This document discusses the classification, recognition and management of shock. It defines shock as acute circulatory failure resulting in inadequate organ perfusion and cellular hypoxia. Shock is classified into four types: hypovolemic, cardiogenic, distributive, and obstructive. Key aspects of each type are discussed in detail, including causes, pathophysiology, diagnosis, and treatment approaches. General management principles for shock include initial resuscitation with fluids, blood products, and vasopressors as needed. Goals of resuscitation are also outlined.

1. Classification, Recognition And
Management Of Shock

2. Shock : Definition
Acute circulatory failure resulting in inadequate organ
perfusion and cellular hypoxia.

3. Introduction
Diagnosis is based on clinical, hemodynamic & biochemical
signs which can be classified in three components :
1.Systemic arterial hypotension
2.Clinical signs of tissue hypoperfusion -
apparent through three “windows” of body-
a. cutaneous signs
b. renal –urine output
c. neurological signs
3.Hyperlactemia ( >1.5 mmol/L )

4. In Normal Conditions: Aerobic
Metabolism
6 O2
GLUCOSE
METABOLISM
6 CO2
2
6 H O
36 ATP
HEAT (417 kcal)

5. In Poor Perfusion States: Anaerobic
Metabolism
GLUCOSE METABOLISM
2 LACTIC ACID
2 ATP
HEAT (32 kcal)

6. Consequences of anaerobic
metabolism
6
Inadequate
Cellular
Oxygenation
Anaerobic
Metabolism
Metabolic
Failure
Metabolic
Acidosis
Inadequate
Energy
Production
Lactic Acid
Production
Cell Death!

7. Classification
1.Hypovolemic Shock
2.Cardiogenic Shock
3.Distributive Shock
a. Septic Shock
b. Anaphylactic Shock
c. Neurogenic Shock
4.Obstructive Shock

8. HYPOVOLEMIC SHOCK
Hemorrhagic :
External hemorrhage:
⚫ Trauma
⚫ Hematoma
Internal
hemorrhage: GIT
Bleeding
Hemothorax/Hemoperitoneum
Non-hemorrhagic
🠶 External:
⚫ Vomiting, Diarrhea
⚫ Polyuria
⚫ Dehydration
⚫ Burns
Internal (third spacing):
⚫ Pancreatitis
⚫ Bowel obstruction
⚫ Ascites

9. HAEMORRHAGIC SHOCK :
History suggestive of hemorrhage
with
Systolic blood pressure<90 mm of Hg
Mean arterial pressure≤60 mm of Hg
Serum lactate>2 mmol/l
🠶Hemorrhagic shock
Leading preventable cause of death in trauma
9

10. ASSESSMENT
🠶Physical Examination
🠶Laboratory tests
10

11. Physical Examination
🠶First step is to recognize its presence
🠶A search for the source of bleeding
🠶This involves a careful head to toe examination
🠶Pelvic examination in obstetric patient
🠶Repeated careful physical examination and monitoring of vital signs
11

12. Clinical Assessment of hemorrhagic shock:
S/S vary depending on severity of blood loss :
**ninth edition,Sept 2012,American Collegeof
Surgeons Committee on Trauma,ATLS

13. Laboratory Investigation
🠶Arterial blood gas : most useful laboratory test.
🠶Metabolic acidosis- an elevated lactate level indicate inadequate tissue
perfusion.
🠶Hemoglobin and hematocrit :
🠶not useful in the diagnosis of shock.
🠶may remain normal in early acute blood loss before resuscitation.
🠶 serial estimate of Hb is helpful in identifying significant blood loss and
potential need for blood transfusion and surgical intervention.
🠶Coagulation studies and Electrolytes
13

14. Diagnostic Options:
Site of Bleeding Diagnostic Modalities
Chest Bedside Chest radiography
Thoracostomy tube output
Abdomen Physical examination
Ultrasound examination (FAST)
Peritoneal lavage
Long bones Physical examination
Plain radiography
Outside the body Physical examination
14

15. Initial management
⚫ABCs
⚫Initial measures to stop bleeding
⚫Initial fluids
⚫Crystalloid
⚫Warming – effects of hypothermia on
mortality
15

16. 🠶Trauma patients are approached systematically, using the principles
of the primary and secondary survey
🠶ATLS emphasizes the ABCDE mnemonic: airway, breathing,
circulation, disability and exposure
🠶 ATLS is based on simultaneous efforts to identify and treat life-
and limb-threatening injuries, beginning with the most immediate
16

17. 🠶After the primary survey when the patient is stabilized, a more deliberate
secondary examination is undertaken
🠶 Any remaining injuries are diagnosed at this time and treatment plans
established
17

18. Initial measures to stop bleeding
⚫Pressure to the bleeding part
⚫Elevation of the bleeding limb
⚫Tourniquet application (not usually recommended)
⚫Immediate placement of a chest tube helps expand the lung
⚫Splinting for fractured extremities
⚫Bimanual uterine compression, administration of oxytocin and uterine evacuation.
18

19. Initial fluids
🠶Warmed isotonic Crystalloid solutions are used for initial resuscitation .
🠶The usual initial dose is 1-2 liters for an adult and 20mL/kg for a pediatric
patient.
🠶 Advantages :
🠶availability, safety, and low cost.
🠶Interstitial losses are replaced.
🠶 Disadvantage: rapid movement from the intravascular to the extravascular space, leading to
three or more times requirement for replacement, and resulting in tissue edema.
19

20.  More effective in rapidly restoring intravascular volume, requiring less
fluid to correct hypovolemia
 Include albumin, hydroxyethyl starch, dextrans, and gelatins.
 Limitation:
-Carries the risk of reaction..
-Are far more expensive
 Nonetheless, the interstitial fluid deficit associated with hypovolemic
shock may be better treated with a crystalloid solution or a combination of
colloids and crystalloids.
20
Colloid solutions

21. Replacement fluids
⚫Ringer’s lactate
 Adv: over NS to avoid hyperchloremic acidosis
 Disadv:- -slightly hypotonic , in large amounts can aggravate cerebral edema.
⚫Hypertonic salt solutions (3% and 7.5% saline) :
 Adv:- less cerebral edema than RL or NS in TBI
-small volumes rapidly expands plasma volume
 Disadv: progressive hypernatremia.
⚫Dextrose containing solutions :
 should be avoided: exacerbate ischemic brain damage
 Given only when documented hypoglycemia.
21

22. Adjuvant therapies
🠶Supplemental oxygen/mechanical ventilation.
🠶Prevention of hypothermia
🠶Treatment of any electrolyte abnormality, specially
hypocalcemia, hypo/ hyperkalemia, hypomagnesaemia
🠶Correction of acid base abnormality, severe metabolic acidosis
🠶Early treatment of hyperglycemia
🠶Corticosteroids. In case of adrenal failure
22

23. 23
Goals for Resuscitation
 Maintain systolic blood pressure at 80 -100 mm Hg
 Maintain hematocrit at 25% to 30%
 Maintain core temperature higher than 35°C
 Maintain SPO2
 Restore normal urine output
 Prevent an increase in serum lactate
 Prevent acidosis from worsening

24. Risks associated with aggressive volume replacement
during early resuscitation
 Increased blood pressure
 Decreased blood viscosity
 Decreased hematocrit
 Decreased clotting factor concentration
 Disruption of electrolyte balance
 Direct immune suppression
 Increased risk for hypothermia
24

25. Reassessment: Response to initial fluids
25

26. Blood transfusion and other products
With hemorrhagic shock, blood products can be life
saving.
⚫Decision to transfuse
⚫Blood Products
⚫Autotransfusion
26

27. Decision to transfuse
🠶If hemodynamic instability persists after approx. 2 L of crystalloid
infusion.
🠶In resource-constrained settings the administration of precious units of
blood should be delayed until hemorrhage is controlled.
🠶Use blood as part of pre-operative resuscitation, when possible.
27

28. INDICATIONS FOR BLOOD COMPONENT THERAPY
Component Indication
Packed RBCs Replacement of O2
carrying capacity
Platelets Thrombocytopenia with
bleeding
Fresh frozen plasma Documented
coagulopathy
Cryoprecipitate Coagulopathy with low
fibrinogen
28

29. Whole Blood vs Component
🠶Advantage of whole blood is
🠶 no special equipment is needed for processing
🠶 supplies plasma volume, red cells, platelets and
coagulation factors, thereby potentially avoiding the
coagulopathy often seen in hemorrhagic shock
29

30. Massive transfusion protocol
🠶Definition : replacement of > 1.5 blood volume in 24 hrs or
replacement of pt. total blood volume by stored homologous bank
blood in 24 hrs
🠶Indication : unresponding unstable pt. who has already transfused 2
units of PRBC with initial resuscitation
🠶It minimize dilutional coagulopathy
🠶1:1:1 (FFP:Platelates:PRBC) initiated early in 1st 2 units of transfused
PRBC

31. VASOPRESSORS
If despite adequate resuscitation with fluids and blood products:
⚫ the CVP <= 8 cm of H2O
⚫ MAP < 60 mm of Hg,
Vasopressors should be considered.
31

32. Damage control resuscitation
 Definition:
Asystematic approach to severe trauma incorporating several strategy to
decrease mortality & morbidity.
Components:
1.Permissive hypotension
2.Hemostatic resuscitation
3.Damage control surgery
 Acute life-threatening bleeding within the abdominal or thoracic cavity is
an indication for operation.

33. MONITORING
Noninvasive monitor:
⚫ECG
⚫BP cuff
⚫Pulse oximeter
⚫ETCO2
⚫Temperature probe
⚫Foley’s catheter-
urine output
Invasive monitor:
⚫Arterial line.
⚫For blood sampling & BP
monitoring
⚫Central venous catheter
⚫For determining patient’s
volume status.
⚫Pulmonary artery catheter.
⚫If the pt. shows signs of heart
failure.
33

34. CARDIOGENIC
SHOCK
34

35. Definition
🠶Cardiac output falls due to the pathology in the heart itself and is
defined as cardiac index less than 2.2 L/ minute/m2. (Cardiac
index is cardiac out put per meter of body surface area)
35

36. Hemodynamic criteria
🠶Sustained hypotension (systolic blood pressure < 90 mm Hg for at least
30 minutes)
🠶Reduced cardiac index (< 2.2 L/min per m2) in the presence of
elevated pulmonary capillary occlusion pressure (>15 mm Hg)
36

37. Pathophysiology of Cardiogenic shock
37

38. Etiology of Cardiogenic Shock
Functional
• Myocardial infarction (most common)
• Blunt Cardiac Injury (trauma)
• Myocarditis
• Cardiomyopathy
• Septic myocardial depression
Mechanical (Structural)
• Valvular failure (stenotic or regurgitant)
• Hypertrophic cardiomyopathy
• Ventricular septal defect
Arrhythmic
• Bradycardia
• Tachycardia Hollenberg Ann Int Med 1999; 131:47-99
38

39. Diagnosis
🠶A focused history and physical examination
🠶Blood tests
🠶Echocardiography
🠶ECG
🠶Chest X-Ray
39

40. 🠶Chest pain
🠶Dyspnea
🠶Pallor
🠶Anxiety
🠶Sweating
🠶Confusion
🠶Agitation
🠶Altered mentation
🠶Tachycardia with feeble
pulse (90–110 beats/m)
🠶Severe bradycardia due to
high-grade heart block may
be present
🠶Systolic blood pressure (BP) is
reduced (<90 mmHg) with a
narrow pulse pressure (<30
mmHg)
🠶Tachypnea and jugular venous
distention.
🠶Characteristic murmurs of MS
and MR may be audible
🠶Rales are audible with LVF
🠶Oliguria (urine output < 30
mL/h) is common
40
HISTORY AND PHYSICAL EXAMINATION

41. LABORATORY TESTS
⚫TLC - ↑
⚫Hepatic transaminases - ↑
⚫BUN & S.Cr - ↑
⚫↑anion gap acidosis
⚫↑ lactic acid level
⚫Arterial blood gases:
⚫hypoxemia and metabolic acidosis with compensatory respiratory alkalosis
⚫Cardiac markers
⚫CPKMB ↑ ↑
⚫TROPONIN - I & T ↑
41

42. ⚫Chest X-Ray
⚫ Shows pulmonary vascular congestion and
often pulmonary edema
⚫Echocardiography
⚫ Excellent tool for confirming the diagnosis
of cardiogenic shock and ruling out other
causes of shock
⚫ECG
⚫ >2-mm ST elevation in multiple leads or
LBBB are usually present.
⚫ 55% of all infarcts associated with shock are
anterior in location.

43. THERAPEUTIC OPTIONS
🠶General measures
🠶Vasopressors
🠶Intra-aortic balloon pumping (IABP)
🠶Reperfusion-revascularization : percutaneous transluminal
coronary angioplasty (PTCA)
43

44. GENERAL MEASURES
🠶Central venous and arterial access, bladder catheterization, and
pulse oximetry are instituted
🠶Hypoxemia and acidosis must be corrected
🠶Most patients require ventilatory support to correct these
abnormalities and reduce the work of breathing
🠶Electrolyte abnormalities should be corrected
🠶Hyperglycemia should be corrected with continuous infusion of
insulin
44

45. 🠶Relief of pain and anxiety with Morphine sulfate (or
fentanyl)
🠶 Bradyarrhythmias and tachyarrhythmias may require
immediate treatment with antiarrhythmic drugs,
cardioversion, or pacing
🠶Hemodynamic goals:
Systolic BP of ~90 mmHg or Mean BP > 60 mmHg and
PCWP of ~15 mmHg
45

46. OBSTRUCTIVE SHOCK
A form of cardiogenic shock that results from
mechanical impediment to circulation leading to
depressed CO rather than primary cardiac failure
 Impaired diastolic filling (decreased
ventricular preload)
- Tension pneumothorax
- Constrictive pericarditis
- Cardiac tamponade
- intrathoracic obstructive tumors

47.  Impaired systolic contraction (increased ventricular afterload)
- Pulmonary embolus (massive)
- Acute pulmonary hypertension
- Aortic dissection
 THERAPEUTIC OPTIONS :
• General measures
• ICTD insersion
• Thoracotomy
• Pericardiocentesis
• embolectomy

48. Distributive Shock
Inadequate perfusion of tissues through maldistribution of
blood flow
Intravascular volume is maldistributed because of alterations
in blood vessels
Cardiac pump & blood volume are normal but blood is not
reaching the tissues
48

49. Distributive Shock :
 Septic (bacterial, fungal, viral)-most common
 Anaphylactic shock
 Neurogenic (spinal shock)
 Endocrinological causes-
• Adrenal crisis
• Thyroid storm

50. Septic shock:
Syndrome of profound
hypotension due to release of
endotoxins / TNF / vasoactive
peptides following bacterial
destruction
Usually associated with
normal blood volume, high CO
and low SVR
Re-distribution of blood to
splanchnic vessels with
resultant poor skin perfusion

51. New definition of sepsis
🠶 The terms SIRS and severe sepsis were eliminated
🠶 Sepsis is now defined as life threatening organ dysfunction caused by a dysregulated
host response to infection
🠶 Organ dysfunction is newly defined in terms of a change in baseline SOFA
(sequential organ failure assessment) score
🠶 Septic shock is defined as the subset of sepsis in which underlying circulatory and
cellular or metabolic abnormalities are profound enough to increase mortality
substantially. **Feb 2016 Society of Critical Care Medicine and
the European Society of Intensive Care Medicine.

52. Quick SOFAscoring
 Anew clinical sepsis screening tool
🠶Components :
1.Respiratory rate >22
2.Glasgow coma score <15
3.Systolic blood pressure <100 mm hg
 ≥2 positive screening.

53. Clinical Manifestations of septic shock
1.Early phase:
 Massive vasodilation – Pink,
warm, flushed skin
 Increased Heart Rate - Full
bounding pulse
 Tachypnea
 Crackles
2.Late phase:
Vasoconstriction – Skin is pale &
cool
Significant tachycardia
Decreased BP
Decreased Urine output
Metabolic & respiratory
acidosis with hypoxemia

54. Management of septic shock

55. SURVIVING SEPSIS CAMPAIGN BUNDLES:
To be completed within 3 hours:
1) Measure lactate level
2) Obtain blood cultures prior to administration of antibiotics
3) Administer broad spectrum antibiotics
4) Administer 30 ml/kg crystalloid for hypotension or lactate ≥4mmol/l

56. SURVIVING SEPSIS CAMPAIGN BUNDLES contn :
To be completed within 6 hours:
5) Apply vasopressors for persistent hypotension- to maintainAMAP 65 mm hg
6) In the event of persistent arterial hypotension despite volume resuscitation (septic shock) or
initial lactate ≥ 4 mmol/l (36 mg/dl):
- Measure CVP and scvo2
7) Remeasure lactate if initial lactate was elevated
*Targets for quantitative resuscitation included in the guidelines are cvp of 8 mm hg, scvo2 of
70%, and normalization of lactate

57. Commonly used Vasopressor and Inotropic
Drugs

58. Drugs Calculation rule
Nor epinephrine
Adrenaline
0.3× body wt in kg is the number of mg to add to make a
final volume of 50 ml
Then, 1ml/hr delivers 0.1µg/kg/min
Dopamine
Dobutamine 3× body wt in kg is the number of mg to add to make a
final volume of 50 ml
Then, 1ml/hr delivers 1µg/kg/min
Arenaline
nor epinephrine .03× body wt in kg is the number of mg to add to make a
final volume of 50 ml
Then, 1ml/hr delivers .01 µg/kg/min
Theformula Ruleof 3hadbeen stated inTheHarriet Lane Handbook is asfollows:
“3 × weight (kg) equals the amount of drug in mg that should be added to 50 ml of solution. The
infusion volume in milliliters per hour (ml/hour) will then equal the mcg/kg/minute dose
ordered.”

59. Neurogenic Shock
59

60. Neurogenic Shock
Results from the loss or suppression of sympathetic tone
venous
Causes massive vasodilatation in the venous vasculature,
return to heart, cardiac output
 Most common etiology: Spinal cord injury above T6
It is rarest form of shock
60

61. P
A
THOPHYSIOLOGY
61
Imbalance between
Sympathetic and
Parasympathetic
stimulation
Massive vasodilation
Vascular tone
SVR
Inadequate C.O
Tissue perfusion
Impaired cellular
metabolism SHOCK

62. DIAGNOSIS
⚫Loss of sympathetic nervous system function
-Relative bradycardia and hypotension
-Warm, flushed skin
-Loss of bladder control
62

63. Treatment strategies
🠶Airway control should be ensured with spinal immobilization and
protection.
🠶Crystalloid IV fluids should be infused
🠶Inotropic agents may be added in titrated doses if needed
🠶Severe bradycardia should be treated with Atropine 0.5 to 1.0 mg IV
(every 5 min for a total dose of 3.0 mg) or with a Pacemaker
 In the presence of Neurologic Deficits, high-dose Methylprednisolone
therapy should be instituted within 8 h of injury
 A30 mg/kg bolus should be administered over 15 min followed by a
continuous infusion of 5.4 mg/kg per h for the next 23 h
63

64. Anaphylactic shock
64

65. 🠶Anaphylactic shock: Immediate hypersensitivity reaction (Type I)
mediated by the interaction of IgE on mast cells and basophils with the
appropriate antigen
🠶Primary mediators include Histamine, Serotonin, Eosinophil,
Chemotactic Factor, and Proteolytic Enzymes
🠶Secondary mediators include PAF, bradykinin, prostaglandins, and
leukotrienes
65

66. CLINICAL FEATURES
⚫Early
• Sensations of warmth, itching especially in axillae and groins
• Feelings of anxiety or panic
⚫Progressive
• Erythematous or urticarial rash
• Oedema of face, neck, soft tissues
⚫Severe
• Hypotension (shock)
• Bronchospasm(wheezing)
• Laryngeal edema(dyspnea, stridor, aphonia, drooling)
• Arrhythmias, cardiac arrest.
66

67. MANAGEMENT
1. TheABCD’s of resuscitation should be followed
2.Administer oxygen by face mask at 6–8 L/minute
3. ADRENALINE
ADULTS: Inject adrenaline 1:1000 intramuscularly:
average adults (50–100 kg) give 0.50 mL
large adults (>100 kg) give 0.75 mL
4. Establish one or preferably two wide bore intravenous lines (16 gauge or larger)
5.If there is severe laryngospasm, bronchospasm, circulatory shock or coma, intubate
and commence IPPV
67

68. ⚫Additional measures :
• Beta2 agonists for bronchospasm
• Antihistaminics
• Corticosteroids
• Nebulised adrenaline
⚫However, do not delay intubation if upper airways obstruction is
progressive.
68

71. 71
Conclusion
Survival and outcomes improve with early perfusion, adequate
oxygenation and identification with appropriate treatment of the
cause of shock
Identification depends on signs and symptoms, basic
investigations, point of care studies: RUSH protocol, TEG
Target the lethal triad in trauma: hypothermia, acidosis and
coagulopathy

72. Conclusion contn :
DCR used during the initial phases of damage control has
further been associated with improved mortality rates and
reduced incidence of complications in major trauma patients
Following surviving sepsis guidelines improve patient outcome
in septic shock.
Choice of vasopressors should be kept in mind for different
types of shock.

73. Thank you