2. Definition
Kumar and Parrillo (1995) - “The state in which
profound and widespread reduction of effective
tissue perfusion leads first to reversible, and then
if prolonged, to irreversible cellular injury.”
Hypovolemic shock- inadequate fluid for vascular
system
Distributive shock- increased size of vascular system
Cardiogenic shock- inadequate pumping action
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Advanced Emergency Trauma Course
4. Basic Physiology
• BP = CO x PR
• CO = SV x HR
4900ml =70ml x 70bpm
• Stroke Volume is a function
• Preload
• Afterload
• Myocardial Contractility
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Advanced Emergency Trauma Course
6. What is Unique about Children
• Poor ability to concentrate urine
• Neonates & infants urine output 1 – 2ml/Kg/hr
• Compare elderly urine outuput <0.5ml/Kg/hr
• Blood vol 8 – 9% of ideal body weight
• Children have more insensible losses compared to adults
7. CLASSIFICATION OF CIRCULATORY SHOCK
• Cardiogenic shock - due to cardiac pump failure related to loss of
myocardial contractility/functional myocardium or
structural/mechanical failure of the cardiac anatomy and
characterized by elevations of diastolic filling pressures and volumes
9. OBSTRUCTIVE SHOCK
• Extra-cardiac obstructive shock - due to obstruction to flow in the
cardiovascular circuit and characterized by either impairment of
diastolic filling or excessive afterload
11. • Distributive shock - caused by loss of vasomotor control resulting in
arteriolar/venular dilatation and characterized (after fluid
resuscitation) by increased cardiac output and decreased VR
13. • Hypovolemic shock - due to decreased circulating blood volume in
relation to the total vascular capacity and characterized by a
reduction of diastolic filling pressures
15. CLINICAL CORRELATES OF HAEMORRHAGE
CLASS I CLASS II CLASS III CLASS IV
BLOOD LOSS
(ml)
= 750 750-1500 1500-2000 >2000
BLOOD LOSS % =15 15-30 30-40 >40
PULSE RATE <100 >100 >120 >140
BP NORMAL NORMAL DECREASED DECREASED
PULSE
PRESSURE
NORMAL/
INCREASED
DECREASED DECREASED DECREASED
ORTHOSTASIS ABSENT MINIMAL MARKED MARKED
CAP REFILL NORMAL DELAYED DELAYED DELAYED
RR 14-20 20-30 30-40 >34
UO (ml/hr) >30 20-30 5-15 <5
CNS MSE SLIGHT ANXIETY MILD ANXIETY ANXIOUS/
CONFUSED
CONFUSED/
LETHARGY
16. PHASES OF SHOCK
• Discrete phases based on physiological changes
• PHASES: (1) compensated phase (2) decompensated phase (3)
terminal shock
• Clinical signs vary with phases
• Prognosis depend on phase
17. Initial Patient Assessment
• Recognition of Shock
• Clinical signs and symptoms depends on the severity of
the shock
• Early manifestations include tachycardia and cutaneous
vasoconstriction
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18. CLINICAL FEATURES
• Hypotension
• Rapid Pulse
• Cold skin and extremities
• Pale skin
• Intense thirst
• Rapid respirations
• Restlessness and coma
• History related to the cause
19. TREATMENT
• According to available protocols
• Pt prep is important
• Need to plan our surgery
• Need good pre op, intra op and post op care
• Anticipate haemorrhage in certain cases
20. • WHAT IF PATIENT COMES BLEEDING
• WHAT IF PATIENT COMES WITH BURNS
• WHAT IF PATIENT COMES WITH IO
21. Treating Hypovolemic Shock
• In SGY we have what we call the golden hour
ABCDEs + call for help
• Airway and Breathing
• Would prefer O2 sat greater than 95%
• Placing O2 on the patient
• Circulation
• Hemorrhage Control
• Vascular Access, Large bore IV x 2
• Xmatch
• IVF
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23. Treating Hemorrhagic Shock
•Identify & reverse the cause
•Restore tissue perfusion
•Restore organ function
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24. Initial Fluid Therapy
• Adult with normal Cardiac Function
• 1 to 2 Liters of LR or NS rapidly
• Pediatric
• 20ml/kg of LR or NS rapidly
• Evaluate patients response to fluid
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25. THE CRYSTAL RANDOMISED TRIAL
• JAMA: effects of fluid resuscitation with colloids Vs crystalloids on
mortality in critically ill patients with hypovolaemic shock
• 359 (25.4%) deaths Colloids Vs 390 (27.0%) deaths in crystalloids. This
outcome was 28 day period mortality
• 434 (30.7%) colloid mortality over 90 days period Vs 493 (34.2%)
crystalloid mortality
26. Evaluation of Treatment
•Assess organ perfusion
•Urinary output
•Mental Status
•Skin exam
•Vitals
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27. MECHANISMS OF CELLULAR INJURY IN SHOCK
1) Cellular ischemia
2) Free radical reperfusion injury
3) Inflammatory mediators (local and circulating)