This document provides an overview of shock, including its classification, causes, pathophysiology, clinical features, and management. It defines shock as a clinical manifestation of inadequate tissue perfusion and cellular hypoxia due to a reduction in effective circulating blood volume. The main types of shock discussed are hypovolemic, cardiogenic, obstructive, distributive, and endocrine shock. The document examines the cellular, microvascular, and systemic pathophysiological changes that occur in shock, as well as compensatory mechanisms and signs of decompensation. Clinical features, diagnosis, and general management principles are also summarized.

1. Aransi Rilwan A.

2.  Introduction
 Classification
 Types
 Causes
 Pathophysiology
 Clinical features
 Management
 Complications

3.  Shock is the most common and most
important cause of death in surgical patients

4.  Shock is the clinical manifestation of failure
of cellular function due to inadequate
tissue perfusion and consequent cellular
hypoxia resulting from a reduction in the
effective circulating blood volume.

5.  Tissue oxidation depends on adequate
pulmonary function together with adequate
perfusion to deliver and release oxygen to the
tissues.
 Oxygen consumption (OC) in an average adult
is 3ml/kg/min
 And oxygen delivery (OD) from arterial blood
= 1000ml/min.
OD:OC = 5 : 1

6.  If ratio is 2:1, tissue hypoxia results in tissue injury
and/or cell damage/death.
 This causes an inflammatory response with the
production of cytokines and secondary mediators.
These may contribute to the development of the
(SIRS)
 If overwhelming or the treatment is late or
ineffective, (MODS) occurs.
 Fortunately, the body has several compensatory
mechanisms which sustain adequate organ perfusion
and lower the risk.

7.  1 . Reduction in Blood Volume
It may result from:
a)Acute Haemorrhage (Haemorrhagic Shock):
It is the commonest cause of shock
May be; internal or external
b) Loss of plasma
c) Loss of Extracellular Fluid

8. 2. Failure of the Cardiac Pump (Cardiogenic
Shock)
3. Obstuctive shock
Reduction in preload from mechanical
obstruction of cardiac filling
4. Distributive shock
This is a pattern of response that characterise
conditions including septic, anaphylactic, and
neurogenic shock

9.  Endocrine shock
Present as a combination of hypovolemic,
cardiogenic, and distributive shock
Causes include hypo and hyper thyroidism and
adrenal insufficiency.
Hypothyroidism
Shock state similar to neurogenic shocck
Disordered vascular and cardiac responsivenes to
circulation catecholaniines +/_ cardiomyopathy

10.  Adrenal insufficiency
 Poor respose to circulating and exogenous
catecholamines.

11.  Cellular
 In the presence of oxygen, glucose is
 metabolized to pyruvate, water and ca rbon
dioxide with
 production of high energy in form of ATP
 As perfusion is reduced, cells are deprived of
o2 and swithc to anaerobic respiration
 The product of anaerobic respiration is lactic
acid
 Accumulation produces systemic metabolic
acidosis

12.  As glucose is exausted, anaerobic
respiaration increases and their is failure of
the na/k pumps in the cell memb and
intracellular organelles.
 Lysosomes release autodigestive enzymes
and the cell lysis
 Intracellular contents are released into the
bloodstream

13.  Microvascular
 As tissues ischaemia progresses, changes in
the local milieu result in activation of the
immune and coagulation systems. Hypoxia
and acidosis activate the complement and
prime neutrophils
 Generation of o2 free radicals and cytokine
release
 This mechanism lead to injury of the capillary
endothelial cells.

14.  Further activation of the immune and
coagulation systems.
 Damaged endothelium loses its integrity and
becomes leaky
 Fluid leaks out and tissue oedema occurs,
exacerbation cellular hypoxia

15.  Systemic
 Cardiovascular
 As preload and afterloas decrases, there is a
compensatory baroreceptorResponse
 Increased sympathetic activity and release of
catecholamines
 Resulting in tachicarida and systemic
vasoconstriction( except in septic shock)

16.  Respiratory
 Metabolic acidosis and icreased sympathetic
response result in an increased respiratory
rate and minite ventilation
 Increase in co2 excretion (compensatory
respiratory alkalosis)

17.  Renal
 Decresed perfusion leads to reduced filtration
and a decrease urine output
 The RAS is stimulated resulting in further
vasicinstricrion and increased sodium and
water reabsorbtuon

18. Endocrine
ADH is released from the hypothalamus in
respone to decreseed preload, results in
vasoconstriction and reabsorption of water.
Cortisol from the adrenal cortex, contributing
to na and water reabsorptrion and sensitizing
the cells to cathecolamines

19.  Ischaemia-reperdusion syndrome
 During hypoperfusion, direct hypoxia and
local activation of inflammation causes
prograssive cellular and organ damage
 Further injury occurs when normal circulation
is restored.
 Acid and potassium leads to direct
myocardial depression, vasodilatation and
further hypotension.

20.  Cellular and humoral elements activated by
hypoxia and flushed back in to circulation.
 This xause further endothelial in jury to
organs such as lungs, kidnit.
 This can be attenuated by reducing the extent
and duration of hypoperfusion.

21.  Compensated shock
 Cardiovascular and endocrine compensatory
resposes reduced flow to non-essential
organs
 Their is adequate compensation to maintain
central blood volume and preservation of flow
to the brain, kidneys, and lungs.
 Tachycardia and cool peripheries may be the
only clinical signs.

22.  Decompensation
 Loss of around 15% of circulationg blood
volume is within mormal compensatory
mechanism
 Blood pressure is usually maintained and falls
after about 30-40% has been lost.
 decompensation progresses from mild, to
moderate to severe which is an irreversible
state.

23. compensated Mild Moderate severe
Level of
consiousness
Normal Mild anxiety Drowsy comatose
Blood
pressure
Normal Normal Mild
hypotension
Severe
hypotension
Pulse rate Mild increase Increased Increased Increased
Respiratory
rate
Normal Increased Increased laboured
Urine output Normal Normal Reduced Anuric
Lactic acidosis + ++ ++ +++

25.  Pitfalls in cardiovascular resposes
 It is important to recorgnise patients who are in
shock despit the absence of clinical signs.
 Capillar refill
 Most patient in hypovolaemic shock will have
cool, pale peripheries with prolonged capillary
refill times.
 This however varies in adults as it is not a
specifec marker in shock.
 Indistributive shock, peripheries are warm and
capillary refill will be brisk despite profound
shock.

26.  Tachycardia
 Patients who are on b- blockers or who have
implanted pacemakers are unable to mount a
tachycardia.
 A pulse rate of 90 in a young fit man who
normally has a pulse of 50 is very abnormal.

27.  Blood pressure
 It is important to note that hypotension is
one of the last signs of shock.
 Children and fit young adults ate able to
maintain blood pressure untill the final stages
of shock by dramatec increase in stroke
volume and peripheral vasoconstiction
 Elderly who are normally hypertensive may
present with a presumably normal BP for the
general population.

28.  Thus, the diagnosis of shock may be difficult
unless one is alert to these pitfalls.

29.  For shock to result from loss of extra-
vascular extracellular fluid, the loss must be
at least 6% of bodyweight
 A rough estimate of the amount of fluid
required may be calculated from the
following formula:
 I - 40 x 20% orB .W.
Hct . of patient

30.  It is a syndrome characterized by two or more
of the following clinical criteria:
 1. Temperature >38°C or <36°c (rectal)
 2. Heart rate >90 beats per min.
 3. Respiratory rate> 20breaths/min
 4. WBC > 12,000mm3 or > 10 % immature
bandforms.

31.  The causes include infections ( bacteria,
viruses, fungi, protozoa)
 non-infectious conditions (acute
pancreatitis, burns, trauma, hypovolaemic
shock.
 Gram-negative bacteria account for 50-60%
an d Gram-positives for 35-40%.

32.  Following tissue injury by microbial, mechanical,
chemical or thermal stimuli, there is a local
inflammatory reaction
during which humoral and cellular responses are
activated to localize the infection/tissue
damage.
The PAMPof the organisms activate the
local monocytes, macrophages, neutrophils and
endothelial cells to produce the release the
pro-inflammatory cytokines TNF-a and IL-l B

33.  These cytokines stimulate the macrophages and
moncytes etc to produce the other pro-
inflammatory cytokines such as lL-6 and secondary
mediators
 These cytokines act in paracrine and aulocrine
fashion.
Their production may be overwhelming and lead to
their spilling over into the general circulation.
They then stimulate secondary mediators from
arachidonic acid metabolites e.g .
 prostaglandins,PAF,thromboxane A2etc.

34.  This may lead to SlRS.
 Progression of the process leads to the
septic shock which may result in the
dysfunction of several organs –MODS,which
has a high mortality

35.  Septic shock is shock resulting from
moderate to severe sepsis or tissue damage;
it is a progression of SIRS.
 It is caused by microorganisms
 gram-negative in nearly two-thirds of cases
and gram positive in one-third
 Also by; viruses, fungi and parasites in a few.

36.  Of the gram-negative organisms, E. coli is
 the commonest.
 Others are Klebsiella, Enterobacter, Proteus
mirabilis/vulgaris, Pseudomonas and
Bacteroides.
 Gram-positive organisms that may cause
shock are Streptococci, Staphylococci,
Clostridia and Pneumococci.

37.  Some predisposing conditions are;
 Gut- Obstruction, Gangrene, Inflammation,
Perforation, surgery.
 Peritoneum- Peritonitis, Abscess
 Biliary tract- Cholecystitis,cholangitis
 Urinary tract-
Infection,obstruclion,Instrumentation , surgery

38.  Female genltal- Abortion, Post partum
sepsis, PlD
 Respiratory- Pneumonia, Mediastinitis
 Vascular system- Venous cuts , Indwelling
catheters
 Others-Haemorrhagic or hypvolaemic shock,
Burns, Severe injuries etc

40.  It is a hypersensivity reaction occurring within
seconds of injection of animal serum or drugs
including antibiotics.
 The generalized vasodilation of peripheral vessels,
increased capillary permeability.
 constriction of bronchioles and oedema of Larynx
 Caused by leukotrienes C4, D4 and E4, histamine,
bradykinin and prostaglandins released from mast
cells in the antigen-antibody reaction.

41.  It occurs as a result sudden loss of
sympathetic tone to the arterioles and
venules resulting in vasdilation of arterioles
and venules of muscles
 This occurs following sudden exposure to
unpleasant events such as pain or fright,
prolonged standing, spinal anaesthesia or
haemorrhage.

42.  Hypovolaemic shock
 Haemorrhage is classified into 4 stages by
the ACS.
 Class I haemorrhage:- up to 15% volume of
blood loss.
 minimal tachycardia occurs with no changes
in respiratory rate or blood pressure.

43.  Class II hemorrhage:15 % to 30% blood volume
loss.
 Increased sympathetic output leads to increased
heart rate and vascular tone.
 This leads to tachycardia (> 100) and narrowed
pulse pressure rather than a drop in blood
pressure.
 There are associated CNS changes like anxiety
and fright.
 Urine output remains at about 30-50ml and
hour.

44.  Class III haemorrhage : 30% - 40% blood
loss.
 By the time blood loss is over 2L , patients
present with the classical signs of shock.
Marked tachycardia (weak, thready pulse),
tachypnoea and mental changes occur.
 The systolic blood pressure falls and the
patient almost always requires transfusion.

45.  Class IV hemorrhage:- More than 40%
blood loss.
The patient is now nearing irreversible shock
with low or unrecordable blood pressure,
barely palpable pulse and negligible urine
output.

46.  In severe degrees of shock the following are
observed
 Pulse and Blood Pressure
 Rapid pulse which because of poor filling of
the vessel with blood is also WEAK and
THREADY and may even be imperceptible.

 Blood pressure, is LOW and may be
UNRECORDABLE especially in the terminal
stages

47.  Skin and Mucous Membranes:
cold, clammy
The Peripheral Veins are collapsed
Respiratory System: rapid and deep
respiration (air hunger).
CNS: confusion, restlessness,
apathetic or comatose, vision is blurred.

48.  Urinary System low urinary output or even
anuria in very severe cases.
 The temperature may be subnormal
 All organs may fail in the end (MODS).

49.  In the early stages of septic shock that is not
associated with hypovolaemia;
 the patient Starts with shivering and malaise
and has warm, dry , flushed skin, moderate
hypotension, hyperventilation,rapid but
bounding pulse
 fever ranging from 38.3° to 41 ° C.
 Sudden circulatory collapse or restlessness,
apprehension and confusion may be the
initial manifestation.

50.  As the condition progresses, the patient may
become semicomatose with cold clammy skin.
 collapsed superficial veins, pale mucosa with a
tinge of cyanosis, rapid and feeble
 pulse, severe hypotension and oliguria.
 With pre-existing hypovolaemia, the clinical
features are those of hypovolemic shock with
superimposed sepsis.

51.  include choking sensation, wheezing, cough,
urticaria, oedema,
 loss of consciousness, severe hypotension
and faint pulse.
 There may be pruritus.

52.  Management of shock is tailored towards the
cause.
 However, The patient is assessed and the
following observations are quickly made;
 I. Respiration:· The rate and depth of
respiration
If a patient is in coma, respiratory obstruction
must be looked for.
 2. Presence of bleeding external wounds
requiring urgent attention, and possible
fractures in cases of trauma .

53.  4. Skin: moist or dry, cool or warm.
 5. State of the veins especially those on the
dorsum of the
 feel: filled or collapsed.
 6. general condition: coma, restlessness, anxiety
or apathy.
 7. Pulse rate and volume, blood pressure and
tempera-
 ture.

54.  Treatment depends on the cause.
 Aims is to;
 I. expand vascular and interstitial fluid
volumes and so improve tissue perfusion,
 2 increase oxygen delivery and
consumption, and
 3. support vital functions.

55. • Control of ongoing haemorrhage-Direct
pressure over the site of haemorrhage
• Adequate airway is secured
• Breathing is maintained
• legs are elevated to increase venous return.
• Wide bore IV access to infuse fluid
• choice of fliud

56.  Bld samples are simultaneously collected for
PCV
Grouping & cross matching
Serum electrolytes urea & creatinine
Serum for bld gases

57.  Oxygen is administered via a passtic nasal
catheter or oxygen mask to increase the
oxygen saturation of the blood.
 Urethral catheter to monitor tissue perfusion
& urinary output

58.  Drugs:
 (i) Morphine : if the patient is in pain, morphine I0mg
may be given l.V.
 (ii) Hydrocortisone: It is not of proven value in
haemorrhagic shock. But it may prevent the onset of
septic shock.
 (iv) Naloxone: It is an opiate antagonist and raises
the B. P.
 It is given intravenously to patients with persistent
hypotension in spite of adequate treatment.

59.  (v) Mannitol: It should not be used to
promote diuresis except in crush injuries
 (vi) Alkalis: The use of sodium bicarbonate
to correct the metabolic acidosis is not
advocated

60.  Gold standard in monitoring: A warm, well
perfused patient with a normal mean arterial
pressure and adequate urine output (>
30ml/h)
 Frequent observation and assessment are
essential.
 I. Clinical Signs:
 2. Urine Output
 3. Pulse and Blood Pressure:
 4. Central Venous Pressure :

61.  5. Lungs and Jugular Veins: The lungs are
auscultated frequently for any evidence of
overloading.
 The external jugular veins are similarly
watched for raised pressure

62.  6. Blood po2, pC02, HCO3/anion gap, lactic
acid level ,pH and bloodsugar and pH :
pO2, pC0 2 and pH of the blood
 are estimated frequently and appropriate
measures taken. pO2 of80mm and pc0 2
of 40mmHg indicate adequate oxygenation.

63.  Management is as for haemorrhagic shock
but it is crystalloids that are needed
urgently, not blood.
 The type of electrolyte solution given
depends on the serum electrolytes and pH.

64.  (i) Adrenaline is most
 (ii). Antihistamine is added if response to
adrenaline is not rapid.
 (iii) Hydrocortisone l00-250mg is also
administered .
 (iv) Aminophylline 0.25-0.5mg in I0ml of
saline is given intravenously slowly to relieve
bronchospasm.
 (v) Adequate airway must be provided and
intravenous fluids administered rapidly.

65.  A complete clinical examination is done to
detect any focus of sepsis e.g PID,
cholecystitis, empyema, pneumonia.
mastoiditis, cerebral abscess.
 Investigations
 FBC
 Culture of blood , urine or any exudate
 Imaging (Ultrasound, CT Scan)

66.  Treatment
 The aims are;
 to improve the haemodynamic state,
 restore tissue
 administer oxygen
 combat the bacteria and cytokine and
eliminate the septic focus.

67. • 1. Volume replacement: There should be
rapid infusion of colloids, albumin containing
solutions or, if these are not available,
crystalloids ·- Ringer's lactate or
dextrose/saline to fill up the vasculature and
improve the haemodynamic state.
• 2. Oxygen is administered via an oxygen
mask to increase oxygen saturation.

68.  3. Antibiotics: Antibiotics are given in large
doses IV to combat infection as soon as the
intravenous infusion has been set up and
blood taken for culture and sensitivity. A
combn of gentamicin 80mg with clindamycin
600mg may be used.Polymyxin E can absorb
the endotoxins.

69.  4. Corticosteroids: Hydrocortisone 2-6g daily
for 2 days is beneficial if given at the onset
Steroids inhibit conversion of membrane
phospholipids to arachidonic acid thereby
inhibiting further release of prostaglandins,
prostacyclin, Thromboxane A, and
leukotrienes. They also inhibit further TNF-
synthesis and release.

70.  5 Ibuprofen It inhibits COX.Hence it blocks
synthesis of PGs & TX.It prevents neutrophil
activation & aggregation,decreases prodn of
superoxide radicals from activated
neutrophils, & stabilises lysosomal membrane
& enzs.

71.  7. Prevention of further coagulopathy. AT III
may prevent further coagulopathy and help
organ function. Protein C is anti-
thrombotic,Profibrinolytic and
antiinflammatory.

72.  8 Naloxone: It raises the blood pressure.
 9. Inotropic agents: lf the heart fails, digitalis
or low doses of dopamine or dobutamine may
be administered to improve myocardial
contractility.

73.  10. Insulin therapy: If hyperglycaemia occurs ,
there should be intensive therapy to maintain
the blood glucose level between the reference
value.
 12. Surgery: If a septic focus , e.g.
gangrenous bowel, is responsible for the
shock, then it must be dealt with as soon as
practicable especially if response to shock
therapy is poor.

74.  1 Pulmonary insufficiency
 2. Cardiac failure/arrest
 3. Cerebral failure
 4. Pre-renal failure/ATN
 5. Metabolic acidosis
 6. Sepsis/SIRS
 7. Liver failure
 8. Failure of coagulation and immune
systems.
 9. Multiple Org an Dysfunction Syndrome

77.  Principles and Practice of Surgical Practice(
Badoe)