Hypovolaemic shock occurs due to a reduction in intravascular volume leading to insufficient oxygen delivery to cells. This results in metabolic acidosis, endoplasmic reticulum swelling, mitochondrial damage, and cell death if untreated. Initial management involves fluid resuscitation to restore intravascular volume and oxygen delivery. Further treatment is aimed at controlling bleeding, preventing complications like hypothermia and coagulopathy, and monitoring for signs of adequate perfusion and organ function during resuscitation. Surgical intervention may be needed to definitively stop blood loss.

1. Hypovolaemic shock
 Reduction in intravascular volume leading to insufficient
oxygen delivery to cells (mitochondria).
 Reduced intravascular volume?
 No oxygen delivery & No aerobic metabolism! Then…
 Metabolic acidosis (lactic acid production), Endoplasmic
recticulum swelling
 Mitochondrial damage and Cell Death!
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2. Hypovolaemic Shock
Mechanisms
Initially;
BP maintained
Brain and heart initially protected through auto regulation
Eventually if untreated; compensatory mechanisms will fail
↓intravascul
ar volume
↓cardiac filling
pressure
↓SV
baroreceptor
stimulated
reflex tachycardia (initially
maintaining CO)
release of endogenous
catecholamine's
↑PVR and myocardial
contractility
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3. Cont.…
 Decreased parameters:
– BP, CVP, PAWP, CO, SV
 Increased parameters:
– HR, SVR
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4. Clinical features
 History : Is there a consistent history?
 Examination
 Resp: tachypnoea
 CVS : cool peripheries, reduced capillary refill, clammy,
tachycardia*, reduced pulse volume, hypotensive (up to
30% blood volume may be lost before fall in systolic
pressure), pulse pressure, reduced JVP.
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5. Class of Hypovolemic Shock
Class I Class II Class III Class IV
Blood Loss (mL) <750 750-1500 1500-2000 >2000
Blood loss
(% volume)
<15% 15-30% 30-40% >40%
Pulse <100 >100 >120 >140
Blood pressure normal normal decreased decreased
Pulse pressure
(mmHg)
normal or
increased
decreased decreased decreased
Respiratory rate 14-20 20-30 30-40 >35
Urine output
(mL /hour)
>30 20-30 5-15 negligible
CNS slightly anxious mildly anxious
anxious,
confused
confused,
lethargic
Fluid
replacement
(3:1)
crystalloid crystalloid
crystalloid and
blood
crystalloid and
blood
Estimated blood loss of patients with haemorrhage
samueldebassu@gmail.com 5These table is based on a 70kg man

6. Cont..
 The previous table is only a guide to severity
 In reality rarely we clinically categorise hypovolaemic shock into
these categories.
 Fluid therapy is guided by clinical response to treatment.
 In addition, many patients will not fit into these categories eg.
paediatric, elderly, pregnant patients, athletes, those unable to
increase their HR.
 Hb concentration or Hct is unreliable at estimating acute blood
loss
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7. Management of Hypovolemic Shock
Initial Definitive bleeding control and
prevention of the lethal triad of hypothermia,
coagulopathy and acidosis.
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8. EFFECTIVE RESUSCITATION
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9. Goals for Early Resuscitation
 Maintain SBP at 80 to 100 mm Hg
 Maintain hematocrit at 25% to 30%
 Maintain the PT & PTT time in normal ranges
 Maintain the platelet count at greater than 50,000
 Maintain core temperature higher than 35°C
 Prevent an increase in serum lactate
 Prevent acidosis from worsening
 Achieve adequate anesthesia and analgesia
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10. Goals of Late Resuscitation
 Maintain SBP higher than 100 mm Hg
 Maintain Hct above individual transfusion threshold
 Normalize coagulation status
 Normalize electrolyte balance
 Normalize body temperature
 Restore normal urine output
 Maximize CO by invasive or noninvasive measurement
 Reverse systemic acidosis
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11. Cont..
 After any intervention reassessment is critical
 Adequate IV access
 Stop the source of loss – surgical intervention may be
required
 Replacement therapy depends on type and volume of
fluid lost
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12.  Estimate of fluid loss is practically very difficult on
initial evaluation
 A rough estimate for amount of crystalloid required is
3 mL for every 1 mL of blood lost (this allows for fluid
loss into interstitial and intracellular compartments)
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13. Hypovolemic Shock Management (cont.)
• Initial fluid therapy - warm fluid bolus 1-2L adults (or
20mls/kg in paeds) this may require a pressure bag
•Further fluid therapy is guided by response to treatment
including adequate end organ perfusion eg UO, peripheral
perfusion and level of consciousness Other parameters which can
be assessed are RR, HR, BP pulse pressure, (CVP, acid/base
balance).
•After any intervention reassessment is critical
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14. Access Gravity Pressure
18 G peripheral IV 50 mL/min 150 mL/min
16 G peripheral IV 100 mL/min 225 mL/min
14 G peripheral IV 150 mL/min 275 mL/min
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15. Rapid Response Transient response No response
Vital Signs
Return to
normal
Transient improvement
but recurrence ↓BP and
↑HR
Remains
abnormal
EBL
Minimal (10-
20%)
Moderate & ongoing
(20-40%)
Severe >40%
Need for more
crystalloid
Low High High
Need for blood Low Moderate
High –
immediate
Blood preparation
Type and
crossmatch
Type-specific
Emergency
blood release
Need for operative
intervention
Possible Likely Highly likely
Early surgical presence Yes Yes Yes
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Response to initial fluid resuscitation after 2L of RL in
patients with haemorrhagic shock

16. • If the amount of fluid required to restore adequate
perfusion greatly exceeds estimates consider
possibility of unidentified or on-going losses
•Avoid hypothermia
Patients with large blood loss may develop a
coagulopathy(compounded by hypothermia)therefore
monitor coagulation and give clotting products as
required/available
•Supportive management as already discussed
Management (cont.)
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17. Treatment of Hemorrhagic Shock
1. RECOGNIZE patient is in shock
2. ATLS (ABCDE’s)
3. Volume, volume, volume
4. Surgical – stop bleeding, correct injury
5. Re-establish normal hemodynamics
6. Re-establish urine flow

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