Physiology of Shock: Beyond Hinshaw-Cox

Matthew Boland MD, FCCP
A definition of SHOCK
 Global tissue hypoxia
 “global” implying systemically while
 “tissue hypoxia” implies inadequate oxygen
May be independent of, or even inversely proportional to
Hypoxia ≠ Hypoxemia
Hinshaw-Cox Approach
 Hypovolemic
 Cardiogenic
 Obstructive
 Distributive
A Physiologic Approach
 Shock ≈ ↓ ḊO2
(inappropriate to V̇O2)
 ḊO2 = CO x CaO2
 CO= HR x SV
 SV ∫ Afterload, Preload and Contractility
 CaO2 = Hgb x SaO2 x 1.34 x (0.003 x PaO2)
 ḊO2 = HR x (∫ Afterload, Preload and Contractility) x
Hgb x SaO2 x 1.34 x (0.003 x PaO2)
So…4 types of Shock
 Circulatory Hypoxia
 This is where Hinshaw-Cox categories really fit…
 Anemic Hypoxia (low hgb)
 Hypoxemic Hypoxia (low SaO2)
 And…
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 O2 delivery.
 Examples: cyanide poisoning, sepsis or anything that
uncouples oxidative phosphorylation
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”
Recognition of Shock
Basic Labs
 Chem 7
 Low bicarb, high anion gap
 Metabolic acidosis ± respiratory alkalosis
 Low SvO2 (though may be high, especially in cellular
 Lactate- elevated (though can be normal if shock is
well compensated)
Recognition of Shock:
 PAC, though rarely used in today’s Critical Care
environment, can be used to determine/narrow the
underlying pattern/cause of shock
Treatment of Shock
 ID and treat underlying cause WHILE
 Optimizing ‘Big 7’ (i.e. goal –directed)
 HR
 Preload
 Afterload
 Contractility
 Hgb
 SaO2
 ↓V̇O2
Decreasing Oxygen Consumption
 Control of fever
 Unloading respiratory muscles
 NIV vs Intubation
 Sedation
 Paralytics
Goal = Nl SvO2
 Vast majority of shock states respond to EARLY
optimization of balancing oxygen delivery and
consumption, BUT…
Exceptions to the rule
 The 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)
 Type A Classic- due to hypoxia and anaerobic metabolism
 Type B Drugs (metformin, HARRT, etc), Cancer, ETOHism,
 Type δ- encountered in short-gut syndrome with
overproduction of δ-isomer of lactate (not assayed by
typical lactate measurements clinically).
Question #1
 Which of the following values is NOT a determinant of
1. Hbg
2. SvO2
3. Preload
4. PaO2
5. Heart rate
Question #2
 Disutilization of oxygen at the mitochondrial level
prompting anaerobic metabolism and lactate
production independent of O2 delivery, can be
1. Circulatory Hypoxia
2. Cytopathic Hypoxia
3. Anemic Hypoxia
4. Hypoxemic Hypoxia
5. Obstructive Hypoxia
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
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
Question #5
 Which of the following is NOT a cause of Type B lactic
2. Alcoholism
3. Lymphoma
4. short-gut syndrome
5. metformin
 Oxygen delivery. Hameed SM. Aird WC. Cohn SM.
Critical Care Medicine. 31(12 Suppl):S658-67, 2003

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