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 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)

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.