5. The degree of shock depends on
Blood loss
Rate at which it was lost
Patient’s ability to activate compensatory
mechanisms
Age
Physical condition
Hypothermia
Pain
6. Organs Involved in Response to
Shock
Brain: brainstem, hypothalamus,
autonomic nervous system
Heart and blood vessels
Kidney
Adrenal Gland
Lungs
7. Three causes of non-septic shock
Hypovolaemia
Neurogenic
Cardiogenic
8. Hypovolaemia
Due to intravascular fluid loss
Causes Haemorrhage (external/internal)
Fractures
Burns
Dehydration (especially children and the
elderly)
9. Cardiogenic
Due to pump failure
Causes Myocardial Infarction
Heart surgery
Pulmonary Embolism
Cardiac Tamponade
Tension Pneumothorax
10. Neurogenic
Due to loss of vasomotor control, leading
to alteration in vessel tone and size which
results in general vasodilation.
Causes Severe brain stem injury
High spinal injury resulting in
damage to sympathetic nervous
system
13. Baroreceptors reduce
vagal tone and
enhances
sympathetic response
Increases heart rate
and enhances
myocardial contractility
Vasoconstriction
occurs – results
in increased
peripheral resistance
Cardiovascular
14. Signs
Decreased colour/warmth of periphery
Increased respirations
Increased heart rate
Blood pressure will not drop until
vasoconstriction and pulse rate has failed
to compensate adequately – usually when
30% of circulating blood volume has been
lost.
15. Renal
Baroreceptors identify
fall in BP
Hypothalamus controls
release of ADH
Water is
re-absorbed
from kidney’s
distal tubules
Conserves
intravascular volume
16. Renin released
by juxtaglomerular
apparatus
Angiotensin produced
Angiotensin I converted
to
Angiotensin II
Stimulates release
of aldosterone
Aldosterone and ADH
promote re-absorption
of sodium & chloride &
excretion of potassium
Increases the
re-absorption of water
– increases blood
volume
18. Respiratory
Chemoreceptors in the carotid body detect
CO2 in hypoxic tissue and the build-up of
lactic acid.
Stimulates the respiratory centre in the
medulla oblongata
Increases the respiratory rate and depth:
to excrete CO2
to maximise oxygenation of red blood
cells
19. Cerebral
Reduction in MAP and CPP causes
autoregulation to fail
This reduction in cerebral blood flow:
- reduces O2 delivery to the brain
- reduces removal of CO2
Results in decreasing level of
consciousness
23. Classification of shock
Estimated blood loss and critical measures (based on 70kg male)
Class I Class II Class III Class IV
Blood loss (mL) Up to 750 750-1500 1500-2000 >2000
Blood loss (%
blood
volume)
Up to 15% 15-30% 30-40% >40%
Pulse rate <100 100-120 120-140 >140
Blood pressure Normal Normal Decreased Decreased
Pulse pressure
(mm Hg)
Normal or
increase
d
Decreased Decreased Decreased
Respiratory
rate
14-20 20-30 30-40 >35
Urine
output(m
L/hr)
> 30 20-30 5-15 Negligible
CNS/mental
status
Slightly
anxious
Mildly
anxious
Anxious,
confused
Confused,
lethargic
Fluid
replaceme
nt
Crystalloid Crystalloid Crystalloid
and
blood
Crystalloid
and
blood
24. Fluid Resuscitation
Electrolyte solutions – 0.9% Normal Saline
Hartmans
1-2 litres initial bolus of warmed fluid
20mL/kg in children
If observations do not improve, assume
that circulating volume is being lost faster
than it can be replaced
Definitive control of haemorrhage is
required
25. Responses to Initial Fluid Resuscitation *
RAPID
RESPONSE
TRANSIENT
RESPONSE
MINIMAL OR
NO RESPONSE
VITAL SIGNS Return to normal Transient
improvement:
recurrence of
decreased BP and
increased HR
Remain abnormal
ESTIMATED
BLOOD LOSS
Minimal (10-20%) Moderate and
ongoing (20-40%)
Severe (> 40%)
NEED FOR
MORE
CRYSTALLOID
Low High High
NEED FOR
BLOOD
Low Moderate to high Immediate
BLOOD
PREPARATION
Type and
crossmatch
Type-specific Emergency blood
release (MHP)
NEED FOR
OPERATIVE
INTERVENTION
Possibly Likely Highly likely
EARLY
PRESENCE OF
SURGEON
Yes Yes Yes
*2000ml of crystalloid in adults; 20mL/kg bolus in children
26. Major Haemorrhage Procedure
Estimated blood loss > 30% of circulating
volume with ongoing bleeding or
haemorrhagic shock
Systolic BP <70mmHg, or <90mmHg after
fluid challenge, with suspected
haemorrhagic cause
27. 2222
Major haemorrhage in A&E,
I am activating the MHP
Send bloods to lab
Order MHP 1
Red cells 4 units
FFP 4 units
O neg can be used in meantime
MHP1 available in 25 mins
Give MHP 1
Re-assess
Stop the bleeding
Haemorrhage control
and
Haemostatic drugs
MHP 2
Red cells 4 units
FFP 4 units
Platelets 1 dose
Cryoprecipitate 2 packs
28. Stop the Bleeding
Haemorrhage Control
Stabilise #’s – pelvic binder
straighten/splint femur
Surgical Intervention
Celox
29. Stop the Bleeding
Haemostatic Drugs
Tranexamic acid – 1g in100mL N.Saline
over 10mins
followed by 1g in 500mL N.Saline
over 8 hours
30. How it works!
Fibrinolysis – a normal body process
preventing the formation/growth of blood
clots.
Plasminogen released from the liver, has
an affinity for fibrin & is incorporated into a
blood clot when it is formed.
Converts to plasmin, an enzyme that
dissolves the fibrin clot.
31. Fibronlysis is an important contributor to
bleeding and coagulopathy in trauma.
Tranexamic acid inhibits fibrinloysis.
CRASH-2 authors report a 32% reduction
in bleeding when tranexamic acid is given
within 1 hour of injury.
33. Elderly
Mortality and morbidity rates increase
directly with age.
Slower blood circulation
Decreased lung volume and compliance
Decreased cardiac function
Slower metabolic rate
Decreased vasoconstrictor response
More likely to be chronically dehydrated
34. Athletes
Blood volume may increase by 15-20 %
Stroke volume increase by 50%
Resting HR can average 50bpm
Ability to compensate for blood loss
Usual responses to hypovolaemia may not
be evident, even when significant blood
loss has occurred
35. Pregnancy
Increased intravascular volume
Uterine compression of the vena cava may
reduce venous return to the heart
Priority is always the mother
Obstetrics should be called as part of the
trauma team
36. Cellular
Blood acidity increases Toxicity increases Tissue necrosis
Death of organ
Cell ruptures and
releases toxins
Multiple organ failure
38. Renal
Continuing reduced urine output occurs
Patient becomes anuric
Kidney fails
Renal tubules become ischaemic and
necrotic
Acute tubular necrosis of the kidney may
lead to acute renal failure.
Contributes to the 3rd peak of death
following trauma.
39. Respiratory
Ventilation and /or perfusion and gas
exchange does not take place resulting in
Atelectasis
Adult Respiratory Distress Syndrome
Respiratory muscle fatigue
Respiratory failure
Respiratory failure is one of the primary causes of death
following initial successful resuscitation of trauma
40. Cerebral
Mean Arterial Pressure drops below 50-
70mm HG, level of consciousness is
reduced
Unconsciousness occurs when less than
50% of the blood volume is in the
circulation
Brain becomes ischaemic
Irreversible brain injury occurs.
41. If shock is not treated adequately,
irreversible shock will occur
Death is inevitable