This document provides an overview of the principles of shock management. It defines shock and describes its causes, including hypovolemic, cardiogenic, obstructive, distributive, and endocrine shock. The pathophysiology of shock is explained at the cellular, microvascular, and systemic levels. The stages of shock - non-progressive, progressive decompensated, and decompensated - are outlined. Signs and symptoms of shock are provided. Finally, the document discusses the general management of shock, which aims to improve oxygen delivery and utilization to prevent organ injury through restoration of perfusion and supportive care.

1. PRINCIPLES OF
MANAGEMENT OF SHOCK
Dr.Bipul Borthakur
Prof and head
Orthopaedics,smc

2. CONTENTS
• Definition
• Classification of shock
• Pathophysiology of shock
• Stages of shock
• Management of shock

3. DEFINITION
 Shock is a systemic state of low tissue perfusion that is
inadequate for normal cellular respiration.
 With insufficient delivery of oxygen and glucose, cells switch
from aerobic to anaerobic metabolism.
 If perfusion is not restored in a timely fashion, cell death
ensues.
 The end result is hypotension and cellular hypoxia and, if
uncompensated, may lead to impaired cellular metabolism and
death.

4.  Shock is the most common and therefore the
most important cause of death of surgical
patients.
 Death may occur rapidly due to profound state
of shock, or be delayed due to consequences of
organ ischaemia and reperfusion injury.

5. CLASSIFICATION OF
SHOCK
Classification of shock on the basis of
initiating mechanism:
 Hypovolaemic shock
 Cardiogenic shock
 Obstructive shock
 Distributive shock
 Endocrine shock

7. 1 HYPOVOLAEMIC SHOCK
 Hypovolaemic shock is due to a reduced circulating volume.
 Hypovolaemia may be due to haemorrhagic or non-haemorrhagic
causes.
 Haemorrhagic causes :
Trauma
Surgery
 Non-haemorrhagic causes:
poor fluid intake (dehydration)
excessive fluid loss due to vomiting, diarrhoea, urinary loss
‘third-spacing’ where fluid is lost into the gastrointestinal tract
and interstitial spaces

8. PATHOPHYSIOLOGY OF HYPOVOLAEMIC
SHOCK

9. CLASSIFICATION OF HYPOVOLAEMIC SHOCK

10. CARDIOGENIC SHOCK
 Cardiogenic shock is due to primary failure of
the heart to pump blood to the tissues.
Causes of Cardiogenic shock include:
- Myocardial infarction
- Cardiac arrhythmia
- Valvular heart disease
- Myocardial injury
- Cardiomyopathy

11. OBSTRUCTIVE SHOCK:
 In obstructive shock there is a reduction in preload due
to mechanical obstruction of cardiac filling.
 Common causes of obstructive shock include;
- Cardiac tamponade
- Tension pneumothorax
- Massive pulmonary embolus or Air embolus
 In each case, there is reduced filling of the left and/or
right sides of the heart leading to reduced preload and a
fall in cardiac output.

12. DISTRIBUTIVE SHOCK
 Distributive shock describes the pattern of
cardiovascular responses characterising a variety of
conditions including;
A) Septic shock
B) Anaphylactic shock
C) Spinal cord injury (Neurogenic shock).

13. A) SEPTIC SHOCK
 It is related to the release of bacterial products
(endotoxin) and the activation of cellular and humoral
components of the immune system.
 There is maldistribution of blood flow at a
microvascular level
 Arteriovenous shunting
 Dysfunction of cellular utilization of oxygen.
 In the later phases of septic shock there is
hypovolaemia from fluid loss into interstitial spaces and
there may be concomitant myocardial depression.

14. SEPTIC SHOCK

15. PATHOPHYSIOLOGY OF
SEPTIC SHOCK

16. B) ANAPHYLACTIC SHOCK
• It is a type of severe hypersensitivity or allergic reaction.
• Causes include allergy to insect stings, medicines or foods (Nuts,
Berries, Sea foods) etc.
• It is caused by a severe reaction to an allergen, leading to the
release of histamine that causes widespread vasodilation and
hypotension.

17. C) NEUROGENIC SHOCK
 It is caused by spinal cord injury usually as a
result of a traumatic injury or accident.
 There is failure of sympathetic outflow and
adequate vascular tone.
 Damage to CNS impairs cardiac function by
reducing heart rate and loosening the blood
vessel tone resulting in severe hypotension.

18. PATHOPHYSIOLOGY OF
SHOCK
Pathophysiology of shock :
A) Cellular level
B) Microvascular level
C) Systemic level

19. A) CELLULAR LEVEL
 As perfusion to the tissues is reduced, cells are deprived
of oxygen and must switch from aerobic to anaerobic
metabolism.
 The product OF anaerobic metabolism lactic acid.
 the accumulation of lactic acid in the blood produces
systemic metabolic acidosis.
 There is failure of the sodium/potassium pumps.
 Intracellular lysosomes release autodigestive enzymes
and cell lysis ensues.
 Intracellular contents, including potassium, are released
into the bloodstream.

20. B) MICROVASCULAR LEVEL
 Activation of the immune and coagulation
systems.
 Generation of oxygen free radicals and
cytokine release.
 These mechanisms lead to injury of the
capillary endothelial cells. These, in turn,
further activate the immune and coagulation
system.

21. C) SYSTEMIC LEVEL
1) CARDIOVASCULAR:
 As preload and afterload decrease, there is a
compensatory baroreceptor response
resulting in increased sympathetic activity and
release of catecholamines into the circulation.
 This results in tachycardia and systemic
vasoconstriction

22. 2) RESPIRATORY SYSTEM:
 Metabolic acidosis and sympathetic response result in an increased
respiratory rate
 Increased minute ventilation lead to increase the excretion of carbon
dioxide.
 It produce a compensatory respiratory alkalosis.

23. 3) RENAL
 Increased afferent arteriolar resistance accounts for
diminished glomerular filtration rate (GFR)
 Increased aldosterone and vasopressin, is responsible for
reduced urine formation.
 Reduced filtration at the glomerulus and a decreased urine
output.
 The stimulated renin–angiotensin–aldosterone system
resulting in further vasoconstriction and increased sodium and
water reabsorption by the kidney.

24. 4)ENDOCRINE
 Vasopressin (antidiuretic hormone) is released from
the hypothalamus in response to decreased preload
and results in vasoconstriction.
 Cortisol is released from the adrenal cortex,
contributing to the sodium and water resorption and
sensitising cells to catecholamines.

25. 5) METABOLIC
 There is disruption of the normal cycles of
carbohydrate, lipid, and protein metabolism.
 Aalanine in conjunction with lactate enhances the
hepatic production of glucose.
 With reduced availability of oxygen, the breakdown of
glucose to pyruvate, and ultimately lactate, represents
an inefficient cycling with minimal net energy
production.

26. SEQUENTIAL EVENTS IN THE
MECHANISM OF SHOCK:
 Decreased effective circulating blood volume.
 Decreased venous return to the heart.
 Decreased cardiac output.
 Decreased blood flow.
 Decreased supply of oxygen.
 Anoxia.
 Shock.

27. CLINICAL FEATURES:

28. CAPILLARY REFILL:
 Most patients in hypovolemic shock will have
cool, pale peripheries, with prolonged capillary
refill times.
 This is not a specific marker of whether a
patient is in shock.
 In septic shock, the periphery will be warm and
capillary refill will be brisk, despite profound
shock.

29.  TACHYCARDIA:
 Tachycardia may not always accompany shock.
 Patients who are on beta-blockers or who have
implanted pacemakers are unable to mount a
tachycardia.
 In young patients, with penetrating trauma
where there is hemorrhage but little tissue
damage, there may be a paradoxical
bradycardia rather than tachycardia.

30.  BLOOD PRESSURE:
 Hypotension is one of the last signs of shock
 Children and young adults are able to maintain
BP until the final stages of shock by increasing
stroke volume and peripheral vasoconstriction.
 These patients can be in profound shock with a
normal blood pressure.

31. STAGES OF SHOCK:
Divided into 3 stages:
 1. Non-progressive (initial, compensated,
reversible) shock
 2. Progressive decompensated shock
 3. Decompensated (Irreversible) shock

32. 1NON-PROGRESSIVE STAGE OF SHOCK:
 In the early stage of shock, an attempt is made to maintain adequate
cerebral and coronary blood supply by redistribution of blood.
 If the cause are adequately treated, the compensatory mechanism may be
able to bring about recovery & re-establish the normal circulation; this is
called compensated or reversible shock.
 These Compensatory mechanisms are:
i) Wide spread vasoconstriction
ii) Fluid conservation by the kidney
iii) Vascular autoregulation

33. PROGRESSIVE DECOMPENSATED
SHOCK:
 This is a stage when the patient suffers from Risk factors (e.g.
Pre-existing cardiovascular and lung disease) besides
persistence of the shock so that there is a progressive
deterioration.
 The effects of progressive decompensated shock are:
a) Pulmonary hypoperfusion with resultant tachypnoea and
ARDS.
b) Anaerobic glycolysis resulting in Metabolic acidosis.

34. DECOMPENSATED (IRREVERSIBLE)
SHOCK:
 When the shock is so severe that inspite of compensatory mechanisms, no
recovery takes place, it is called decompensated or irreversible shock.
 Effects due to widespread cell injury include:
a) Deterioration in cardiac output.
b) Severe metabolic acidosis
c) Pulmonary oedema, tachypnoea and ARDS
d) Ischemic cell death of brain, heart and kidneys due to reduced blood
supply to these organs.
 Clinically the patient has features of coma, worsened heart function and
progressive renal failure.

35. MANAGEMENT OF SHOCK:
General principles of shock management:
1. The overall goal of shock management is to improve
oxygen delivery/utilisation in order to prevent cellular
and organ injury.
2. Effective therapy requires treatment of underlying
etiology.
3. Restoration of adequate perfusion, monitoring and
comprehensive supportive care.
4. Interventions to restore perfusion centre, increasing
cardiac output and optimising oxygen content.
5. Oxygen demand should also be reduced.

36. PHYSICAL EXAMINATION:
 Increased HR
 Tachypnea
 Mean arterial pressure less than 60 mmHg (not
always present)
 Confusion and encephalopathy
 Oliguria
 Decreased capillary refill and cold skin.

37. PHYSICAL EXAMINATION:
 Site of an untreated infection
 GI Hemorrhage on rectal examination.
 Pulsus paradox and elevated JVP seen in
cardiac tamponade
 Paucity of breath sounds, deviation of trachea
away from the affected side, subcutaneous
emphysema seen in tension pneumothorax

38. DIAGNOSTIC TESTING:
 The laboratory evaluation is directed toward the dual aim of assessing the
extent of end organ dysfunction and of gaining insight into the possible
etiology of shock.

39. DIAGNOSTIC TESTING:
 BLOOD TESTS:
 Blood urea nitrogen (BUN), creatinine, transaminase
evaluation show extent of end organ damage
 Urine electrolytes, FE Na, FE urea indicate hypovolemia
status
 Increased WBCs show infective process
 Increased cardiac enzymes show primary cardiac problem
 Blood cultures, urine cultures and sputum cultures should be
obtained.
 Lactate measurement

40. MONITORING:

41. MONITORING:
 Echocardiography: an echocardiogram should be
obtained in patients with suspected cardiogenic shock.
 Advanced hemodynamic monitoring: recently new
central venous catheter systems linked with computer
based algorithms provides continuous monitoring of
hemodynamic parameters.
 Cardiac catheterization and coronary angiography
indicated in all patients with cardiogenic shock.

42. SYSTEMIC AND ORGAN
PERFUSION:
 The best measure of organ perfusion and the best monitor
of adequacy of shock therapy remains the urine output.

43. RESUSCITATION:
 Resuscitation should not be delayed in order to
definitively diagnose the source of the shocked state.
 If there is initial doubt of cause of shock, it is safer to
assume the cause is hypovolemia. And begin fluid
resuscitation.
 Intravenous fluids should be given through short, wide
bore catheters.
 The oxygen carrying capacity of crystalloid and colloids
is zero
 If blood is being lost, the ideal replacement is blood,
although crystalloid therapy may be required while
awaiting blood products.

44. VASOPRESSOR AND INOTROPIC
SUPPORT:
 Vasopressor agents (phenylephrine,
noradrenaline) are indicated in distributive
shock.
 When vasodilation is resistant to
catecholamines, vasopressin may be used as
an alternative vasopressor.
 In cardiogenic shock, inotropic therapy
required to increase cardiac output, dobutamine
is the agent of choice.

45. END POINTS OF
RESUSCITATION:
 Traditionally, patients have been resuscitated until they
have a normal pulse, BP, and urine output.
 Occult hypoperfusion: state of normal vital signs and
continued underperfusion.
 With current monitoring techniques, occult
hypoperfusion is manifested only by a persistent lactic
acidosis and low mixed venous oxygen saturation.
 Resuscitation algorithms directed at correcting global
perfusion end points ( base deficits, lactate, mixed
venous oxygen saturation ) rather than traditional end
points have been shown to improve mortality and
morbidity in high risk surgical patients.

46. MANAGEMENT OF
HYPOVOLAEMIC SHOCK:
• Maximise oxygen delivery-completed by ensuring
adequacy of ventilation
• Control further blood loss.
• Fluid resuscitation.

47. MANAGEMENT OF
HYPOVOLAEMIC SHOCK:

48. MANAGEMENT OF SEPTIC SHOCK:
 The most important aspects of therapy for patients with septic shock/sepsis
include:
1. Adequate oxygen delivery.
2. Crystalloid fluid administration-normal saline (0.9% NaCl), Ringer
lactate.
3. Broad spectrum antibiotics- cefotaxim, clindamycin, ceftriaxone,
ciprofloxacin, metronidazole, cefepime, levofloxacin, vancomycin.
4. Alpha and beta adrenergic agonists-nor epinephrine, dopamine,
dobutamine, epinephrine, vasopressin, phenylephrine.
5. Corticosteroids like hydrocortisone, dexamethasone.

49. MANAGEMENT OF SEPTIC SHOCK:

50. MANAGEMENT OF SEPTIC
SHOCK:
 General Supportive Care :
 Patients requiring a vasopressor should have an arterial catheter placed
as soon as is practical.
 Hydrocortisone is not suggested in septic shock.
 Continuous or intermittent sedation should be minimized in
mechanically ventilated sepsis patients.
 A protocol-based approach to blood glucose management should be
used in ICU patients with sepsis, with insulin dosing initiated when two
Consecutive blood glucose levels are >180 mg/dL.
 Continuous or intermittent renal replacement therapy should be used in
patients with sepsis and acute kidney injury.
 Stress ulcer prophylaxis should be given to patients with risk factors
for gastrointestinal bleeding.

51. MANAGEMENT OF NEUROGENIC
SHOCK:
 Immobilization: if the patient has a suspected case of spinal cord
injury.
 High dose steroid to reduce inflammation
 IV fluids: administration of IV fluids is done to stabilize the patient’s
blood pressure.
 Inotropic agents such as dopamine may be infused for fluid
resuscitation.
 Atropine is given intravenously to manage severe bradycardia.

52. MANAGEMENT OF CARDIOGENIC
SHOCK:
 Management of Cardiogenic shock includes supportive measures which
includes:
 Oxygen therapy
 Judicious use of fluids with careful monitoring of central venous pressure
or pulmonary wedge pressure.
 Other monitoring include continuous ECG, 12 lead ECG, urine output,
urea and electrolytes & blood gases.
 Patient should be preferably managed in coronary care unit.
 Drugs like morphine 5-10mg IV helps to relieve pain and anxiety
associated with myocardial infarction.
 Inotropic support, vasodilators and mechanical support may be needed.

53. MANAGEMENT OF ANAPHYLACTIC
SHOCK:
 During an anaphylactic attack, cardiopulmonary
resuscitation (CPR) may be needed if breathing or heart
beat is stopped.
 Medications in Anaphylactic shock includes:
1. Epinephrine (adrenaline) to reduce body’s allergic
response.
2. Oxygen, which helps in breathing.
3. Intravenous anti histaminics and cortisone to reduce
inflammation of air passages and improve breathing.
4. Beta agonist (e.g. Albuterol) to relieve breathing
symptoms.

54. THANK YOU