an overview

1. Shock : Pathophysiology &
Causes
Idris Khalil
400L
MB;BS

2. outline
 Introduction
 Pathophysiology
 Types of shock
 Clinical features
 Management
 conclusion

3. Introduction
Shock is the term used to describe
acute circulatory failure with
inadequate or inappropriately
distributed tissue perfusion
resulting in generalized cellular
hypoxia

4. Types of shock
 Hypovolaemic
 Cardiogenic
 Obstructive
 Distributive

5. Pathophysiology
Cellular response
 Inadequate delivery of oxygen
leads to a decrease in oxidative phosphorylation
 This causes cells to go into anaerobic respiration
, increasing lactic acid production and lactic
acidosis

6. Cellular response
There is also an increased
production of vasodilatory
substances including
• Hydrogen ion
• Potassium ion
• Adenosine
• Histamine, NO
This is an autoregulatory
mechanism for local perfusion

7. In response to hypovolemia or reduced
blood pressure, there is an increase in
the sympathetic output. This results in
• Increased Heart rate ( beta 1)
• Vasoconstriction (alpha 1)
• Production of renin (beta 1). This is
also mediated by the tubuloglomerular
feedback
Chemoteceptors
Neuroendocrine
response

8. Hormonal response
 Stimulation of renin angiotensin system
for vasoconstriction ( angiotensin) and
salt and water retention ( aldosterone)
 Release of ADH to conserve
water

9. Release of pro and anti-
inflammatory mediators
 Inflammatory response with systemic
activation of leukocytes and release of
potentially damaging mediators
including cytokines and complements
triggered by:
1. Severe infection (often with
bacteremia or endotoxemia )

10. 2. the presence of large amounts of
damaged tissue
3. Hypoxia or prolonged repeated
episodes of hypoperfusion

11. Phases of shock
Phases
- Compenseted
- Decompenseted
- Irreversible

12. Hypovolemic shock
 Most common form of shock (low circulatory
volume)
 Due to loss of blood, plasma, extravascular
sequestration
 severity depends upon amount of volume lost

13. Hypovolemic shock
 Causes
- Trauma
- Burns
- Severe dehydration
• vomiting, diarrhea Diabetes
mellitus, insipidus

14.  Class 1
 <15 %
 min. fast heart rate, normal blood
pressure
 Class II
 15-30 %
 fast heart rate, min. low blood
pressure

15.  Class III
 30-40
 very fast heart rate, low blood
pressure, confusion
 Class IV
 >40 %
 critical blood pressure and heart rate

16. Cardiogenic shock
The clinical definition of cardiogenic shock is
decreased cardiac output and evidence of tissue
hypoxia in the presence of adequate
intravascular volume

17. Causes
 Restriction of filling
 Volume overload
 Pressure overload
 Contraction impairment
 Arrhythmias

18. Obstructive shock
 Obstruction to blood flow outside the
heart.
 Cardiac tamponade
 Pulmonary embolism
 Constrictive pericarditis
 Tension pneumothorax

19. Distributive shock
 Abnormal distribution of blood flow at
the level of small vessels
 Different from the rest in that cardiac
output ia at or above the normal level

20. Causes
 Systemic inflammatory response
syndrome(SIRS). Caused by:
– Sepsis (SIRS + antecedent infection)
– Trauma
– Burns
– Severe acute pancreatitis
– Hemorrhage
Pathogenesis: Activation of the cytokine
storm

21. Criteria
 Fever of more than 38°C (100.4°F) or
less than 36°C (96.8°F)
 Heart rate of more than 90 beats per
minute
 Respiratory rate of more than 20
breaths per minute or PaCO 2 <
4.3Kpa
 Abnormal white blood cell count
(>12,000/µL or < 4,000/µL or >10%
immature [band] forms)

22. Distributive shock
 Other causes include
 Toxic shock syndrome
– Gram + bacteria superantigens. T-cell polyclonal
activation and cytokine storm
 Adrenal crisis
 Anaphylaxis
 Neurogenic shock
– Spinal cord injury, loss of sympathetic tone
 Drugs

23. Septic shock
 Manifestation of excessive & inflammatory
response of endogenous immune mechanism
 Sepsis is SIRS with established focus of
infection
 gram –ve bacteria most common. But also
by viruses fungi and parasites

24. Clinical features
 Hypovolemic shock
– Inadequate perfusion
 Cold skin, paleness, slow capillary refill
 Kidneys: Oliguria, Andria
 CNS: drowsiness, confusion
– Increased sympathetic tone
 Tachycardia, weak pulse
 Sweating
– Metabolic acidosis
 Compensatory tachypnoea

25. Clinical features
 Cardiogenic shock
– Signs of myocardial failure
 Raised jugular venous pressure, pulsus
alternans, pulmonary edema, crackles
 Obstructive shock
– Elevated JVP
– Pulsus paradoxes
– Muffled heart sounds in cardiac
tamponade
– Features of P.E

26. Clinical features
 Anaphylactic shock
– Warm peripheries
– Tachycardia
– Erythema, urticaria
– Bronchospasm, rhinitis
– Edema of face

27. Clinical features
 Septic shock
– Pyrexia and rigors (hypothermia
sometimes)
– Nausea vomiting
– Bouncing pulse
– Hypotension. Etc

28. Management
 Initially empirical
 Air way secured
+ oxygenation
 I.V. fluids NS/BSS
 Catheterisation
 Insertion of central venous catheter
 Hb, CBC, Blood sugar, urea, creatinine, electrolytes
 ABG

29. References
 Medscape
 Kumar and clark