Shock

By
Dr. Nabeela Zeeshan
Department of Pathology
Shock: Objectives
• Define Shock
• Describe the major causes of shock and
explain giving examples the pathophysiology

of each
• Explain the physiological basis of signs and
symptoms of different types of shock
• Explain the short and long term physiological
compensation of shock
• List the factors which make the shock
refractory
 Shock
Shock is defined as:

• Systemic hypotension due either to reduced cardiac

output or to reduced effective circulating blood volume.

• The end results are impaired tissue perfusion, and

cellular hypoxia.

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 Etiological Types of Shock
• There are three general etiological types
of shock:
• Cardiogenic Shock
• Hypovolemic Shock, and
• Septic Shock
• Less commonly
• Neurogenic Shock
• Anaphylactic Shock
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 Cardiogenic Shock
Principal Mechanism / Pathophysiology

It results from low cardiac output due to failure of

myocardial pump.

Clinical examples:
• Myocardial damage e.g., MI
• Ventricular arrhythmias
• Extrinsic compression e.g., cardiac tamponade
• Outflow obstruction e.g., pulmonary embolism
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 Hypovolemic Shock
• Principal Mechanisms / Pathophysiology
• Inadequate blood or plasma volume
leading to hypovolumia and hypotension

• Clinical Examples
• Blood loss
• e.g., Hemorrhage
• Fluid loss
• e.g., vomiting, diarrhea, burns, or
trauma 6
 Anaphylactic shock
• Anaphylaxis – a severe systemic
hypersensitivity reaction
characterized by systemic
vasodilation and increased
vascular permeability caused by
an immunoglobulin E
hypersensitivity reaction

• SIGN & SYMPTOMS

• First- Pruritus, flushing,
urticaria appear
• Next- Throat fullness, anxiety,
chest tightness, shortness of
breath and lightheadedness
• Finally- Altered mental status,
respiratory distress and
circulatory collapse
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 Neurogenic shock
• Less commonly, shock
may occur due to
neurogenic condition like:
• anesthetic accident or
• spinal cord injury

resulting in
• loss of vascular tone
(vasodilation,
hypotension) and
• peripheral pooling of
blood.
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 Septic Shock
• Septic shock ranks first among the causes of death in
intensive care units and accounts for more than 200,000
deaths annually in the United States.

• It carries 20-50% risk of mortality .

• Its most common victims are children, immunocompromised

individuals, and the elderly, as their immune system cannot
deal with infection as effectively as those of healthy adults.
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 Septic Shock
Principal Mechanisms / Pathophysiology

• It results from arterial vasodilation and venous blood pooling

as a result of the toxins released from the microbial
organisms

• Cardiac output is preserved or even initially increased.

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 Etiology: Septic Shock

• Gram-positive bacteria (at present constitute the most common cause

of septic shock (eg: Staph aureus infection) followed by

• Gram-negative organisms. eg.:
• E coli
• Proteus
• Klebsiella
• Bacteroides
• Pseudomonas (burns)
• Meningococci

• Fungi
• Viruses
• Parasites 11
Septic Shock

Clinical examples of bacterial spread

• Infected burns
• Septicaemia
• Localised infections
• Instrumentation e.g. Urogenital
• Immunosuppression

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 Pathogenesis of Septic Shock
• In septic shock the cardiac output is preserved or even initially increased.
• The toxins from bacteria damage endothelium which causes the released
of Nitric oxide (NO) which in turn causes:
• increased capillary permeability,
• decreased systemic vascular resistance,
• vasodilatation, and hypotension
• Unlike hypovolaemic shock there is no vasoconstriction phase.
• The endothelial cell damage and activation may lead to DIC:
• Damaged endothelium releases thromboplastins which trigger the
coagulation cascade: this results in disseminated intravascular
coagulation (DIC). Blood clotting factors are consumed and the patient
therefore has a bleeding tendency
• In addition, septic shock is associated with disturbance of metabolism
that directly suppress cell and tissue function.
• The net effect of these abnormalities is hypoperfusion and
dysfunction of multiple organs.
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Exotoxic (gram + ve) and Endotoxic (gram –ve)
shock

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 Septic Shock:
Example: Infected Burns

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 Septic Shock:
Example: Severe localized infection

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 Septic Shock:
Example: Meningococcal meningitis

The brain is
covered in
purulent exudate

17
University of Newcastle upon
Tyne
Outcomes in patients with septic shock
• Difficult to predict

• In general those with widespread infections and co-

morbid diseases have the highest mortality rates,

• But even young healthy individuals with virulent

infections (e.g., meningococcal sepsis) can succumb
within hours.

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 END RESULTS
Hemorrhage Septic shock , Anaphylactic
Fluid Loss shock & Neurogenic Shock
increased capillary permeability,
Hypovolemia Peripheral vasodilatation
Pooling of blood in dilated BV

↓ venous return and low cardiac output

Reflex vasoconstriction in non vital organ leading to

hypoperfusion and cellular hypoxia in various organs
Which along with
failure to remove toxic metabolic end products

if not corrected can lead to multi-organ failure like

• Cardiac Depression
• Respiratory distress
• Renal failure
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• DIC
 Stages of Shock
• Shock is a progressive disorder that if
uncorrected leads to death.

• Unless the damage is massive and rapidly

lethal, shock tends to evolve through three
general stages.

• These stages have been documented most

clearly in hypovolemic shock but are common
to other forms as well:
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 Stages of Shock
• An initial nonprogressive stage during which reflex
compensatory mechanisms are activated and
perfusion of vital organs is maintained.

• A progressive stage characterized by tissue

hypoperfusion and onset of worsening circulatory and
metabolic imbalances.

• An irreversible stage that sets in after the body has

incurred cellular and tissue injury (due to persistent
hypoxia) so severe that even if the hemodynamic
defects are corrected, survival is not possible
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 Nonprogressive Phase:
Compensatory Physiological basis of
mechanisms signs and symptoms
• In the early, nonprogressive • The net effect is tachycardia,
phase of shock, various peripheral vasoconstriction,
neurohumoral mechanisms help and renal conservation of fluid.
maintain cardiac output and
blood pressure.
• For example Cutaneous
• These include
vasoconstriction, is
• Baroreceptor reflexes
responsible for the
• Release of catecholamines characteristic coolness and
• Activation of the renin- pallor of skin in shock
angiotensin axis • (although septic shock may
• Antidiuretic hormone initially cause cutaneous
vasodilation and thus present with
release, warm, flushed skin).
• Generalized sympathetic
stimulation 22
 Progressive Phase
If the underlying causes are not corrected, shock passes
imperceptibly to the progressive phase, during which there is
widespread tissue hypoxia

Persistent oxygen deficit will lead to anaerobic respiration and

glycolysis, with excessive production of lactic acid and
consequent ↓ in tissue pH.

As a result: arterioles dilate and blood begins to pool in the

microcirculation leading to hypotension

Peripheral pooling also puts endothelial cells at risk of

developing anoxic injury with subsequent DIC.
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 Irreversible Stage
• Unless there is intervention, the process eventually enters an irreversible stage
which will be manifested as:

• Reflex peripheral vasoconstriction fails, as a result of persistent hypoxia and

acidosis.

• Widespread vasodilation and hypoperfusion to the vital organ occur

• Cardiac depression: decreased in cardiac contractility, because of nitric

oxide synthesis released from injured endothelium further decrease
cardiac output.

• Brain dysfunction, edema and neuronal degenaration

• Renal failure: At this point, the patient has complete renal shutdown due
to ischemic acute tubular necrosis.

• Reduced intestinal perfusion (ischemia) allows intestinal flora to enter the

circulation, endotoxic shock may also be superimposed. 24
 Refractory Shock
• In some patients shock persists for hours and gradually
progresses. It eventually reaches a state in which there
is no longer any response to vasopressor drugs and
even if the blood volume is returned to normal, cardiac
output remains depressed.
• This condition is known as refractory shock.
• It used to be called irreversible shock, and patients still
die despite vigorous treatment

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 Various factors appear to make shock refractory
• Cerebral ischemia depresses vasomotor and cardiac
discharge, causing blood pressure to fall and making the
shock worse.
• This, in turn, causes a further reduction in cerebral blood flow.
• Myocardial blood flow is reduced .
• Myocardial failure makes the pumping action of the
heart less effective and consequently makes the shock
worse and further lowers myocardial blood flow.
• Pulmonary damage with production of acute
respiratory distress syndrome .
• A complication of shock that has a very high mortality
rate.
• Due to damage to endothelial cells of capillaries and
alveolar epithelial cells with the release of cytokines
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 Morphology
• The cellular and tissue changes induced by
shock are essentially those of hypoxic injury
(ischemic necrosis).

• Since shock is characterized by failure of

many organ systems, the cellular changes
may appear in any tissue.

• Nevertheless, they are particularly evident in

the brain, heart, kidneys, adrenal glands, and
gastrointestinal tract 27
 Clinical Course
The clinical manifestations of shock depend on the
precipitating insult.
In hypovolemic and cardiogenic shock, the patient presents with
• Tachycardia due to widespread cellular
• a weak, rapid pulse hypoxia occurring in heart,
• Tachyponea lung and brain
• Loss of consciousness

• Cool, clammy, cyanotic skin Due to peripheral

vasoconstriction

In septic shock, however the

Skin may be warm and flushed as a result of peripheral

vasodialation
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 Clinical Course (cont)
• Afterwards, the cardiac, cerebral, and pulmonary
changes occur secondary to the shock state.

• If patients survive the initial complications, they enter a

second phase, dominated by renal insufficiency and
marked by a progressive fall in urine output as well as
acidosis, and severe fluid and electrolyte imbalances.
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JAZAK ALLAH

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