Matthew Boland MD, FCCP Pulmonary/CCM

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

Hinshaw-Cox Approach Hypovolemic Cardiogenic Obstructive Distributive

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 )

So… D ̇ O 2 = HR x (∫ Afterload, Preload and Contractility) x Hgb x SaO 2 x 1.34 x (0.003 x PaO 2 )

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…

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

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 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)

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 Shock ID and treat underlying cause WHILE Optimizing ‘Big 7’ (i.e. goal –directed) HR Preload Afterload Contractility Hgb SaO 2 ↓V ̇ O 2

Decreasing Oxygen Consumption Control of fever Unloading respiratory muscles NIV vs Intubation Sedation Paralytics

Goal = Nl SvO 2 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) 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)

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).

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

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

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 acidosis? 1. HAART 2. Alcoholism 3. Lymphoma 4. short-gut syndrome 5. metformin

Bibliography Oxygen delivery. Hameed SM. Aird WC. Cohn SM. Critical Care Medicine. 31(12 Suppl):S658-67, 2003 Dec.