Shock and its treatment Jozsef Stankovics Department of Paediatrics, Medical University of Pécs 2008.

What is shock after all? circulatory failure? cardiac insufficiency? low blood pressure? etc.

Practical definition of shock A frightened look on a doctor's face: we have a low blood pressure here, call someone to help me…..

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

The simple truth of shock VO 2 > DO 2 VO 2 = oxygen consumption DO 2 = oxygen delivery

The basic triad of life functioning brain stem functioning respiratory system functioning circulatory system

Causes of shock I. Cardiogenic Shock Causes low contractility valve malfunction heart rate disturbances: too fast too slow arrhythmias

Causes of shock II. Obstructive Shock Causes Tension pneumothorax Massive pulmonary embolism Cardiac tamponade HOCM

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)

Causes of shock IV. Hypovolemic Shock Excessive blood loss (trauma) Excessive plasma loss (burn) Excessive fluid loss (diarrhea, vomiting)

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)

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.

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

Clinical approach to assess tissue perfusion Pulse Pressure Perfusion Periphery (CRT < 2”) Pee ( 1 ml/kg/hr)

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

Treatment of shock Increase DO 2 Decrease VO 2 Then have a nice day

Treatment of shock A B C as always

How to increase DO 2 Perfusion: MAP – CVP MAP: CO X SVR CO: SV X Fr SV: preload, contractility, valve function

Practical approach I. SVR is low (few instances), extremities are warm: sepsis anaphylaxis spinal cord injury vasodilator drugs → volume resuscitation, use of vasoconstrictors

Practical approach II. SVR is high: cold extremities → CO is low: -preload ≈ CVP (fill up) -contractility (inotropes) -afterload („inodilatatores”) -treat rhythm abnormalities

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

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  ↑↑ Dobutamine     ↑↑↑ Dopexamine      DR ↑↑ 0 - ↑ VasopressinAngiotensin III 0 -  AmrinonePDI  (  g/kg/min)

How to lower VO2 ? O 2 supplementation pain management sedation temperature control mechanical ventilation (early consideration after 2-3 fluid boluses)

Protocol for Early Goal Directed Therapy in the ED: (Adapted from NEJM 2001; 345: , in which patients receiving this goal directly therapy had improved in-hospital mortality compared to those with “standard” therapy, 31% to 47%.)