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Published bySamuel Cooper Modified over 9 years ago
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Matthew Boland MD, FCCP Pulmonary/CCM
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A definition of SHOCK Global tissue hypoxia “global” implying systemically while “tissue hypoxia” implies inadequate oxygen delivery/utilization May be independent of, or even inversely proportional to “perfusion” Hypoxia ≠ Hypoxemia
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Hinshaw-Cox Approach Hypovolemic Cardiogenic Obstructive Distributive
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A Physiologic Approach Shock ≈ ↓ D ̇ O 2 (inappropriate to V ̇ O 2 ) D ̇ O 2 = CO x CaO 2 CO= HR x SV SV ∫ Afterload, Preload and Contractility CaO 2 = Hgb x SaO 2 x 1.34 x (0.003 x PaO 2 )
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So… D ̇ O 2 = HR x (∫ Afterload, Preload and Contractility) x Hgb x SaO 2 x 1.34 x (0.003 x PaO 2 )
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So…4 types of Shock Circulatory Hypoxia This is where Hinshaw-Cox categories really fit… Anemic Hypoxia (low hgb) Hypoxemic Hypoxia (low SaO 2 ) And…
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Cellular Hypoxia AKA cytopathic hypoxia or cytotoxic hypoxia Disutilization of oxygen at the cellular level (usually mitochondrial) prompts anaerobic metabolism and lactate production independent of O 2 delivery. Examples: cyanide poisoning, sepsis or anything that uncouples oxidative phosphorylation
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Recognition of Shock Physical Exam Shock Index= SBP/HR; the lower the quotient, the “shockier” the patient Decreased Cap refill or pulses Skin exam “warm shock” vs “cold shock”
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Recognition of Shock Basic Labs Chem 7 Low bicarb, high anion gap ABG Metabolic acidosis ± respiratory alkalosis VBG Low SvO 2 (though may be high, especially in cellular hypoxia) Lactate- elevated (though can be normal if shock is well compensated)
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Recognition of Shock: PAC PAC, though rarely used in today’s Critical Care environment, can be used to determine/narrow the underlying pattern/cause of shock
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Treatment of Shock ID and treat underlying cause WHILE Optimizing ‘Big 7’ (i.e. goal –directed) HR Preload Afterload Contractility Hgb SaO 2 ↓V ̇ O 2
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Decreasing Oxygen Consumption Control of fever Unloading respiratory muscles NIV vs Intubation Sedation Paralytics
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Goal = Nl SvO 2 Vast majority of shock states respond to EARLY optimization of balancing oxygen delivery and consumption, BUT…
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Exceptions to the rule The pattern of rising lactate despite normal (or even more ominous, high) SvO 2 frequently implicates three clinical scenarios… Cellular hypoxia (? Role for steroids) DIC (0bstruction of the micro-vasculature does not allow delivery of oxygenated blood to tissues on other side) (? Role for rhAPC) Uncontrolled source of shock (typically ongoing hemorrhage, infection, etc)
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Hyperlactatemia Type A- Classic- due to hypoxia and anaerobic metabolism Type B- Drugs (metformin, HARRT, etc), Cancer, ETOHism, HIV Type δ- encountered in short-gut syndrome with overproduction of δ-isomer of lactate (not assayed by typical lactate measurements clinically).
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Question #1 Which of the following values is NOT a determinant of D ̇ O 2 ? 1. Hbg 2. SvO 2 3. Preload 4. PaO 2 5. Heart rate
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Question #2 Disutilization of oxygen at the mitochondrial level prompting anaerobic metabolism and lactate production independent of O 2 delivery, can be termed… 1. Circulatory Hypoxia 2. Cytopathic Hypoxia 3. Anemic Hypoxia 4. Hypoxemic Hypoxia 5. Obstructive Hypoxia
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Question #3 Optimizing which of the following is NOT a treatment option for shock? 1. Urine Output 2. Contractility 3. Work of breathing 4. Arterial Oxygen Saturation 5. Hgb
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Question #4 Which of the following is NOT an example of obstructive shock? 1. Tension pneumothorax 2. Atrial myxoma 3. Pulmonary embolism 4. Pericardial tamponade 5. Papillary muscle rupture
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Question #5 Which of the following is NOT a cause of Type B lactic acidosis? 1. HAART 2. Alcoholism 3. Lymphoma 4. short-gut syndrome 5. metformin
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Bibliography Oxygen delivery. Hameed SM. Aird WC. Cohn SM. Critical Care Medicine. 31(12 Suppl):S658-67, 2003 Dec.
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