PATHOPHYSIOLOGY

1. Shock
DONE BY
AISWARYA THOMAS
ND
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2. of Shock
• Inadequate oxygen delivery due to reduction
of effective circulating blood volume.
• Results in global tissue hypoperfusion and
metabolic acidosis.
• If uncompensated it leads to impaired
cellular metabolism and death.
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3. Shock?• Restless
• Confused
• Skin cool and mottled
or hot and flushed
• Weak or absent
peripheral pulses
• Low BP
• Tachycardia
• Drowsiness, coma
3
Yes!
These are all signs
and symptoms of
shock

4. NESIS
All forms of shock involves following 3 derangement :
•Reduced effective circulating blood volume
•Reduce supply of oxygen to the cells and tissues results
anoxia.
•Inflammatory mediators and toxins released from shock
induced cellular injury.
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5. 5

6. 1)REDUCED EFFECTIVE
CIRCULATORY BLOOD
VOLUME
• By actual loss of blood volume occurs in
hypovolaemic shock
•By decreased cardiac output without actual
loss of blood occurs in cardiogenic shock and
septic shock.
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7. 2) IMPAIRED TISSUE OXYGENATION
Reduction in the effective circulatory blood volume from either above
or other etiologic agents, there is a decreased venous return to the heart
resulting in decreased cardiac output.
This consequently causes reduced supply of oxygen to the organs and
tissues and hence tissue anoxia, which sets in cellular injury.
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8. 3) RELESE OF INFLAMATORY
MEDIATORS
•As a response to cell injury inflammatory mediators are
released but eventually these agents themselves become the
cause of cell injury.
•Endotoxins in bacterial wall in septic shock stimulate
massive release of pro- inflammatory mediators (cytokines)
but a similar process of release of agents takes place in late
stages of shock from other causes. 8

9. • Several pro inflammatory mediators are
released from monocytes-macrophages,
other leucocytes and other body cells, the
most important being the tumour necrosis
factor (TNF)-α and interleukin-1 (IL-1)
cytokines.
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10. Types of
Shock
• Hypovolaemic
• Septic
• Cardiogenic
• Other types
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Traumatic Shock
Neurogenic Shock
Hypoadrenal shock

11. Hypovolae
mic Shock
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Results from inadequate
circulatory blood volume
Due to loss of red cell mass and
plasma or from loss of plasma
volume alone

12. ETIOLOGY
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1. Loss of whole blood
Hemorrhage
Trauma
Gastrointestinal ulcer
Surgery
Inadequate clotting
2. Loss of other body fluids
Vomiting
Diarrhea
Diuretic therapy
Burns(>10% surface)

13. Pathogenes
is
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Hypovolaemia
Decreased circulatory volume
Decreased venous return to heart
Decreased stroke volume
Decreased cardiac output
Decreased cellular oxygen supply
Decreased tissue perfusion
Impaired cellular metabolism
Shock

14. Clinical
features
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Increased heart rate(Tachycardia)
Low BP (hypotension)
Low urinary output
Pallor , cool and clammy skin
Anxiety , confusion , agitation
Absent bowel sounds
Diagnostic
findings
 Decreased hematocrit
 Increased lactate
 Increased urine specific gravity

15. Septic Shock
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Septic shock is the result of bacterial
infections or septicemia along with the
presence of tissue perfusion abnormalities.
Gram positive septicemia(exotoxic shock)
Gram negative septicemia(endotoxic shock)
– more common

16. Etiology
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Gram negative septicaemia
Example: infection with E.coli
Proteus
Pseudomonas
Bacteroides
Gram positive septicaemia
Example: infection with Streptococci
Pneumococci

17. s of Sepsis
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18. Features• Hyperthermia or hypothermia
• Tachycardia
• Wide pulse pressure
• Low blood pressure (SBP<90)
• Mental status changes,agitation,coma
• Hypoxemia
• Urine output
• Gastro intestinal bleeding
Diagnostic
findings
Increase or decrease of WBC
Decrease platelets
Increase urine specific gravity
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19. ic
Shock
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Acute circulatory failure with sudden fall in cardiac
output from acute diseases of the heart without
actual reduction of the blood volume
(normovolaemia)

20. Etiologies
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• MI
• Cardiac arrhythmias
• Myocarditis
• Pulmonary embolism
• Rupture of heart, ventricle or
papillary muscles
• Acute aortic insufficiency
•Tension pneumothorax

21. Pathogenesis
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22. Clinical Features• Cool, mottled skin
• Tachypnea, Nausea, omitting
• Altered mental status , anxiety , confusion
• Narrowed pulse pressure and hypotension
• Decreased renal blood flow and urine output
• Chest pain may or may not be present
• Decreased capillary refill time
DIAGNOSTIC FINDINGS
 Increase blood glucose
Increase cardiac marks
ECG
Echocardiogram
Chest X ray
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23. 4) OTHER TYPES
1.Neurogenic shock:- Arise due to interruption of sympathetic
vasomotor supply.
2.Hypoadrenal shock :- Arise from unknown adrenal insufficiency,
patients fails to respond normally to stress 0f Trauma, surgery or
illness.
3.Traumatic shock :- Shock resulting from trauma is initially due to
hypovolemia but even after haemorrhage has been controlled, these
patient continue to suffer loss of plasma volume into the interstitial
of injured tissue.
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24. Stages Of
Shock
Deterioraton of the circulation in shock is a
progressive phenomenon and can be divided
arbitrarily into 3 ways:-
Non-Progressive
(Initial,compensated,reversible shock)
Progressive Decompensated Shock
Decompensated (Irreversible) Shock
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25. • COMPENSATED (NON-PROGRESSIVE,
INITIAL, REVERSIBLE) SHOCK
• In early stages of shock, an attempt is made to
maintain adequate cerebral and coronary blood
supply by redistribution of blood so that the vital
organs(brain and heart) are adequately perfused
and oxygenated.
• These is achieved by activation of various neuro
hormonal mechanism causing widespread vaso
constriction,fluid conservation by the kidney and by
stimulation of adrenal medulla. 25

26. 1)WIDESPREAD
CONSTRICTION
• The neural and humeral
factors(baroreceptor,chemoreceptors,catacholamines
, renin and angiotensin II) are activated,in turn
brings vasoconstriction particular in the vessel in
the skin and abdominal viscera
• Wide spread vasoconstriction is a protective
mechanism which increase peripheral resistance
increased heart rate and increased blood pressure.
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27. 2) FLUID
CONSERVATION BY THE
KIDNEY
Following factors may assist in restoring the blood
volume(caused by shock) and improve venous return to the
heart.
Release of aldosterone from hypoxic kidney by activation of
renin-angiotensin- aldosterone mechanism.
Release of ADH due to decreased effective circulating
blood volume.
Reduced GFR due to arteriolar constriction.
Shifting of tissue fluids into the plasma due to lowered
capillary hydro static pressure. 27

28. 3) STIMULATION OF
ADRENAL MEDULA
• In response to cardiac out put adrenal
medulla is stimulated to release excess of
catecholamine's ( epinephrine and non
epinephrine) which increase heart rate and
try to increase cardiac output.
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29. PROGRESSIVE
DECOMPENSATED
SHOCK
Patient suffers from some other stress or risk factors
( eg:- pre existing cardiovascular & lung disease)
The effect of progressive decompensated shock due to
tissue hypoperfusion are:-
1)PULMONARY HYPOPERFUSION
It increase vascular permeability resulting in tachypnea
and adult respiratory distress syndrome.
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30. 2) TISSUE ISCHAEMIA
•It cause switch from aerobic to anaerobic
glycolysis resulting in metabolic lactic acidosis
which reduces the tissue pH which makes
vasomotor response ineffective.
•It cause vasodilation and peripheral pooling of
blood.
•The patient develops confusion and worsening of
renal function.
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31. IRREVERSIBLE
DECOMPENSATED
SHOCK
• Shock is so severe that in spite of compensatory mechanisms
and despite therapy and control of etiologic agent no
recovery is taking place, it is called Irreversible
Decompensated Shock.
1)PROGRESSIVE VASODILATION
• Anoxia damages the capillary and venular wall. Arterioles
become unresponsive to vasoconstriction and begin to dilate
which results in peripheral pooling of blood which further
deteriorate the effective circulating blood volume.
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32. 2)INCREASED
VASCULAR
PERMEABILITY
• Anoxic damage to tissue release
inflammatory mediators which cause
increased vascular permeability.
• This results in escape of fluid from
circulation into the interstitial tissue,
thus deteriorating effective circulating32

33. 3)MYOCARDIAL
DEPRESSANT FACTOR
• Decreased BP and persistently reduce blood flow to
myocardium causes coronary insufficiency and
myocardial ischemia due to release of myocardial
depressant factor.
• It make depression of cardiac function, reduced
cardiac output and decreased blood flow.
4)WORSENING PULMONARY
HYPOPERFUSION
• It cause respiratory distress due to pulmonary
oedema, tachypnoea and adult respiratory distress
syndrome. 33

34. 5)ANOXIC DAMAGES TO
HEART, KIDNEY, BRAIN
• There is release of inflammatory
cytokines and other inflammatory
mediators and generation of free
radicals.
• There will be ischaemic cell death in the
tissue due to aerobic respiration for ATP
generation.
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35. 6)HYPERCOAGULABILIT
Y OF BLOOD
• Tissue damages in shock activates coagulation cascade
with release of clot promoting factor, thromboplastin
and release of platelet aggregator, which slows blood-
stream and vascular thrombosis.
• It cause hypercoagulability of blood, impair the blood
flow and cause tissue necrosis.
• Clinically, patient features coma, worsened heart
function and progressive renal failure due to acute
tubular necrosis.
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36. 36

37. MANAGEMENT
• Critical factors in the successful
management of a patient experiencing
shock relate to early recognition of shock
more precisely determination the correct
stage of shock and it can very well help in
the treatment of shock. Management may
include:-
• FLUID REPLACEMENT
• DRUG THERAPY
• NUTRITIONAL THERAPY 37

38. FLUID REPLACEMENT
 The cornerstone of therapy for shock other than cardiogenic
shock is volume expansion with administration of the
appropriate fluid. Both crystalloid (Eg:-Normal saline
solution)and colloid (Eg:-Albumin) have a role in fluid
resuscitation
 Crystalloid such as normal saline are used in the initial shock
resuscitation, eventhough approximately 2/3 of the
crystalline volume will diffuse out of the vascular space and
into the intestinal space.
 Colloids are effective volume expanders because the size of
their molecules keeps them in vascular space for a longer
time.
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39. DRUG THERAPY
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