Post on 17-Dec-2015
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Physiology of Shock:Beyond Hinshaw-Cox
Matthew Boland MD, FCCPPulmonary/CCM
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
Hinshaw-Cox ApproachHypovolemicCardiogenicObstructiveDistributive
A Physiologic ApproachShock ≈ ↓ D ̇O2
(inappropriate to V ̇O2)
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)
So…D ̇O2 = HR x (∫ Afterload, Preload and Contractility) x
Hgb x SaO2 x 1.34 x (0.003 x PaO2)
So…4 types of ShockCirculatory Hypoxia
This is where Hinshaw-Cox categories really fit…
Anemic Hypoxia (low hgb)Hypoxemic Hypoxia (low SaO2)And…
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
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”
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)
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
Treatment of ShockID and treat underlying cause WHILEOptimizing ‘Big 7’ (i.e. goal –directed)
HRPreloadAfterloadContractilityHgbSaO2
↓V̇O2
Decreasing Oxygen ConsumptionControl of feverUnloading respiratory muscles
NIV vs IntubationSedationParalytics
Goal = Nl SvO2Vast majority of shock states respond to
EARLY optimization of balancing oxygen delivery and consumption, BUT…
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)
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).
Question #1Which of the following values is NOT a
determinant of D ̇O2?
1. Hbg2. SvO2
3. Preload4. PaO2
5. Heart rate
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
Question #3Optimizing which of the following is NOT a
treatment option for shock?1. Urine Output2. Contractility3. Work of breathing4. Arterial Oxygen Saturation5. Hgb
Question #4Which of the following is NOT an example of
obstructive shock?1. Tension pneumothorax2. Atrial myxoma3. Pulmonary embolism4. Pericardial tamponade5. Papillary muscle rupture
Question #5Which of the following is NOT a cause of
Type B lactic acidosis?1. HAART2. Alcoholism3. Lymphoma4. short-gut syndrome5. metformin
BibliographyOxygen delivery. Hameed SM. Aird WC. Cohn
SM. Critical Care Medicine. 31(12 Suppl):S658-67, 2003 Dec.