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
6 H2O
36 ATP
HEAT (417 kcal)
5. In Poor Perfusion States: Anaerobic
Metabolism
GLUCOSE METABOLISM
2 LACTIC ACID
2 ATP
HEAT (32 kcal)
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
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 College of
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
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
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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.
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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.
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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.
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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
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26. Blood transfusion and other products
With hemorrhagic shock, blood products can be life
saving.
Decision to transfuse
Blood Products
Autotransfusion
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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.
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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
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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
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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:
A systematic 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
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)
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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)
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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.
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
Impaired diastolic filling (decreased
ventricular preload)
- Tension pneumothorax
- Constrictive pericarditis
- Cardiac tamponade
- intrathoracic obstructive tumors
A form of cardiogenic shock that results from
mechanical impediment to circulation leading to
depressed CO rather than primary cardiac failure
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
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 SOFA scoring
A new 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
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 maintain A MAP 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
58. Drugs Calculation rule
Nor epinephrine 0.3× body wt in kg is the number of mg to add to make a
final volume of 50 ml
Adrenaline
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
The formula Rule of 3 had been stated in The Harriet Lane Handbook is as follows:
“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.”
60. Neurogenic Shock
Results from the loss or suppression of sympathetic tone
Causes massive vasodilatation in the venous vasculature, venous
return to heart, cardiac output
Most common etiology: Spinal cord injury above T6
It is rarest form of shock
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62. DIAGNOSIS
Loss of sympathetic nervous system function
-Relative bradycardia and hypotension
-Warm, flushed skin
-Loss of bladder control
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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
A 30 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
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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
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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.
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67. MANAGEMENT
1. The ABCD’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
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68. Additional measures :
• Beta2 agonists for bronchospasm
• Antihistaminics
• Corticosteroids
• Nebulised adrenaline
However, do not delay intubation if upper airways obstruction is
progressive.
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69.
70.
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.