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SHOCK
Dr. Salman Ansari
Kanachur Institute of Medical Sciences
Contents
● Definition
● Types of shock with examples
● Hypovolemic shock
● Cardiogenic shock
● Septic shock
● Stages of shock: non-progressive, progressive and
irreversible
Shock
Definition: pathological process characterised by
intense failure of the circulatory system to maintain
an appropriate blood supply to the microcirculation
● This results in life-threatening hypoperfusion to
vital organs
Types of shock
1. Cardiogenic
2. Hypovolemic
3. Septic
4. anaphylactic shock
5. neurogenic shock
Type Causes
Cardiogenic ● MI
● Ventricular rupture
● Arrhythmia
● Cardiac tamponade
● Pulmonary embolism
Hypovolemic Fluid loss(bleeding, vomiting, diarrhoea, burns)
Septic Severe bacterial or fungal infections
neurogenic Spinal cord injury, anesthetic accident
anaphylactic Drug reaction, insect sting, food allergy
Cardiogenic shock
Definition: Shock due to low cardiac output as a result of:
- myocardial damage or
- external compression of the heart or
- obstruction to outflow of blood from ventricles
Causes:
● MI
● Ventricular rupture
● Arrhythmia
● Cardiac tamponade
● Pulmonary embolism
Pathogenesis of cardiogenic shock
Various causes of cardiogenic shock(e.g: MI)
↓
LV dysfunction
↓
Decreased cardiac output
↓
Decreased perfusion of tissues
Hypovolemic shock
Hypovolemia=abnormal decrease in volume of circulating blood
Definition: Shock due to low cardiac output as a result of:
- Loss of blood: massive hemorrhage
- Loss of plasma: severe burns
- Loss of fluid: vomiting, diarrhoea, severe gastroenteritis
Causes: Fluid loss due to:
● Hemorrhage
● Vomiting
● Diarrhoea
● burns
Pathogenesis of hypovolemic shock
Inadequate blood or plasma volume and fluid loss
↓
hypovolemia
↓
low cardiac output
↓
hypotension
↓
inadequate perfusion of tissue.
Septic shock
Definition: Shock due to severe sepsis with
hypotension
Causes:
● Infection by Gram-positive bacteria most
commonly. E.g: Staphylococcus aureus,
Streptococcus pneumoniae
● Gram-negative bacteria
Main factors contributing to septic shock
1. Inflammatory response:
Activation of neutrophils, macrophages and cytokine release
1. Endothelial cell activation and injury:
Increased vascular permeability → widespread edema
1. Pro-coagulant state:
endotoxin activates factor XII → activation of coagulation system
→ thrombosis of small vessels - complication called
4. Metabolic abnormalities:
- hyperglycemia, insulin resistance
- Decreased glucocorticoid production - due to adrenal
gland insufficiency - life-threatening complication called
Waterhouse-Friderichsen syndrome(WFS)
5. Organ dysfunction: decreased contractility of the heart
and cardiac output → failure of multiple organs like liver,
lung, kidneys and heart → death
6. Immune suppression: hyperinflammatory state leads to
suppression of immune system
Pathogenesis of septic shock(short version)
Major factors contributing to septic shock are:
1. Inflammatory response: Activation of neutrophils,
macrophages and cytokine release
2. Endothelial cell activation and injury: Increased
vascular permeability → widespread edema
3. Pro-coagulant state: endotoxin causes activation of
coagulation system → Disseminated intravascular
coagulation(DIC)
4. Metabolic abnormalities: hyperglycemia, insulin
resistance, adrenal gland insufficiency
5. Organ dysfunction: decreased cardiac output → failure
of multiple organs like liver, lung, kidneys and heart →
death
6. Immune suppression
Activation of host’s immune system:
neutrophils and cytokines released
Endothelial cell injury
Vasodilation and pooling of blood in
peripheries
↑ permeability: widespread edema
Decreased tissue perfusion
Multi-organ failure
Endotoxin
Activation of coagulation
Micro-thrombi - Disseminated
intravascular coagulation(DIC)
Tissue ischemia
Microbial products
Stages of shock
3 phases
1. Non-progressive (compensated/reversible) phase
2. Progressive phase
3. Irreversible phase
1. Nonprogressive/compensated/reversible
phase
- Various compensatory mechanisms are activated
- Blood is redistributed to maintain perfusion to vital
organs
2. Progressive phase
- If the underlying cause of shock is not corrected,
shocks passes into the progressive phase
- Widespread tissue hypoperfusion, hypoxia and
blood pools in the microcirculation
- Cardiac output worsens and there will be
widespread hypoxic damage to vital organs and
they begin to fail
3. Irreversible phase
- If there is no intervention, shock enters into irreversible
stage
- Widespread cell injury further worsens shock
- Acute renal failure
- Death
Prognosis
- Hypovolemic shock: can survive with appropriate
management
- Septic shock, cardiogenic shock with massive MI:
poorer prognosis
Clinical features of shock
● Hypotension - low systolic blood pressure <90 mmHg
● Tachycardia - heart rate >100/minute
● Cold, clammy skin
● Cyanosis
● Tachypnoea - rapid respiratory rate
● Low urine output
● Confusion
● In septic shock: warm extremities(called ‘’warm shock’’)
Treatment of shock
Goal of management:
1. Treat reversible causes
2. Protect ischemic myocardium
3. Improve blood supply to tissues
ABC protocol - Airway, Breathing and Circulation
- Airway:
- Check if airway is patent
- If airway is blocked, patient needs to be intubated
- Glasgow Coma Scale(GCS) of <8 - intubation required
- Breathing:
- If airway is patent, patient is to be started on oxygen
- 100% O2 via NRBM face mask
- Circulation:
- Check pulses, extremities
- Vitals: pulse, blood pressure - connect to monitor
- Insert 2 large bore cannulas
- Start on IV fluids - but be careful in case of cardiogenic
shock
- Disability:
- Assessment for any neurological deficit
- Ask to move each limb, if responsive
- Blood sugar: check glucose level
- Glasgow coma scale(GCS):
- it is used to assess level of consciousness
- 3 components: E.V.M
1) Eye response
2) Verbal response
3) Motor response
- Total score of 15
GCS: score interpretation
Normal: 15
Coma: 8 or less
Unresponsive/death: 3
E - Exposure
- Remove clothing
- Examine for trauma, skin rashes or any abnormalities
- Use of vasopressor agents to raise blood pressure
- E.g dobutamine, dopamine, vasopressin
- Use of iv fluids such as crystalloids(normal saline), colloid,
blood
- Stop any bleeding
- Treat the cause of shock
- Cardiogenic shock: tamponade - pericardiocentesis
- Septic shock: antibiotics, vasopressors for low BP
- Anaphylactic shock: adrenaline
Anaphylactic shock
Definition: life-threatening form of type 1 hypersensitivity
reaction mediated by IgE
Causes:
Allergy to
- foods(peanuts, fish, egg)
- Drugs: antibiotics(penicillin), hormones(insulin), latex
- Vaccines
- Insect bite: honey bee
Mechanism:
Sensitisation following an initial exposure to the allergen.
Repeat exposure leads to IgE-induced degranulation of
mast cells and basophils, which leads to release of
mediators like histamine, which cause vasodilation and
smooth muscle contraction
Clinical features:
Sudden onset of dyspnea, wheezing, hypotension, skin
rashes, angioedema
Treatment:
Inj. Adrenaline(epinephrine) intramuscularly - 1:1000
concentration
Dose: Adults and children above 12 years - 0.5 ml
6-12 years old - 0.3 ml
>6 years old - 0.15 ml
Site: deltoid muscle or anterolateral aspect of middle third of
thigh
Questions
LE:
SE: Anaphylactic shock
Classify shock and write brief note on ABC protocol
Types of shock. Brief note on hypovolemic shock.
SA: ABC protocol
Adrenaline

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Shock: types of shock, treatment - General Medicine - ATOT

  • 1. SHOCK Dr. Salman Ansari Kanachur Institute of Medical Sciences
  • 2. Contents ● Definition ● Types of shock with examples ● Hypovolemic shock ● Cardiogenic shock ● Septic shock ● Stages of shock: non-progressive, progressive and irreversible
  • 3. Shock Definition: pathological process characterised by intense failure of the circulatory system to maintain an appropriate blood supply to the microcirculation ● This results in life-threatening hypoperfusion to vital organs
  • 4. Types of shock 1. Cardiogenic 2. Hypovolemic 3. Septic 4. anaphylactic shock 5. neurogenic shock
  • 5. Type Causes Cardiogenic ● MI ● Ventricular rupture ● Arrhythmia ● Cardiac tamponade ● Pulmonary embolism Hypovolemic Fluid loss(bleeding, vomiting, diarrhoea, burns) Septic Severe bacterial or fungal infections neurogenic Spinal cord injury, anesthetic accident anaphylactic Drug reaction, insect sting, food allergy
  • 6. Cardiogenic shock Definition: Shock due to low cardiac output as a result of: - myocardial damage or - external compression of the heart or - obstruction to outflow of blood from ventricles Causes: ● MI ● Ventricular rupture ● Arrhythmia ● Cardiac tamponade ● Pulmonary embolism
  • 7. Pathogenesis of cardiogenic shock Various causes of cardiogenic shock(e.g: MI) ↓ LV dysfunction ↓ Decreased cardiac output ↓ Decreased perfusion of tissues
  • 8. Hypovolemic shock Hypovolemia=abnormal decrease in volume of circulating blood Definition: Shock due to low cardiac output as a result of: - Loss of blood: massive hemorrhage - Loss of plasma: severe burns - Loss of fluid: vomiting, diarrhoea, severe gastroenteritis Causes: Fluid loss due to: ● Hemorrhage ● Vomiting ● Diarrhoea ● burns
  • 9. Pathogenesis of hypovolemic shock Inadequate blood or plasma volume and fluid loss ↓ hypovolemia ↓ low cardiac output ↓ hypotension ↓ inadequate perfusion of tissue.
  • 10. Septic shock Definition: Shock due to severe sepsis with hypotension Causes: ● Infection by Gram-positive bacteria most commonly. E.g: Staphylococcus aureus, Streptococcus pneumoniae ● Gram-negative bacteria
  • 11. Main factors contributing to septic shock 1. Inflammatory response: Activation of neutrophils, macrophages and cytokine release 1. Endothelial cell activation and injury: Increased vascular permeability → widespread edema 1. Pro-coagulant state: endotoxin activates factor XII → activation of coagulation system → thrombosis of small vessels - complication called
  • 12. 4. Metabolic abnormalities: - hyperglycemia, insulin resistance - Decreased glucocorticoid production - due to adrenal gland insufficiency - life-threatening complication called Waterhouse-Friderichsen syndrome(WFS) 5. Organ dysfunction: decreased contractility of the heart and cardiac output → failure of multiple organs like liver, lung, kidneys and heart → death 6. Immune suppression: hyperinflammatory state leads to suppression of immune system
  • 13.
  • 14. Pathogenesis of septic shock(short version) Major factors contributing to septic shock are: 1. Inflammatory response: Activation of neutrophils, macrophages and cytokine release 2. Endothelial cell activation and injury: Increased vascular permeability → widespread edema 3. Pro-coagulant state: endotoxin causes activation of coagulation system → Disseminated intravascular coagulation(DIC)
  • 15. 4. Metabolic abnormalities: hyperglycemia, insulin resistance, adrenal gland insufficiency 5. Organ dysfunction: decreased cardiac output → failure of multiple organs like liver, lung, kidneys and heart → death 6. Immune suppression
  • 16. Activation of host’s immune system: neutrophils and cytokines released Endothelial cell injury Vasodilation and pooling of blood in peripheries ↑ permeability: widespread edema Decreased tissue perfusion Multi-organ failure Endotoxin Activation of coagulation Micro-thrombi - Disseminated intravascular coagulation(DIC) Tissue ischemia Microbial products
  • 17. Stages of shock 3 phases 1. Non-progressive (compensated/reversible) phase 2. Progressive phase 3. Irreversible phase
  • 18. 1. Nonprogressive/compensated/reversible phase - Various compensatory mechanisms are activated - Blood is redistributed to maintain perfusion to vital organs
  • 19. 2. Progressive phase - If the underlying cause of shock is not corrected, shocks passes into the progressive phase - Widespread tissue hypoperfusion, hypoxia and blood pools in the microcirculation - Cardiac output worsens and there will be widespread hypoxic damage to vital organs and they begin to fail
  • 20. 3. Irreversible phase - If there is no intervention, shock enters into irreversible stage - Widespread cell injury further worsens shock - Acute renal failure - Death
  • 21. Prognosis - Hypovolemic shock: can survive with appropriate management - Septic shock, cardiogenic shock with massive MI: poorer prognosis
  • 22. Clinical features of shock ● Hypotension - low systolic blood pressure <90 mmHg ● Tachycardia - heart rate >100/minute ● Cold, clammy skin ● Cyanosis ● Tachypnoea - rapid respiratory rate ● Low urine output ● Confusion ● In septic shock: warm extremities(called ‘’warm shock’’)
  • 23. Treatment of shock Goal of management: 1. Treat reversible causes 2. Protect ischemic myocardium 3. Improve blood supply to tissues
  • 24. ABC protocol - Airway, Breathing and Circulation - Airway: - Check if airway is patent - If airway is blocked, patient needs to be intubated - Glasgow Coma Scale(GCS) of <8 - intubation required
  • 25. - Breathing: - If airway is patent, patient is to be started on oxygen - 100% O2 via NRBM face mask
  • 26. - Circulation: - Check pulses, extremities - Vitals: pulse, blood pressure - connect to monitor - Insert 2 large bore cannulas - Start on IV fluids - but be careful in case of cardiogenic shock
  • 27. - Disability: - Assessment for any neurological deficit - Ask to move each limb, if responsive - Blood sugar: check glucose level - Glasgow coma scale(GCS): - it is used to assess level of consciousness - 3 components: E.V.M 1) Eye response 2) Verbal response 3) Motor response - Total score of 15
  • 28.
  • 29.
  • 30.
  • 31. GCS: score interpretation Normal: 15 Coma: 8 or less Unresponsive/death: 3
  • 32.
  • 33. E - Exposure - Remove clothing - Examine for trauma, skin rashes or any abnormalities
  • 34. - Use of vasopressor agents to raise blood pressure - E.g dobutamine, dopamine, vasopressin - Use of iv fluids such as crystalloids(normal saline), colloid, blood - Stop any bleeding - Treat the cause of shock - Cardiogenic shock: tamponade - pericardiocentesis - Septic shock: antibiotics, vasopressors for low BP - Anaphylactic shock: adrenaline
  • 35. Anaphylactic shock Definition: life-threatening form of type 1 hypersensitivity reaction mediated by IgE Causes: Allergy to - foods(peanuts, fish, egg) - Drugs: antibiotics(penicillin), hormones(insulin), latex - Vaccines - Insect bite: honey bee
  • 36. Mechanism: Sensitisation following an initial exposure to the allergen. Repeat exposure leads to IgE-induced degranulation of mast cells and basophils, which leads to release of mediators like histamine, which cause vasodilation and smooth muscle contraction Clinical features: Sudden onset of dyspnea, wheezing, hypotension, skin rashes, angioedema
  • 37. Treatment: Inj. Adrenaline(epinephrine) intramuscularly - 1:1000 concentration Dose: Adults and children above 12 years - 0.5 ml 6-12 years old - 0.3 ml >6 years old - 0.15 ml Site: deltoid muscle or anterolateral aspect of middle third of thigh
  • 38. Questions LE: SE: Anaphylactic shock Classify shock and write brief note on ABC protocol Types of shock. Brief note on hypovolemic shock. SA: ABC protocol Adrenaline