1. SHOCK By : O. Ahmadi, MD. Professor Assistant of Esfahan medical School, Emergency Department of Al-Zahra Hospital

2.  Shock is defined as circulatory insufficiency that creates an imbalance between tissue oxygen supply and oxygen demand  Nutrient requirements are not fulfilled  Toxic metabolites are not removed  If untreated, inevitable progression from inadequate perfusion to organ dysfunction and ultimately to death

3. Shock is classified into four categories by etiology (1)Hypovolemic (caused by inadequate circulating volume) (2) Cardiogenic (caused by inadequate cardiac pump function) (3) Distributive (caused by peripheral vasodilatation and maldistribution of blood flow) (4) Obstructive (caused by extra cardiac obstruction to blood flow)

4. Effect of cytokine exposure, arterial hypotension, and acidosis on cardiac function can be generalized Indirectly depressed in shock conditions by coronary hypotension The contribution of acidosis to depressed heart function is probably minimal

5. Hemorrhagic Shock Rapid reduction in blood volume Baroreceptor activation Vasoconstriction Strength of cardiac contraction Heart rate

6. The first clinical manifestations of hemorrhage are tachycardia, then a slight increase in the diastolic BP Causing the pulse pressure (difference between systolic and diastolic BP) to narrow.

7. The base deficit is defined as the amount of strong base that would have to be added to 1 L of blood to normalize the pH. Distinguish simple hemorrhage from hemorrhagic shock occurs when the base deficit worsens (the total body base deficit increases)

8. Arterial hypotension Systolic arterial BP less than 90 mm Hg Systolic arterial BP less than 100 mm Hg in patients with known systemic hypertension and in patients older than age 60 years The second phase of organ injury from hemorrhagic shock occurs during resuscitation

9. Septic shock Septic shock causes three major effects that must be addressed during resuscitation: Hypovolemia, Cardiovascular depression, and Induction of systemic inflammation More recently the incidence of gram-positive infections has increased to a frequency equal to that of gram-negative infections Hypoxemia is more severe with septic shock than hemorrhagic shock

10. Cardiogenic Shock Results when more than 40% of the myocardium becomes necrosed from ischemia Severe left ventricular dysfunction is evident on echocardiography early in the course of cardiogenic shock

11. Anaphylactic Shock IgE-mediated systemic response to an allergen IgE mast cells to release histamine vascular smooth muscle relaxation + bronchial smooth muscle constriction + capillary leak of plasma into interstitial spaces

12. Platelets PAF peripheral vasodilation + bronchial constriction + pulmonary arterial and coronary vasoconstriction PAF an important mediator of anaphylaxis that is refractory to antihistamine treatments.

13. CLINICAL FEATURES Shock can be strongly supported by the presence of a worsening base deficit or lactic acidosis Arterial BP as a sole measurement remains an unreliable marker of circulatory status The HR-to-systolic BP ratio (a normal ratio is less than 0.8 )

14. Excellent indicator of organ perfusion Urine output Measuring urine output requires at least 30 minutes, however, to determine accurately if output is normal (>1mL/kg/hr), reduced (0.5 to 1 mL/kg/hr), or severely reduced (<0.5 mL/kg/hr)

15. 1-Empiric Criteria for Diagnosis of Circulatory Shock Ill appearance or altered mental status Heart rate >100 beats/min Respiratory rate >22 breaths/min or PaCO2 <32 mm Hg Arterial base deficit 4 mM/L Urine output <0.5 mL/kg/hr Arterial hypotension >20 minutes duration Regardless of cause. Four criteria should be met

16. 2-Classify the cause of shock

18. Rectal temperature should be performed on every patient with suspected shock. A hemoglobin level less than 8 g/dL strongly suggests the need for blood transfusion if other criteria for shock are present Some emergency departments have bedside ultrasound capability, and cardiac and abdominal scanning can be performed rapidly at the bedside

19. Septic Shock Systemic inflammatory response syndrome (SIRS) Two or more of the following: 1. Temperature >38° C or 90 beats/min 3. Respiratory rate >20 breaths/min or PaCO2 12,000/mm3, 10% band neutrophilia Sepsis syndrome SIRS associated with organ dysfunction or hypotension; organ dysfunction may include presence of lactic acidosis, oliguria, or altered mental status Septic shock SIRS with hypotension despite adequate fluid resuscitation; septic shock should still be diagnosed if vasopressor therapy has normalized blood pressure

20. Hemorrhagic Shock Simple hemorrhage Suspected bleeding with pulse <100 beats/min, normal respiratory rate, normal blood pressure, and normal base deficit Hemorrhage with hypoperfusion Suspected bleeding with base deficit 100 beats/min Hemorrhagic shock Suspected bleeding with at least four criteria

21. Cardiogenic Shock Cardiac failure Clinical evidence of impaired forward flow of the heart presence of dyspnea, tachycardia, pulmonary rales, peripheral edema, or cyanosis Cardiogenic shock Cardiac failure plus four criteria

22. Goal-directed therapy

23. Resuscitation should continue until the lactate concentration decreases to less than 2 mM/L

24. Hemorrhagic Shock Ensure adequate ventilation/oxygenation Provide immediate control of hemorrhage, when possible (e.g., traction for long bone fractures, direct pressure) Initiate judicious infusion of lactated Ringer's solution (10-20 mL/kg) or 5% hydroxyethyl starch (5 mL/kg) With evidence of poor organ perfusion and 30-minute anticipated delay to hemorrhage control, begin packed red blood cell (PRBC) infusion (5-10 mL/kg) With suspected central nervous system trauma or Glasgow Coma Scale score <9, immediate PRBC transfusion may be preferable as initial resuscitation fluid Treat severe acidosis (pH <6.8) Treat coincident dysrhythmias (e.g., atrial fibrillation with synchronized cardioversion)

25. Cardiogenic Shock Ameliorate increased work of breathing; provide oxygen and positive end-expiratory pressure (PEEP) for pulmonary edema Begin inotropic support; dobutamine(5µg/kg/min) is common empiric agent Seek to reverse the insult (e.g., initiate thrombolysis, arrange percutaneous transluminal angioplasty, or administer charcoal for drug overdose) Consider intra-aortic balloon pump counterpulsation for refractory shock

26. Septic Shock Ensure adequate oxygenation; remove work of breathing. Administer 20 mL/kg of crystalloid or 5 mL/kg of colloid, and titrate infusion to adequate urine output Begin antimicrobial therapy; attempt surgical drainage or debridement If volume restoration fails to improve organ perfusion, begin vasopressor support; initial choice includes dopamine, infused at 5-15µg/kg/min, or norepinephrine, infused at 0.1-1µg/kg/min

27. Anaphylactic Shock Control airway and ventilation Administer 10-20 mL/kg of crystalloid Test an intravenous bolus of epinephrine (50- 100µg), then mix 5 mg of epinephrine in 500 mL of normal saline. Begin infusion at 10 cc/hr, and titrate to arterial blood pressure response Administer 5-10 mg/kg of hydrocortisone or 1-2 mg/kg of methylprednisolone