Frank Meissner, profile picture
Uploaded byFrank Meissner
KEY, PPTX1,855 views

Shock 2011

(250ml/5mins) 250ml/ 5mins or transfusion 1) This document provides guidance on evaluating and treating shock in patients. It discusses the different types of shock (hypovolemic, cardiogenic, distributive), their causes, signs, and treatments. 2) The initial approach involves taking a thorough history, performing a full physical exam, and obtaining basic lab tests to help identify the type and cause of shock. 3) Mixed venous oxygen saturation (SvO2) and central venous pressure (CVP) measurements can help guide fluid resuscitation and vasopressor use depending on whether the values are low or normal. Fluid challenges are recommended initially

Embed presentation

Download as KEY, PPTX
1 / 170
2 / 170
3 / 170
4 / 170
5 / 170
6 / 170
7 / 170
8 / 170
9 / 170
10 / 170
11 / 170
12 / 170
13 / 170
14 / 170
15 / 170
16 / 170
17 / 170
18 / 170
19 / 170
20 / 170
21 / 170
22 / 170
23 / 170
24 / 170
25 / 170
26 / 170
27 / 170
28 / 170
29 / 170
30 / 170
31 / 170
32 / 170
33 / 170
34 / 170
35 / 170
36 / 170
37 / 170
38 / 170
39 / 170
40 / 170
41 / 170
42 / 170
43 / 170
44 / 170
45 / 170
46 / 170
47 / 170
48 / 170
49 / 170
50 / 170
51 / 170
52 / 170
53 / 170
54 / 170
55 / 170
56 / 170
57 / 170
58 / 170
59 / 170
60 / 170
61 / 170
62 / 170
63 / 170
64 / 170
65 / 170
66 / 170
67 / 170
68 / 170
69 / 170
70 / 170
71 / 170
72 / 170
73 / 170
74 / 170
75 / 170
76 / 170
77 / 170
78 / 170
79 / 170
80 / 170
81 / 170
82 / 170
83 / 170
84 / 170
85 / 170
86 / 170
87 / 170
88 / 170
89 / 170
90 / 170
91 / 170
92 / 170
93 / 170
94 / 170
95 / 170
96 / 170
97 / 170
98 / 170
99 / 170
100 / 170
101 / 170
102 / 170
103 / 170
104 / 170
105 / 170
106 / 170
107 / 170
108 / 170
109 / 170
110 / 170
111 / 170
112 / 170
113 / 170
114 / 170
115 / 170
116 / 170
117 / 170
118 / 170
119 / 170
120 / 170
121 / 170
122 / 170
123 / 170
124 / 170
125 / 170
126 / 170
127 / 170
128 / 170
129 / 170
130 / 170
131 / 170
132 / 170
133 / 170
134 / 170
135 / 170
136 / 170
137 / 170
138 / 170
139 / 170
140 / 170
141 / 170
142 / 170
143 / 170
144 / 170
145 / 170
146 / 170
147 / 170
148 / 170
149 / 170
150 / 170
151 / 170
152 / 170
153 / 170
154 / 170
155 / 170
156 / 170
157 / 170
158 / 170
159 / 170
160 / 170
161 / 170
162 / 170
163 / 170
164 / 170
165 / 170
166 / 170
167 / 170
168 / 170
169 / 170
170 / 170
Eval & Rx of Shock Frank W Meissner, MD, RDMS FACP, FACC, FCCP, FASNC, CPHIMS, CCDS
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?
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
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
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
Cellular Shock
MOSF Rapid Progression to death Prompt recognition early syms key to survival
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
Stages Pre-shock Shock End-organ dysfunction
Stages: Pre-shock Warm or compensated shock Regulatory mechanisms are able to compensate for diminished perfusion.
Stages: Cold Shock Compensatory mechanisms become overwhelmed, resulting in: Tachycardia Tachypnea Metabolic acidosis Oilguria Cool, clammy skin High SVR
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
Sepsis: end-organ dysfunction Decreasing urine output Restlessness =>agitation =>obtundation =>coma Mutiple organ system failure than death
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]
Physiologic determinants Cardiac Output (CO) = HR x SV Stroke volume ∫ (preload, myocardial contractility, afterload)
Pre-Load
Myocardial Contractility Slope of End-systolic pressure volume relationship = Emax or Ees independent measure of contractility
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
Do Hemodynamics Matter? Maybe NOT in Septic Shock
Classification Hypovolemic Cardiogenic Distributive
Physiologic Determinants SVR & CO can reliably differentiate shock states Assuming SVR is accurate
Hypovolemic shock #1 Cause of Death Worldwide Hemorrhage Trauma GI bleeding Ruptured aneurysm or hematoma Hemorrhagic pancreatitis Fractures
Hypovolemic shock Fluid loss Diarrhea Vomiting Heat stroke Inadequate repletion of insensible losses Burns
Cardiogenic shock 2ndary 2 pump failure & decreased cardiac output Main categories: Myopathies Arhythmia Mechanical Obstructive
Cardiogenic shock Cardiomyopathies: Infarction > 40% of LV mass RV infarction Dilated cardiomyopathies Stunned myocardium 2ndary prolonged ischemia or cardiopulmonary bypass
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)
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
Cardiogenic shock Obstructive Pulmonary embolism Tension pneumothorax Constrictive pericarditis Pericardial tamponade Severe pulmonary hypertension
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)
Distributive shock Causes: Addisonian crisis Myxedema coma Neurogenic shock 2ndary spinal cord trauma MI + SIRS Cardiopulmonary bypass
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
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
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
Common features Mental status changes Begins with agitation Progresses to confusion/delirium Ends in obtundation/coma
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
Initial approach History: Food/medicine allergies Recent medication changes Potential acute/chronic drug intoxication Preexisting diseases
Initial approach Physical exam: HEENT Scleral icterus Dry conjunctivae Dry mucous membranes Pinpoint pupils Fixed/dilated pupils
Initial approach Physical exam: Neck JVD Delayed carotid upstroke Carotid bruits Meningeal signs
Initial approach Physical exam: lungs Tachypnea Shallow respirations Crackles/rales Consolidation Egophony
Initial approach Physical exam: cardiovascular Arrhythmia Murmurs or S3 gallop Diffuse PMI Right or left ventricular heave
Initial approach Physical exam: Abdomen Tenseness Distension Tenderness Rebound/guarding Absent bowel sounds
Initial approach Physical exam: rectal Decreased tone Blood (hematochezia or melena)
Initial approach Physical exam: extremities Calf swelling/palpable cords Unequal pulses Disparity of blood pressure between upper extremities
Initial approach Physical exam: neurologic Agitation Confusion Delirium Obtundation
Initial approach Physical exam: skin Cold, clammy Warm, hyperemic Rashes Petechiae Urticara
Initial approach Lab evaluation CBC with manual differential Basic chemistries Liver function tests Amylase/lipase Fibrinogen & fibrin split products
Initial approach Lab evaluation ABG’s & SVO2 Toxicology screen Chest x-ray Abdominal x-ray
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
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
Insert CVP/SvcO2
Insert CVP/SvcO2 SvO2 >70%
Insert CVP/SvcO2 SvO2 >70% CVP N or low
Insert CVP/SvcO2 SvO2 >70% CVP N or low Sepsis?
Insert CVP/SvcO2 SvO2 >70% CVP N or low Sepsis? Repeat Fluid challenge 250ml/ 5mins
Insert CVP/SvcO2 SvO2 >70% CVP N or low Sepsis? Repeat Fluid challenge 250ml/ 5mins Haemodynamic improvement ?
Insert CVP/SvcO2 SvO2 >70% CVP N or low Sepsis? Repeat Fluid challenge 250ml/ 5mins Continue until normal values obtained Haemodynamic improvement ? Yes
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
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
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
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
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
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
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
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
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
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
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
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
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
PA Catheterization Can also help with: Monitoring fluid resuscitation Titration of vasopressors Measuring effects of changes in ventilator settings (PEEP) on hemodynamics
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
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
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 ± +
Pressure Measurements Doppler US
RUSH Exam
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.
“The Pump” SubCostal View 4-V Enlargement
“The Pump” Large Pericardial Effusion
Studies examining the incidence of pericardial effusions in Emergency Department or “The Pump” Fig. 4. Subxiphoid view: cardiac tamponade. Cardiac Tamponade
“The Pump” Acute RV Strain => Massive PE
a et al “The Pump” Thrombus in RA Apical view: floating thrombus in right atrium.
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
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”
“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
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
Perera et al “The Tank” Fig. 11. Right upper quadrant/hepatorenal view: free fluid. FAST Eval Liver/Kidney R-hypochondrium view
“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
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,
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.
The RUSH RUSH Exam - Probe Sites 6. RUSH step 3. Evaluation of the pipes. “The Pipes”
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
“The Pipes” Fig. 18. Short-axis view: aortic dissection. Acute Aortic Dissection
“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-
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
Macro Vs Micro Assessment of Shock Resuscitation
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.
Capillary flow in sepsis
Orthogonal polarization spectral (OPS) imaging
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
Sepsis is a disease of the microcirculation Spronk P, Zandstra D, Ince C (2004) Critical Care 8:462-468
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
Functional and Morphologic Consequences of Decreased ATP During Cell Injury Ischemia Oxidative Phosphorylation ATP
Functional and Morphologic Consequences of Decreased ATP During Cell Injury Ischemia Oxidative Phosphorylation ATP Anaerobic glycolysis Glycogen pH Clumping chromatin
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
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
Hemodynamic Vs mitochondrial failure Energy failure BE - Lactate
Hemodynamic Vs mitochondrial failure Energy Volume failure test BE - Lactate
Hemodynamic Vs mitochondrial failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate
Hemodynamic Vs mitochondrial failure Hemodynamic failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate
Hemodynamic Vs mitochondrial failure Hemodynamic failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate VO2 →↓ Lactate →↓
Hemodynamic Vs mitochondrial failure Hemodynamic failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate VO2 →↓ Lactate →↓ Pump failure or mitochondrial dysfunction
Hemodynamic Vs mitochondrial failure Hemodynamic failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate VO2 →↓ Dobutamine Lactate →↓ test Pump failure or mitochondrial dysfunction
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
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
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
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
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.
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.
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
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’
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
Initial management Signs of inadequate organ perfusion: Cool, vasoconstricted skin due to redirection of bloodflow to vital organs Obtundation/restlessness Oliguria/anuria Lactic acidosis
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
Physiologic Classification of Acute Circulatory Insufficiency Volume Vessel Heart tone function Fluids / blood Vasopressors Inotropes
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
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
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
“Will my patient respond to fluids?” CO Preload
“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
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
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
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
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
Properties of Vasopressors Arterial Drug HR Contractility constriction Dobutamine + +++ - Dopamine ++ ++ ++ Epinephrine +++ +++ ++ Norepinephrine ++ ++ +++ Phenylephrine 0 0 +++ Amrinone + +++ --
Monitoring therapy response All patients require close monitoring Evidence of deterioration => prompt re-evaluation
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
Monitoring therapy response Ebb phase: Restore arterial perfusion pressures to pre- sepsis levels Flow phase: Maintain oxygen delivery to meet ongoing tissue needs
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
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%
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
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
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)
Control of septic focus Prompt identification & treatment infectious source is critical All previously discussed treatments are supportive - not definitive
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
Control of septic focus Investigational methods: TREM-1 (triggering receptor expressed on myeloid cells) Elevated serum procalcitonin
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
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
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
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
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
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)
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
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
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
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
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)
Concluding Advice
Concluding Advice • Fluid resuscitation to keep a CI > 2.5 l/min/m2 with a Ppao < 20 mm Hg
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
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
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.
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

More Related Content

PPTX
Pulmonary embolism 21jan21
byBest Doctors
 
PPTX
Management of Massive & Submassive Pulmonary Embolism
bySun Yai-Cheng
 
PPT
Pulmonaryembolism final
byLPS Institute of Cardiology Kanpur UP India
 
PPSX
Pulmonary embolism@ghanem@.2013
byIslam Ghanem
 
PPTX
Pulmonary Embolism- Diagnosis by Dr.Tinku Joseph
byDr.Tinku Joseph
 
PPT
Pulmonary embolism
byTeleClinEd
 
KEY
Pe final
byFrank Meissner
 
PPT
Pe 2
byTroy Pennington
 
Pulmonary embolism 21jan21
byBest Doctors
 
Management of Massive & Submassive Pulmonary Embolism
bySun Yai-Cheng
 
Pulmonaryembolism final
byLPS Institute of Cardiology Kanpur UP India
 
Pulmonary embolism@ghanem@.2013
byIslam Ghanem
 
Pulmonary Embolism- Diagnosis by Dr.Tinku Joseph
byDr.Tinku Joseph
 
Pulmonary embolism
byTeleClinEd
 
Pe final
byFrank Meissner
 
Pe 2
byTroy Pennington
 

What's hot

PDF
Case Report On Dic &amp; Dvt
byTshering Namgyal Wangdi
 
PPT
Pulmonary Embolism - (PE)
bysteveclaydon1970
 
PPTX
Acute Pulmonary Embolism: Introduction, Clinical presentation, Classification...
byRichardKhoi
 
PPTX
Acute pulmonary embolism
byKhurram Wazir
 
PPT
Acute pulmonary thromboembolism
byDr. Mohammed Sadiq Azam M.D.
 
PPTX
Cardiology exam MCQ
byPRAVEEN GUPTA
 
PPTX
Pulmonary embolism
byRamin Sadeghi
 
PPTX
Management of Venous Thromboembolism
byAbhishek Agrawal
 
PPT
Pulmonary embolism dr.bayazid
byDrMuhammad Bayazid
 
PPT
Acute pulmonary embolism - risk stratification and management
byPrithvi Puwar
 
PPTX
Venous thromboembolism, THROMBOPROPHYLAXIS and management
bymauryaramgopal
 
PPTX
Pulmonary embolism,overview
byEman Mahmoud
 
PPT
Venous Thromboembolism
byAndrew Ferguson
 
PPTX
Pulmonary embolism
byKapil Vasanth
 
PPT
CTA OF PULMONARY EMBOLISM
byXiu Srithammasit
 
PPT
Pulmonary Embolism
bycairo1957
 
PPT
Pulmonaryembolism
byMohankumar Thekkinkattil
 
PPTX
Pulmonary embolism 2
bysamirelansary
 
PPT
Moore Chapter: Visceral Ischemic Syndromes
byagucwa
 
PPT
ipertensione polmonare postembolica-cteph
byPAH-GHIO
 
Case Report On Dic &amp; Dvt
byTshering Namgyal Wangdi
 
Pulmonary Embolism - (PE)
bysteveclaydon1970
 
Acute Pulmonary Embolism: Introduction, Clinical presentation, Classification...
byRichardKhoi
 
Acute pulmonary embolism
byKhurram Wazir
 
Acute pulmonary thromboembolism
byDr. Mohammed Sadiq Azam M.D.
 
Cardiology exam MCQ
byPRAVEEN GUPTA
 
Pulmonary embolism
byRamin Sadeghi
 
Management of Venous Thromboembolism
byAbhishek Agrawal
 
Pulmonary embolism dr.bayazid
byDrMuhammad Bayazid
 
Acute pulmonary embolism - risk stratification and management
byPrithvi Puwar
 
Venous thromboembolism, THROMBOPROPHYLAXIS and management
bymauryaramgopal
 
Pulmonary embolism,overview
byEman Mahmoud
 
Venous Thromboembolism
byAndrew Ferguson
 
Pulmonary embolism
byKapil Vasanth
 
CTA OF PULMONARY EMBOLISM
byXiu Srithammasit
 
Pulmonary Embolism
bycairo1957
 
Pulmonaryembolism
byMohankumar Thekkinkattil
 
Pulmonary embolism 2
bysamirelansary
 
Moore Chapter: Visceral Ischemic Syndromes
byagucwa
 
ipertensione polmonare postembolica-cteph
byPAH-GHIO
 

Viewers also liked

PPT
ChemBio Tutorial
byFrank Meissner
 
PPT
Giuseppe Vaciago Profili giuridici dell'indagine digitale 08 09 18 Ordine Ber...
byAndrea Rossetti
 
PPTX
Utilidad De Cateter Arteria Pulmonar
byuniversidad del valle
 
PPT
Point of Care Cardiac U/S
byFrank Meissner
 
PPTX
Big Data In Medicine
byFrank Meissner
 
PPT
Practical thanatology
byFrank Meissner
 
KEY
Chronotropic Incompetence
byFrank Meissner
 
KEY
Therapeutic hypothermia
byFrank Meissner
 
KEY
Differential Dx Chest Pain
byFrank Meissner
 
PPS
10 Na Hraně PtáK
byjedlickak07
 
KEY
Acute Coronary Syndrome
byFrank Meissner
 
PPTX
Land and Light
byAlan Doherty
 
PDF
Adv 410 Quiz 2
bytoenail23
 
PPTX
GeoNews - La Niña
byAlan Doherty
 
PPS
For You
byguestd58738
 
PPT
İ N S A N B E Y Nİ
bykirbiyik
 
KEY
Dining With Cannibals
byFrank Meissner
 
PDF
TV Distribution reloaded
byBertram Gugel
 
PPT
TLL Sicily: Building Partnerships for Territorial Living Labs for
byjexxon
 
PPT
Kios
bybeowulf
 
ChemBio Tutorial
byFrank Meissner
 
Giuseppe Vaciago Profili giuridici dell'indagine digitale 08 09 18 Ordine Ber...
byAndrea Rossetti
 
Utilidad De Cateter Arteria Pulmonar
byuniversidad del valle
 
Point of Care Cardiac U/S
byFrank Meissner
 
Big Data In Medicine
byFrank Meissner
 
Practical thanatology
byFrank Meissner
 
Chronotropic Incompetence
byFrank Meissner
 
Therapeutic hypothermia
byFrank Meissner
 
Differential Dx Chest Pain
byFrank Meissner
 
10 Na Hraně PtáK
byjedlickak07
 
Acute Coronary Syndrome
byFrank Meissner
 
Land and Light
byAlan Doherty
 
Adv 410 Quiz 2
bytoenail23
 
GeoNews - La Niña
byAlan Doherty
 
For You
byguestd58738
 
İ N S A N B E Y Nİ
bykirbiyik
 
Dining With Cannibals
byFrank Meissner
 
TV Distribution reloaded
byBertram Gugel
 
TLL Sicily: Building Partnerships for Territorial Living Labs for
byjexxon
 
Kios
bybeowulf
 

Similar to Shock 2011

PPT
Hemodynamic Stabilisation In Septic Shock
bychandra talur
 
PDF
Shock
bySugunakar Rao
 
PPTX
shock medicine, surgery , medicine clinical 11 2024.pptx
bymothanaafnan12
 
PPTX
Shock
byProf. Ahmed Mohamed Badheeb
 
PPTX
Shockในศัลยกรรม
byสปสช นครสวรรค์
 
PPTX
hemodynamicstabilisationinsepticshock-090814084800-phpapp01.pptx
byDr Shabeer D
 
PPT
shock
byKhalid Ali Diriye
 
PPTX
Shock
byMeghanPowers10
 
PPT
Shock
byAndrew Ferguson
 
PPTX
Shock Emergency Medicine seminar work.pptx
byAwsSbool1
 
PPTX
Shock its pathopysiology and management
bySHAKIL JAWED
 
PPTX
2013 Pediatric Subspecialty Boot Camp_SHOCK
byDanny Castro
 
PPT
High output cardiac failure
byUscom - Presentations
 
PPTX
Shock
bysalaheldin abusin
 
PPT
Shock: A review of hypovolemic, septic, cardiogenic and neurogenic shock.
byJoseph A. Di Como MD
 
PPTX
learning on easy education on CME Shock .pptx
bydontforgetyourself19
 
PPTX
SHOCK .pptx
byYuveneshwari
 
PPTX
ICU INTERNSHIP REGULATION AT HOPITAL LAQUINTINIE FROM 3.pptx
byDanielleMade
 
PPTX
SHOCK.pptx...............................
byNanduPadmakumar3
 
PPT
Conshock
bykk 555888
 
Hemodynamic Stabilisation In Septic Shock
bychandra talur
 
Shock
bySugunakar Rao
 
shock medicine, surgery , medicine clinical 11 2024.pptx
bymothanaafnan12
 
Shock
byProf. Ahmed Mohamed Badheeb
 
Shockในศัลยกรรม
byสปสช นครสวรรค์
 
hemodynamicstabilisationinsepticshock-090814084800-phpapp01.pptx
byDr Shabeer D
 
shock
byKhalid Ali Diriye
 
Shock
byMeghanPowers10
 
Shock
byAndrew Ferguson
 
Shock Emergency Medicine seminar work.pptx
byAwsSbool1
 
Shock its pathopysiology and management
bySHAKIL JAWED
 
2013 Pediatric Subspecialty Boot Camp_SHOCK
byDanny Castro
 
High output cardiac failure
byUscom - Presentations
 
Shock
bysalaheldin abusin
 
Shock: A review of hypovolemic, septic, cardiogenic and neurogenic shock.
byJoseph A. Di Como MD
 
learning on easy education on CME Shock .pptx
bydontforgetyourself19
 
SHOCK .pptx
byYuveneshwari
 
ICU INTERNSHIP REGULATION AT HOPITAL LAQUINTINIE FROM 3.pptx
byDanielleMade
 
SHOCK.pptx...............................
byNanduPadmakumar3
 
Conshock
bykk 555888
 

More from Frank Meissner

PDF
Cardiomyopathy
byFrank Meissner
 
PDF
EKG Patterns of SCD - Can't Miss EKG Patterns for Generalist & Psychiatrist
byFrank Meissner
 
PDF
Pediatric delirium
byFrank Meissner
 
PDF
Curanderos presentation
byFrank Meissner
 
PDF
Eating D/O
byFrank Meissner
 
PDF
Bipolar D/O
byFrank Meissner
 
PDF
Schistomasis
byFrank Meissner
 
PDF
Visceral leishmanasis
byFrank Meissner
 
PDF
PE case
byFrank Meissner
 
PDF
Taktosubo cardiomyopathy verona june2018
byFrank Meissner
 
PDF
Pills & Thrills
byFrank Meissner
 
PDF
Hemmorhagic fever zagreb
byFrank Meissner
 
PDF
Chest pain perals
byFrank Meissner
 
PDF
Tropical cardiology
byFrank Meissner
 
PDF
Drug induced brugadda apa
byFrank Meissner
 
PDF
Burns zagreb presentation
byFrank Meissner
 
PDF
Malaria
byFrank Meissner
 
PDF
Verona sleep hx presentation
byFrank Meissner
 
PDF
Onchocerciasis
byFrank Meissner
 
PPTX
BigDataInMedicine.pptx
byFrank Meissner
 
Cardiomyopathy
byFrank Meissner
 
EKG Patterns of SCD - Can't Miss EKG Patterns for Generalist & Psychiatrist
byFrank Meissner
 
Pediatric delirium
byFrank Meissner
 
Curanderos presentation
byFrank Meissner
 
Eating D/O
byFrank Meissner
 
Bipolar D/O
byFrank Meissner
 
Schistomasis
byFrank Meissner
 
Visceral leishmanasis
byFrank Meissner
 
PE case
byFrank Meissner
 
Taktosubo cardiomyopathy verona june2018
byFrank Meissner
 
Pills & Thrills
byFrank Meissner
 
Hemmorhagic fever zagreb
byFrank Meissner
 
Chest pain perals
byFrank Meissner
 
Tropical cardiology
byFrank Meissner
 
Drug induced brugadda apa
byFrank Meissner
 
Burns zagreb presentation
byFrank Meissner
 
Malaria
byFrank Meissner
 
Verona sleep hx presentation
byFrank Meissner
 
Onchocerciasis
byFrank Meissner
 
BigDataInMedicine.pptx
byFrank Meissner
 

Shock 2011

  • 1.
    Eval & Rxof Shock Frank W Meissner, MD, RDMS FACP, FACC, FCCP, FASNC, CPHIMS, CCDS
  • 2.
    Case Study 58 y/omale 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 physiologicstate 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 initiallyreversible, but lead to cellular hypoxia with: Cell membrane and ion pump dysfunction Intracellular edema Leak intracellular contents into extracelluar space Dysregulation of intracellular pH
  • 6.
  • 7.
    MOSF Rapid Progression todeath 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
  • 9.
  • 10.
    Stages: Pre-shock Warm orcompensated shock Regulatory mechanisms are able to compensate for diminished perfusion.
  • 12.
    Stages: Cold Shock Compensatorymechanisms become overwhelmed, resulting in: Tachycardia Tachypnea Metabolic acidosis Oilguria Cool, clammy skin High SVR
  • 13.
    Stages: shock Usually occurwith: 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.
  • 18.
    Myocardial Contractility Slope of End-systolic pressure volume relationship = Emax or Ees independent measure of contractility
  • 20.
    Newer Non-Invasive HemodynamicMeasures 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? MaybeNOT in Septic Shock
  • 22.
  • 23.
    Physiologic Determinants SVR & CO can reliably differentiate shock states Assuming SVR is accurate
  • 25.
    Hypovolemic shock #1 Causeof 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 2pump 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, clammyskin 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 statuschanges Begins with agitation Progresses to confusion/delirium Ends in obtundation/coma
  • 38.
    Common features Metabolicacidosis 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.
  • 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 beused 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 alsohelp with: Monitoring fluid resuscitation Titration of vasopressors Measuring effects of changes in ventilator settings (PEEP) on hemodynamics
  • 74.
    PA Catheterization PA cathetersentail 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 VsUS 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.
  • 78.
  • 79.
    maximal impulse ofthe 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.
  • 81.
  • 82.
    Studies examining theincidence of pericardial effusions in Emergency Department or “The Pump” Fig. 4. Subxiphoid view: cardiac tamponade. Cardiac Tamponade
  • 83.
    “The Pump” Acute RVStrain => 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 theIVC 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 etal 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 thesepatients, 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 linearlines, 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 abdominal14). 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 5cm.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 thevein (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 microcirculationis 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.
  • 101.
  • 106.
    Shunting model ofsepsis 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 adisease of the microcirculation Spronk P, Zandstra D, Ince C (2004) Critical Care 8:462-468
  • 108.
    Mitochondrial Dysfunction inCell 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 MorphologicConsequences of Decreased ATP During Cell Injury Ischemia Oxidative Phosphorylation ATP
  • 110.
    Functional and MorphologicConsequences of Decreased ATP During Cell Injury Ischemia Oxidative Phosphorylation ATP Anaerobic glycolysis Glycogen pH Clumping chromatin
  • 111.
    Functional and MorphologicConsequences 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 MorphologicConsequences 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 mitochondrialfailure Energy failure BE - Lactate
  • 114.
    Hemodynamic Vs mitochondrialfailure Energy Volume failure test BE - Lactate
  • 115.
    Hemodynamic Vs mitochondrialfailure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate
  • 116.
    Hemodynamic Vs mitochondrialfailure Hemodynamic failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate
  • 117.
    Hemodynamic Vs mitochondrialfailure Hemodynamic failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate VO2 →↓ Lactate →↓
  • 118.
    Hemodynamic Vs mitochondrialfailure Hemodynamic failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate VO2 →↓ Lactate →↓ Pump failure or mitochondrial dysfunction
  • 119.
    Hemodynamic Vs mitochondrialfailure Hemodynamic failure VO2 ↑ Lactate ↓ Energy Volume failure test BE - Lactate VO2 →↓ Dobutamine Lactate →↓ test Pump failure or mitochondrial dysfunction
  • 120.
    Hemodynamic Vs mitochondrialfailure Hemodynamic failure VO2 ↑ Lactate ↓ VO2 ↑ Energy Volume Lactate ↓ failure test BE - Lactate VO2 →↓ Dobutamine Lactate →↓ test Pump failure or mitochondrial dysfunction
  • 121.
    Hemodynamic Vs mitochondrialfailure 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 mitochondrialfailure 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 mitochondrialfailure 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 TherapyResults 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 measuresto 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 oftissue 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 ofinadequate organ perfusion: Cool, vasoconstricted skin due to redirection of bloodflow to vital organs Obtundation/restlessness Oliguria/anuria Lactic acidosis
  • 130.
    Initial management Restoration oftissue 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 AcuteCirculatory Insufficiency Volume Vessel Heart tone function Fluids / blood Vasopressors Inotropes
  • 132.
    Initial management IVfluids 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 patientrespond to fluids?” CO Preload
  • 136.
    “Will my patientrespond 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 Mayrepeat 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 septicfocus Prompt identification & treatment infectious source is critical All previously discussed treatments are supportive - not definitive
  • 152.
    Control of septicfocus 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 septicfocus Investigational methods: TREM-1 (triggering receptor expressed on myeloid cells) Elevated serum procalcitonin
  • 154.
    Control of septicfocus 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 isnot 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 ProteinC (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 ProteinC (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 ProteinC (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 ProteinC (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 ProteinC (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 optimalimmune 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 illpatients 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.
  • 166.
    Concluding Advice • Fluidresuscitation to keep a CI > 2.5 l/min/m2 with a Ppao < 20 mm Hg
  • 167.
    Concluding Advice • Fluidresuscitation 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 • Fluidresuscitation 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 • Fluidresuscitation 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 • Fluidresuscitation 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

Editor's Notes