This document discusses shock, including its definition, pathophysiology, stages, types (hypovolemic, distributive, cardiogenic), and management. Shock is defined as inadequate tissue perfusion with oxygenated blood. It outlines the initial, compensatory, progressive, and irreversible stages of shock. Hypovolemic shock is the most common type in trauma patients and results from blood or fluid loss. Initial fluid resuscitation for trauma patients in hemorrhagic shock consists of 2 L of isotonic saline as rapidly as possible. Ongoing fluid resuscitation is guided by monitoring the patient's response and signs of end organ perfusion. Blood transfusion may be needed for patients who are transient or non

2. How do you define Shock?
Systemic imbalance between oxygen
supply and demand…
“Shock is inadequate tissue perfusion
with oxygenated blood”
Shock is not a blood pressure diagnosis!!

3. Pathophysiology of Shock

4. Whom to blame?

5. Principle Mechanisms
In CVS,
Pressure gradient =Flow x Resistance
Blood Pressure = Cardiac output x Resistance
HR x SV
Volume of blood in
ventricle
Resistance to
contraction
Force applied

6. Improving Stroke Volume:
Therapy for Cardiovascular Support
Preload Volume
Contractility Inotropes
Afterload Vasodilators

7. Principle Mechanisms
Flow = Perfusion
Adequate Flow =
Adequate
Perfusion
Inadequate Flow =
Indequate
Perfusion
(Hypoperfusion)
Hypoperfusion = Shock

8. Types of Shock
• Hypovolemic Shock
• Distributive Shock
– Neurogenic shock
– Septic shock
– Anaphylactic shock
• Cardiogenic Shock

9. Stages of Shock
• Initial Stage
• Compensatory Stage
• Progressive Stage
• Irreversible Stage

10. Stages of Shock
• Initial Stage
• Compensatory Stage
• Progressive Stage
• Irreversible Stage

11. Initial Stage
• Initially, the body compensates with the
onset of shock.
• No changes are noted clinically.
• Changes are beginning to occur on the
cellular level.

12. Stages of Shock
• Initial Stage
• Compensatory Stage
• Progressive Stage
• Irreversible Stage

13. Compensatory Stage
• Fluid shift from insterstital to intravascular
space.
• Activation of SNS - activation of epinephrine
and norepinephrine.
• Kidneys release renin into blood
formation of angiotension & release of
aldosterone, ADH

14. Decreased CO
SNS stimulation
Epinephrine &
norepinephrine
released
Vasoconstriction
Increased SVR
Renin secreted by
kidney
Angiotension
Aldosterone
ADH
Increase blood volume
hydrostatic pressure
fluid pulled into
capillary
Blood Pressure Maintained

15. • Initial Stage
• Compensatory Stage
• Progressive Stage
• Irreversible Stage
Stages of Shock

16. Progressive Stage
• Vicious circle of compensation eventually
leads to decompensation.
• Blood pressure starts to fall - SBP below 80 is
considered danger signal.
• Tachycardia; tachypnea; decreased urine
output; decreased body temperature; cold,
pale clammy skin.

17. • Initial Stage
• Compensatory Stage
• Progressive Stage
• Irreversible Stage
Stages of Shock

18. Irreversible Stage
• Body attempts at compensation have failed -
death is imminent.
• Pooling and sludging of blood; thrombosis of
small vessels occurs.
• Tissue hypoxia and anoxia occur - lactic acid
accumulation contributes to cell death.

19. HYPOVOLEMIC SHOCK IN
POLYTRAUMA PATIENT
• Shock is a common and frequently treatable
cause of death in injured patients and is
second only to traumatic brain injury as the
leading cause of death from trauma.
• ATLS (ADVANCED TRAUMA LIFE SUPPORT)

20. WHEN A PATIENT ARRIVES….
• Primary survey-
• ●Airway assessment and protection (maintain cervical
spine stabilization when appropriate)
• ●Breathing and ventilation assessment (maintain
adequate oxygenation)
• ●Circulation assessment (control hemorrhage and
maintain adequate end-organ perfusion)
• ●Disability assessment (perform basic neurologic
evaluation)
• ●Exposure, with environmental control (undress
patient and search everywhere for possible injury,
while preventing hypothermia)

21. Is the patient in SHOCK?????
• BLOOD PRESSURE- Not reliable ….
( BP falls when 30% blood volume lost )
Look for- Pulse Rate
Respiratory rate
Skin circulation
Pulse pressure (SBP-DBP)
ANY INJURED PATIENT WHO IS COOL & HAS
TACHYCARDIA IS CONSIDERED TO BE IN SHOCK
UNTIL PROVEN OTHERWISE.

22. • Haematocrit / Haemoglobin- Not reliable in
Acute blood loss.
• MASSIVE BLOOD LOSS MAY PRODUCE ONLY
MINIMAL DECREASE.
• SO, a VERY LOW HAEMATOCRIT SHORTLY
AFTER INJURY- MASSIVE BLOOD LOSS OR PRE
EXISTING ANAEMIA while a normal doesn’t
exclude significant blood loss.

23. CAUSE OF SHOCK IN TRAUMA PATIENT
• Can be HAEMORRHAGIC OR
• NON HAEMHORRHAGIC SHOCK.
( CARDIOGENIC SHOCK d/t Blunt cardiac injury,
Cardiac tamponade
Tension Pneumothorax
Neurogenic shock- ISOLATED INTRACRANIAL INJURIES DON’T
CAUSE SHOCK.
Cervical or upper thoracic spinal cord injury produce hypotension
d/t loss of sympathetic tone.
CLASSIC PICTURE – HYPOTENSION WITHOUT TACHYCARDIA OR
CUTANEOUS VASOCONSTRICTION
FAILURE OF FLUID RESUSCITATION TO RESTORE ORGAN PERFUSION
SUGGESTS EITHER CONTINUING HEMORRHAGE OR NEUROGENIC
SHOCK

24. HEMORRHGIC SHOCK???
• Try to find source----
“ ON THE FLOOR PLUS FOUR MORE “
CHEST
ABDOMEN
PELVIS
EXTREMITIES
ANY EXTERNAL BLEEDING

25. WHAT TO DO
• Xray abdomen , chest and pelvis
• Focussed Assesment Sonography in Trauma
(FAST)
• Diagnostic Peritoneal Lavage (DPL)
• Computed Tomography (CT)

26. Haemodynamically Unstable Patient

27. Haemodynamically Stable Patient

28. CHEST INJURY

29. HEMORRHAGIC SHOCK
• Advanced Trauma Life Support (ATLS) manual
describes four classes of hemorrhage to
emphasize the early signs of the shock state.
• Normal Adult blood volume = Approximately-
7% of body weight ( 70 kg= 5 L)
• Children= 8-9% of Body weight (80-90 ml/kg).
• Volume replacement is determined by
patient’s response to initial therapy.

30. • Hemhorrhage control & balanced fluid
resusicitation must be initiated when early S/S of
blood loss are apparent or suspected- NOT WHEN
BP IS FALLING OR ABSENT.
• BLEEDING PATIENT NEEDS BLOOD….otherwise

31. CLASS I HEMORRHAGE
• ● Blood volume loss of up to 15 percent.
• The heart rate is minimally elevated or
normal, and there is no change in blood
pressure, pulse pressure, or respiratory rate.
• Usually don’t require blood.

32. CLASS II HEMORRHAGE
• 15 to 30 percent blood volume loss
• Manifested clinically as
Tachycardia (heart rate of 100 to 120), Tachypnea
(respiratory rate of 20 to 24),
• Decreased pulse pressure, although systolic blood
pressure changes minimally if at all.
• Skin may be cool and clammy, and capillary refill
may be delayed.
• Most stabilized with CRYSTALLOID, few may
require blood….

33. CLASS III HEMORRHAGE
• 30 to 40 percent blood volume loss, resulting in a
significant drop in blood pressure and changes in
mental status.
• Any hypotension (SBP less than 90 mmHg) or drop
in BP greater than 20 to 30 percent of the
measurement at presentation is cause for concern.
• Heart rate (≥120 and thready) and RR are markedly
elevated, while urine output is diminished. Capillary
refill is delayed.
• Mg- Stop BLEEDING & BLOOD TRANSFUSION-ASAP

34. CLASS IV HEMORRHAGE
• More than 40 percent blood volume loss
• LIFE THREATENING….
• Patients are hypotensive ( SBP less than 90 mmHg).
• Pulse pressure is narrowed (≤25 mmHg), and
tachycardia is marked (>120).
• Urine output is minimal or absent.
• The skin is cold and pale, and capillary refill is
delayed.
• Mg- Rapid fluid transfusion and surgical
intervention depending on initial fluid response.

35. FRACTURES & SOFT TISSUE INJURIES
Blood loss at fracture site
TIBIA/HUMERUS-750ml
FEMUR- Double 1500ml
RETROPERITONEUM- Liters…
Edema in injured soft tissue d/t
release of inflammatory
mediators.
Depletes intravascular volume

36. HOW TO USE IT..
• 70 kg patient and
• Clinically femur fracture
• ESTIMATED BLOOD LOSS???
• CLASSIFICATION OF SHOCK??
• FLUIDS??

37. • Estimated blood volume- 7% of 70 kg= 5 L
• Blood loss = 1470 ml
• 30%
• CLASS III
• CRYSTALLOIDS+ BLOOD PRODUCTS

38. FLUID THERAPY-OPTIONS
– Crystalloids
– Colloids
– Blood Products
• Blood
• Plasma
• Blood Substitutes

39. CRYSTALLOIDS
Solutions that contain small molecules that
flow easily across the cell membranes,
allowing for transfer from the bloodstream
into the cells and body tissues.
This will increase fluid volume in both the
interstitial and intravascular spaces
(Extracellular)

40. Commonly used CRYSTALLOIDS
0.9% sodium chloride (0.9% NaCl)
lactated Ringer's solution
 5% dextrose in water (D5W)
Ringer's solution-RL with out lactate

41. 0.9% sodium chloride (Normal Saline)
 Simply salt water that contains only water, sodium (154 mEq/L),
and chloride (154 mEq/L).
 It's called "normal saline solution" because the percentage of
sodium chloride in the solution is similar to the concentration of
sodium and chloride in the intravascular space.
It’s the fluid of choice for resuscitation efforts.
It's the only fluid used with administration of blood products.
Solutions Na+ K+ Ca2+ Mg2+ Cl- HCO3
- Dextrose mOsm/L
0.9% NaCl 154 154 308

42. o is the most physiologically adaptable fluid because its
electrolyte content is most closely related to the
composition of the body's blood serum and plasma.
o Another choice for first-line fluid resuscitation for certain
patients, such as those with burn injuries.
B- Ringer's lactate or Hartmann solution
Solutions Na
+
K
+
Ca
2+
Mg
2+
Cl
-
HCO3
-
Dextrose mOsm/L
Lactated
Ringer’s
130 4 3 109 28 273

43. Both 0.9% sodium chloride and LR may be used in many
clinical situations, but patients requiring electrolyte
replacement (such as surgical or burn patients) will benefit
more from an infusion of LR.
- LR is metabolized in the liver, which converts the lactate to
bicarbonate. LR is often administered to patients who have
metabolic acidosis not patients with lactic acidosis
- Don't give LR to patients with liver disease as they can't
metabolize lactate
- used cautiously in patients with sever renal impairment
because it contains some potassium
- LR shouldn't be given to a patient whose pH is greater than
7.5

44. Solutions that contain large molecules that don't pass the
cell membranes.
When infused, they remain in the intravascular
compartment and expand the intravascular volume and
they draw fluid from extravascular spaces via their higher
oncotic pressure.
-ALBUMIN
-MANNITOL
-DEXTRAN
-HETASTARCH
COLLOIDS

45. Colloid solutions
Precautions when using Colloid solutions:
-The patient is at risk for developing fluid volume overload
- Colloid solutions can interfere with platelet function
and increase bleeding times, so monitor the patient's
coagulation indexes.
- Anaphylactoid reactions are a rare but potentially
lethal adverse reaction to colloids

46. Colloid versus crystalloid
• Saline versus Albumin Fluid Evaluation(SAFE) trial, 6997
severe sepsis critically. No diff between groups for any
end point (mortality)
(Finfer, S, Bellomo, et al. A comparison of albumin and saline for fluid resuscitation : a
systematic review. Critcare med 1999; 358-2247.)
• Randomized trial compared penstarchto modified RLS
in severe sepsis; no difference in 28 day mortality.
(Brunkhorst, FM et al. intensive therapy in sepsis, N EnglJ Med 2008;385:125.)
• •Crystalloid versus colloid –clinic trials have failed to
consistently demonstrate a difference between colloid
and crystalloid in treatment of septic shock.
• (choi, PT, Yip, G. crystalloid vs. colloids in fluid resuscitation in the intensive care unit. N EnglJ Med
2004; 350:2247.)
OVERALL Crystalloids PREFERRED
-cheap
-readily available
-No alteration in coagulation

47. INITIAL FLUID
• Initial fluid resuscitation for trauma patients in
hemorrhagic shock consist of 2 L of isotonic
saline (ie, normal saline, NS) given as rapidly as
possible through short, large gauge (16 or larger)
peripheral IVs.
• Central venous catheters are used when
peripheral IVs are not available.
• Monitor patient response to initial fluids
resuscitation and identify evidence of end organ
perfusion.

48. DANGERS OF EXCESSIVE FLUIDS
• Infusions of large volumes of NS can lead to the
development of a nonanion gap hyperchloremic
metabolic acidosis.
• PERSISTANT INFUSION OF LARGE VOLUME OF FLUID
AND BLOOD IN AN ATTEMPT TO ACHIEVE NORMAL BP
IS NOT SUBSTITUTE FOR DEFINITIVE CONTROL OF
BLEEDING.
• TRIAD- COAGULOPATHY
- ACIDOSIS
- HYPOTHERMIA
• SO MONITOR…..

49. WHAT TO MONITOR
• BP, PP PR-A mean arterial pressure (MAP) around 65
mmHg or a systolic blood pressure (SBP) around 90
mmHg is a reasonable goal in penetrating trauma (MAP
= [(2 x diastolic) + systolic]/3).
• CVP STATUS & SKIN PERFUSION- Improvement is
evidence of evidence of enhanced perfusion but
difficult to quantitate.
• URINE OUTPUT- 0.5 ml/kg/hr in adults
1 ml/kg/hr in children
ACID BASE BALANCE- Initially resp alkalosis-d/t
tachypnea f/b metabolic acidosis in long standing
shock d/t anaerobic metabolism.

50. CVP
• Reflects the pressure in the central veins.
• CVP (right atrial pressure) indicates pressure and not
volume.
• DIFFICULTY-
• Shocked patients: low intravascular volume with
compensatory vasoconstriction: CVP low.
• Rapid resuscitation: fluid poured into a constricted
patient will increase BP & push CVP up rapidly, but the
vasculature may still be constricted.
• Redistribution: normally the patient's vasculature will
dilate a little and the fluid will redistribute slowly. CVP
falls to zero but the patient remains constricted.

51. ON BASIS OF INITIAL FLUID RESPONSE
• Decide course of subsequent therapy.
• Differntiate between
• On basis of fluid response -3 groups
HEMODYNAMICALLY STABLE HEMODYNAMICALLY
NORMAL
May have persistant
tachycardia,tachypnea &
oliguria.
Patient exhibit no signs of
inadequate tissue perfusion
Patient is clearly under
resuscitated & still in shock

52. RAPID RESPONSERS
• Responds to initial fluid bolus & remains
hemodynamically NORMAL in maintaience
phase.
• Estimated blood loss- 20%
• Blood & further surgical evaluation may be
needed

53. TRANSIENT RESPONDERS
• Initially improve but deteriorate when fluids
slowed to maintenance level d/t- Ongoing
blood loss or inadequate resuscitation.
• Estimated blood loss- 20-40%
• Blood transfusion & in transiently respond to
blood- Urgent surgical intervention.

54. NON RESPONDERS
• Failure to respond to crystalloids or Blood-
IMMEDIATE &URGENT SURGICAL
INTERVENTION (OPERATION
/ANGIOEMBOLIZATION ) to control
exsanguinating hemorrhage.
• ALSO CONSIDER- NON HEMOHRRGIC SHOCK
(CVP Monitoring and Cardiac ultrasound rules
out)

55. BLOOD TRANSFUSION
• Transient responders or Non responders
• Class III or IV hemohrrage
• Full crossmatched blood preferred – but takes
min 1 hour.
• O Packed cells can be used- O Negative in
females of child bearing age group
( TO avoid sensitization & pregancy
complications)

57. LATEST GUIDELINES FOR MASSIVE
BLOOD TRANSFUSION IN TRAUMA
PATIENTS
• Damage control Approach i.e.
1:1:1 (FFP:platelets:RBCs)
- Conventional resuscitation with crystalloid will rapidly
lead to greater than 50 percent dilution of coagulation
factors and a diminution of thrombin generation.
- Calcium gluconate to be used -10 to 20 mL should be
given intravenously (into another vein) for each 500 mL
of blood infused.
- Monitoring of patient should be PT, aPTT and platelet
count preferably after each five units of blood replaced.

58. MASSIVE TRANSFUSION
• Massive transfusion, historically defined as the
replacement by transfusion of 10 units of red
cells in 24 hours, is a response to massive and
uncontrolled hemorrhage.
• With more rapid and effective therapy,
definitions such as five units over three hours are
more effective in identifying patients needing
rapid issue of blood products for serious injuries
because of uncontrolled hemorrhage

59. COAGULATION CASCADE

60. Risk associated
• COAGULOPATHY-
Activation and consumption of coagulation factors
secondary to tissue trauma, such as massive head
injury or muscle damage
Reduced activity of coagulation factors from
prolonged shock, hypoxia, hypothermia, or failure
to clear activation peptides that act as competitive
inhibitors.
Such trauma-associated coagulopathy can be
diagnosed as Acute disseminated intravascular
coagulation (acute DIC).

61. Other explanations for
COAGULOPATHY
• Tissue injury/trauma and shock, and their
associated physiologic changes (ie, acidosis,
hypothermia, consumption of coagulant
proteins, and fibrinolysis) combined with
extensive blood loss and the dilutional effects
of physiologic vascular refill and fluid
replacement therapy.
• Acidosis and Hypothermia also alters
coagulation.

62. • Decrease platelet count-
• D/t dilutional effect of massive transfusion.
• In an adult, each 10 to 12 units of transfused
RBCs are associated with a 50 percent fall in
the platelet count; thus, significant
thrombocytopenia can be seen after 10 to 20
units of blood, with platelet counts
below 50,000/microL
Reed RL Jr, Ciavarella D, Heimbach DM, et al. Prophylactic platelet administration during massive
transfusion. A prospective, randomized, double-blind clinical study. Ann Surg 1986; 203:48.

63. MONITORING
• PT, aPTT, fibrinogen concentration, and
platelet count