Shock is a state of tissue hypoperfusion where there is inadequate oxygen delivery for normal cellular function. Symptoms include cold skin, tachycardia, hypotension, and decreased urine output. At the cellular level, shock causes hypoxia, switches metabolism to anaerobic pathways producing lactic acidosis, and eventually cell lysis. Microvascular changes include endothelium damage and fluid leaks causing edema. Cardiovascular changes are decreased preload and afterload with tachycardia. Respiratory changes include tachypnea. Renal changes are decreased perfusion and urine output. Treatment involves ensuring a patent airway, giving crystalloid fluids like Hartmann's solution to restore circulating volume, and identifying and treating the
6. Cellular
In shock at cellular level decrease supply of oxygen
( hypoxia) and nutrient supply ( such as glucose)
So,
Hypoxia
Switch to anaerobic metabolism
Increase lactic acid production
Systemic metabolic acidosis
7. Glucose exhausted
Ceasation of anaerobic respiration (So no production of ATP)
Failure of sodium-potassium pump
Release of intracellular lysosomal autodigestive enzymes
Cell lysis
Release of intracellular potassium and cellular content into
blood
8. So there release of
Acid
Potassium
Cellular and humoral content ( complement ,
neutrophil)
Into blood
9. cre
Microvascular
Hypoxia and acidosis activate complement and prime neutrophil
Endothelium damaged and become leaky
Fluid leak out and causes tissue edema, excerbating hypoxia
12. Endocrine
Activation of adrenaline and RAAS axis
Increase release ADH
Vasoconstriction and resorption of water in renal collecting
system
Cortisol also causes sodium and water reabsorption
14. Due to reduced circulating volume
Causes
1. Haemorrhagic
2. Non –haemorrhagic
Poor fluid intake – dehydration
Excessive fluid loss-vomiting , diarrhea, urinary loss (diabetes)
Third space loss in GIT, interstitial space- e.g. intestinal obstruction,
pancratitis
15. Primary failure of heart to pump blood to tissues
Causes
Myocardial infarction
Cardiac dysrhythmia
Valvular heart disease
Cardiomyopathy
Myocardial depression
16. Reduced in preload due to mechanical obstruction in
cardiac filling
Causes
Cardiac tamponade
Tension pneumothorax
Massive pulmonary embolus
17. Distributive shock
Events in distributive shock
Vascular dilatation
Low systemic vascular resistance
Inadequate afterload
Inadequate organ perfusio
Causes
Anaphylaxis ( due to histamine release)
Septic shock
Spinal cord injury (failure of sympathetic outflow)
18. Endocrine shock
May present as combination of hypovolaemic,
cardiogenic, distributive shock.
Causes
Hypothyroidism – cardiac output fall due to low inotropy and
bradycardia.
Hyperthyroidism- high output cardiac failure
Adrenal insufficiency
21. Pitfalls
Capillary refill- it is not a specific marker. In distributive shock peripheries are warm and capillary
refill are brisk.
Tachycardia- may not always accompany shock. Pateint on beta blocker or implanted pacemaker
unable to mount tachycardia. Yo ng patient in penetrating trauma with hemorrhage but
little tissue damage show paradoxical bradycardia.
Blood pressure – last sign of shock. Young patient and adult are able to maintain blood pressure
untill final stage.
22. Immediate
ABCD Management
Ensure patent airway adequqte oxygenation
Determine the type, nature of shock, if not possible
safer to assume as hypovolemic shock
25. Some notes
If patient with active bleeding (major trauma, GIT hemorrhage) must
control bleeding and fluid resuscitation run simultaneously. Transfused
blood if required.
Patient with bowel obstruction – hypovolaemic shock resuscitate
adequately before undergoing surgery