Shock is defined as inadequate organ perfusion and tissue oxygenation. It can be caused by hypovolaemia from blood loss, cardiac issues, or neurogenic factors. The body activates compensatory mechanisms through the cardiovascular, renal, respiratory, and cerebral systems but these fail over time without treatment. Signs of shock include decreased consciousness, fast heart rate, pale skin, and low urine output. Treatment involves fluid resuscitation, controlling bleeding, and monitoring the patient's color, breathing, pulse, and consciousness. Without adequate treatment, shock leads to multiple organ failure and death.

1. Pathophysiology of
Shock

2. Objectives
 What is shock?
 3 causes of non-septic shock
 Compensatory mechanisms
 Signs & symptoms
 Responses to fluid therapy
 Outcome of inadequate treatment

4. Definition
 Inadequate organ perfusion and tissue
oxygenation

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

11. How does the body react
to shock?

12. Cellular
Resorts to
anaerobic
metabolism
Deprivation of O2 –
cell unable to
maintain
aerobic metabolism
Produces
lactic acid
Metabolic acidosis
Death of cell

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

17. Signs
 Earliest response is a reduction of urine
output
 Does not become apparent immediately

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

20. Signs
 Anxiety
 Agitation
 Aggression
 Drowsiness
 Lethargy
 Loss of consciousness

21. Recognising Clinical Signs of
Shock

22. Recognising Clinical Signs of
Shock
 Mental state alterations
 Pale, cool, clammy skin
 pulse
 Capillary refill > 2 secs
 Narrowing pulse
pressures – as
decompensation occurs
pulse pressures will
widen
 Urine output
 Absent bowel sounds
 Feeling thirsty
 respirations
 Feeling cold
 Oxygen saturation

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.

32. Special Considerations
 Elderly
 Athletes
 Pregnancy

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

37. Cardiovascular
Reduced
arterial
pressure
Reduced coronary
blood flow
Reduced
ventricular
function
Pooling of blood
in peripheries

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

42. To summarise….

43.  Patient colour, skin temperature
 Respiratory pattern
 Pulse
 Oxygen saturation
 Level of conciousness

44.  Oxygenation
 Fluid replacement
 Haemorrhage control
 Frequent observations
 Consider transfer to trauma centre/theatre

45. Shock can be considered a pause on the
way to death, giving the trauma team a
chance to intervene.