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Shock and its treatment Jozsef Stankovics Department of Paediatrics, Medical University of Pécs 2008.
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What is shock after all? circulatory failure? cardiac insufficiency? low blood pressure? etc.
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Practical definition of shock A frightened look on a doctor's face: we have a low blood pressure here, call someone to help me…..
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Scientific definition of shock Is a condition where the perfusion of organs is too low to meet the metabolic demands and leads to anaerobic metabolism
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The simple truth of shock VO 2 > DO 2 VO 2 = oxygen consumption DO 2 = oxygen delivery
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The basic triad of life functioning brain stem functioning respiratory system functioning circulatory system
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Causes of shock I. Cardiogenic Shock Causes low contractility valve malfunction heart rate disturbances: too fast too slow arrhythmias
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Causes of shock II. Obstructive Shock Causes Tension pneumothorax Massive pulmonary embolism Cardiac tamponade HOCM
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Causes of shock III. Distributive Shock Inappropriate vasodilatation of peripheral blood vessels Causes Septic shock Neurogenic shock Anaphylaxis Adrenal insufficiency High output failure (fistula, pregnancy)
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Causes of shock IV. Hypovolemic Shock Excessive blood loss (trauma) Excessive plasma loss (burn) Excessive fluid loss (diarrhea, vomiting)
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Stages of shock Stages of shock - 1st and 2nd stages 1st stage = Initial phase. The CO is insufficient to meet the metabolic needs of the body but not low enough to produce symptoms (patient is anxious with tachypnoe). 2nd stage = Compensatory stage. Due to catecholamine release BP is normal/slightly reduced, but patient will have : Increased HR. Increase CO. Vasoconstriction (cold periphery)
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Stages of shock 3 rd stage = Progressive stage. Unfavorable signs & symptoms more apparent Progressive fall in BP despite Thx. Persistent tachycardia Oliguria. MOF Shock to be reversed at this time, otherwise death results.
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Stages of shock 4 th stage = Irreversible Stage During this stage despite all efforts the outcome is death resistant myocardial depression resistant capillary dilation/leak blood remains pooled in the extremities irreversible intracellular destruction
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Clinical approach to assess tissue perfusion Pulse Pressure Perfusion Periphery (CRT < 2”) Pee ( 1 ml/kg/hr)
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Physiologic approach to assess tissue perfusion DO2 = CO x 10 [(1.34 x Hb x SaO2) + (0.003 x PaO2)] ≈ CO x 13 x Hb x SaO2 VO2 ≈ CO x Hb x 13 x (SaO2 – SvO2) O2ER = (VO2 / DO2) x 100
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Treatment of shock Increase DO 2 Decrease VO 2 Then have a nice day
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Treatment of shock A B C as always
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How to increase DO 2 Perfusion: MAP – CVP MAP: CO X SVR CO: SV X Fr SV: preload, contractility, valve function
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Practical approach I. SVR is low (few instances), extremities are warm: sepsis anaphylaxis spinal cord injury vasodilator drugs → volume resuscitation, use of vasoconstrictors
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Practical approach II. SVR is high: cold extremities → CO is low: -preload ≈ CVP (fill up) -contractility (inotropes) -afterload („inodilatatores”) -treat rhythm abnormalities
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Volume replacement (≈ to manage CVP) crystalloid (normal saline or RL) colloid (gelatin or starch) human albumin (not preferred) blood (volumetric effect with increased O 2 delivery !!!) for sure: 20 ml/kg/20 min, until CVP is normalized
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Medical treatment ( to manage contractility and SVR) Drug Receptor CO SVR Dose Range Epinephrine ↑↑↑ 0.02 – 0.5 Norepinephrine 0 - ↑↑↑↑ 0.05 – 0.5 Dopamine DR ↑↑ 2 -12 Dobutamine ↑↑↑ 2 - 12 Dopexamine DR ↑↑ 0 - ↑ 0.9 - 5 VasopressinAngiotensin III 0 - 5 - 20 AmrinonePDI 5 -10 ( g/kg/min)
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How to lower VO2 ? O 2 supplementation pain management sedation temperature control mechanical ventilation (early consideration after 2-3 fluid boluses)
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Protocol for Early Goal Directed Therapy in the ED: (Adapted from NEJM 2001; 345:1368-77, in which patients receiving this goal directly therapy had improved in-hospital mortality compared to those with “standard” therapy, 31% to 47%.)
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