superficial introduction to the topic for bachelor level

1. Dr. Saugat Chapagain
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

24. THANK YOU