1) Shock is defined as inadequate tissue perfusion and can be cardiogenic, hemorrhagic, distributive, or neurogenic in type. Traditionally defined as a systolic blood pressure under 90 mmHg, studies show mortality increases sharply below 110 mmHg. 2) The shock index (heart rate divided by systolic blood pressure) and modified shock index (heart rate divided by mean arterial pressure) can help assess shock severity and predict outcomes. Lactate and base deficit also correlate with injury severity and outcomes. 3) Compensatory mechanisms in shock include shunting blood to vital organs, increased sympathetic activity, renal sodium retention, and fluid shifts. The "lethal triad"

1. SHOCK
Dr Kaushal Deep Singh
Lecturer, Department of Surgery
UPUMS, Saifai

2. Introduction
■ Definition: Inadequate perfusion of tissue.
■ Types:
1. Cardiogenic Shock
2. Hemorrhagic Shock
3. Distributive Shock
4. Neurogenic Shock
■ Hypotension has been traditionally set, arbitrarily, at
< 90 mm Hg.
■ Eastridge suggested that hypotension be redefined
as < 110 mm Hg.
■ In 2008, Bruns and colleagues confirmed the
concept, showing that a prehospital BP < 110 mm Hg
was associated with a sharp increase in mortality and
that 15% of patients with BP < 110 mm Hg would
eventually die in the hospital.

3. Shock Index (SI)/Modified Shock Index (MSI)
■ SI is defined as heart rate divided by systolic BP.
■ Utility not only in trauma patients but also in sepsis, obstetrics, myocardial infarction, stroke,
and other acute critical illnesses.
■ Also useful for paediatric and geriatric population.
■ Correlates with need for interventions (blood transfusion and invasive procedures including
operations).
■ MSI is defined as heart rate divided by mean arterial pressure.
■ High MSI indicates a value of stroke volume and low systemic vascular resistance, a sign of
hypodynamic circulation.
■ MSI has been considered a better marker than SI for mortality rate prediction.
■ Age, mechanism of injury, Glasgow Coma Scale (GCS) score, lactate levels, hemoglobin levels,
and other physiologic parameters - addition of variables would be more predictive of outcome.

4. Lactate and Base Deficit
■ Lactate - marker of injury, and possibly ischemia.
■ Lactate - byproduct of anaerobic metabolism. Routinely perceived to be an end waste product that is
completely unfavourable.
■ In humans, lactate may be the preferred fuel in the brain and heart; in these tissues, infused lactate is
used before glucose at rest and during exercise.
■ Because it is glucose sparing, lactate allows glucose and glycogen levels to be maintained.
■ Lactate fuels the human brain during exercise and protective role in traumatic brain injury.
■ Base deficit, a measure of the number of millimoles of base required to correct the pH of a liter of
whole blood to 7.4.
■ Seems to correlate well with lactate level, at least in the first 24 hours after an injury.
■ Rutherford, in 1992, showed that a base deficit of 8 was associated with a 25% mortality rate in
patients older than 55 years without a head injury or in patients younger than 55 years with a head
injury.
■ When base deficit remains elevated, it is an indication of ongoing shock.

5. Compensatory Mechanisms in Shock
■ Blood is shunted from less critical organs (e.g., skin,
skeletal muscle, and splanchnic circulation) to more
critical organs (e.g., brain, liver, and kidneys).
■ Shock → ↑ Sympathetic activity, ↓ Parasympathetic
activity → ↑ Epi- & Norepinehrine → ↑ Myocardial
contractility and rate, vasoconstriction
■ Kidneys – Vasoconstriction, ↓ blood flow → Renin →
Angiotensin → Aldosterone, Na+ resorption
■ Carotid baroreceptors, ANP → Supraoptic,
paraventricular nuclei of brain → ADH → Water
resorption
■ ↓ water in intravascular space, Precapillary
constriction > Postcapillary → ↓ Hydrostatic
pressure. Shift of water from extravascular to
intravascular compartment.

6. LethalTriad
■ Triad of acidosis, hypothermia, and coagulopathy.
■ Shock → Inadequate tissue perfusion
↓
→ ↑ Lactate → MetabolicAcidosis → ↓ Enzymatic action → Coagulation abnormality
→ ↓ O2 → ↓ ATP → ↓ Heat production → ↓ Enzymatic action → Coagulation abnormality
(Hypothermia)

7. Acidosis
■ Double edged sword.
■ Correction – NaHCO3 ,THAM (tromethamine; tris[hydroxymethyl] aminomethane).
■ THAM - biologically inert amino alcohol of low toxicity that buffers CO2 and acids. Sodium free and limits the generation of
CO2 in the process of buffering. At 37° C, the pKa of THAM is 7.8, making it a more effective buffer than sodium
bicarbonate in the physiologic range of blood pH.
■ Unlike sodium bicarbonate, which requires an open system to eliminate CO2 to exert its buffering effect, THAM is effective
in a closed or semiclosed system, and it maintains its buffering ability during hypothermia.
■ Initial loading dose ofTHAM acetate (0.3 M, pH 8.6) for the treatment of academia:
THAM (in mL of 3M solution) = lean body weight (in kilograms) × the base deficit (in mmol/liter)
■ Maximal daily dose - 15 mmol/kilogram/day for an adult (3.5 liters of a 0.3 M solution in a patient weighing 70 kg).
■ Indications –
– Treatment of respiratory failure (acute respiratory distress syndrome [ARDS] and infant respiratory distress syndrome);
– Use during hypothermia and permissive hypercapnia (controlled hypoventilation).
– Diabetic and renal acidosis, salicylate and barbiturate intoxication, and increased intracranial pressure (ICP) associated
with brain trauma.
– Used in cardioplegic solutions and during liver transplantation.

8. Hypothermia
■ Double edged sword.
■ Trauma patients with a
postoperative core
temperature below 35° C have a fourfold increase in death; below 33° C, a sevenfold
increase in death.
■ The survival rates after accidental hypothermia range from about 12% to 39%. The
average temperature drop is to about 30° C.
■ Trauma-associated hypothermia - survival rate falls dramatically with the core
temperature, reaching 100% mortality when it reaches 32° C.
■ Beilman and coworkers demonstrated that hypothermia was associated with more
severe injuries, bleeding, and a higher rate of multiple-organ dysfunction in the ICU, but
not with death.

10. Coagulopathy
■ Causes - Acidosis, hypothermia, consumption, dilution, disease.
■ Measured by PT,APTT, INR, thromboelastography and rotational thromboelastometry.
■ Thromboelastography parameters include R, reaction time; α, alpha angle; and MA, maximum
amplitude.
■ The R time reflects the latent time until fibrin formation begins.An increase in this time may
result from factor deficiency or decreased factor activity, whereas a decrease in R time reflects a
hypercoagulable state.
■ The steepness of the α angle reflects the rate of fibrin formation.
■ The measure of clot strength is MA, which reflects clot elasticity.The value of MA is a measure
of the strength of interaction between the coagulation factors and platelets.Qualitative or
quantitative defects in either of these would result in decreased MA.
■ Thromboelastography provides the additional ability to measure the fibrinolytic arm of the
coagulation cascade. LY30 and LY60 indices provide a measure of the fibrinolysis rate by
calculating the decrease in clot strength at 30 and 60 minutes, respectively. A large lysis index
reflects rapid fibrinolysis and may help guide the use of antifibrinolytic therapy in these patients,
which has been shown to reduce mortality if it is used within 3 hours of injury.

12. ■ Treatment –
1. Stop bleeding
2. Correct acidosis and hypothermia
3. Fresh frozen plasma
4. Platelet transfusion
5. Vitamin K injection
6. Recombinant factorVIIa (rFVIIa) – Definite role inTBI
7. Factor IX or prothrombin complex concentrate (PCC) –
■ Has become popular for the treatment of surgical coagulopathy.
■ For patients taking warfarin, PCC is the recommended treatment of choice.
■ Particular benefit in elderly patients with TBI, in whom treatment with fresh-frozen plasma (FFP) can
potentially be a problem if the patient has comorbid cardiac disease and could induce cardiac heart
failure from volume overload.
■ Additional benefit of using PCC is that the time to reversal of coagulopathy is shorter than when FFP is
used.PCC actually has many factors (factors II, VII, IX, X) in it, including variable amounts of factor VIIa,
depending on the brand of PCC used.
■ Costs only one-tenth the cost of rFVIIa.
8. Tranexamic acid (TXA) is a synthetic analogue of the amino acid lysine. It is an antifibrinolytic
that competitively inhibits the activation of plasminogen to plasmin. Thus, it prevents
degradation of fibrin.

13. Oxygen Delivery
■ DO2 = CO × CaO2 oxygen delivery (DO2); cardiac output (CO); content of oxygen carried
by a volume of blood (CaO2)
■ CaO2 = (1.34×Hgb×SaO2) + (0.003×PaO2)
oxygen saturation (SaO2) of the red cell; partial pressure of
oxygen in the arterial blood (PaO2)
■ Cardiac output is heart rate multiplied by the stroke volume.
■ VO2 = CO×(CaO2 −CvO2)
Oxygen consumption (VO2) by cells; content of oxygen in the
venous system (CvO2)
■ VO2 = CO×1.34×Hgb×(SaO2 −SvO2)
■ Average mixed venous sample is 75% saturated, so the oxygen consumption is thought to be on
average 25% of the oxygen delivered.

14. Optimization (Supernormalization)