shock

1. Shock Gordon R. Bernard, M.D. Division of Allergy, Pulmonary, and Critical Care Medicine Vanderbilt University

2. Overall Objectives Understand the pathophysiology of shock Know the types of shock and how they differ Understand the therapeutic approaches to shock

3. Definition (Gross, 1882) �A manifestation of the rude unhinging of the machinery of life.� (Guyton, 1966) �An abnormal state of the circulation in which cardiac output is reduced enough that the tissues of the body are damaged from lack of blood flow.�

4. Types of Shock Hypovolemic Loss of blood or plasma Cardiogenic Myocardial infarction Cardiac trauma Distributive e.g., septic shock Obstructive Pulmonary embolism

5. Arterial Resistance Controlled by: a) Arteriolar tone b) Precapillary sphincter Control capillary hydrostatic pressure c) Postcapillary sphincter

7. Factors Causing Reduced Cardiac Output A. Reduced venous return Hypovolemic shock Endotoxic shock Anaphylactic shock Obstruction to venous return B. Reduced pumping ability Cardiogenic shock

8. Hemorrhagic shock Due to volume loss: Blood Plasma Fluid/electrolyte

9. 10% of blood volume can be lost with minimal hemodynamic effects. 20% loss followed by initiation of BP reduction. Sympathetic activity increases. Vasoconstriction occurs (cerebral and coronary circulation protected).

10. CORRELATION OF MAGNITUDE OF VOLUME DEFICIT AND CLINICAL PRESENTATION

11. Clinical Features Sensorium Anxiety to obtundation Weakness or prostration Pallor Sweating Tachycardia Thready pulse Hypotension Tachypnea

12. Hypovolemic Shock

13. Laboratory Changes Hematocrit - No change until dilution occurs Blood Gas Studies: Indicate degree of acid-base disturbance and lactic acidosis (anaerobic metabolism) Electrolytes and Renal Function Tests: Important baseline information Blood - Type and crossmatch Urine Output - Monitor continuously

14. Time Required for Blood Typing Procedures

15. Compensatory Mechanisms To maintain perfusion pressure Sympathetic discharge Catecholamines increase Heart rate and contractility increased Afferent arterioles in vascular beds constrict Peripheral resistance Venous capacitance vessels constricted Increase in venous return

16. Aim is to effectively perfuse coronary and carotid arteries. Catecholamines produce greater contraction of precapillary sphincter than postcapillary sphincter. Therefore, cappilary hydrostatic pressure is reduced. In early stages of shock this is important in pulling fluid into the intravascular space and increasing blood volume (Hct reduced).

17. Overall Effect: Constriction of arterioles and venules Increase in central blood volume Increase in cardiac output (circulates the available blood more rapidly) Draws interstitial fluid into intravascular space

18. Sympathetic Discharge Negative effects if sustained Sludging of blood Disseminated intravascular coagulation Profound acidosis Tissue hypoxia-cell death Acidosis, metabolites and hypoxia relax precapillary sphincter more than post capillary sphincter.

19. Late Shock Postcapillary sphincter resistance greater than precapillary Therefore, hydrostatic pressure increased Interstitial edema produced

20. Capillary Injury Important part of the shock process Maybe due to: Increased platelet adhesiveness Release of vasoactive materials Leads to further loss of plasma volume. Also, if in pulmonary bed may contribute to shock lung.

21. Shock Lung (ARDS) Pulmonary edema Alveolar hemorrhage Pulmonary vascular congestion Loss of surfactant Increased lymph flow

22. Hypovolemic Shock Control bleeding Establish and maintain airway + O2 Assist ventilation (if necessary) Replace volume Acid-base correction

23. Fluids Any fluid can improve perfusion, at least temporarily Only RBC�s carry oxygen

24. Fluids Crystalloids (electrolyte solutions) Colloids (large molecular weight) Red blood cells

25. Selection of Replacement Fluid Electrolyte solutions (crystalloids) Rapidly escape from intravascular space into the interstitium. Therefore, short-lived volume expansion.

26. Colloids (large molecules) Increase plasma onocotic pressure Draw fluid into plasma space Remain in circulation longer than crystalloids Raise interstitial onocotic pressure May cause pulmonary edema

27. Colloid vs Crystalloid Controversy

28. Cardiogenic Shock Myocardial infarction Rhythm disturbance

29. Cardiogenic Shock Systolic BP < 80 mm Cardiac Index < 2.1 liters/min/m2 Urinary output < 20 ml/hr Reduced cerebral perfusion (Confusion Obtundation)

30. Cardiogenic Shock Incidence 15% of M.I. Mortality 70-90% Usually > 40% of left ventricle infarcted

31. Potentially Repairable Lesions Ruptured chordae tendinae Intraventricular septal defects

32. Cardiogenic Shock

33. Dobutamine �1 Stimulant Mainly inotropic effects Probably drug of choice in cardiogenic shock

34. Septic Shock Endotoxin or other mediator release Activation of vasoactive kinins Activation of intrinsic coagulation system Increasing capillary permeability Decreased peripheral vascular resistance Disseminated intravascular coagulation Mortality 40-50%

35. Hemodynamics: Peripheral resistance fails C.O. and HR rise (but not enough) BP falls

36. Therapy for Septic Shock General supportive measures Specific antibacterial therapy Corticosteroids? Activated protein C

37. Recent Randomized Studies Suggest:

38. Treatment of Shock

39. Vasoconstrictors Phenylephrine Vasoconstricts Elevates blood pressure but increases myocardial work Decrease cardiac output Decrease tissue perfusion Rarely used except in anesthesia for management of drug induced vasodilation

40. Dopamine

41. Vasopressin in Septic Shock Redistributes blood flow Away from muscle, skin, gut To brain and heart High dose: coronary vasoconstriction Antidiuretic effect Inexpensive No proven effect on ultimate outcome

42. BP and Vasopressin Levels After AVP for Septic Shock

44. Primary Analysis: 28-Day All-Cause Mortality