to achieve comparable plasma volumes and resuscitation endpoints .

• The basis considerations: • 1.Substitute fluid loss or dehydration using crystalloid infusions • 3.Infusion management: A rational strategy • Two different therapies for two different diagnosis fluid substitution and fluid resuscitation.Replace volume loss or hypovolemia with colloidal tetrastarch solutions until normalization of the circulating blood volume .Save the endothelial glycocalyx from degradation due to hyperinfusion • 2.

Colloid • The intravascular COP after colloid infusion is influenced by baseline COP. the degree of hemodilution and the COP of the infused volume and its plasma retention. determined by the molecular weight distribution. • Albumin solutions are monodisperse (MW of 69 kDa kDa) ) • Gelatins are polydisperse and in excess of 75% of the molecules are to be smaller than the renal threshold of 30 kDa. . kDa .

polydisperse. • The greater of degree of substitution the greater the resistance of degradation prolongs the effectiveness of HES as a plasma expander • Colloid with a low COP50/COP10 ratio will be lost more rapidly from intravascular space • The resulting sealing effect may attenuate fluid extravasation independently of the COP by albumin. defined by degree of substitution and by MW. .Colloid • HydroxyHydroxy-ethylethyl-starch solutions is very polydisperse.

Hypotonic infusion • 5% dextrose increases ICF > ECF Replace Replace Normal Normal loss loss (IWL + urine) urine) ICF ICF 660 660 ml ml ISF ISF 255 255 ml ml Plasma Plasma 85 85 ml ml Cairan .

Infus Isotonic • Ringer’s acetate • Ringer’s lactate • Normal saline Replace acute/ abnormal loss RL 2liter/15 menit Plasma Plasma 200 ml increases ECF ICF ICF ISF ISF 800 ml .

Perdarahan • Mulai segera resusitasi cairan agressif agressif: : • Rule 3:1 untuk perdarahan akut • Pengobatan disesuaikan dengan respon pasien pada terapi awal .

20 > 30 sedikit Cemas Kristaloid ----------------------------------------------------------- • • • • • • • • • • .Tanda perdarahan • • Klas I Perdarahan ml Perdarahan (%BV) Nadi Tensi Tek Nadi (mmHg) Nafas Urine ml/jam SSP/status mental Penggantian cairan (hukum 3:1) (BB 70 Kg) sampai 750 sampai 15% < 100 Normal Normal atau naik 14 .

Tanda perdarahan • • • • • • • • • • • Perdarahan ml Perdarahan (%BV) Nadi Tensi Tek Nadi (mmHg) Nafas Urine ml/jam SSP/status mental Penggantian cairan (hukum 3:1) Klas II 750750 -1500 15-30% 15>100 Normal Turun 20-30 2020-30 20Cemas sedang Kristaloid • ----------------------------------------------------------- .

Tanda perdarahan • • • • • • • • • • • Perdarahan ml Perdarahan (%BV) Nadi Tensi Tek Nadi (mmHg) Nafas Urine ml/jam SSP/status mental Penggantian cairan (hukum 3:1) Klas III 15001500-2000 3030-40% > 120 Turun Turun 30 30-40 5-15 5Cemas gelisah Kristaloid & darah • ----------------------------------------------------------- .

Tanda perdarahan • • • • • • • • • Perdarahan ml Perdarahan (%BV) Nadi Tensi Tek Nadi (mmHg) Nafas Urine ml/jam SSP/status mental Klas IV >2000 >40% >140 turun turun >35 tak ada gelisah/letargi kristaloid & darah • ----------------------------------------------------------- • Penggantian cairan • (hukum 3:1) .

Perdarahan bermakna perlu konsultasi BEDAH • . .

Keputusan Pengobatan • Respon pasien pada resusitasi cairan merupakan penentu terapi berikutnya • INGAT • Bedakan antara “hemodinamik stabil” dan “hemodinamik normal” .

Keputusan Terapi • • • • • Respon cepat *< 20% perdarahan *Stabil : respon pada penggantian cairan *Lanjutkan monitor *Evaluasi dan konsultasi bedah .

Keputusan Terapi • • • • • • • Respon transient 20 20-40% perdarahan Tidak stabil : memburuk setelah terapi cairan awal Lanjutkan cairan dan darah Evaluasi dan konsultasi bedah Perdarahan berlanjut : operasi .

hemorrhagik Operasi segera .Keputusan terapi • • • • • • Tak ada respon (minimal) > 40% perdarahan Tak ada respon pada terapi cairan Singkirkan kemungkinan shock nonnon .

Diagnosis & pengobatan • Pitfalls • • • • • • *Tensi tidak sama dengan cardiac output *Umur *Atlit *Hipotermi *Pengobatan *Pacu Pacu-jantung .

Differential Diagnosis • • • • Distributive shock Hypovolemic shock Obstructive shock Cardiogenic shock .

hyperglycemia) • Capillary leak and third spacing (burns.DD • Hypovolemic shock • Dehydration (low fluid intake. sweating or diabetes insipidus) insipidus) • Diuresis (diuretics. diarrhea. bowel obstruction. surgical stress) • Hemorrhage (trauma . GIT bleeding. etc) • Anemia . fractures. sepsis. vascular injuries. ectopic pregnancy. pancreatitis.

Secure the airway and on mechanical ventilation if necessary highhigh-flow oxygenation oxygen saturation > 92% & PaO2 > 60 • Put 3.Management and Therapy • The basic goal of shock therapy is the restoration of effective perfusion to vital organs and tissue before the onset of cellular injury.bore i. • Basic resuscitation : • 1.Foley catheter .Rapid placement of a large large.v line or a highhigh -flow central line as a route for fluid resuscitation • 2.

000 • + thrombocyte • Massive red blood cell transfusion microfilter • .• Fluid resuscitation • 2/3 crystalloid + 1/3 colloid • Loss of blood volume: • > 25% erythrocyte concentration • > 60% 4 erythrocyte concentration • + FFP • > 80% polytransfusion + AT < 50.

.• . Diagnose and treat underlying cause concomittantly.

lactate. creatinine BGA & pH. coagulation parameter Transaminases.• • • • • • Laboratory: Crossmatching Hb/Hct/AT Electrolyte. albumin .

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General goals for support of shock patients • • • • Hemodynamic support MAP > 6060-65 mmHg PCWP= 1515-18 mmHg Cardiac index > 2. or hemorrhagic shock . traumatic.0 L/min per m2 body surface area for septic.1 L/min per m2 of body surface area for cardiogenic and obstructive shock • Cardiac index > 4.

General goals • Optimization of oxygen delivery Hb level > 10 g/dl Arterial oxygen saturation > 92% • Reversal of organ system dysfunction • Maintain urine output > 0.5 ml/kg per hour .

A Fluid Challenge • A diagnostic intervention designed to give an indication of whether a patient with hemodynamic compromise will benefit from further fluid replacement • To administer a prepre-determined volume of iv fluid over a short period of time while measuring a change in the patient’s cardiovascular parameters .

• The aim: • To differentiate hypovolemia. which might improve with further fluid. from cardiac failure or a full intravascular volume in which case further fluid will not improve things and may cause deterioration . or relative hypovolemia.

5 l/min/m2 Systolic BP < 90 mmHg HR > 120 bpm Oliguria (urine output < 2525-30 ml/hr) Lactic acidosis Oxygen delivery < 600 ml/min/m2 Cool extremities The need for vasoactive drug Pulmonary arteri occlusive pressure (PAOP) < 18 mmHg .5-3.5<2.Indication fluid challenge • • • • • • • • • Cardiac index <2.

• The Surviving Sepsis Resuscitation Bundle recommends: 1000 ml crystalloid or 300300-500 ml of colloid over 30 minutes. • In ICU : 250 ml colloid run 55-10 minutes .

WAIT & reassess Following fluid challenge increase 33-5 Increase 33-7 WAIT & reassess Following fluid challenge increase < 3 Increase < 3 Safe to repeat fluid bolus if indicated ----------------------------------------------------------------------------------------------------- .Protocol ----------------------------------------------------------------------------------------------------CVP PAOP ACTION mmHg mmHg ----------------------------------------------------------------------------------------------------During fluid challenge increase > 5 Increase > 7 Stop infusion.

drain.Balans Cairan • Tiap pemberian cairan harus dibuat balans cairan: tiap 6 atau 8 jam. muntah/NGT. IWL (insensibel water loss) . dihitung total tiap 24 jam. • Semua cairan masuk dihitung: oral dan infus • Setiap cairan keluar dihitung: urine. diare.

Avoid / prevent tissue injury 4. ABC 2. Collaboration to allied surgeon . Restored tissue oxygenation 3.• • • • • • Fluid resuscitation in traumatic shock: shock: 1. Monitor vital sign 5.

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