Topic: Shock
Faculty: Medicine
Course: BSc ATOT - 2nd year
Definition
Types of shock with examples
Hypovolemic shock
Cardiogenic shock
Septic shock
Clinical features
Treatment of shock
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
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
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
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
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