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A
SEMINAR
ON
CONTENT
 Definition
 Pathophysiology of shock
 Types of Shock
 Hypovolaemic Shock
 Traumatic Shock
 Cardiogenic Shock
 Neurogenic Shock
 Septic Shock
 Crush Syndrome
DEFINITION
It is difficult to define shock in one sentence.
However,
It may be defined as a condition in which circulation
fails to meet the nutritional needs of the cells and at
the same time fails to remove the metabolic waste
products.
TYPES OF SHOCK
 There are various types of shock, of which
haematogenic or hypovolaemic shock is the most
common and important.
 Various types of shock are as:
 Haematogenic or hypovolaemic shock
 Traumatic shock
 Neurogenic shock
 Cardiogenic shock
 Septic shock
 Miscellaneous types
HYPOVOLAEMIC SHOCK
 Pathophysiology – Such shock is usually due to
sudden loss of blood volume or loss of fluid from
the vascular space.
Loss of blood
Dec. filling of right heart
Dec. filling of pulmonary vasculature
Dec. filling of left atrium and
ventricle
Dec. in stroke volume
Drop in arterial
blood pressure
Shock
COMPENSATORY MECHANISMS
 After hemorrahge this mechanism follows:
1. Adrenergic discharge
2. Hyperventilation
3. Release of vasoactive hormones
4. Collapse
5. Resorption of fluid from the interstitial space
6. Resorption of fluid from the intercellular to the
extracellular space
7. Renal conservation of body water and electroytes.
CLINICAL FEATURES
 Depends on the degree of loss of blood volume and
on the duration of shock.
 MILD SHOCK: loss of less than 20% of blood
voluyme is included in this category.
 Feet become pale and cool
 Sweating
 Urinary output pulse rate and blood pressure remai
normal
 Thirst and cold.
 Moderate shock: Loss of bloos volume from 20 –
40% cause this shock.
 Oliguria
 Pulse rate increased to 100 beats / min.
 Normal blood pressure.
 Severe Shock: Loss of blood volume more than
40% usually causes severe shock.
 Paller occurs
 Low urinary output
 Rapid pulse rate
 Low blood pressure.
INVESTIGATIONS
 Monitoring a shock includes:
 Blood pressure- measurement of blood pressure is very
essential in shock
 Respiration: hyperventilation is and important indicator
of shock.
 Urine- urine is affected quite early even in moderate
shock. It is a good index of adequacy of replacement
therapy.
 CVP: Measurement of CVP is quite important in
assessing shock.
 In hypovolumic shock there is dec. in the blood volume
ans so is the CVP.
 ECG: in severe shock it may show signs of myocardial
ischemia
 SWAN-GANG CATHETER:
TREATMENT
1 Resuscitation: This should begin immediately as the
patient is admitted with hypovolaemic shock.
 Establish clear airway
 Maintain adequate ventilation and oxugenation.
 Lowering of head to prevent pheripheral pooling of blood
and odema.
 Increases cerebral circulation.
2 Immediate control of bleeding is highly important in
case of heamorrhagic shock.
Raise the footend of the bed and by compression bandage
to tamponade external haemorrhage
Bleeding can be stoppped surgically as well.
 3 Extracellular fluid replacement is probably the
most important point in the treatment of
hypovolaemic shock.
 Ringer’s lactate, ringer’s acetate or normal saline
can be administered.
 A few points to be remembered in case of
extracellular fluid replacement:
 The I.V fluid particularly the crystalloid, ehich
should be given first, is administered with rapidly so
that replacemnet is done as quickly as possible
 B.P, pulse rate, urine output, CVP and other
laboratory tests should be performed.
 If there is blood loss, it is replaced by blood
 DRUGS: A few drugs are commonly used different
shock.
 Sedatives: Morphine is quite good in this respect
and sholud be given IV.
Injection pethidine can be also be used
intramuscularly.
Chronotropic Agents: Atropine is the most widely
used in this group Followed by isoproterenol.
Inotropic agents: Most commonly used drugs in this
cateogory are the dopamine and dobutamine these
should be used in low dosages.
Othr used agents are vasodialators, vasoconstrictors,
betablockers, Diuretics.
654 × 668 - esicm.org
TRAUMATIC SHOCK
 Pathophysiology:
 The pecularity of this shock is that traumatised
tissues activate the coagulation system and release
microthrombi into the circulation. These may
occlude or constrict parts of pulmonary
microvasculature to increse pulmonary vascular
resistance. This inc. right ventricular diastolic and
right atrial pressures. Inc. in capillary permeability.
Loss of plasma depletion of the vascular volume to
a great extent.
CLINICAL FEATURE
 Presence of peripheral and pulmonary oedema in
this type of shock
 Infusion of large volumes of fluid whih may be
adequate for pure hypovolaemic shock is usually
inadequate for traumatic shock.
TREATMENT
 Resuscitation: In this type of shock shock
mechanical ventilatory support is more needed.
 Local treatment of trauma and control of bleeding:
This is almost similar to hypovolaemic shock.
Surgical debridement of ischaemic and dead
tissues and immobilisation of fractures may be
required.
 Fluid replacement: adquate fluid replacemnet
should be done with a dose of 10,000 units of
heparin seemes to be effective.
CARDIOGENIC SHOCK
 Pathophysiology:
Dysfunction of the
right ventricle
Right heart unable to pump
blood to lungs
Filling of left heart decreases
Left ventricular output
decreases.
Dysfunction of the
left ventricle
Unable to maintain adequate
stroke volume
Left ventricle output and
systemic arterial blood
pressure dec.
Engorgement of pulmonary
vasculature results in failure of
left heart.
CARDIAC COMPRESSIVE SHOCK
 This arises when the heart is compressed enough from
outside to decrease cardiac output.
 Causes: Tension pneumothorax, pericardial tamponade and
diaphragmatic rupture with herniation of the bowel into chest.
 Clinical features: In the beginning the skin is pale and cool
and the urine output is low.
 Pulse becomes rapid
 Arterial blood flow becomes low
 Left ventricular dysfuctional the patient has broncheal rales
and a third heart sound is heard.
 Gradually the heart becomes enlarged and when the right
ventricle also fails distended neck veins will be visible.
TREATMENT
 Airway must be clear with adequate oxygenation.
 In case of right sided failure large doses of heparin
intravenously are given.
 If pain is complained of left heart failure proper
sedation E.g. morphine should be prescribed.
 Fluminant pulmonary oedema should be treated
with a diuretic.
 Treatment of cardiogenic shock is complex.
NEUROGENIC SHOCK
 Pathophysiology:
Dialatation of systemic vasculature
Dec. arterial pressure
Blood pools in the systemic venules and small veins
Right heart filling and stroke volume dec.
Dec. in pulmonary blood volume and left
heart filling
Left ventricular output dec.
Compensatory
mechanisms of
adrenergic nervous
system fail.
shock
CLINICAL FEATURES
 Skin remains warm
 Pink in color
 Well perfused in contarry to the hypovolumic shock
 Urine output may be normal.
 Heart rate is rapid.
 Blood pressure is low.
TREATMENT
 Elevation of the legs is effective in treating patients
with neurogenic shock.
 Assumption of Trendelenburg position displaces
blood from the systemic venules and small veins
into the right heart and thus inc. cardiac output.
 Administration of fluid is important though not so as
in hypovolaemic shock. This increase filling of the
right heart which in its increases cardiac output.
 Neurogenic shock is probably the only form of
shock that can be safely treated with a
vasocaonstrictor drug.
SEPTIC SHOCK
 Pathophysiology: High mortality rate
 Most frequently causitive organisms are gram
positive and gram negative bacteria,
 Because of effective antibiotic treatment available
for most gram positive infections, the majority of
cases of septic shock are now caused by gram
negative bacteria.
COMMON ORGANISMS CONCERNED WITH
SEPTIC SHOCK
 E.Coli
 Klebsiells aerobacter
 Proteus
 Pseudomonas
 Bacteriods
Gram- positive sepsis and shock: Clostridium tetani
or Clostridium perfringes, streptococcus,
staphylococcus, pseudomonas.
Gram- negative sepsis and shock: Genitourinary
system associated with instrumentation.
CLINICAL FEATURE:
Recognized by development of chills and elevated
temperature above 100 F.
Two types:
Early warm shock
Late cold shock
In early warm shock there is cutaneous vasodialation.
Inc. in body temperature.
Cutaneous dilation.
Pulse rate high
Intermittent spikes of fever alternating with bouts of
chills.
 Late cold Shock: inc. permeability due to liberation
of toxic products into the center circulation.
Clinically difficult to differentiate b/w hemorrahgic ,
traumatic shock.
 Only guide is the knowlegde of septic focus.
 Treatment:
 Treatment can be classified into two groups :
 Treatment of the infection by early surgical
debridement or drainage and by use of appropriate
antibiotics
 Treatment of shock which includes fluid
replacement , steroid administration and use of
vasoactive drugs.
 Cephalothin (6-8gm/day I.V in 4 -6 divided doses)
 Gentamicin (5mg/kg/day)
 Clindamycin (bacteroides)
 Chloromycetin
 Fluid replacement is of great importance.
 Mechanical ventilation along with endotracheal
intubation.
 Steriods can be used sometimes.
 Use of vasoactive drugs with mixed alpha and beta
adrenergic effects may be indicated.
CRUSH SYNDROME
 It is a symptom complex in which a portion of the body
becomes crushed due to a heavy weight falls on that potion of
the body and is kept there for sometime to crush all the
tissues in that portion of the body.
 This type of injury is come across after earthquakes, mine
injuries, air raids, collapse of a building or use of tourniquiet
for longer period.
 In this syndrome oligaemic shock occurs due to extravasation
of blood into the muscle in the affceted portion of the body.
 Sweeling of the muscles, myohaemoglobin enter the
circulation
 At this stage the limbs fills tense and the patient complains of
severe pain in the limb.
 Urine output will be obviously reduced if uraemia supervenes,
the patient may show restlessness, mild delirium.
TREATMENT
 As a first aid measure application of tourniquet to
the affected limb above the crush injury is a good
method to reduce admission of deleterious
substances into the general circulation.
 Parallel incisions ,ay be applied to relieve temsion,
through which muscles protruded.
 Low molecular weight dextran (40000)or
Rheomacrodex is effective in this condition as it
prevents sludging of red cells in small blood vessels
and maintain circulation to the kidneys.
.
 Mannitol is also very effective in this condition
1gm/kg body weight of mannitol is given IV as 20%
solution in 12 hours.
 Catheterisation of the bladder should be performed
before instituting mannitol.
 Tourniquet should be removed as scheduled, blood
transfusion should be done.
 Haemodialysis should be used as life saving
procedure in grave conditions.

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SHOCK

  • 2. CONTENT  Definition  Pathophysiology of shock  Types of Shock  Hypovolaemic Shock  Traumatic Shock  Cardiogenic Shock  Neurogenic Shock  Septic Shock  Crush Syndrome
  • 3. DEFINITION It is difficult to define shock in one sentence. However, It may be defined as a condition in which circulation fails to meet the nutritional needs of the cells and at the same time fails to remove the metabolic waste products.
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  • 8. TYPES OF SHOCK  There are various types of shock, of which haematogenic or hypovolaemic shock is the most common and important.  Various types of shock are as:  Haematogenic or hypovolaemic shock  Traumatic shock  Neurogenic shock  Cardiogenic shock  Septic shock  Miscellaneous types
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  • 10. HYPOVOLAEMIC SHOCK  Pathophysiology – Such shock is usually due to sudden loss of blood volume or loss of fluid from the vascular space. Loss of blood Dec. filling of right heart Dec. filling of pulmonary vasculature Dec. filling of left atrium and ventricle Dec. in stroke volume Drop in arterial blood pressure Shock
  • 11. COMPENSATORY MECHANISMS  After hemorrahge this mechanism follows: 1. Adrenergic discharge 2. Hyperventilation 3. Release of vasoactive hormones 4. Collapse 5. Resorption of fluid from the interstitial space 6. Resorption of fluid from the intercellular to the extracellular space 7. Renal conservation of body water and electroytes.
  • 12. CLINICAL FEATURES  Depends on the degree of loss of blood volume and on the duration of shock.  MILD SHOCK: loss of less than 20% of blood voluyme is included in this category.  Feet become pale and cool  Sweating  Urinary output pulse rate and blood pressure remai normal  Thirst and cold.
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  • 14.  Moderate shock: Loss of bloos volume from 20 – 40% cause this shock.  Oliguria  Pulse rate increased to 100 beats / min.  Normal blood pressure.  Severe Shock: Loss of blood volume more than 40% usually causes severe shock.  Paller occurs  Low urinary output  Rapid pulse rate  Low blood pressure.
  • 15. INVESTIGATIONS  Monitoring a shock includes:  Blood pressure- measurement of blood pressure is very essential in shock  Respiration: hyperventilation is and important indicator of shock.  Urine- urine is affected quite early even in moderate shock. It is a good index of adequacy of replacement therapy.  CVP: Measurement of CVP is quite important in assessing shock.  In hypovolumic shock there is dec. in the blood volume ans so is the CVP.  ECG: in severe shock it may show signs of myocardial ischemia  SWAN-GANG CATHETER:
  • 16. TREATMENT 1 Resuscitation: This should begin immediately as the patient is admitted with hypovolaemic shock.  Establish clear airway  Maintain adequate ventilation and oxugenation.  Lowering of head to prevent pheripheral pooling of blood and odema.  Increases cerebral circulation. 2 Immediate control of bleeding is highly important in case of heamorrhagic shock. Raise the footend of the bed and by compression bandage to tamponade external haemorrhage Bleeding can be stoppped surgically as well.
  • 17.  3 Extracellular fluid replacement is probably the most important point in the treatment of hypovolaemic shock.  Ringer’s lactate, ringer’s acetate or normal saline can be administered.  A few points to be remembered in case of extracellular fluid replacement:  The I.V fluid particularly the crystalloid, ehich should be given first, is administered with rapidly so that replacemnet is done as quickly as possible  B.P, pulse rate, urine output, CVP and other laboratory tests should be performed.  If there is blood loss, it is replaced by blood
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  • 19.  DRUGS: A few drugs are commonly used different shock.  Sedatives: Morphine is quite good in this respect and sholud be given IV. Injection pethidine can be also be used intramuscularly. Chronotropic Agents: Atropine is the most widely used in this group Followed by isoproterenol. Inotropic agents: Most commonly used drugs in this cateogory are the dopamine and dobutamine these should be used in low dosages. Othr used agents are vasodialators, vasoconstrictors, betablockers, Diuretics.
  • 20. 654 × 668 - esicm.org TRAUMATIC SHOCK  Pathophysiology:  The pecularity of this shock is that traumatised tissues activate the coagulation system and release microthrombi into the circulation. These may occlude or constrict parts of pulmonary microvasculature to increse pulmonary vascular resistance. This inc. right ventricular diastolic and right atrial pressures. Inc. in capillary permeability. Loss of plasma depletion of the vascular volume to a great extent.
  • 21. CLINICAL FEATURE  Presence of peripheral and pulmonary oedema in this type of shock  Infusion of large volumes of fluid whih may be adequate for pure hypovolaemic shock is usually inadequate for traumatic shock.
  • 22. TREATMENT  Resuscitation: In this type of shock shock mechanical ventilatory support is more needed.  Local treatment of trauma and control of bleeding: This is almost similar to hypovolaemic shock. Surgical debridement of ischaemic and dead tissues and immobilisation of fractures may be required.  Fluid replacement: adquate fluid replacemnet should be done with a dose of 10,000 units of heparin seemes to be effective.
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  • 24. CARDIOGENIC SHOCK  Pathophysiology: Dysfunction of the right ventricle Right heart unable to pump blood to lungs Filling of left heart decreases Left ventricular output decreases. Dysfunction of the left ventricle Unable to maintain adequate stroke volume Left ventricle output and systemic arterial blood pressure dec. Engorgement of pulmonary vasculature results in failure of left heart.
  • 25. CARDIAC COMPRESSIVE SHOCK  This arises when the heart is compressed enough from outside to decrease cardiac output.  Causes: Tension pneumothorax, pericardial tamponade and diaphragmatic rupture with herniation of the bowel into chest.  Clinical features: In the beginning the skin is pale and cool and the urine output is low.  Pulse becomes rapid  Arterial blood flow becomes low  Left ventricular dysfuctional the patient has broncheal rales and a third heart sound is heard.  Gradually the heart becomes enlarged and when the right ventricle also fails distended neck veins will be visible.
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  • 27. TREATMENT  Airway must be clear with adequate oxygenation.  In case of right sided failure large doses of heparin intravenously are given.  If pain is complained of left heart failure proper sedation E.g. morphine should be prescribed.  Fluminant pulmonary oedema should be treated with a diuretic.  Treatment of cardiogenic shock is complex.
  • 28. NEUROGENIC SHOCK  Pathophysiology: Dialatation of systemic vasculature Dec. arterial pressure Blood pools in the systemic venules and small veins Right heart filling and stroke volume dec. Dec. in pulmonary blood volume and left heart filling Left ventricular output dec. Compensatory mechanisms of adrenergic nervous system fail. shock
  • 29. CLINICAL FEATURES  Skin remains warm  Pink in color  Well perfused in contarry to the hypovolumic shock  Urine output may be normal.  Heart rate is rapid.  Blood pressure is low.
  • 30. TREATMENT  Elevation of the legs is effective in treating patients with neurogenic shock.  Assumption of Trendelenburg position displaces blood from the systemic venules and small veins into the right heart and thus inc. cardiac output.  Administration of fluid is important though not so as in hypovolaemic shock. This increase filling of the right heart which in its increases cardiac output.  Neurogenic shock is probably the only form of shock that can be safely treated with a vasocaonstrictor drug.
  • 31. SEPTIC SHOCK  Pathophysiology: High mortality rate  Most frequently causitive organisms are gram positive and gram negative bacteria,  Because of effective antibiotic treatment available for most gram positive infections, the majority of cases of septic shock are now caused by gram negative bacteria.
  • 32. COMMON ORGANISMS CONCERNED WITH SEPTIC SHOCK  E.Coli  Klebsiells aerobacter  Proteus  Pseudomonas  Bacteriods Gram- positive sepsis and shock: Clostridium tetani or Clostridium perfringes, streptococcus, staphylococcus, pseudomonas. Gram- negative sepsis and shock: Genitourinary system associated with instrumentation.
  • 33. CLINICAL FEATURE: Recognized by development of chills and elevated temperature above 100 F. Two types: Early warm shock Late cold shock In early warm shock there is cutaneous vasodialation. Inc. in body temperature. Cutaneous dilation. Pulse rate high Intermittent spikes of fever alternating with bouts of chills.
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  • 35.  Late cold Shock: inc. permeability due to liberation of toxic products into the center circulation. Clinically difficult to differentiate b/w hemorrahgic , traumatic shock.  Only guide is the knowlegde of septic focus.  Treatment:  Treatment can be classified into two groups :  Treatment of the infection by early surgical debridement or drainage and by use of appropriate antibiotics  Treatment of shock which includes fluid replacement , steroid administration and use of vasoactive drugs.
  • 36.  Cephalothin (6-8gm/day I.V in 4 -6 divided doses)  Gentamicin (5mg/kg/day)  Clindamycin (bacteroides)  Chloromycetin  Fluid replacement is of great importance.  Mechanical ventilation along with endotracheal intubation.  Steriods can be used sometimes.  Use of vasoactive drugs with mixed alpha and beta adrenergic effects may be indicated.
  • 37. CRUSH SYNDROME  It is a symptom complex in which a portion of the body becomes crushed due to a heavy weight falls on that potion of the body and is kept there for sometime to crush all the tissues in that portion of the body.  This type of injury is come across after earthquakes, mine injuries, air raids, collapse of a building or use of tourniquiet for longer period.  In this syndrome oligaemic shock occurs due to extravasation of blood into the muscle in the affceted portion of the body.  Sweeling of the muscles, myohaemoglobin enter the circulation  At this stage the limbs fills tense and the patient complains of severe pain in the limb.  Urine output will be obviously reduced if uraemia supervenes, the patient may show restlessness, mild delirium.
  • 38. TREATMENT  As a first aid measure application of tourniquet to the affected limb above the crush injury is a good method to reduce admission of deleterious substances into the general circulation.  Parallel incisions ,ay be applied to relieve temsion, through which muscles protruded.  Low molecular weight dextran (40000)or Rheomacrodex is effective in this condition as it prevents sludging of red cells in small blood vessels and maintain circulation to the kidneys. .
  • 39.  Mannitol is also very effective in this condition 1gm/kg body weight of mannitol is given IV as 20% solution in 12 hours.  Catheterisation of the bladder should be performed before instituting mannitol.  Tourniquet should be removed as scheduled, blood transfusion should be done.  Haemodialysis should be used as life saving procedure in grave conditions.