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Shock 2011
- 1. Eval & Rx of Shock Frank W Meissner, MD, RDMS FACP, FACC, FCCP, FASNC, CPHIMS, CCDS
- 2. Case Study 58 y/o male Day 1 S/P CABG Persistent Shock @ 18 hrs post CABG Shock developed about 8 hr after off-pump - Nursing followed post CABG protocols, but Doubutamine @ 12 mcg/kg/min & freq ectopy Hemodynamic parameters: RAP 4, PA 28/5, PAOP 10, C.O. 12 l/min, SVR 400, P 110, T 98.4°F, SVO2 85 Thoughts?
- 3. Hemodynamic profiles of shock states Physiologic Preload Pump function Afterload Tissue perfusion variable Cardiac output SVR MV O2Sat Clinical PCWP/PAOP Myocardial Myocardial pH measurement IVC Dimensions Contractility Contractility Lactic Acid Hypovolemic Cardiogenic Distributive
- 4. Introduction Definition: a physiologic state caused by inadequate tissue perfusion leading to decreased tissue oxygen delivery (DO2) & decreased tissue oxygen uptake (VO2) Not a blood pressure or an isolated vital sign abnormality A pattern of physiological dysfunction = inadequate tissue perfusion
- 5. Introduction Effects are initially reversible, but lead to cellular hypoxia with: Cell membrane and ion pump dysfunction Intracellular edema Leak intracellular contents into extracelluar space Dysregulation of intracellular pH
- 7. MOSF Rapid Progression to death Prompt recognition early syms key to survival
- 8. Prognosis Despite extensive research, mortality rates remain high in the published literature Septic: 35-40% Cardiogenic: 60-90% Hypovolemic: variable, depends on etiology and time to treatment
- 10. Stages: Pre-shock Warm or compensated shock Regulatory mechanisms are able to compensate for diminished perfusion.
- 12. Stages: Cold Shock Compensatory mechanisms become overwhelmed, resulting in: Tachycardia Tachypnea Metabolic acidosis Oilguria Cool, clammy skin High SVR
- 13. Stages: shock Usually occur with: Loss of 20-25% of effective blood volume Fall in cardiac index to 2.5 L/min/M2 Activation of mediators of the sepsis syndrome
- 14. Sepsis: end-organ dysfunction Decreasing urine output Restlessness =>agitation =>obtundation =>coma Mutiple organ system failure than death
- 15. Physiologic Determinants Systemic Vascular Resistance (SVR) Vessel length - or length of vessel bed Blood viscosity - incr Hgb => incr resistance Vessel diameter - majority of resistance in small arteriolar vessels (resistance vessels) - 450 to 100 µm SG definition = 80*[(MAP-MPAOP)/CO]
- 16. Physiologic determinants Cardiac Output (CO) = HR x SV Stroke volume ∫ (preload, myocardial contractility, afterload)
- 17. Pre-Load
- 18. Myocardial Contractility Slope of End-systolic pressure volume relationship = Emax or Ees independent measure of contractility
- 20. Newer Non-Invasive Hemodynamic Measures Systolic Pressure Variation (MaxSBP-MinSBP) Pulse Pressure Variation[(MaxArterialPulsePressure- MinArterialPulsePressure)/MeanArterialPulsePressure] Stroke Volume Variation [(MaxSV-MinSV)/MeanSV] Measurements made during one controlled vent breath If SPV>10, SVV>10%, PPV>13% => Volume Responsiveness
- 21. Do Hemodynamics Matter? Maybe NOT in Septic Shock
- 23. Physiologic Determinants SVR & CO can reliably differentiate shock states Assuming SVR is accurate
- 25. Hypovolemic shock #1 Cause of Death Worldwide Hemorrhage Trauma GI bleeding Ruptured aneurysm or hematoma Hemorrhagic pancreatitis Fractures
- 26. Hypovolemic shock Fluid loss Diarrhea Vomiting Heat stroke Inadequate repletion of insensible losses Burns
- 27. Cardiogenic shock 2ndary 2 pump failure & decreased cardiac output Main categories: Myopathies Arhythmia Mechanical Obstructive
- 28. Cardiogenic shock Cardiomyopathies: Infarction > 40% of LV mass RV infarction Dilated cardiomyopathies Stunned myocardium 2ndary prolonged ischemia or cardiopulmonary bypass
- 29. Cardiogenic shock Arrhythmia Lost synchrony of filling of atria & ventricles 2ndary atrial fibrillation (Atrial Kick) Complete loss of CO with ventricular fibrillation Symptomatic bradycardia & heart block with decrease in CO (CO = HR * SV)
- 30. Cardiogenic shock Mechanical Mitral regurgitation from chordae tendineae rupture Aortic insufficiency due to dissection of ascending aorta into the aortic valve ring Critical aortic stenosis
- 31. Cardiogenic shock Obstructive Pulmonary embolism Tension pneumothorax Constrictive pericarditis Pericardial tamponade Severe pulmonary hypertension
- 32. Distributive shock Causes: Sepsis Activation of systemic inflammatory response system (pancreatitis, burns, multiple trauma) Anaphylaxis Drug or toxin reactions (insect bites, transfusion reactions, heavy metal poisoning)
- 33. Distributive shock Causes: Addisonian crisis Myxedema coma Neurogenic shock 2ndary spinal cord trauma MI + SIRS Cardiopulmonary bypass
- 34. Common features Hypotension SBP < 90, MAP < 60 Occurs in most shock patients Initially relative to patient’s baseline blood pressure Drop in SBP > 40 early indicator Progresses profound hypotension, often requiring vasopressors
- 35. Common features Cool, clammy skin Regulatory processes compensate 4 decreased effective tissue perfusion Blood flow redirected to vital organs maintain coronary, cerebral and splanchnic perfusion Lack of peripheral flow leads to classic cool, clammy picture of shock
- 36. Common features Oliguria Result of shunting of renal bloodflow to other vital organs Objective measure of intravascular volume depletion Related signs: tachycardia, orthostatic hypotension, poor skin turgor, absent axillary sweat, dry mucous membranes
- 37. Common features Mental status changes Begins with agitation Progresses to confusion/delirium Ends in obtundation/coma
- 38. Common features Metabolic acidosis Initially unexplained respiratory alkalosis Acidosis eventually prevails Accumulation of lactate due to lack of clearance by liver, kidneys and skeletal muscle Increased anaerobic metabolism 2ndary tissue hypoxia in later stages
- 39. Initial approach History: Food/medicine allergies Recent medication changes Potential acute/chronic drug intoxication Preexisting diseases
- 40. Initial approach Physical exam: HEENT Scleral icterus Dry conjunctivae Dry mucous membranes Pinpoint pupils Fixed/dilated pupils
- 41. Initial approach Physical exam: Neck JVD Delayed carotid upstroke Carotid bruits Meningeal signs
- 42. Initial approach Physical exam: lungs Tachypnea Shallow respirations Crackles/rales Consolidation Egophony
- 43. Initial approach Physical exam: cardiovascular Arrhythmia Murmurs or S3 gallop Diffuse PMI Right or left ventricular heave
- 44. Initial approach Physical exam: Abdomen Tenseness Distension Tenderness Rebound/guarding Absent bowel sounds
- 45. Initial approach Physical exam: rectal Decreased tone Blood (hematochezia or melena)
- 46. Initial approach Physical exam: extremities Calf swelling/palpable cords Unequal pulses Disparity of blood pressure between upper extremities
- 47. Initial approach Physical exam: neurologic Agitation Confusion Delirium Obtundation
- 48. Initial approach Physical exam: skin Cold, clammy Warm, hyperemic Rashes Petechiae Urticara
- 49. Initial approach Lab evaluation CBC with manual differential Basic chemistries Liver function tests Amylase/lipase Fibrinogen & fibrin split products
- 50. Initial approach Lab evaluation ABG’s & SVO2 Toxicology screen Chest x-ray Abdominal x-ray
- 51. Factors influencing mixed & central venous SO2 75% _ + ↑VO2 ↓DO2 ↑ DO2 ↓VO2 Stress ↓ PaO2 ↑ PaO2 Hypothermia Pain ↓ Hb ↑ Hb Anesthesia Hyperthermia ↓ Cardiac output ↑ Cardiac output Shivering
- 52. Interp of SVO2 • Like the CO, a low SvO2 tells you something is wrong, but not what and what should be done (fluids? inotropes?). • If SvO2 is normal or high - in septic patients ScvO2 may be elevated 2ndary low O2 extraction
- 53. Insert CVP/SvcO2
- 54. Insert CVP/SvcO2 SvO2 >70%
- 55. Insert CVP/SvcO2 SvO2 >70% CVP N or low
- 56. Insert CVP/SvcO2 SvO2 >70% CVP N or low Sepsis?
- 57. Insert CVP/SvcO2 SvO2 >70% CVP N or low Sepsis? Repeat Fluid challenge 250ml/ 5mins
- 58. Insert CVP/SvcO2 SvO2 >70% CVP N or low Sepsis? Repeat Fluid challenge 250ml/ 5mins Haemodynamic improvement ?
- 59. Insert CVP/SvcO2 SvO2 >70% CVP N or low Sepsis? Repeat Fluid challenge 250ml/ 5mins Continue until normal values obtained Haemodynamic improvement ? Yes
- 60. Insert CVP/SvcO2 SvO2 >70% CVP N or low Sepsis? Repeat Fluid challenge 250ml/ 5mins Continue until normal values obtained Haemodynamic improvement ? Yes No Vasopressors
- 61. Insert CVP/SvcO2 SvO2 >70% SvO2 <70% CVP N or low Sepsis? Repeat Fluid challenge 250ml/ 5mins Continue until normal values obtained Haemodynamic improvement ? Yes No Vasopressors
- 62. Insert CVP/SvcO2 SvO2 >70% SvO2 <70% CVP low CVP N or low Sepsis? Repeat Fluid challenge 250ml/ 5mins Continue until normal values obtained Haemodynamic improvement ? Yes No Vasopressors
- 63. Insert CVP/SvcO2 SvO2 >70% SvO2 <70% CVP low CVP N or low Hypovolaemic/ Sepsis? Haemorrhagic/ cause? Repeat Fluid challenge 250ml/ 5mins Continue until normal values obtained Haemodynamic improvement ? Yes No Vasopressors
- 64. Insert CVP/SvcO2 SvO2 >70% SvO2 <70% CVP low CVP N or low Hypovolaemic/ Sepsis? Haemorrhagic/ cause? Repeat fluid Repeat Fluid challenge challenge (250ml/5mins) 250ml/ 5mins or transfusion if necessary. Continue until normal values obtained Haemodynamic improvement ? Yes No Vasopressors
- 65. Insert CVP/SvcO2 SvO2 >70% SvO2 <70% CVP low CVP N or low Hypovolaemic/ Sepsis? Haemorrhagic/ cause? Repeat fluid Repeat Fluid challenge challenge (250ml/5mins) 250ml/ 5mins or transfusion if necessary. Continue until normal values obtained Continue until normal Haemodynamic values obtained improvement ? Yes Haemodynamic No improvement Vasopressors
- 66. Insert CVP/SvcO2 SvO2 >70% SvO2 <70% CVP low CVP N or low Hypovolaemic/ Sepsis? Haemorrhagic/ cause? Repeat fluid Repeat Fluid challenge challenge (250ml/5mins) 250ml/ 5mins or transfusion if necessary. Continue until normal values obtained Continue until normal Haemodynamic values obtained improvement ? No response Yes Haemodynamic No improvement Vasopressors
- 67. Insert CVP/SvcO2 SvO2 >70% SvO2 <70% CVP low CVP N or low Hypovolaemic/ Sepsis? Haemorrhagic/ cause? Repeat fluid Repeat Fluid challenge challenge (250ml/5mins) 250ml/ 5mins or transfusion if necessary. Continue until normal values obtained Continue until normal Haemodynamic values obtained improvement ? No response Yes Haemodynamic No improvement Echocardiography that preceeds Vasopressors CO monitoring
- 68. Insert CVP/SvcO2 SvO2 >70% SvO2 <70% CVP high CVP low CVP N or low Hypovolaemic/ Sepsis? Haemorrhagic/ cause? Repeat fluid Repeat Fluid challenge challenge (250ml/5mins) 250ml/ 5mins or transfusion if necessary. Continue until normal values obtained Continue until normal Haemodynamic values obtained improvement ? No response Yes Haemodynamic No improvement Echocardiography that preceeds Vasopressors CO monitoring
- 69. Insert CVP/SvcO2 SvO2 >70% SvO2 <70% CVP high CVP low CVP N or low Hypovolaemic/ Sepsis? Consider global/right Haemorrhagic/ ventricular failure cause? Repeat fluid Repeat Fluid challenge challenge (250ml/5mins) 250ml/ 5mins or transfusion if necessary. Continue until normal values obtained Continue until normal Haemodynamic values obtained improvement ? No response Yes Haemodynamic No improvement Echocardiography that preceeds Vasopressors CO monitoring
- 70. Insert CVP/SvcO2 SvO2 >70% SvO2 <70% CVP high CVP low CVP N or low Hypovolaemic/ Sepsis? Consider global/right Haemorrhagic/ ventricular failure cause? Repeat fluid Repeat Fluid challenge challenge Echocardiography that preceeds (250ml/5mins) 250ml/ 5mins cardiac output monitoring or transfusion if necessary. Continue until normal values obtained Continue until normal Haemodynamic values obtained improvement ? No response Yes Haemodynamic No improvement Echocardiography that preceeds Vasopressors CO monitoring
- 71. Insert CVP/SvcO2 SvO2 >70% SvO2 <70% CVP high CVP low CVP N or low Hypovolaemic/ Sepsis? Consider global/right Haemorrhagic/ ventricular failure cause? Repeat fluid Repeat Fluid challenge challenge Echocardiography that preceeds (250ml/5mins) 250ml/ 5mins cardiac output monitoring or transfusion if necessary. Continue until normal values obtained Continue until normal Haemodynamic values obtained improvement ? No response Yes Haemodynamic No improvement Echocardiography that preceeds Vasopressors CO monitoring
- 72. PA Catheterization Can be used to provide hemodynamic measurements such as: Cardiac output Pulmonary artery wedge pressure SVR Helpful in determining a cause when the differential is broad
- 73. PA Catheterization Can also help with: Monitoring fluid resuscitation Titration of vasopressors Measuring effects of changes in ventilator settings (PEEP) on hemodynamics
- 74. PA Catheterization PA catheters entail significant clinical risks & have never been proven to improve clinical outcomes in a RCT Bedside PA Cath ≠ Right Heart Catheterization
- 75. Hemodynamic Shock profiles Physiologic Preload Pump function Afterload Tissue perfusion variable Pulmonary Clinical Systemic vascular Mixed venous capillary wedge Cardiac output measurement resistance oxygen saturation pressure Hypovolemic Decreased Decreased Increased Decreased Cardiogenic Increased Decreased Increased Decreased Distributive Decreased Increased Decreased Increased
- 76. PA Cath Vs US Measurement PA Cath US RAP + + CO + + (Pulm CO & Aortic CO) PAOP + + LAP ≠ + RV + + PVR + ± SVR + ± SVO2 + - Core body temp + - Cardiac Chamber Sizes - + Ccontractile State - + Valve Function ± + Detection of Shunts ± + Pericardial Dz ± +
- 77. Pressure Measurements Doppler US
- 78. RUSH Exam
- 79. maximal impulse of the heart. It is important for the EP to know RUSH Exam - Probe Sites “The Pump” d Ultrasound in SHock (RUSH) step 1. Evaluation of the pump.
- 80. “The Pump” SubCostal View 4-V Enlargement
- 81. “The Pump” Large Pericardial Effusion
- 82. Studies examining the incidence of pericardial effusions in Emergency Department or “The Pump” Fig. 4. Subxiphoid view: cardiac tamponade. Cardiac Tamponade
- 83. “The Pump” Acute RV Strain => Massive PE
- 84. a et al “The Pump” Thrombus in RA Apical view: floating thrombus in right atrium.
- 85. T RUSH Exam - Probe Sites step 2. Evaluation of the tank. IVC exam, inferior vena ca “The Tank” graphy in Trauma), right upper quadrant, left upper quadran
- 86. change of the IVC with respiratory variation to central venous pressure (CVP) using an indwelling catheter. A smaller caliber IVC (<2 cm diameter) with an inspiratory collapse “The Tank” Fig. 8. Inferior vena cava sniff test: low cardiac filling pressures. Eval IVC with “Sniff Test”
- 87. “The Tank” Perera et al Fig. 9. Inferior vena cava sniff test: M-mode Doppler showing collapsible IVC. Eval IVC with “Sniff Test” m-mode greater than 50% roughly correlates to a CVP of less than 10 cm of water. This
- 88. reversed. In these patients, the IVC is also less compliant and more distended “The Tank” throughout all respiratory cycles. However, crucial physiologic data can still be Fig. 10. Inferior vena cava sniff test: high cardiac filling pressures. Eval IVC with “Sniff Test” High Filling Pressures
- 89. Perera et al “The Tank” Fig. 11. Right upper quadrant/hepatorenal view: free fluid. FAST Eval Liver/Kidney R-hypochondrium view
- 90. “The Tank” The RUSH Exam Fig. 12. Left upper quadrant: pleural effusion. e-FAST Eval L-pleural space Free fluid in the peritoneal or thoracic cavities in a hypotensive patient in whom
- 91. repeating horizontal linear lines, demonstrating a lack of lung sliding or absence of “The Tank” the ‘‘beach’’ (see Fig. 14). Although the presence of lung sliding is sufficient to rule The RUSH Exam 45 Fig. 13. Long-axis view: normal lung. Fig. 14. M-mode: normal lung versus pneumothorax. e-FAST Eval R/O PTX out pneumothorax, the absence of lung sliding may be seen in other conditions in addition to pneumothorax, such as a chronic obstructive pulmonary disease bleb,
- 92. as ruptured abdominal 14). Although the presence of lung dissections, are life-threat- the ‘‘beach’’ (see Fig. aortic aneurysms (AAA) and aortic sliding is sufficient to rule “The Tank” ening causes of hypotension. The survival of such patients may often be measured in minutes, and the ability to quickly diagnose these diseases is crucial. A ruptured AAA is classically depicted as presenting with back pain, hypotension, and a pulsatile abdominal mass. However, fewer than half of cases occur with this triad, and some cases will present with shock as the only finding.84 A large or rupturing AAA can also mimic a kidney stone, with flank pain and hematuria. Fortunately for the EP, ultrasound can be used to rapidly diagnose both conditions.85 Numerous studies have shown that EPs can make the diagnosis of AAA using bedside ultrasound, with a high sensitivity and specificity.86–89 The sensitivity of EP-performed ultrasound for the detection of AAA ranges from 93% to 100%, with specificities approaching 100%.86–88 A complete ultrasound examination of the abdominal aorta involves imaging from the epigastrium down to the iliac bifurcation using a phased-array or curvilinear Fig. 13. Long-axis view: normal lung. e-FAST Eval Pulmonary Edema Fig. 15. Lung ultrasound: edema with B lines.
- 93. The RUSH RUSH Exam - Probe Sites 6. RUSH step 3. Evaluation of the pipes. “The Pipes”
- 94. larger than 5 cm.90 Studies have also confirmed that the EP can reliably make a correct “The Pipes” determination of the size of an AAA.87,91 Fig. 17. Short-axis view: large abdominal aortic aneurysm. Abdominal Aorta
- 95. “The Pipes” Fig. 18. Short-axis view: aortic dissection. Acute Aortic Dissection
- 96. “The Pipes” The RUSH Exam Fig. 19. Suprasternal view: aortic dissection. Acute Aortic Dissection ‘‘Clogging of the pipes’’: venous thromboembolism Bedside ultrasound for DVT In the patient in whom a thromboembolic event is sus-
- 97. walls of the vein (Fig. 20).98,99 In contrast, a normal vein will completely collapse with “The Pipes” simple compression. Most distal deep venous thromboses can be detected through Fig. 20. Femoral vein deep venous thrombosis with fresh clot. Femoral Vein U/S Eval
- 98. Macro Vs Micro Assessment of Shock Resuscitation
- 99. Why the microcirculation is important in shock! 1. It is where oxygen exchange takes place. 2. It plays a central role in the immune system. 3. During septic shock it is the first to go and last to recover. 4. Rescue of the microcirculation = resuscitation end-point.
- 100. Capillary flow in sepsis
- 101. Orthogonal polarization spectral (OPS) imaging
- 106. Shunting model of sepsis Implication : that active recruitment of the microcirculation is an important component of resuscitation. O2 a v lactate CO2 Ince C & Sinaasappel M (1999) Crit Care Med 27:1369-1377
- 107. Sepsis is a disease of the microcirculation Spronk P, Zandstra D, Ince C (2004) Critical Care 8:462-468
- 108. Mitochondrial Dysfunction in Cell Injury Increased cytosolic Ca2+, oxidative stress, lipid peroxidation Mitochondrial Cytochrome c and other PermeabilityTransition pro-apoptotic proteins Robbins & Cotran Pathologic Basis of Disease: 2005 Apoptosis
- 109. Functional and Morphologic Consequences of Decreased ATP During Cell Injury Ischemia Oxidative Phosphorylation ATP
- 110. Functional and Morphologic Consequences of Decreased ATP During Cell Injury Ischemia Oxidative Phosphorylation ATP Anaerobic glycolysis Glycogen pH Clumping chromatin
- 111. Functional and Morphologic Consequences of Decreased ATP During Cell Injury Ischemia Oxidative Phosphorylation ATP Anaerobic Na pump glycolysis Influx of Ca2+ Glycogen H20, and Na+ pH Efflux of K+ ER swelling Clumping Cell swelling chromatin Blebs
- 112. Functional and Morphologic Consequences of Decreased ATP During Cell Injury Ischemia Oxidative Phosphorylation ATP Anaerobic Detachment Na pump glycolysis of ribosomes Influx of Ca2+ Glycogen Protein synthesis H20, and Na+ pH Efflux of K+ ER swelling Clumping Lipid deposition Cell swelling chromatin Blebs
- 113. Hemodynamic Vs mitochondrial failure Energy failure BE - Lactate
- 114. Hemodynamic Vs mitochondrial failure Energy Volume failure test BE - Lactate
- 115. Hemodynamic Vs mitochondrial failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate
- 116. Hemodynamic Vs mitochondrial failure Hemodynamic failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate
- 117. Hemodynamic Vs mitochondrial failure Hemodynamic failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate VO2 →↓ Lactate →↓
- 118. Hemodynamic Vs mitochondrial failure Hemodynamic failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate VO2 →↓ Lactate →↓ Pump failure or mitochondrial dysfunction
- 119. Hemodynamic Vs mitochondrial failure Hemodynamic failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate VO2 →↓ Dobutamine Lactate →↓ test Pump failure or mitochondrial dysfunction
- 120. Hemodynamic Vs mitochondrial failure Hemodynamic failure VO2 ↑ Lactate ↓ VO2 ↑ Energy Volume Lactate ↓ failure test BE - Lactate VO2 →↓ Dobutamine Lactate →↓ test Pump failure or mitochondrial dysfunction
- 121. Hemodynamic Vs mitochondrial failure Hemodynamic failure Pump failure VO2 ↑ Lactate ↓ VO2 ↑ Energy Volume Lactate ↓ failure test BE - Lactate VO2 →↓ Dobutamine Lactate →↓ test Pump failure or mitochondrial dysfunction
- 122. Hemodynamic Vs mitochondrial failure Hemodynamic failure Pump failure VO2 ↑ Lactate ↓ VO2 ↑ Energy Volume Lactate ↓ failure test BE - Lactate VO2 →↓ Dobutamine Lactate →↓ test Pump failure or VO2 → mitochondrial Lactate →↑ dysfunction
- 123. Hemodynamic Vs mitochondrial failure Hemodynamic failure Pump failure VO2 ↑ Lactate ↓ VO2 ↑ Energy Volume Lactate ↓ failure test BE - Lactate VO2 →↓ Dobutamine Lactate →↓ test Pump failure or VO2 → mitochondrial Lactate →↑ dysfunction Mitochondrial dysfunction
- 124. Nitroglycerin promotes microvascular recruitment in septic and cardiogenic shock patients Sublingual OPS imaging in a patient Same patient after subsequent with septic shock after pressure nitroglycerin 0.5 mg IV bolus guided volume resuscitation Spronk, Ince, Gardien, Mathura, Oudemans-van Straaten, Zandstra DF. (2002) The Lancet 360:1395-1396.
- 125. Early Goal-Directed Therapy Results 28-day Mortality 60 49.2% 50 P = 0.01* 40 33.3% 30 20 10 0 Standard Therapy EGDT n=133 n=130 *Key difference was in sudden CV collapse, not MODS Rivers E. N Engl J Med 2001;345:1368-77.
- 126. Therapeutic priorities Supportive measures to treat hypoxemia, hypotension and impaired tissue oxygenation Distinguish between sepsis and SIRS (systemic inflammatory response syndrome) so medical/ surgical treatment of the source of infection can be started Assess for adequate tissue perfusion
- 127. Initial management Resuscitation Assess airway, respiration, perfusion Supplemental O2 to all patients Intubation often required to protect airway Mechanical ventilation often needed => development of lung injury or ARDS is common - ‘Shock Lung’
- 128. Initial management Monitoring of tissue perfusion Hypotension is typically present Prompt volume resuscitation & restoration of perfusion pressure can limit end organ damage Arterial catheterization if restoration of perfusion pressure is expected to be protracted process
- 129. Initial management Signs of inadequate organ perfusion: Cool, vasoconstricted skin due to redirection of bloodflow to vital organs Obtundation/restlessness Oliguria/anuria Lactic acidosis
- 130. Initial management Restoration of tissue perfusion - Goal Directed Therapy CVP 8 - 12 MAP > 65 Urine output > 0.5 ml/kg/hr Mixed venous O2 > 70% Use IV fluids, PRBC’s & pressors to achieve goals depending on patient’s intravascular volume, cardiac status & severity of shock
- 131. Physiologic Classification of Acute Circulatory Insufficiency Volume Vessel Heart tone function Fluids / blood Vasopressors Inotropes
- 132. Initial management IV fluids Rapid, large volume infusions CHF is primary relative contraindication Relative hypovolemia is often severe Not unusual for a patient to require 10 liters within the first 24 hours
- 133. Initial management IV fluids Should be given in well-defined, rapidly infused boluses (Preferably within 15min) Effects of 1Liter/hr =25% effects of 1liter/15 min = 4liters an hr without the longterm volume effects Assess volume status, tissue perfusion, blood pressure, and for pulmonary edema before/after each bolus Colloids have not been proven to be superior to crystalloids - but have a role in hypoalbuminemia
- 134. PRELOAD Assessment-Volume • LOOK @ CVP/ PAOP • Always Eval CVP in relation to CO Volume unresponsive Preload OK Volume responsive Failing Heart Add dopamine or dobutamine
- 135. “Will my patient respond to fluids?” CO Preload
- 136. “Will my patient respond to fluids?” Fluid Responsiveness is a dynamic parameter that reflects the degree by which the CO responds to changes in preload CO Preload
- 137. Initial management May repeat IV fluid boluses until: B/P, tissue perfusion & oxygen delivery are @ goal PAWP > 18 Development of pulmonary edema Septic patients can develop pulmonary edema with normal wedge pressures due to capillary leak
- 139. Initial management IV fluids: how much? Central venous catheters monitor central venous pressures - Continuous SVO2 monitoring sheaths - SVV measurements + continuous C.O. monitors Also can estimate mixed venous oxygen content Simultaneous MV 02 & Arterial O2 sats + Hgb measurement allow 4 calculation of C.O. by Fick eq
- 140. Initial management Vasopressors Second-line agents Useful in patients who fail to reach adequate blood pressures despite adequate volume resuscitation Also useful in patients who develop cardiogenic pulmonary edema
- 141. Initial management Vasopressors Dopamine & levophed recommended are first-choice drugs - RCT neither superior Phenylephrine (pure α-adrenergic) useful when tachycardia or arrhythmia with β- adrenergic activity limit their use- no data showing efficacy in septic shock Vasopressin is added to patients refractory to first-choice agents
- 142. Properties of Vasopressors Arterial Drug HR Contractility constriction Dobutamine + +++ - Dopamine ++ ++ ++ Epinephrine +++ +++ ++ Norepinephrine ++ ++ +++ Phenylephrine 0 0 +++ Amrinone + +++ --
- 143. Monitoring therapy response All patients require close monitoring Evidence of deterioration => prompt re-evaluation
- 144. Monitoring therapy response Monitoring parameters: Respiratory: PaO2/FiO2 ratio Renal: hrly U/O, BUN, creatinine Hematologic: CBC, %Bands, platelet counts CNS: Glascow coma scale Hepatobiliary: bilirubin, LFT’s CV: P, B/P, arterial lactate, SVO2 GI: ileus, blood in NG aspirate
- 145. Monitoring therapy response Ebb phase: Restore arterial perfusion pressures to pre- sepsis levels Flow phase: Maintain oxygen delivery to meet ongoing tissue needs
- 146. Monitoring therapy response Detection of tissue hypoxia Arterial lactate concentration is most useful measure of tissue perfusion Limited in that it is a global measure and can miss significant injury to a specific organ system
- 147. Monitoring therapy response Treatment of tissue hypoxia Study compared standard treatment (MAP>65, CVP>8, urine output>0.5 ml/kg/ hr) to maintaining central venous O2 saturation > 70%
- 148. Monitoring therapy response Results: Decreased in-hospital mortality (30% vs. 46%) Lower arterial lactate concentration following 6 hours of therapy Lower APACHE II and SAPS II scores Decreased evidence of multiple organ dysfunction
- 149. Monitoring therapy response Red blood cell transfusions were used aggressively in this study to maintain DO2 (70% in study arm vs. 45% in control arm) Recommend maintaining Hct > 30 to maintain adequate tissue oxygen delivery
- 150. Monitoring therapy response If arterial lactate concentrations fail to fall with adequate transfusion, cardiac output must be increased Further IV fluid therapy can be given Dobutamine is given when arterial pressures are adequate to tolerate afterload reduction (phenylephrine/norepineprhine can be added if needed)
- 151. Control of septic focus Prompt identification & treatment infectious source is critical All previously discussed treatments are supportive - not definitive
- 152. Control of septic focus Identification of septic focus: Blood cultures (2 sets, aerobic and anaerobic) Urine Gram stain and culture Sputum in a patient with productive cough Intra-abdominal collection in post-operative patients
- 153. Control of septic focus Investigational methods: TREM-1 (triggering receptor expressed on myeloid cells) Elevated serum procalcitonin
- 154. Control of septic focus Eradication of infection Potentially infected foreign bodies (vascular access devices) Percutaneous or surgical drainage of abscesses Soft-tissue debridement or amputation if necessary
- 155. Antibiotics Antimicrobial regimen Started promptly after cultures are obtained Inappropriate antibiotic selection is depressingly common & can increase mortality Time to initiation of treatment is shown to be the strongest predictor of mortality
- 156. Antibiotics If pseudomonas is not likely, vancomycin (+) 3rd/4th generation cephalosporin β-lactam/β-lactamase inhibitor Carbapenem Up to 60% Septic Shock patient’s with negative cultures
- 157. Antibiotics If pseudomonas likely, vancomycin and 2 of the following (Synergistic Pseudomona Coverage): Antipseudomonal cephalosporin Antipseudomonal penicillin/β-lactamase inhibitor Antipseudomonal carbepenem Floroquinolone with good antipseudomonal activity Aminolgycoside
- 158. Recombinant Human Activated Protein C (Xigris) Coagulation abnormalities are common in septic shock Several reports have suggested that protein C supplementation may produce clinical benefit, esp with purpura fulminans
- 159. Recombinant Human Activated Protein C (Xigris) PROWESS trial: Lower 28-day mortality rate (24.7 vs. 30.8%) Non-significant increase in serious bleeding Was of greater benefit in the most acutely ill patients (APACHE II > 25)
- 160. Recombinant Human Activated Protein C (Xigris) PROWESS trial limitations: Excluded patients with chronic renal failure Patients with metastatic cancer, pancreatitis and organ transplant recipients were excluded after 720 patients were enrolled Cell line used to produce drug was changed during the trial
- 161. Recombinant Human Activated Protein C (Xigris) ENHANCE trial: Similar 28-day all-cause mortality rates Increase in incidence of serious bleeding (specifically intracranial hemorrhage) was significant Treatment within 24 hours of first sepsis- related organ dysfunction showed significantly lower mortality than those treated after 24 hours
- 162. Recombinant Human Activated Protein C (Xigris) ADDRESS trial Patients with APACHE II scores < 25 Designed to enroll 11,000 patients Stopped after 2,600 patients were enrolled because it was unlikely to show any benefit
- 163. Nutrition Essential for optimal immune function Beneficial in both treatment of & prevention of sepsis Early enteral nutrition offers > benefit than parenteral nutrition & less risk + maintains gut integrity & lowers risk of GIB Results in higher neutrophil counts and higher albumin levels
- 164. Glucose control Critically ill patients can develop hyperglycemia and insulin resistance regardless of a history of diabetes Several papers have shown improvement in outcome with aggressive glucose control (goal Glucose = 80-110 mg/dl)
- 165. Concluding Advice
- 166. Concluding Advice • Fluid resuscitation to keep a CI > 2.5 l/min/m2 with a Ppao < 20 mm Hg
- 167. Concluding Advice • Fluid resuscitation to keep a CI > 2.5 l/min/m2 with a Ppao < 20 mm Hg • Add inotropic support if unable to sustain CI within this Ppao limit
- 168. Concluding Advice • Fluid resuscitation to keep a CI > 2.5 l/min/m2 with a Ppao < 20 mm Hg • Add inotropic support if unable to sustain CI within this Ppao limit • Vasopressors to maintain a mean arterial pressure > 65 mm Hg
- 169. Concluding Advice • Fluid resuscitation to keep a CI > 2.5 l/min/m2 with a Ppao < 20 mm Hg • Add inotropic support if unable to sustain CI within this Ppao limit • Vasopressors to maintain a mean arterial pressure > 65 mm Hg • If measures of organ perfusion available (urine output, ΔPCO2, tissue blood flow, Serum lactate, base deficit ) use them to guide response to therapy.
- 170. Concluding Advice • Fluid resuscitation to keep a CI > 2.5 l/min/m2 with a Ppao < 20 mm Hg • Add inotropic support if unable to sustain CI within this Ppao limit • Vasopressors to maintain a mean arterial pressure > 65 mm Hg • If measures of organ perfusion available (urine output, ΔPCO2, tissue blood flow, Serum lactate, base deficit ) use them to guide response to therapy. • Trends may be more important than absolute values
Hinweis der Redaktion
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