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SHOCK
Dr HARSHA NANDINI TALASILA
M.S. Ortho
DEFINITION
• Shock is a systemic state of low tissue perfusion which is inadequate
for normal cellular respiration.
PATHOPHYSIOLOGY
Decreased tissue perfusion
Cells switch from aerobic to anaerobic respiration
Lactic acid
Systemic metabolic acidosis
• Hypoxia and acidosis activate complement and neutrophils
• Oxygen free radicals and cytokines released
• Injury to the capillary endothelial cells
• Loss of integrity of the endothelium
• Tissue oedema
EFFECTS OF SHOCK ON ORGANS
1. CARDIOVASCULAR
• preload and afterload decrease
• Compensatory baroreceptor response
• Increased sympathetic activity
• TACHYCARDIA
2. RESPIRATORY
• Metabolic acidosis and increased sympathetic response
• Increased respiratory rate and minute ventilation
• Compensatory respiratory alkalosis
3. RENAL
• Decreased renal perfusion
• Decreased urine output
4. ENDOCRINE
• ADH is released
• Vasoconstriction and water resorption
5. CNS
• Decreased perfusion DROWSY
6. BLOOD
• Coagulation abnormalities DIC
TYPES OF SHOCK
1. Hypovolaemic shock
2. Cardiogenic shock
3. Obstructive shock
4. Distributive shock
HYPOVOLEMIC SHOCK
• Haemorrhagic
• Non haemorrhagic:
Dehydration
Vomiting
Diarrhoea
Urinary loss
CARDIOGENIC SHOCK
• Myocardial infarction
• Cardiac arrhythmias
• Valvular heart disease
• Cardiomyopathy
OBSTRUCTIVE SHOCK
• Cardiac tamponade
• Tension pneumothorax
• Massive pulmonary embolus
DISTRIBUTIVE SHOCK
• Septic shock
• Anaphylactic shock
• Spinal cord injury
SEPTIC SHOCK
• CLINICAL SIGNS: hyperthermia
tachycardia
wide pulse pressure
low blood pressure
Altered mental status
NEUROGENIC SHOCK
• Acute spinal cord injury
• Sympathetic outflow is disrupted
• Unopposed vagal tone
• Hypotension, bradycardia and hypothermia
SPINAL SHOCK
• Temporary dysfunction of spinal cord leading to loss of spinal reflexes
and sensorimotor function caudal to the level of injury.
• Manifested by flaccid paralysis, absence of anal wink and
bulbocavernous reflexes.
• Temporary phenomenon and recovers in 24 to 48 hours.
CLINICAL FEATURES
MILD SHOCK :
• Patient is anxious
• Cool peripheries
• Prolonged capillary refill time
• Tachycardia
• Tachypnoea
• Reduction in urine output
MODERATE SHOCK
• Patient is confused and drowsy
• Further tachycardia
• Urine output < 0.5ml /kg/hour
SEVERE SHOCK:
• Patient unconscious with laboured respiration
• Profound tachycardia and hypotension
• Urine output fall to zero
STAGES OF SHOCK
1. Initial stage : switch from aerobic to anaerobic respiration
2. Non progressive ( compensated stage ) : attempt to correct the
metabolic derangement
3. Progressive ( decompensated stage ) : compensatory mechanism
fail
4. Refractory: organ damage which cannot be reversed
MANAGEMENT
GOALS OF TREATMENT
1. Treat the cause
2. Improve cardiac output
3. Improve tissue perfusion
HYPOVOLEMIC SHOCK
• Airway, Breathing, Circulation
• Direct control of obvious bleeding: direct pressure control or
clamping of vessels
• Large bore venous access
• Fluid resuscitation
• Blood replacement
• Traction with Thomas splints, extremity splints to limit haemorrhage
from unstable fractures.
SEPTIC SHOCK
• INVESTIGATIONS: CBC,ABG with lactate,Blood culture, urine culture.
• TREATMENT : IV FLUIDS
Supplemental oxygen
Emperic antibiotics
NEUROGENIC SHOCK
• ABC
• Fluid resuscitation
• Bradycardia: Atropine
Pacemaker
• Methylprednisolone : used for blunt spinal cord injury.
High doses for first 24hours.
MONITORING
• Blood pressure
• Heart rate
• Respiratory rate
• Urine output
• Blood CBC
• Pulse- oximetry
• ECG
• U/S , CT , X-ray
SPECIAL MONITORING
Central venous pressure
• Normal : 5-10cmH2O,
• If CVP<5cmH2O: Inadequacy of blood volume
• CVP>12cmH2O: Cardiac dysfunction
Cardiac output
• Pulmonary catheter
• Doppler ultrasound
SYSTEMIC & ORGAN PERFUSION
• Clinical : urine output & LOC
• Sr. Lactate estimation & Base deficit
• Blood gas analysis
• PO2 / PCO2 / pH
END POINTS OF RESUSCITATION
• MAP : 65 to 90 mm of hg
• Urine output: >0.5ml/kg/hr
• CVP: 5 to 10 cm of H2O
• Central venous oxygen concentration >70%
THANK YOU

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Shock

  • 1. SHOCK Dr HARSHA NANDINI TALASILA M.S. Ortho
  • 2. DEFINITION • Shock is a systemic state of low tissue perfusion which is inadequate for normal cellular respiration.
  • 3. PATHOPHYSIOLOGY Decreased tissue perfusion Cells switch from aerobic to anaerobic respiration Lactic acid Systemic metabolic acidosis
  • 4. • Hypoxia and acidosis activate complement and neutrophils • Oxygen free radicals and cytokines released • Injury to the capillary endothelial cells • Loss of integrity of the endothelium • Tissue oedema
  • 5. EFFECTS OF SHOCK ON ORGANS 1. CARDIOVASCULAR • preload and afterload decrease • Compensatory baroreceptor response • Increased sympathetic activity • TACHYCARDIA
  • 6. 2. RESPIRATORY • Metabolic acidosis and increased sympathetic response • Increased respiratory rate and minute ventilation • Compensatory respiratory alkalosis
  • 7. 3. RENAL • Decreased renal perfusion • Decreased urine output 4. ENDOCRINE • ADH is released • Vasoconstriction and water resorption
  • 8. 5. CNS • Decreased perfusion DROWSY 6. BLOOD • Coagulation abnormalities DIC
  • 9. TYPES OF SHOCK 1. Hypovolaemic shock 2. Cardiogenic shock 3. Obstructive shock 4. Distributive shock
  • 10. HYPOVOLEMIC SHOCK • Haemorrhagic • Non haemorrhagic: Dehydration Vomiting Diarrhoea Urinary loss
  • 11. CARDIOGENIC SHOCK • Myocardial infarction • Cardiac arrhythmias • Valvular heart disease • Cardiomyopathy
  • 12. OBSTRUCTIVE SHOCK • Cardiac tamponade • Tension pneumothorax • Massive pulmonary embolus
  • 13. DISTRIBUTIVE SHOCK • Septic shock • Anaphylactic shock • Spinal cord injury
  • 14. SEPTIC SHOCK • CLINICAL SIGNS: hyperthermia tachycardia wide pulse pressure low blood pressure Altered mental status
  • 15. NEUROGENIC SHOCK • Acute spinal cord injury • Sympathetic outflow is disrupted • Unopposed vagal tone • Hypotension, bradycardia and hypothermia
  • 16. SPINAL SHOCK • Temporary dysfunction of spinal cord leading to loss of spinal reflexes and sensorimotor function caudal to the level of injury. • Manifested by flaccid paralysis, absence of anal wink and bulbocavernous reflexes. • Temporary phenomenon and recovers in 24 to 48 hours.
  • 17. CLINICAL FEATURES MILD SHOCK : • Patient is anxious • Cool peripheries • Prolonged capillary refill time • Tachycardia • Tachypnoea • Reduction in urine output
  • 18. MODERATE SHOCK • Patient is confused and drowsy • Further tachycardia • Urine output < 0.5ml /kg/hour
  • 19. SEVERE SHOCK: • Patient unconscious with laboured respiration • Profound tachycardia and hypotension • Urine output fall to zero
  • 20. STAGES OF SHOCK 1. Initial stage : switch from aerobic to anaerobic respiration 2. Non progressive ( compensated stage ) : attempt to correct the metabolic derangement 3. Progressive ( decompensated stage ) : compensatory mechanism fail 4. Refractory: organ damage which cannot be reversed
  • 22. GOALS OF TREATMENT 1. Treat the cause 2. Improve cardiac output 3. Improve tissue perfusion
  • 23. HYPOVOLEMIC SHOCK • Airway, Breathing, Circulation • Direct control of obvious bleeding: direct pressure control or clamping of vessels • Large bore venous access • Fluid resuscitation • Blood replacement • Traction with Thomas splints, extremity splints to limit haemorrhage from unstable fractures.
  • 24. SEPTIC SHOCK • INVESTIGATIONS: CBC,ABG with lactate,Blood culture, urine culture. • TREATMENT : IV FLUIDS Supplemental oxygen Emperic antibiotics
  • 25. NEUROGENIC SHOCK • ABC • Fluid resuscitation • Bradycardia: Atropine Pacemaker • Methylprednisolone : used for blunt spinal cord injury. High doses for first 24hours.
  • 26. MONITORING • Blood pressure • Heart rate • Respiratory rate • Urine output • Blood CBC • Pulse- oximetry • ECG • U/S , CT , X-ray
  • 27. SPECIAL MONITORING Central venous pressure • Normal : 5-10cmH2O, • If CVP<5cmH2O: Inadequacy of blood volume • CVP>12cmH2O: Cardiac dysfunction Cardiac output • Pulmonary catheter • Doppler ultrasound
  • 28. SYSTEMIC & ORGAN PERFUSION • Clinical : urine output & LOC • Sr. Lactate estimation & Base deficit • Blood gas analysis • PO2 / PCO2 / pH
  • 29. END POINTS OF RESUSCITATION • MAP : 65 to 90 mm of hg • Urine output: >0.5ml/kg/hr • CVP: 5 to 10 cm of H2O • Central venous oxygen concentration >70%