Shock is an acute clinical syndrome involving hypoperfusion and dysfunction of vital organs due to cardiovascular collapse, characterized by low blood pressure and inadequate tissue perfusion. It progresses through three stages: compensated, progressive decompensated, and irreversible decompensated shock, each marked by increasing severity and risk of complications such as acute respiratory distress syndrome and multiple organ dysfunction. Different types of shock include hypovolemic, cardiogenic, obstructive, and distributive, each requiring specific treatments to restore blood volume, improve cardiac function, or address underlying causes.

1. PATHOGENESIS OF SHOCK

2. CONTENTS
• Definition
• Pathogenesis of shock
• Stages of shock
• Clinical features and complications
• Classification
• References

3. DEFINITION
• Shock is defined as an acute clinical syndrome characterised by
hypoperfusion and severe dysfunction of vital organs .
• There is a failure of circulatory system to supply blood in sufficient
quantities or under sufficient pressure necessary for the optimal
function of organs vital for survival

4. • Shock is a life-threatening clinical syndrome of cardiovascular collapse
characterised by:
• Acute reduction of effective circulating blood volume (hypotension);
• inadequate perfusion of cells and tissues (hypoperfusion)
If uncompensated, these mechanisms may lead
to impaired cellular metabolism and death

5. PATHOGENESIS
• In general, shock involve following 3 derangements:
 Reduced effective circulating blood volume.
Impaired oxygenation
Release of Inflammatory mediators

6. REDUCED EFFECTIVE CIRCULATING BLOOD
VOLUME
• It may result by either of the following mechanisms:
 by actual loss of blood volume as occurs in hypovolaemic shock;
 by decreased cardiac output without actual loss of blood
(normovolaemia) as occurs in cardiogenic shock and septic shock

7. IMPAIRED TISSUE OXYGENATION
• Following reduction in the effective circulating blood volume from either of the above two
mechanisms and from any of the etiologic agents.

Decreased venous return

Decreased cardiac output

Reduced oxygenation

Celluar injury

8. RELEASE OF INFLAMMATORY MEDIATORS.

9. STAGES OF SHOCK
• Deterioration of the circulation in shock is a progressive and continuous
phenomenon and compensatory mechanisms become progressively less
effective, historically shock has been divided arbitrarily into 3 stages :
1. Compensated (non-progressive, initial, reversible) shock.
2. Progressive decompensated shock.
3. Irreversible decompensated shock

10. COMPENSATED SHOCK
• In the early stage 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.
• This is achieved by activation of various neurohormonal mechanisms causing
widespread vasoconstriction
fluid conservation by the kidney

11. PROGRESSIVE DECOMPENSATED SHOCK
• This is a stage when the patient suffers from some other stress or risk factors
(e.g. pre-existing cardiovascular and lung disease) besides persistence of the
shock so that there is progressive deterioration. The effects of progressive
decompensated shock due to tissue hypoperfusion are as under
Pulmonary hypoperfusion
Tissue ischaemia

12. IRREVERSIBLE DECOMPENSATED SHOCK
When the shock is so severe that in spite of compensatory mechanisms and
despite therapy and control of etiologic agent which caused the shock, no
recovery takes place, it is called decompensated or irreversible shock. Its
effects due to widespread cell injury include the follow
Progressive vasodilation
Increased vascular permeability

13. Myocardial depressant factor
Worsening pulmonary hypoperfusion
Anoxic damage to heart, kidney, brain
Hypercoagulability of blood

14. CLINICAL FEATURES AND COMPLICATIONS
• The classical features of decompensated shock are characterised by depression of
4 vital processes:
Very low blood pressure
Subnormal temperature
Feeble and irregular pulse ,Shallow and sighing respiration
In addition, the patients in shock have pale face, sunken eyes, weakness, cold and
clammy skin.

15. • Life-threatening complications in shock are due to hypoxic cell injury resulting in
immuno-inflammatory responses and activation of various cascades which
includes
1. Acute respiratory distress syndrome (ARDS)
2. Disseminated intravascular coagulation (DIC)
3. Acute renal failure (ARF)
4. Multiple organ dysfunction syndrome (MODS)
With progression of the condition, the patient may develop stupor,
coma and death

16. CLASSIFICATION
• Hypovolaemic shock
• Cardiogenic shock
• Obstructive shock
• Distributive shock
 Neurogenic shock
Septic shock
 Anaphylactic shock

17. Hypovolaemic shock
• This form of shock results from inadequate circulatory blood volume
by various etiologic factors
• Hemorrhagic causes – trauma,surgery
• Non hemorrhagic causes –dehyadration,vomiting,diuretics

18. • The severity of clinical features depends upon degree of blood volume
lost, haemorrhagic shock is divided into 4 types:
 < 1000 ml: Compensated
 1000-1500 ml: Mild
 1500-2000 ml: Moderate
 >2000 ml: Severe

19. TREATMENT
• Replace the lost blood volume.
• The primary goal is to restore tissue perfusion and oxygenation to
normal as early as possible.
• Crystalloids: If crystalloids are used to replace blood loss, 2–3 times
the volume lost needs to be given. Ringer lactate is the crystalloid of
choice..

20. • Large volumes of saline infusion can cause hyperchloraemic metabolic
acidosis. 5% dextrose is not used to expand the intravascular volume
as it is hypotonic once the dextrose is metabolised.
• Colloids: When colloids are used to replace lost blood volume, a
volume equal to the lost volume may be given. However, they are not
preferred

21. CARDIOGENIC SHOCK
• Cardiogenic shock results from a severe left ventricular dysfunction
from various causes.
• The resultant decreased cardiac output has its effects in the form of
decreased tissue perfusion and movement of fluid from pulmonary
vascular bed into pulmonary interstitial space initially (interstitial
pulmonary oedema) and later into alveolar spaces

22. TREATMENT
• The primary goal is to improve cardiac muscle function.
• Oxygenation can be improved by administering oxygen, either by face mask or by
endotracheal intubation and ventilation as necessary.
• Inotropes improve cardiac muscle contractility
• Vasodilators such as nitroglycerine may dilate the coronary arteries and
peripheral vessels to improve tissue perfusion. Lowering systemic vascular
resistance reduces impedance to forward cardiac output (afterload)

23. • Intra-aortic balloon pump or ventricular assist devices may be used to
augment cardiac output.
• If hypotension continues to be unresponsive, revascularisation
(surgical or interventional) or valve replacement may be considered
on an emergency basis

24. OBSTRUCTIVE SHOCK
• It can be due to cardiac tamponade or due to tension pneumothorax.
Cardiac Tamponade Features
• In obstructive shock, there is impedance to either inflow or outflow
of blood into or out of the heart.
• • In cardiac tamponade, the pericardium is filled with blood and
hampers venous filling as well as outflow.
• The filling pressures of the left-sided and right-sided chambers
equalise

25. • The central venous pressure is high and the blood pressure is low.
• The patients also have pulsus paradoxus where there is at least 10% decrease in
systolic blood pressure with inspiration.
Treatment
• To maintain preload with fluids or blood as indicated.
• Relief of obstruction, drain the pericardial cavity as early as possible

26. TENSION PNEUMOTHORAX
Causes
• Injury to the lung due to trauma
• Ventilator-induced barotrauma
• Rupture of emphysematous bulla in a patient with chronic obstructive
pulmonary disease.

27. TREATMENT
• A wide (large) bore needle/cannula (needle thoracostomy) must be
inserted into the pleural cavity to drain the air.
• Traditionally, it was advised that the needle should be inserted in the
midclavicular line in the 2nd intercostal space on the affected side.
The recommendation remains the same for children

28. • In adults diagnosed to have a tension pneumothorax, the current
advanced trauma life support (ATLS) guidelines advise that the needle
is inserted in the 5th intercostal space in the midaxillary line. This is
followed by tube thoracostomy.

29. SEPTIC SHOCK
• Septic shock results most often from Gram-negative bacteria entering
the body from genitourinary tract, alimentary tract, respiratory tract
or skin, and less often from Gram-positive bacteria. In septic shock,
there is immune system activation and severe systemic inflammatory
response to infection as follows

31. TREATMENT
• Removal of the septic focus is an essential step
• Early empirical antibiotic therapy to treat the precipitating infection.
This must be given in the first hour of arrival
• Supportive care: Oxygenation and, if necessary, endotracheal
intubation and mechanical ventilation should be administered

32. • Intravenous fluids: Restoration of intravascular filling pressures must be
done using crystalloids, colloids and blood as necessary. Crystalloids,
such as isotonic saline or Ringer’s lactate, may be used
• Vasoactive agents, such as norepinephrine to produce vasoconstriction
and raise the systemic vascular resistance to normal, may be used.
Dopamine, dobutamine or adrenaline may need to be added.

33. • Vasopressin infusion may be useful in patients with refractory shock
• Measure and monitor serum lactate. Aim to eliminate lactic acidosis
with fluid resuscitation and better perfusion

34. NEUROGENIC SHOCK
a) High cervical spinal cord injury
b) Accidental high spinal anaesthesia
c) Severe head injury

36. • Treatment: Intravenous fluids, inotropes and vagolytics as necessary

37. ANAPHYLACTIC SHOCK
• Occurs on exposure to an allergen the patient is sensitive to. It may be pollen,
foodstuffs, preservatives in the food or a medication
• The reaction may be in the form of
• mild rashes with or without bronchospasm
• It may be a full blown anaphylactic shock wherein the patient presents with
rashes, generalised oedema including laryngeal oedema, bronchospasm and
hypotension and if not treated in time, cardiac arrest

38. TRERATMENT
• Oxygen and, if necessary, endotracheal intubation and ventilation.
• Adrenaline, 0.5–1 mg IM or 50–100 μg intravenous boluses as
necessary to maintain blood pressure.
• Intravenous fluids—isotonic saline or ringer lactate
• Chlorpheniramine maleate
• hydrocortisone 100 mg intravenously

39. REFERENCES
• Davidsons principles and practise of medicine(22nd
edition)
• Manipal manual of surgery(5th
edition)
• Robbins and cotran pathologic basis of diseases(10th
edition)
• Harsh mohan textbooh of pathology(6th
edition)
• Hinshaw LB, Peterson M, Huse WM, Stafford CE, Joergenson EJ. Regional
blood flow in haemorrhagic shock. Am J Surg 1961;102:224-234.