Shock is defined as inadequate tissue perfusion and oxygenation. There are five main types of shock: hypovolemic, cardiogenic, obstructive, distributive, and endocrine. Shock causes a decrease in cardiac output, vasoconstriction, and activation of stress responses in an attempt to maintain perfusion to vital organs. If shock persists, cellular damage occurs due to hypoxia, acidosis, and organ dysfunction. Treatment focuses on restoring circulating volume and oxygen delivery through fluid resuscitation, vasopressors, and inotropes while addressing the underlying cause. Septic shock involves an inflammatory response to infection that can lead to multiple organ dysfunction syndrome if not promptly treated with antibiotics and circulatory

1. SHOCK
LT COL SM SHAHADAT HOSSAIN
MCPS,FCPS( Surgery),FCPS(Thoracic Surgery)
Adv Trg on Thoracoscopy,CNUH,South Korea

2. DEFINITION
Shock is a systemic state of low tissue
perfusion that is inadequate for normal
cellular respiration.

3. What happened ?

4. CLASSIFICATION OF SHOCK
1. Hypovolaemic shock
2. Cardiogenic shock
3. Obstructive shock
4. Distributive shock
5. Endocrine shock

5. CAUSE
1. Hypovolaemic shock
a. Haemorrhage.
b. Severe burns.
c. Peritonitis, intestinal obstruction.
d. Vomiting and diarrhoea.

6. CAUSE
2.Cardiogenic
a. Valvular heart disease.
b. Myocardial infarction.
c. Cardiac arrhythmias.
d. Cardiomyopathy.

7. CAUSE
3. Obstructive
a. Cardiac Tamponade
b. Pulmonary Embolism
c. Tension Pneumothorax
d. Air embolism

8. CAUSE
4.Distributive shock
a. Septic shock
b. Anaphylaxis
c. Spinal cord injury

9. NEUROGENIC ETIOLOGY
Neurogenic
a. Paraplegia.
b. Quadriplegia.
c. Trauma to spinal cord.
d. Spinal anesthesia.

10. ANAPHYLACTIC
a. Injections - Penicillins
b. Anaesthetics.
c. Stings.
d. Shelfish.

11. SEPTIC
a. Gram +
b. Gram-
c. Fungi / Virus
d. Protozoa

12. CAUSE
5.Endocrine
a. Hypo & Hyperthyroidism.
b. Adrenal insufficiency.

13. PATHOPHYSIOLOGY OF SHOCK
Any cause of shock
↓
Low cardiac output
↓
Vasoconstriction
↓
Dynamic circulation increases
↓
Tachypnoea
↓
Peripheral veins constrict

14. PATHOPHYSIOLOGY OF SHOCK
Decreased urine output
↓
Renin angiotensin mechanism activated
↓
Salt and water retention
↓
ADH is released
↓
If shock persists cardiac output falls further
↓
Hypotension and tachycardia

15. PATHOPHYSIOLOGY OF SHOCK
Hypoxia—metabolic acidosis
↓
Anaerobic metabolism
↓
Lactic acidosis
↓
Cell wall damage
↓
Sodium and calcium enter the cell and potassium
leaks out of the cell
↓
Causes hyperkalaemia, hyponatraemia and
hypocalcaemia

16. PATHOPHYSIOLOGY OF SHOCK
Lysosomes break down
↓
SICK CELL SYNDROME
Platelets are activated forming small clots
↓
Disseminated intravascular coagulation (DIC)
↓
Further bleeding.

17. SHOCK – EFFECTS ON ORGAN
o Heart – ↓ CO / hypotension / myocardial
depressants
o Lung - ↓gas exchange / tachypnoea /
pulmonary edema
o Endocrine – ADH → ↑ reabsorption of water

18. SHOCK – EFFECTS ON ORGAN
o CNS – perfusion ↓ – drowsy
o Blood - Coagulation abnormalities – DIC
o Renal - ↓ GFR - ↓ urine output
o GIT – mucosal ischaemia – bleeding &
hepatic - ↑ enzyme levels

19. STAGES OF SHOCK
Stage1 compensatory shock by
neuroendocrine response to maintain the
perfusion of the vital organs like brain, heart,
kidney, liver.
Stage2 decompensatory shock where there is
persistent shock with severe hypotension,
oliguria, tachycardia.
Stage3 irreversible shock with severe hypoxia
and MODS.

20. CLINICAL FEATURES
Types
a. Mild shock.
b. Moderate shock.
c. Severe shock.

21. MILD SHOCK
 Conscious level- mild anxiety.
 Pulse rate- increased.
 Respiratory rate- increased.
 Blood pressure- normal.
 Urine output -normal.
 Extremities pale and cool.
 Sweat on forehead, hand and feet.

22. MODERATE SHOCK
 Conscious level- drowsy.
 Pulse rate- increased.
 Respiratory rate- increased.
 Blood pressure- mild hypotension.
 Urine output- reduced.

23. SEVERE SHOCK
 Conscious level- comatose.
 Pulse rate- increased.
 Respiratory rate- laboured.
 Blood pressure- severe hypotension.
 Urine output -anuric.

24. MONITORING
Minimum
a.ECG
b.Pulse oximetry
c.Blood pressure
d.Urine output

25. MONITORING
Additional modalities
a. Central venous pressure
b. Invasive blood pressure
c. Cardiac output
d. Base deficit and serum lactate

26. MONITORS FOR ORGAN/SYSTEMIC PERFUSION.
Systemic perfusion
I. Base deficit
II. Lactate
III. Mixed venous oxygen saturation
Kidney Urine output

27. MONITORS FOR ORGAN/SYSTEMIC PERFUSION
Muscle
a. Near-infrared spectroscopy
b. Tissue oxygen electrode
Gut
a. Sublingual capnometry
b. Gut mucosal pH
c. Laser Doppler flowmetry

28. MONITORS FOR ORGAN/SYSTEMIC PERFUSION
Brain
a. Conscious level
b. Tissue oxygen electrode
c. Near-infrared spectroscopy

29. TREATMENT
GOAL:
 Increase O2 delivery
 Decrease demand

30. PRINCIPLES OF RESUSCITATION
A: Airway
Patent upper airway
B: Breathing
Adequate ventilation and oxygenation
C: Circulation
Placement of adequate IV access

31. FLUID THERAPY IN SHOCK
Crystalloid Solutions
I. Normal saline
II. Ringers Lactate solution
III. Hartmann’s solution
IV. Colloid Solutions
V. Blood transfusion

32. DYNAMIC FLUID RESPONSE
Infusing 250-500ml of Fluid rapidly in 5 - 10
mts.
1. Responders – Improvement
2. Transient responders – revert back
3. Non – responders

33. VASOPRESSORS / INOTROPIC DRUGS
Vasopressors – Phenylephrine / NA
Distributive shock states
Septic shock / Neurogenic
Inotropics - Dobutamine
Cardiogenic shock / Severe septic shock
To increase the cardiac output

34. OTHER TREATMENTS
1. Correction of Acid – base balance
2. Steriods - Hydrocortisone
3. Antibiotics
4. Catheterisation
5. Nasal O2 / Ventilatory support
6. CVP Line
7. Control of Pain
8. ICU – Critical care management

35. SEPTIC SHOCK
• Septic shock may be due to gram-positive
organisms, gram negative organisms, fungi,
viruses or protozoal origin.
• Gram-negative septicaemia/gram-negative
septic shock is called as endotoxic shock.

36. PATHOPHYSIOLOGY OF SEPTIC SHOCK
Toxins/endotoxins from organisms like E. Coli, Klebsiella,
Pseudomonas, and Proteus
↓
Inflammation, cellular activation of macrophages,
neutrophils,
monocytes
↓
Release of cytokines, free radicals
↓
Chemotaxis of cells, endothelial injury, altered
coagulation
cascade—SIRS
↓

37. PATHOPHYSIOLOGY OF SEPTIC SHOCK
Reversible hyperdynamic warm stage of septic
shock with
fever, tachycardia, tachypnoea
↓
Severe circulatory failure with MODS (failure of
lungs, kidneys, liver, heart) with DIC
↓
Hypodynamic, irreversible cold stage of septic
shock.

38. TREATMENT
• Appropriate antibiotics—third generation
cephalosporins/ aminoglycosides.
• Correction of fluid and electrolyte by crystalloids,
blood transfusion.