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Dr. Saugat Chapagain
SHOCK
WHAT IS IT???
Life threatening clinical syndrome of cardiovascular collapse
characterised by:
• An acute reduction of effective circulating blood volume
(hypotension)
• An inadequate perfusion of cells and tissues (hypoperfusion)
AETIOLOGICAL CLASSIFICATION
• Hypovolemic shock
• Cardiogenic shock (normovolemia)
• Septic shock – gram negative (endotoxic) or gram
positive (exotoxic)
• Neurogenic shock
• Anaphylactic shock
PATHOGENESIS
• Reduced effective circulating blood volume.
• Reduced supply of oxygen to the cells and tissues with resultant
anoxia.
• Inflammatory mediators and toxins released from shock-induced
cellular injury.
COMPENSATED SHOCK
• Non-progressive, initial, reversible
• In early stage, body acts to provide supply to the vital organs (brain
and heart)
• Peripheral vasoconstriction (widespread) and kidneys retain fluid.
• After prompt management, body’s homestasis may be returned
easily
PROGRESSIVE DECOMPENSATED SHOCK
Usu. a/w pre existing co-morbidity.
Persistence of shock + progressive deterioration.
Circulatory and metabolic imbalance (incl. met acidosis)
Effects:
• Pulmonary hypoperfusion
• Tissue ischemia
IRREVERSAL/ DECOMPENSATED
• Severe shock.
• Recovery poor or absent despite compensatory mechanism as well
as therapy.
• MODS common.
MORPHOLOGY IN SHOCK
Brain
Gross –
• Area supplied by the most distal branches of cerebral
arteries suffer from severe ischemic necrosis.
Microscopic –
• Changes are prominent if ischemia lasts for 12-24 hrs at
least.
• Cytoplasm of affected neurons are intensely eosinophilic
and nucleus is small and pyknotic.
• Dead neurons replaced by gliosis.
Heart
2 types of changes:
• Haemorrhages and necrosis –
• Zonal lesions –
Lung
More prominenet changes in septic shock
Not much effect in hypovolemic shock
Gross –
• Heavy and wet
Microscopic –
• ARDS changes seen
• Congestion, interstitial and alveolar oedema, interstitial
lymphocytic infiltrate, alveolar hyaline membranes, etc.
Kidney
End result is almost always anuria and death.
Gross –
• Soft and swollen
• Section shows blurred margins
Microscopic –
• Tubular lesions seen at all levels of nephron (ATN)
Adrenals
• Show stress response
• Release of aldosterone in response to hypoxic kidney, release of
glucocorticoid (from cortex)
• Release of adrenaline from medulla.
• Acute adrenal haemorrhagic necrosis may occur in serious conditions.
GIT –
• May show mucosal haemorrhage and necrosis.
Liver –
• May show fatty changes and central necrosis.
CLINICAL FEATURES
• Very low pressure.
• Subnormal temperature.
• Feeble and irregular pulse.
• Shallow and sighing respiration.
• Other features:
• Pale face, sunken eyes, weakness, cold and clammy skin.
CLINICAL FEATURES
Symptoms:
• Restlessness
• Sweating, coldness
• Rapidly shallow breathing
Signs:
• Altered level of consciousness, rapid and weak pulse
• Hypotention, oliguria, anxiety
• Cold clammy skin.
SPECIFIC FEATURES
In septic shock:
• Fever
• Skin – pink and well perfused
In cardiogenic shock:
• Raised CVP/ JVP
• Lungs – b/l basal crepts +
• Liver – enlarged d/t decreased pumping of the venous return.
In anaphylactic shock:
• Rashes.
• Vomiting.
• SoB.
• Headache, body ache.
COMPLICATIONS
• Acute Respiratory Distress Syndrome.
• Disseminated Intravascular coagulation.
• Acute renal failure
• Multiple organ dysfunction syndrome
• Stupor, coma and death.
• Septic shock • Neurogenic shock
PATHOPHYSIOLOGY
Tissue death/ necrosis
Tissue Hypoperfusion
Vasodialation and hypotention
Production of cytokines
Release of bacterial endotoxins
Unconsciousness (hypoxia/
ischemia)
Reduced supply to the brain
Decreased cardiac output
Hypotension and decreased
heart rate
Decreased sympathetic activity
controling vascular tone
Anaesthesia, brain or spinal
injury
• Type I hypersensitivity
reaction
• IgE mediated rxn.
• Systemic vasodilation and
increased vascular
permeability
ANAPHYLACTIC SHOCK
a/w bronchoconstriction and
skin rashes
Venous pooling of blood and
hpotension.
Vasodilation
Systemic release of
mediators (histamine/
bradykinin)
Allergic substance enters
circulation/ organism
MANAGEMENT
Principles
• Clinical monitoring
• Maintenance of ABC
• Clearing the Airway
• Maintenance of Respiration
• Maintenance of Circulation
• Prevention of Renal Shut down
• Correction of Acid base balance
• Treatment of underlying cause
CLINICAL MONITORING
• History
• Vitals
• Pulse
• Pressure
• Temperature
• Respiration rate
• CVP
• Urinary output
MAINTENANCE OF RESPIRATION
• Keep patient in well ventilated room.
• Extend neck and support jaw
• Place in left lateral position
• Airway in mouth to prevent fallback of tongue
• Supplement of nasal O2
• ET intubation and ventilation (if needed)
MAINTENANCE OF CIRCULATION
• Control of bleeding (hemorrhagic shock)
• IV access and start suitable IV fluid (RL, NS, DNS, 5-D, dextran,
hemacele)
• Necessary investigation incl. blood grouping and cross matching
• Blood transfusion if needed.
SUPPORTIVE CARE
• Prevention of renal shut down (AKI/ MODS)
• Foley’s catheterization
• I/O charting strictly
• Correction of acid base balance
• Identification and treatment of underlying cause
• Septic shock-
• Broad spectrum antibiotics
• TT prophylaxis
• Excision of source of sepsis
CARE OF ANAPHYLACTIC SHOCK
• Stop drug/ agent causing anaphylaxis
• Clear the airway
• IV antihistamine (phenargan, promethazine, avil, meperamine)
• IV steroid (hydrocort)
• IV adrenaline 0.5ml or SC 1:1000
THANK YOU

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8. shock

  • 2. WHAT IS IT??? Life threatening clinical syndrome of cardiovascular collapse characterised by: • An acute reduction of effective circulating blood volume (hypotension) • An inadequate perfusion of cells and tissues (hypoperfusion)
  • 3. AETIOLOGICAL CLASSIFICATION • Hypovolemic shock • Cardiogenic shock (normovolemia) • Septic shock – gram negative (endotoxic) or gram positive (exotoxic) • Neurogenic shock • Anaphylactic shock
  • 4. PATHOGENESIS • Reduced effective circulating blood volume. • Reduced supply of oxygen to the cells and tissues with resultant anoxia. • Inflammatory mediators and toxins released from shock-induced cellular injury.
  • 5. COMPENSATED SHOCK • Non-progressive, initial, reversible • In early stage, body acts to provide supply to the vital organs (brain and heart) • Peripheral vasoconstriction (widespread) and kidneys retain fluid. • After prompt management, body’s homestasis may be returned easily
  • 6. PROGRESSIVE DECOMPENSATED SHOCK Usu. a/w pre existing co-morbidity. Persistence of shock + progressive deterioration. Circulatory and metabolic imbalance (incl. met acidosis) Effects: • Pulmonary hypoperfusion • Tissue ischemia
  • 7. IRREVERSAL/ DECOMPENSATED • Severe shock. • Recovery poor or absent despite compensatory mechanism as well as therapy. • MODS common.
  • 8. MORPHOLOGY IN SHOCK Brain Gross – • Area supplied by the most distal branches of cerebral arteries suffer from severe ischemic necrosis. Microscopic – • Changes are prominent if ischemia lasts for 12-24 hrs at least. • Cytoplasm of affected neurons are intensely eosinophilic and nucleus is small and pyknotic. • Dead neurons replaced by gliosis.
  • 9. Heart 2 types of changes: • Haemorrhages and necrosis – • Zonal lesions – Lung More prominenet changes in septic shock Not much effect in hypovolemic shock Gross – • Heavy and wet Microscopic – • ARDS changes seen • Congestion, interstitial and alveolar oedema, interstitial lymphocytic infiltrate, alveolar hyaline membranes, etc.
  • 10. Kidney End result is almost always anuria and death. Gross – • Soft and swollen • Section shows blurred margins Microscopic – • Tubular lesions seen at all levels of nephron (ATN) Adrenals • Show stress response • Release of aldosterone in response to hypoxic kidney, release of glucocorticoid (from cortex) • Release of adrenaline from medulla. • Acute adrenal haemorrhagic necrosis may occur in serious conditions.
  • 11. GIT – • May show mucosal haemorrhage and necrosis. Liver – • May show fatty changes and central necrosis.
  • 12. CLINICAL FEATURES • Very low pressure. • Subnormal temperature. • Feeble and irregular pulse. • Shallow and sighing respiration. • Other features: • Pale face, sunken eyes, weakness, cold and clammy skin.
  • 13. CLINICAL FEATURES Symptoms: • Restlessness • Sweating, coldness • Rapidly shallow breathing Signs: • Altered level of consciousness, rapid and weak pulse • Hypotention, oliguria, anxiety • Cold clammy skin.
  • 14. SPECIFIC FEATURES In septic shock: • Fever • Skin – pink and well perfused In cardiogenic shock: • Raised CVP/ JVP • Lungs – b/l basal crepts + • Liver – enlarged d/t decreased pumping of the venous return. In anaphylactic shock: • Rashes. • Vomiting. • SoB. • Headache, body ache.
  • 15. COMPLICATIONS • Acute Respiratory Distress Syndrome. • Disseminated Intravascular coagulation. • Acute renal failure • Multiple organ dysfunction syndrome • Stupor, coma and death.
  • 16. • Septic shock • Neurogenic shock PATHOPHYSIOLOGY Tissue death/ necrosis Tissue Hypoperfusion Vasodialation and hypotention Production of cytokines Release of bacterial endotoxins Unconsciousness (hypoxia/ ischemia) Reduced supply to the brain Decreased cardiac output Hypotension and decreased heart rate Decreased sympathetic activity controling vascular tone Anaesthesia, brain or spinal injury
  • 17. • Type I hypersensitivity reaction • IgE mediated rxn. • Systemic vasodilation and increased vascular permeability ANAPHYLACTIC SHOCK a/w bronchoconstriction and skin rashes Venous pooling of blood and hpotension. Vasodilation Systemic release of mediators (histamine/ bradykinin) Allergic substance enters circulation/ organism
  • 18. MANAGEMENT Principles • Clinical monitoring • Maintenance of ABC • Clearing the Airway • Maintenance of Respiration • Maintenance of Circulation • Prevention of Renal Shut down • Correction of Acid base balance • Treatment of underlying cause
  • 19. CLINICAL MONITORING • History • Vitals • Pulse • Pressure • Temperature • Respiration rate • CVP • Urinary output
  • 20. MAINTENANCE OF RESPIRATION • Keep patient in well ventilated room. • Extend neck and support jaw • Place in left lateral position • Airway in mouth to prevent fallback of tongue • Supplement of nasal O2 • ET intubation and ventilation (if needed)
  • 21. MAINTENANCE OF CIRCULATION • Control of bleeding (hemorrhagic shock) • IV access and start suitable IV fluid (RL, NS, DNS, 5-D, dextran, hemacele) • Necessary investigation incl. blood grouping and cross matching • Blood transfusion if needed.
  • 22. SUPPORTIVE CARE • Prevention of renal shut down (AKI/ MODS) • Foley’s catheterization • I/O charting strictly • Correction of acid base balance • Identification and treatment of underlying cause • Septic shock- • Broad spectrum antibiotics • TT prophylaxis • Excision of source of sepsis
  • 23. CARE OF ANAPHYLACTIC SHOCK • Stop drug/ agent causing anaphylaxis • Clear the airway • IV antihistamine (phenargan, promethazine, avil, meperamine) • IV steroid (hydrocort) • IV adrenaline 0.5ml or SC 1:1000