2. Slide 2 Section of Critical Care Medicine Section of Infectious Diseases University of Manitoba, Winnipeg, Canada UMDNJ-Robert Wood Johnson Medical School Cooper Hospital, NJ Anand Kumar, MD SHOCK Classification and Approach to Management

3. Slide 3 Shock Cardiogenic Shock -a major component of the mortality associated with cardiovascular disease Hypovolemic Shock -the major contributor to early mortality from trauma Septic Shock -most common cause of death in American ICUs

4. Slide 4 Definition Kumar and Parrillo (1995): “the state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then if prolonged, to irreversible cellular injury”

5. Slide 5 Shock: Classification Hypovolemic Shock -due to decreased circulating blood volume Cardiogenic Shock -due to cardiac pump failure related to loss of myocardial contractility/functional myocardium or structural/mechanical failure Extra-cardiac Obstructive Shock -due to obstruction to flow in the cardiovascular circuit Distributive Shock -caused by loss of vasomotor control

6. Slide 6 Shock Hemodynamics CO SVR PWP EDV hypovolemic cardiogenic obstructive afterload preload distributive pre-resusc post-resusc

7. Slide 7 Classification of Shock Hypovolemic CardiogenicExtracardiac ObstructiveDistributive (e.g. Hemorrhage) Preload Diastolic filling (e.g. Myocardial infarction) Myocardial damage Systolic and diastolic function Diastolic filling (e.g. tension pneumothorax or pericardial tamponade) Diastolic functionSystolic function Ventricular afterload (e.g. massive pulmonary embolus) Preload ( Diastolic filling) ( Systolic and Diastolic function) (e.g. septic) Myocardial depression CO ( SVR) MAP Shock MODS Maldistribution of flow SVR ( CO) CO = cardiac output; SVR = systemic vascular resistance; MAP = mean arterial blood pressure; MODS = multiple organ dysfunction syndrome. Kumar and Parrillo, 2001

8. Slide 8 Hypovolemic Shock degree of volume loss response –10% well tolerated (tachycardia) –20-25% failure of compensatory mechanisms (hypotension, orthostasis, decreased CO) –>40% loss associated with overt shock (marked hypotension, decreased CO, lactic acidemia)

9. Slide 9 Hypovolemic Shock rate of volume loss and pre-existing cardiac reserve response acute 1 L blood loss results in mild to moderate hypotension with decreased CVP and PWP

10. Slide 10 Cardiogenic Shock #1 cause of in-hospital mortality from Q-wave MI requires at least 40% loss of functional myocardium usually involves left main or left anterior descending obstruction historically, incidence of cardiogenic shock post-Q wave MI has run 8-20%with mortality 70-90%

11. Slide 11 Cardiogenic Shock mortality substantially better for cardiogenic shock due to surgically remediable lesions –aortic valve failure –papillary muscle rupture ischemic form seen 3-7 days post-LAD territory infarct v wave of > 10 mm often seen in PWP trace –VSD (post-infarct, rarely traumatic) post-infarct seen 3-7 days post-LAD occlusion 5-10% oxygen saturation step-up

12. Slide 12 Obstructive Shock rate of development of obstruction to blood flow response –acute, massive PE involving 2 or more lobar arteries and 40-50% pulmonary bed can cause shock –acute cardiac tamponade can occur with 150 mL fluid but over 2L can be well tolerated if slow accumulation similar variability based on presence of pre-existing cardiopulmonary disease

13. Slide 13 Distributive Shock defining feature: loss of peripheral resistance dominantly septic shock, anaphylactic and neurogenic shock less common clinical form of shock with greatest contribution of other shock elements i.e., hypovolemia, cardiac failure

14. Slide 14 Compensatory Responses to Shock Maintain mean circulatory pressure Volume –Fluid redistribution to vascular space –Decrease Renal losses Pressure –Decreased venous capacitance Kumar and Parrillo, 2001

15. Slide 15 Compensatory Responses to Shock Maximize cardiac performance Increase contractility Redistribute perfusion Optimize oxygen unloading Kumar and Parrillo, 2001

16. Slide 16 hypovolemia intravascular volume sepsis venous capacitance venous pressure myocardial dysfunction (e.g. MI) cardiovascular obstruction (e.g. massive PE) renal perfusion stretch receptors right atrial pulmonary artery renal juxtaglomerular apparatus cardiac contractility vasoconstriction flow redistribution sympathetic response hormonal epinepherine norepinephrine renin/angiotensin aldosterone Na/H 2 O retention cardiac contractility vasoconstriction flow redistribution cardiovascular stress circulatory shock ( MAP) baroreceptors aortic arch, carotid body vascular chemoreceptors carotid, aorta medullary chemoreceptor CNS pituitary response neural ACTH/ADH cortisol aldosterone Na retention maintain cardiovascular catecholamine responsiveness Kumar and Parrillo, 2001

17. Slide 17 ORGAN SYSTEM DYSFUNCTION CNSEncephalopathy (ischemic or septic) Cortical necrosis HeartTachycardia, bradycardia Supraventricular tachycardia Ventricular ectopy Myocardial ischemia Myocardial depression PulmonaryAcute respiratory failure Adult respiratory distress syndrome (ARDS) KidneyPrerenal failure Acute tubular necrosis GIIleus Erosive gastritis Pancreatitis Acalculous cholecystitis Colonic submucosal hemorrhage Transluminal translocation of acteria/endotoxin ORGAN SYSTEM MANIFESTATIONS Kumar and Parrillo, 2001

18. Slide 18 Organ System Dysfunction LiverIschemic hepatitis “Shock” liver Intrahepatic cholestasis HematologicDisseminated intravascular coagulation Dilutional thrombocytopenia MetabolicHyperglycemia Glycogenolysis Gluconeogenesis Hypoglycemia (late) Hypertriglyceridemia Immune SystemGut barrier function depression Cellular immune depression Humoral immune depression ORGAN SYSTEMMANIFESTATIONS Kumar and Parrillo, 2001

19. Slide 19 Shock Suspected Hypotension Tachycardia Peripheral hypoperfusion Oliguria Encephalopathy DIAGNOSTIC THERAPEUTIC Clinical Approach to Diagnosis and Management

20. Slide 20 Diagnosis and Evaluation Clinical Signs –primary diagnosis –differential Dx

21. Slide 21 Diagnosis and Evaluation Laboratory –Hgb, WBC, platelets –PT/PTT –Electrolytes, arterial blood gases –BUN, Cr –Ca, Mg –serum lactate –ECG

22. Slide 22 Clinical Approach to Diagnosis and Management Initial Diagnostic Steps CXR abdominal views* CT scan abdomen or chest* echocardiogram* pulmonary perfusion scan*

23. Slide 23 Diagnosis and Evaluation Invasive Monitoring –arterial pressure catheter –CVP monitoring –ScvO2

24. Slide 24 Clinical Approach to Diagnosis and Management Admit to Intensive Care Unit (ICU) Venous access Central venous catheter Arterial catheter EKG monitoring Pulse oximetry Hemodynamic support (MAP <60 mmHg)

25. Slide 25 Clinical Approach to Diagnosis and Management Diagnosis Remains Undefined or Hemodynamic Status Requires Repeated Fluid Challenges of Vasopressors Pulmonary Artery Catheterization Echocardiography

26. Slide 26 Diagnosis Using Pulmonary Artery Catheterization Pulmonary Artery Cardiac Miscellaneous Diagnosis Occlusion Pressure Output Comments Cardiogenic Shock Cardiogenic shock  Usually occurs with due to myocardial evidence of extensive dysfunction myocardial infarction (40% of LV infarcted), severe cardiomyopathy, or myocarditis. Cardiogenic shock due to a mechanical defect Acute VSD  LVCO  Predominant shunt is  and RVCO left to right, pulmonary >LVCOblood flow is greater than systemic blood flow: oxygen “step-up” occurs at RV level. Kumar and Parrillo, 2001

27. Slide 27 Diagnosis Using Pulmonary Artery Catheterization Pulmonary Artery Cardiac Miscellaneous Diagnosis Occlusion Pressure Output Comments Cardiogenic Shock Acute mitral  ForwardV waves in pulmonary regurgitation CO  artery occlusion pressure tracing. Right ventricular Normal or  Elevated RA and RV filling infarction pressures with low or normal pulmonary artery occlusion pressures. Extracardiac obstructive forms of shock Pericardial  or  RA mean, RV end- tamponade diastolic, pulmonary artery occlusion mean pressures are elevated and within 5 mmHg of one another. Kumar and Parrillo, 2001

28. Slide 28 Diagnosis Using Pulmonary Artery Catheterization Pulmonary Artery Cardiac Miscellaneous Diagnosis Occlusion Pressure Output Comments Extracardiac obstructive forms of shock Massive pulmonary Normal or   Usual finding is embolism elevated right-sided pressures. Hypovolemic shock  Distributive forms of shock Septic shock  or normal  or normal, Pre-resuscitation rarely  cardiac output is Anaphylactic  or normal  or normal decreased shock Kumar and Parrillo, 2001

29. Slide 29 Clinical Approach to Diagnosis and Management Immediate Goals in Shock Hemodynamic support MAP >60mmHg PAOP = 12-18 mmHg Cardiac Index >2.2 L/min/m 2 Maintain oxygen delivery Hemoglobin >9 g/dL Arterial saturation >92% Supplemental oxygen and mechanical ventilation Reversal of oxygen dysfunction Decreasing lactate (<2.2 mM/L) Maintain urine output Reverse encephalopathy Improving renal, liver function tests MAP = mean arterial pressure; PAOP = pulmonary artery occlusion pressure.

30. Slide 30 Clinical Approach to Diagnosis and Management Hypovolemic Shock Rapid replacement of blood, colloid orcrystalloid Identify source of blood or fluid loss

31. Slide 31 Clinical Approach to Diagnosis and Management Cardiogenic Shock RV infarction –fluid and inotropes with PA catheter monitoring Mechanical abnormality

32. Slide 32 Results of Current Therapy Inotropic support 90 + Thrombolysis80-90 + IABP 80 + CABG50-60 + PTCA if successful50-60 if unsuccessful80-90 Treatment In-hospital StrategyMortality Rate (%) From Klein L. W.: Intra-aortic balloon pumping. In Parrillo J.E., Bone R.C. (eds), Critical Care Medicine: Principles of diagnosis and management, St. Louis, 1995: Mosby.

33. Slide 33 Clinical Approach to Diagnosis and Management Extracardiac Obstructive Shock Pericardial tamponade

34. Slide 34 Courtesy of David Hunter, MD University of Minnesota

35. Slide 35 Clinical Approach to Diagnosis and Management Distributive Shock Septic shock - Identify site of infection and drain, if possible Goals: –SV02 >70% –improving organ function –decreasing lactate levels

36. Slide 36 Fluid Therapy Crystalloids Colloids Packed red blood cells Infuse to physiologic endpoints

37. Slide 37 Relative Potency: Vasopressors/Inotropes CARDIAC PERIPHERAL VASCULAR Agent Dose Heart Contractility Vasoconstriction Vasodilation Dopaminergic Rate Dopamine1-4 (  /k)/min1+1+01+4+ 4-20 (  g/kg)/min2+2-3+2-3+02+ Norepi2-20  g/min1+2+4+00 Dobutamine2-15 (  g/kg)/min 1-2+3-4+02+0 Isoproterenol 1-5  g/min4+4+04+0 Epinephrine1-20  g/min4+4+4+3+0 Phenylephrine20-200  g/min003+00 Vasopressin0.01-0.04 u/min004+00 Milrinone37.5-75  g/kg1+3+02+0 bolus; then 0.375- 0.75 ug/kg/min Kumar and Parrillo, 2001

38. Slide 38 Conclusion This concludes the presentation.