The document discusses shock, including its pathophysiology, classification, severity, consequences, and resuscitation. It aims to provide medical students an understanding of shock. Shock is defined as a systemic state of low tissue perfusion inadequate for cellular respiration. Different types of shock are classified including hypovolemic, cardiogenic, obstructive, distributive, and endocrine shock. The severity of shock ranges from compensated to decompensated to multiple organ failure. Consequences include cellular damage, organ dysfunction, and death. Resuscitation focuses first on fluid therapy and addressing hypovolemia, with vasopressors and inotropes as adjuncts depending on the shock type.

1. NUR FARRA NAJWA BINTI ABDUL AZIM
082015100035

2. AT THE END OF SEMINAR, STUDENT SHOULD
BE ABLE TO
 Understand what is shock.
 Explain patho-physiology of shock.
 Classify shock.
 Know the severity of shock.
 Know the consequences of shock.
 Know the resuscitation in shock in brief .

3.  Shock is most common and important cause
of death of surgical patient
 Death occur due to
◦ Rapidly profound state of shock
◦ Delayed consequences causing organ ischemia and
reperfusion injury

4.  Systemic state of low tissue perfusion,
 which inadequate for normal cellular
respiration.
 With insufficient delivery of oxygen and
glucose,
 cell switch from aerobic to anaerobic
metabolism
 If no reperfusion in timely fashion, cell death
ensue

5. Systemic state of low tissue perfusion,
which inadequate for normal cellular
respiration. With insufficient delivery
of oxygen and glucose, cell switch
from aerobic to anaerobic
metabolism. If no reperfusion in
timely fashion, cell death ensue

6. 1. Cellular
2. Microvascular
3. Systemic
4. Ischemic reperfusion syndrome

7. Tissue perfusion
reduce, cell deprived of
oxygen
Change from aerobic to
anaerobic metabolism
Lactic acid accumulate,
systemic metabolic
acidosis ensue
Glucose within cell
exhausted,
Anaerobic
metabolism cease
Failure of sodium
potassium pump
Lysosome release
autodigestive enzyme
Cell lysis ensue

8. Progression of tissue ischemia (hypoxia and acidosis), changes the internal
cell milieu, activate the coagulation and immune system
Generation of oxygen free radicle and cytokine release
Injured capillary endothelium, further activate immune and coagulation
system
Capillary loss integrity and become leaky
Edema ensue and exacerbate tissue hypoxia

9. •Decreasea preload and afterload
•Compensatory baroreceptor activation
•Increase sympathetic and cathecholamine
•Tachcardia and systemic vasoconstriction ensue
CVS
•Metabolis acidosis and increased sympoathetic activation
•Increase respiratory rate and minute ventilation (excretion of carbon
dioxide)
•Respiratory alkalosis ensue
RS
•Kidney decrease perfusion, reduce filtration, reduce urine output
•Activate RAAS
•Resulting in water and salt retention and vasoconstriction
RENAL
•Activation of adrenal and RAAS, release of ADH, release of cortisol
•Result in vasoconstriction, water resorbtion, cell sentisation to
cathecholamine
ENDO

10.  During period of systemic hypoperfusion
◦ Tissue hypoxia and local inflammation cause cellular and
organ damage
 When normal circulation is restored
◦ Further injury occur
1. Acid and potassium buildup
2. Cellular and humoral immune
response are flushed back to
circulation
THIS LEADS TO
1. Acute lung injury
2. Acute renal injury
3. MOF
4. Death
REPERFUSION INJURY CAN BE ATTENUATED ONLY BY
REDUCING THE EXTENT AND DURATION OF
HYPOPOERFUSION

11. 1. HYPOVOLEMIC SHOCK
2. CARDIOGENIC SHOCK
3. OBSTRUCTIVE SHOCK
4. DISTRIBUTIVE SHOCK
5. ENDOCRINE SHOCK

12.  DUE TO : REDUCED CIRCULATION VOLUME
 Cause of hypovolemia
◦ Hemorhagic
◦ Non-haemorhagic
LESS FLUID INTAKE : Dehydration
FLUID LOSS : Vomitting, diarrhae, urine
loss (diabetic mellitus)
3 SPACE FLUID LOSS,
EVAPORATION
: Bowel obstruction and
pancretitis

13.  DUE TO : PRIMARY FAILURE OF HEART FAILS
TO PUMP BLOOD TO TISSUE
 Cause
◦ Myocardial infarction
◦ Dyarrythmias
◦ Valvular heart diseases
◦ Blunt heart injury
◦ Cardiomyopathy
◦ Cardiac depression
ENDOGENOUS FACTOR EXOGENOUS FACTOR
Bacterial and humoral
agent on sepsis
Drugs

14.  DUE TO : MECHANICAL OBSTRUCTION OF
CARDIAC FILLING REDUCE CARDIAC PRELOAD
 Cause:
◦ Tension pneumothorax
◦ Massive air emboli, pulmonary emboli
◦ Cardiac tamponade
Reduce filling
of both side
of heart
Reduce
preload
Reduce
cardiac
output

15.  It is a pattern of
cardiovascular
response
characterize a
variety of
condition
DISTRIBUTIVE SHOCK
Spinal cord
injury
Anaphylaxis
Septic
shock

16. In-
adequate
organ
perfusion
Vascular
dilatation
with
hypotension
Low systemic
vascular
resistance
Inadequate
afterload
ABNORMAL
HIGH
CARDIAC
OUTPUT

17. ANAPHYLAXIS : Histamine release, vasodilatation
SPINAL CORD INJURY : Failure sympathetic outflow, loss
vessel tone (neurogenic shock)
SEPSIS : Bacterial endotoxin release and
activation of immune and
coagulation system

18.  Combination of hypovolemic, cardiogenic and
distributive shock
 Cause
◦ hypo/hyper thyroid
◦ Adrenal insufficiency
HYPOTHYROIDISM Disorder vascular and cardiac
response to cathecholamine ,
low cardiac output due to
bradycardia and lown inotropy
HYPERTHYROIDISM High output cardiac failure
ADRENAL INSUFFICIENCY Hypovolemia and poor
response to cathecholamine

20. 1. Compensated shock
2. Decompensation
3. Mild shock
4. Moderate shock
5. Severe shock
6. Pitfalls

21.  As shock progress, cardiovascular and
endocrine compensatory response
◦ Reduce flow to non-essential organ
◦ Preserve flow to essential organ (lung, brain)
 In compensated shock,
◦ Central blood volume maintain and preserve flow to
essential organ
 Clinical sign of hypovolemia
◦ Tachycardia
◦ Cool peripheries

22.  However
◦ Compensation state only reduce perfusion to skin,
gut, muscle
◦ In underperfused organ, there is met acidosis and
activation of humoral and cellular element (clinically
occult condition)
◦ Will lead to multiple organ failure and death if
prolonged (due to ischemic-reperfusion syndrome)
 Patient with occult hypoperfusion > 12 hrs
◦ Higher mortality, infection and incidence of MOF
OCCULT HYPOPERFUSION :
metabolic acidosis with normal urine output and cvs vital sign

23.  Further loss of circulating volume > body
compensatory mechanism
 There is progressive renal, respiratory and
cardiovascular decompensation.
 ∼15% blood loss is within normal
compensatory mechanism
 After 30-40% of circulating volume been lost
= fall of well maintained blood pressure

24.  Initially
◦ Tachycardia, tachypnea, mild reduction in urine
output and mild anxiety
◦ Blood pressure in maintained (though pulse
pressure decrease)
◦ Cold peripheries with sweaty
◦ Prolonged capillary refill time

25.  As shock progress
◦ Renal compensatory fails
 Fall of renal perfusion
 Urine output dip below 0-5ml/kg per hour
 Further tachycardia, and blood presurre start
to fall
 Patient will be drowsy and mildly confused

26.  Severe shock
◦ Profound tachycardia and hypotension
◦ Urine output fall to zero
◦ Patient unconsious with laboured breathing

27.  Classical cardiovascular response is not seen
in every patient

30.  Most hypovolemic patient have
◦ Cool and pale peripheries
◦ With prolonged capillary refill time.
 However, capillary refill time varies in adult
and not a specific marker of weather patient
is in shocked.

31.  It is not always accompany shock
 Patient on beta blocker and implanted
pacemaker unable to mount
tachycardia
 Young patient with
◦ Penetrating trauma
 haemorrhage, but little tissue damage
 paradoxically bradycardia in shock
state

32.  Important as it is a last sign of shock is
hypotension
 Child and fit young man able to maintained
normal value till end by
◦ Dramatic increase of stroke volume
◦ Dramatic peripheral vasconstriction
 Elderly who is hypertensive may come with
normal blood pressure but it is hypotensive
compared to their usual blood pressure.
 Drug also can prevent tachycardia response

33. 1. UNRESUSCITABLE SHOCK
2. MULTIPLE ORGAN FAILURE (MOF)

34.  Unresuscitable = prolonged period of
profound shock
 Death follow due to
◦ Cellular damage
◦ Lost of body ability to compensate
 Death is inventible result
HEART •Myocardial depression
•Unresponse to fluid and
inotrophy therapy
PERIPHERIES •Fails to maintaned vascular
response and further
hypotension ensues

35.  Cause
◦ Delayed and inappropiate resuscitation in early
stage of shock
◦ Severity of insult
 At this stage, patient has
◦ Minimal response to maximal therapy

36.  Due to prolonged systemic ischemia and
reperfusion injury
 End organ damage and multiple organ failure
 To has a rapid and uncomplicated recovery
◦ timely intervention and reduce period of shock
LUNG ARDS
KIDNEY Acute liver insufficinecy
CLOTTING Coaguloapathy
CARDIAC Cardiovascular failure

37.  Management is more on supporting the organ
system till their resume recovery
◦ Ventilation
◦ Cardiovascular support
◦ Hemofiltration
◦ Dialysis
 Mortality of 60%
 Prevention is vital by :
◦ Aggressive identification and shock reversal

38.  Conduction of fluid therapy
 Fluid therapy
 Vasopressor and inotropic support

39. Ensure a airway and
adequate oxygenation
and ventilation
Once ‘airway’ and
‘breathing’ are assessed
and controlled,
Attention given for
cardiovascular
resuscitation.

40.  Resuscitation should not be delayed to find
the diagnose and source of the shocked
state.
 The timing and nature of resuscitation will
depend on
◦ type of shock
◦ timing and severity of the insult

41. Rapid clinical examination
will provide adequate clues
If there is initial doubt about
the cause of shock, safe to
assume the cause is
hypovolaemia and begin
with fluid resuscitation
then assess the response.

42. Patients who are actively
bleeding (major trauma,
aortic aneurysm rupture,
gastrointestinal
haemorrhage),
It is counterproductive to
institute high-volume fluid
therapy without controlling
the site of haemorrhage.

43. Increasing blood pressure merely
increases bleeding from the site
while, fluid therapy cools the
patient and dilutes available
coagulation factors.
Operative haemorrhage control
should not be delayed and
resuscitation should proceed in
parallel with surgery.
A patient with bowel obstruction
and hypovolaemic shock must
be adequately resuscitated
before undergoing surgery
Otherwise the additional surgical
injury and hypovolaemia induced
during the procedure
exacerbate the inflammatory
activation
Increase the incidence and
severity of end-organ insult.

44.  Hypovolaemia and inadequate preload must be
addressed first
 First-line therapy
◦ intravenous access and administration of intravenous fuids.
 Access through
◦ Short, wide-bore catheters that allow rapid infusion of fluids
as necessary.
◦ Long, narrow lines, such as central venous catheters, have
too high a resistance (more appropriate for monitoring)

46. Administration of inotropic or chronotropic
agents to an empty heart
Deplete the myocardium of oxygen stores
Reduce diastolic filling and coronary
perfusion.
Patients will enter the unresuscitatable stage
of shock
Myocardium becomes more ischaemic and
unresponsive to resuscitative attempts.

47.  No ideal resuscitation fluid
 No difference in response between crystalloid
solutions or colloids.
 Colloids are more expensive and have worse
side-effect.

48.  Most importantly, the oxygen carrying
capacity of crystalloids and colloids is zero.
 If blood lost, the ideal replacement fluid is
blood.
 Hypotonic solutions are poor volume
expanders and should not be used in the
treatment of shock unless the decit is free
water loss (eg. diabetes insipidus) or patients
are sodium overloaded (eg. cirrhosis).

49.  Shock response determined dynamically by
cardiovascular response to rapid
administration of fluid bolus
 Total of 250-500ml given over 5-10 min
 Response look for in terms of
◦ Heart rate
◦ Blood pressure
◦ Central venous pressure
 Divided to further 3

50. DYANAMIC FLUID
RESPONSE
RESPONDER
Improvement in cvs
status and sustained it
Not actively losing
fluid but requires
filling to normal
volume status
TRANSIENT
RESPONDER
There is improvement
but then revert back to
previous condition
over next 10-20 min
Has moderate ongoing
fluid loss
NON-RESPONDER
Severely volume
depleted
Persistent uncontrolled
haemorrhage

51.  Not indicated as first-line therapy in hypovolaemia.
1. Vasopressor agents are indicated in distributive shock
states ,in which there is peripheral vasodilatation and a
low systemic vascular resistance (resistant to
catecholamines, use vasopressin)
2. In cardiogenic shock or when myocardial depression
complicates a shock state, inotropic therapy may be
required to increase cardiac output and, therefore,
oxygen delivery (Dobutamine)

52. AT THE END OF SEMINAR, STUDENT SHOULD
BE ABLE TO
 Understand what is shock.
 Explain patho-physiology of shock.
 Classify shock.
 Know the severity of shock.
 Know the consequences of shock.
 Know the resuscitation in shock in brief .

53.  Bailey & Loves Short Practice of Surgery. 26th
Ed., Rev. by A.J. Harding Rains and W. Melville
Capper, with Chapters by John Charnley,
William P. Cleland and Geoffrey Knight.
Consulting Editor: McNeill Love. Lippincott,
1965. Chapter 2: Shock and Blood
Transfusion