SHOCK IN EMERGENCY SETTING

1. SHOCK
Presenter : Haashveeni & Amalina
Supervisor : Dr Gan Kiat Kee

2. DEFINITION
• Shock is a state of circulatory insufficiency that creates an
imbalance between tissue oxygen supply (delivery) and
demand (consumption), resulting in end-organ dysfunction
( Tintinalli emergency medicine 9th ed )

3. • Aorebic respiration : glucose + oxygen  32 ATP + CO2 + H20 + heat
• 32 ATP used by Na+K+ATPase channel to maintain the balance
between the intracellular and extracellular ion
• In state of shock ( hypoxia ) anaerobic respiration occur and glucose is
converted to lactate and released only 2 ATP which is inaqeduate for
cell metabolism
• Resulting in the leakage of intracellular K+ to extracellular and influx
of Na+ and water to intracellular region causing cell edema and cell
death, apart from resulting in high lactate, hyperkalemia and
hyponatremia
PATHOPHYSIOLOGY

4. PATHOPHYSIOLOGY
Oxygen delivery (DO2)
• DO2 = CO × ([1.34 ×Hb × SaO2 ]+[PaO2 × 0.003])
• SaO2: arterial haemoglobin (Hb) oxygen saturation
• PaO2: arterial oxygen partial pressure
• haemoglobin O2-carrying capacity constant : 1.34 mL O2/g Hb
• Assuming adequate arterial oxygen content, CO is the main determinant of
DO2.
• CO = HR × SV (preload, afterload, contractility)
• Alterations in any of these determinants of CO will eventually lead to the
development of different ‘types’ of circulatory shock

5. • DO2 in adults at rest is approximately 1000 mL/min,
while oxygen consumption (VO2) is about 250 mL/
min.
• Under normal circumstances, the ‘extra’ O2 being
supplied is not required to meet metabolic demand 
‘reserve’ supply (O2 supply independency).
• If DO2 decreases, VO2 initially remains unchanged as
the ‘reserve’ O2 is utilised.
• If DO2 falls further, oxygen extraction from Hb is
increased to maintain adequate oxygen supply to the
tissues
• Further reduction of DO2 results in oxygen being
maximally extracted from Hb  VO2 becomes
dependent on DO2 (O2 supply dependency) and
energy production in cells is limited by the supply of
oxygen

6. Inadequate O2 supply
Anaerobic cellular
metabolism
Less efficient adenosine
triphosphate (ATP)
production
Cellular and organ
dysfunction
Ongoing limitation of
oxygen supply affects cell
membrane ion channels
Influx of sodium and water,
cellular oedema, breaching
of cell membrane integrity,
cell injury and eventually
cell death
If shock
persists

7. • The heart and brain have high metabolic requirements with a relatively
high oxygen extraction  more vulnerable to reduced oxygen supply
• Kidney and skin have relatively lower metabolic requirements and lower O2
extraction  more tolerant of decreased DO2.
• Critical DO2 also varies between individuals and is affected by metabolic
demand, age, disease states and medications.

11. HYPOVOLAEMIC SHOCK
• Occurs when acute blood loss or excessive fluid losses lead to decreased circulating blood volume
 reduce preload and SV
• Total blood volume is 70 mL/kg
• About 10% of circulating volume loss can be restored by the movement of interstitial fluid into
the circulation.
• Blood loss beyond this invokes cardiovascular compensatory mechanisms in order to restore
preload and maintain CO and systemic blood pressure.
• Priorities in the management of hypovolaemic shock are:
• to control the source of blood and/or volume loss
• restoring the circulating volume

13. Causes - hypovolemic shock
● GI losses - the setting of
vomiting, diarrhea, NG suction, or
drains.
● Renal losses - medication-
induced diuresis, endocrine
disorders such as
hypoaldosteronism.
● Skin losses/insensible losses -
burns, Stevens-Johnson
syndrome, Toxic epidermal
necrolysis, heatstroke, pyrexia.
● Third-space loss - in the setting
of pancreatitis, cirrhosis,
intestinal obstruction, trauma.
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Main problem – inadequate
volume
Fluid resuscitation 1 to 2L
crytalloids should be started
while assessing the response
Paedicatric patient – fluid
challenge with boluses
20ml/kg
Vasopressor agent should only
be considered after adequate
volume replacement

14. Causes - haemorrhagic shock
● Gastrointestinal bleed (both
upper and lower gastrointestinal
bleed (e.g., variceal bleed, portal
hypertensive gastropathy bleed,
peptic ulcer, diverticulosis) trauma
● Vascular etiologies (e.g.,
aortoenteric fistula, ruptured
abdominal aortic aneurysm,
tumour eroding into a major
blood vessel)
● Spontaneous bleeding in the
setting of anticoagulant use (in
the setting of therapeutic INR
from drug interactions)
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Main problem – inadequate volume and
oxygen carrying capacity
Fluid resuscitation does not stop the
hemorrhage
Control all external hemorrhage and
obtain urgent review by surgical
In general :
-Prior to definitive surgical hemorrhagic
control, avoid excessive fluid resuscitation
-If patient hypotensive with ongoing blood
loss or MTP criteria are met, transfuse
without delay

20. INITIAL MANAGEMENT OF PATIENT
SUSPECTED HAVING SHOCK
• All patients exhibiting features of shock
should urgently transferred to monitored
critical care for assessment and
stabilization
• Prompt recognisition and initiation of
treatment
• Supplemental oxygen if hypoxemic
• Maintained airway. Prepare for
intubation if necessary
• 2 large bore branula
• Small fluid challenges – 250ml IV
crytalloids
RESUSCITATION STRATERGIES
GENERALLY TARGET THREE
MECHANISM TO REPAY OXYGEN
DEBT AND RESTORE OXYGEN
DEFICIT IN THE TISSUE
1. Intravascular volume (preload
and afterload)
2. Cardiac output (pump)
3. Oxygen delivery capacity and
delivery (Hb content)

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23. ABCDE
1) Fluid therapy
2 Large-bore peripheral lines (14- to 16-gauge in adults)
Begin with isotonic crystalloid, IV bolus 500-1000 ml (10-15ml/kg) for 5-20mins and reassess
Consider using lactated ringer’s/ Hartmann or plasmalyte to avoid hyperchloremic metabolic acidosis.
*metabolic acidosis has negative inotropic and pro-arrhythmogenic effects.
2) Vasopressor : Inadequate response to volume resuscitation or if there are contraindications to volume
infusion*.
May decrease capillary blood flow in certain tissue beds, especially the GI tract and peripheral
vasculature.

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For patients with hypovolemic shock, the three major classes of replacement fluids are:
• Crystalloid solutions (eg, saline solutions, Lactated Ringer, Hartmann solution) – FIRST
LINE
• Colloid-containing solutions (eg, albumin solutions, hyperoncotic starch, dextran,
gelatin).
• Blood products (eg, packed red blood cells) or blood substitutes.
Vasopressors — Vasopressors (eg, norepinephrine) generally should not be administered.
• do not correct the primary problem
• in the absence of adequate resuscitation, tend to further reduce tissue perfusion
• However, in patients with refractory shock, vasopressors may be administered while
ongoing measures are being taken to treat hypovolemia.
CHOICE OF REPLACEMENT FLUID

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26. BASIC INVESTIGATIONS
• ECG
• Capillary blood glucose
• UPT
• FBC
• Urea/electrolytes
• Blood gas analysis
• Lactate
• Blood culture
• Cardiac troponin
• Gxm