2. SAMUEL V GROSS, 1872
“Shock is the
manifestation of
the rude unhinging
of the machinery
of life”
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3. HISTORICAL
PERSPECTIVE
• Ambroise Paré (1510) – Fluids to injured patients
• ‘Shock’ – 1743 – act of impact/ collision
• Guthrie (1815) – described physiological instability
• Crile (1899) – Importance of measuring BP
• Claude Bernard – Milieu intérieur
• Walter B. Cannon – Homeostasis
• WW I – Disturbance of nervous system
• Alfred Blalock (1934) – 4 categories of shock
• Carl John Wiggers (1950) – Wiggers prep
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4. Definition
A systemic state of tissue hypo-perfusion, which is inadequate for
normal cellular respiration
Systemic – global phenomenon
Hypoperfusion (relative/ absolute)
Inadequate cellular respiration
Anaerobic, dysfunction
Body responses thereof
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8. Cardiogenic shock
• Hemodynamic criteria:
1. Sustained Hypotension (i.e. SBP <90 mm Hg
for at least 30 minutes)
2. Reduced Cardiac Index (<2.2 L/min per
square meter) &
3. Elevated Pulmonary Artery Wedge Pressure
(>15 mm Hg)
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9. SEPTIC SHOCK
• Four sepsis-related clinical syndromes = Four steps of
increasingly exaggerated systemic inflammatory responses
SIRS
Sepsis
Severe Sepsis (Sepsis Syndrome)
Septic Shock
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10. DEFINITIONS DESCRIBING THE
CONDITION OF SEPTIC PATIENTS
Bacteremia: Bacteria in blood
Positive blood cultures
Septicemia: Microbes or their toxins in blood
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11. DEFINITIONS DESCRIBING THE
CONDITION OF SEPTIC PATIENTS
SIRS: Two or more of the following
(1) Temperature >38°C or <36°C
(2) Heart Rate > 90/ min
(3) Respi rate > 24/ min
(4) TLC >12,000/mm3 or <4,000/mm3)
or >10% bands on PBS
◦ SIRS may have a noninfectious etiology
Sepsis: SIRS that has a proven/ suspected microbial etiology
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12. DEFINITIONS DESCRIBING THE
CONDITION OF SEPTIC PATIENTS
Severe Sepsis (Similar to sepsis syndr): Sepsis with one or more signs of
organ dysfunction:
1. Cardiovascular
2. Renal
3. Respiratory
4. Hematologic
5. Unexplained metabolic acidosis
6. Adequate fluid resuscitation
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13. DEFINITIONS DESCRIBING THE
CONDITION OF SEPTIC PATIENTS
Septic Shock: Sepsis + Hypotension
or
Need for vasopressors to
maintain systolic BP 90 mmHg
or MAP70 mmHg
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14. DEFINITIONS DESCRIBING THE
CONDITION OF SEPTIC PATIENTS
Refractory septic shock: Septic shock
◦ lasting for >1 h
◦ Not responding to fluid or pressor administration
MODS: Dysfunction of more than one organ system,
requiring intervention (individual organ support) to maintain
homeostasis
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15. NEUROGENIC SHOCK
• Acute loss of sympathetic vascular tone
• Loss of vascular resistance
◦ Pooling in capacitance vessels
◦ Reduced preload
◦ Poor cardiac output
◦ Inadequate pressure in arterial system to
maintain capillary perfusion
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16. NEUROGENIC SHOCK
Etiology:
◦ High cervical spinal cord injury (vertebral body #)
◦ inadvertent cephalad migration of spinal anaesthesia
◦ epidural hematoma or devastating head injury
Failure of fluid resuscitation to improve hemodynamics, where no source of blood
loss or sepsis can be identified
Vasopressors are necessary to treat this condition
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17. TRAUMATIC SHOCK
• Hemorrhage overtly controlled, but
patients continues to lose plasma volume
into the interstitium
• Secondary microcirculatory injury
• Excessive pro-inflammatory response
• Third spacing
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18. OBSTRUCTIVE SHOCK
• Reduction in preload due to mechanical
obstruction of cardiac filling
•Common causes: cardiac tamponade,
tension pneumothorax, massive pulmonary
embolus or air embolus
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19. PATHOPHYSIOLOGY OF SHOCK
• Initial response driven by
• Tissue hypoperfusion
• Developing cellular energy deficit.
• Demand-supply mismatch
• Neuro-endocrine & inflammatory response (proportional
to degree & duration of shock)
• The specific responses depends on etiology of shock
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26. 31
• Arterial vasoconstriction with regional
variations
• Shunting of blood away from less essential
organ beds such as the intestine, kidney, and
skin
• Brain & heart – autoregulatory mechanisms
CARDIOVASCULAR
PATHOPHYSIOLOGY
39. Severity of shock
Compensated shock
◦ Loss of up to 15% of circulatory volume
◦ Maintain central blood volume
◦ If prolonged (>12 hrs) Ischaemia-Reperfusion effect
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40. Severity of shock
Decompensation
◦ Loss of > 15% of circulating volume.
◦ Progressive Renal, Respiratory & Cardiovascular decompensation.
◦ Hypotension >30-40% volume loss.
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45. Hemorrhagic shock
Approach to Hemorrhagic shock
Identify haemorrhage
Immediate resuscitative maneuvers
Identify the site of haemorrhage
Haemorrhage control
Damage control resuscitation
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53. Hemorrhagic shock
Fluid therapy : Dynamic Fluid Response
To determine shock status
250-500ml bolus over 5-10min
HR, BP & CVP are measured
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54. Hemorrhagic shock
Responders
• Sustained improvement in CVS status after bolus
• No active bleeding, require fluids to attain normal volume status
Transient Responders
• Initial improvement followed by reverting to previous state over 10-20 min
• Moderate ongoing fluid losses
Non responders
• No improvement in CVS status following bolus
• Severely volume depleted and likely to have ongoing loss( persistent uncontrolled
Hemorrhage)
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61. SEPSIS SIX
The Sepsis Six is the name given to a bundle of medical therapies designed to reduce
the mortality of patients with sepsis.
The Sepsis Six consists of three diagnostic and three therapeutic steps – all to be
delivered within one hour of the initial diagnosis of sepsis.
◦ Deliver high-flow oxygen.
◦ Take blood cultures.
◦ Administer empiric intravenous antibiotics.
◦ Measure serum lactate and send full blood count.
◦ Start intravenous fluid resuscitation.
◦ Commence accurate urine output measurement.
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62. Management of severe sepsis
Initial Resuscitation and Infection Issues
Hemodynamic Support and Adjunctive Therapy
Supportive Therapy of Severe Sepsis
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63. Initial Resuscitation and Infection Issues
A. Initial Resuscitation
B. Screening for Sepsis and Performance Improvement
C. Diagnosis
D. Antimicrobial Therapy
E. Source Control
F. Infection Prevention
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64. A. Initial Resuscitation
Resuscitation of patients with sepsis- induced tissue
hypoperfusion
◦ defined as hypotension persisting after initial fluid challenge or blood
lactate concentration ≥ 4 mmol/L
EGDT (first 6 hrs of resuscitation)
◦ a) CVP 8–12 mm Hg
◦ b) MAP ≥ 65 mm Hg
◦ c) Urine output ≥ 0.5 mL/kg/hr
◦ d) Scvo2 or Svo2 70% or 65%, respectively
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65. B. Screening for Sepsis and Performance
Improvement
Routine screening of seriously ill patients for severe sepsis to
increase the early identification of sepsis
allow implementation of early sepsis therapy
Performance improvement efforts to improve patient outcomes
and decrease sepsis-related mortality.
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Treatment: Initially pay attention to the ‘A’ ‘B’ & ‘C’ of resuscitation basics. Control ongoing haemorrhage. Early stabilization of fractures, debridement of devitalized or contaminated tissues, and evacuation of hematoma → ↓ subsequent inflammatory response to the initial insult & ↓ damaged-tissue release of DAMPs and subsequent diffuse organ injury. Supplementation of depleted endogenous antioxidants → ↓ subsequent organ failure and mortality.
Cultures as clinically appropriate before antimicrobial therapy if no significant delay (> 45 mins) in the start of antimicrobial(s) (grade 1C). At least 2 sets of blood cultures (both aerobic and anaerobic bottles) be obtained before antimicrobial therapy with at least 1 drawn percutaneously and 1 drawn through each vascular access device, unless the device was recently (<48 hrs) inserted
Colloids as well as crystalloids recommended in SSC 2008. Fluid challenge with 1ltr crystalloid or 300-500 ml colloid within 30 min recommended in SSC 2008.