Shock presentation medical students

1. Shock
Dr. Mohamed Jukaku
www.mjortho.com

2. Define Shock?
Systemic state of low tissue perfusion
That is inadequate
for normal cellular respiration

3. Insufficient delivery of oxygen & glucose
Cell metabolism
Aerobic --- Anaerobic
Cell death
What happens in shock?

5. Classify Shock
Based on Cause

6. Hypovolaemic shock
• Reduced circulating volume
• Haemorrhagic or Non-Haemorrhagic
• Hypovolaemia is probably the most common form of shock,
• Is a component of all other forms of shock.
• Hypovolaemia must be excluded or treated
in the management of the shocked state, regardless of cause.

7. • Dehydration
• Excessive fluid loss- Vomiting / Diarrhoea
• Urinary loss (e.g. diabetes) / Sweating
• ‘3rd-spacing’ fluid is lost into the GI tract & interstitial Spaces
eg. bowel obstruction or pancreatitis
Non Haemorrhagic

8. • Primary failure of the heart to pump blood to the tissues.
• Causes:
• MI, cardiac dysrhythmias, valvular heart disease,
blunt myocardial injury & cardiomyopathy.
• Cardiac insufficiency may also be due to myocardial depression caused by
endogenous factors
• (e.g. bacterial &chemical agents released in sepsis)
• or Exogenous factors, such as pharmaceutical agents/ drug abuse.
• Evidence of venous hypertension with pulmonary or systemic oedema may
coexist.
Cardiogenic shock

9. • Reduction in preload due to mechanical obstruction of cardiac filling.
• Common causes of obstructive shock:
• 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 & a fall in cardiac output.
Obstructive shock

10. Septic shock, Anaphylaxis & Spinal cord injury
• Inadequate organ perfusion + vascular dilatation  Low
systemic vascular resistance  Inadequate afterload
+ a resulting abnormally high cardiac output
Distributive Shock

11. Sepsis
Release of bacterial products (endotoxin)
+ activation of cellular & humoral components of Immune system
Maldistribution of blood flow at microvascular level
+ arteriovenous shunting & dysfunction of cellular utilization of
oxygen
Late phase of septic shock  hypovolaemia from fluid loss into
interstitial spaces + myocardial depression

12. Anaphylaxis
Histamine release
Vasodilation

13. Spinal cord injury
failure of sympathetic outflow
inadequate vascular tone
Neurogenic shock

14. • May present as a combination of hypovolaemic,
cardiogenic or distributive shock.
• Causes:
• Hypo/ hyperthyroidism & Adrenal insufficiency.
Endocrine Shock

15. • Shock state similar to that of neurogenic shock
• due to disordered vascular & cardiac responsiveness to
circulating catecholamines.
• Cardiac output falls due to low inotropy & bradycardia.
• associated cardiomyopathy also present.
• Thyrotoxicosis may cause high-output cardiac failure.
Hypothyroidism

16. • Shock due to hypovolaemia & poor response to circulating &
exogenous catecholamines.
• Adrenal insufficiency:
• Primary - Addison’s disease
• Secondary (Systemic sepsis)
Adrenal insufficiency

17. Clinical features of Shock
• Tachycardia & Tachypnea
• Feeble/absent pulse & Hypotension
• Cold extremities & Pale skin
• Decreased capillary refill
• Mental status changes (Drowziness, fainting)
• Decreased Urine output (concentrated urine)

20. A B C
• Airway
• Breathing
• Circulation

21. Vitals
• Pulse rate
• Blood pressure
• SpO2
• GRBS

22. •Control Bleeding
•IV Fluids (NS, RL)
•Blood transfusion
•Vasopressors & Inotropes

23. Insert IV Line
• First-line therapy  Intravenous access & Administration of IV
fluids
• Short, wide-bore catheters
Allow rapid infusion of fluids as necessary.

24. Colloids vs Crystalloids
• No overt difference in response or outcome between
• Crystalloid solutions -Normal saline, Hartmann’s solution,
Ringer’s lactate)
• Colloids (albumin or Haemaccel)
• Colloids more side-effects, more expensive

25. •If blood is being lost, the ideal
replacement fluid is…
•Blood

26. Vasopressor & Inotropic support
• Administration of these agents in the absence of adequate preload
rapidly leads to
• Decreased coronary perfusion & depletion of myocardial oxygen
reserves.

27. • Vasopressor agents  Adrenaline & Noradrenaline
• Indicated in distributive shock states (sepsis, neurogenic
shock)
• Where the vasodilatation is resistant to catecholamines (eg.
absolute or relative steroid deficiency)
• Vasopressin may be used as an alternative vasopressor.

28. •Cardiogenic Shock  Dobutamine

32. www.mjortho.com
@mjorthopedics