physiology of shock: beyond hinshaw -cox
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Physiology of Shock: Beyond Hinshaw -Cox. Matthew Boland MD, FCCP Pulmonary/CCM. A definition of SHOCK. Global tissue hypoxia “global” implying systemically while “tissue hypoxia” implies inadequate oxygen delivery/utilization - PowerPoint PPT PresentationTRANSCRIPT
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Physiology of Shock:Beyond Hinshaw-Cox
Matthew Boland MD, FCCPPulmonary/CCM
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A definition of SHOCKGlobal 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 ApproachHypovolemicCardiogenicObstructiveDistributive
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A Physiologic ApproachShock ≈ ↓ D ̇O2
(inappropriate to V̇O2)
D ̇O2 = CO x CaO2
CO= HR x SV
SV ∫ Afterload, Preload and Contractility
CaO2 = Hgb x SaO2 x 1.34 x (0.003 x PaO2)
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So…D ̇O2 = HR x (∫ Afterload, Preload and Contractility) x
Hgb x SaO2 x 1.34 x (0.003 x PaO2)
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So…4 types of ShockCirculatory Hypoxia
This is where Hinshaw-Cox categories really fit…
Anemic Hypoxia (low hgb)Hypoxemic Hypoxia (low SaO2)And…
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Cellular HypoxiaAKA cytopathic hypoxia or cytotoxic hypoxiaDisutilization of oxygen at the cellular level
(usually mitochondrial) prompts anaerobic metabolism and lactate production independent of O2 delivery.
Examples: cyanide poisoning, sepsis or anything that uncouples oxidative phosphorylation
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Recognition of ShockPhysical Exam
Shock Index= SBP/HR; the lower the quotient, the “shockier” the patient
Decreased Cap refill or pulsesSkin exam
“warm shock” vs “cold shock”
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Recognition of ShockBasic Labs
Chem 7Low bicarb, high anion gap
ABGMetabolic acidosis ± respiratory alkalosis
VBGLow SvO2 (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 ShockID and treat underlying cause WHILEOptimizing ‘Big 7’ (i.e. goal –directed)
HRPreloadAfterloadContractilityHgbSaO2
↓V̇O2
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Decreasing Oxygen ConsumptionControl of feverUnloading respiratory muscles
NIV vs IntubationSedationParalytics
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Goal = Nl SvO2Vast majority of shock states respond to
EARLY optimization of balancing oxygen delivery and consumption, BUT…
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Exceptions to the ruleThe pattern of rising lactate despite normal
(or even more ominous, high) SvO2 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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HyperlactatemiaType A-
Classic- due to hypoxia and anaerobic metabolism
Type B-Drugs (metformin, HARRT, etc), Cancer,
ETOHism, HIVType 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 #1Which of the following values is NOT a
determinant of D ̇O2?1. Hbg2. SvO2
3. Preload4. PaO2
5. Heart rate
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Question #2Disutilization of oxygen at the mitochondrial
level prompting anaerobic metabolism and lactate production independent of O2 delivery, can be termed…1. Circulatory Hypoxia2. Cytopathic Hypoxia3. Anemic Hypoxia4. Hypoxemic Hypoxia5. Obstructive Hypoxia
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Question #3Optimizing which of the following is NOT a
treatment option for shock?1. Urine Output2. Contractility3. Work of breathing4. Arterial Oxygen Saturation5. Hgb
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Question #4Which of the following is NOT an example of
obstructive shock?1. Tension pneumothorax2. Atrial myxoma3. Pulmonary embolism4. Pericardial tamponade5. Papillary muscle rupture
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Question #5Which of the following is NOT a cause of
Type B lactic acidosis?1. HAART2. Alcoholism3. Lymphoma4. short-gut syndrome5. metformin
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BibliographyOxygen delivery. Hameed SM. Aird WC. Cohn
SM. Critical Care Medicine. 31(12 Suppl):S658-67, 2003 Dec.