SHOCK_Dr BZ scrptic shock University.pptx

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1. SHOCK Dr Blessing Zambuko

2. SHOCK Shock (cardiovascular collapse) is final common pathway for several potentially lethal clinical events Severe haemorrhage massive pulmonary embolism microbial sepsis etc.

3. SHOCK Reduction in cardiac output or effective circulating volume causes hypoperfusion which is systemic Hypoperfusion causes reversible then irreversible hypoxic and metabolic effects which may be lethal

4. THREE MAJOR TYPES OF SHOCK Three major types Hypovolaemic } low Cardiogenic } cardiac Output Septic shock - more Complex Mechanisms

5. CARDIOGENIC SHOCK Results from myocardial pump failure May be caused by intrinsic myocardial damage Infarction ventricular arrythmias extrinsic compression (tamponade) outflow obstruction (P.E.)

6. HYPOVOLAEMIC SHOCK Blood or plasma volume loss Haemorrhage, burns, diarrhoea trauma, etc

7. Septic shock Systemic microbial infection especially gram negative infections (endotoxic shock) Fungal and gram positive infections also occur

8. NEUROGENIC SHOCK Less common Anaesthetic accident or spinal cord injury Due to loss of vascular tone and peripheral pooling of blood

9. ANAPHYLACTIC SHOCK Initiated by generalised IgE – mediated hyper-sensitivity responses Associated with systemic vasodilatation and ↑ vascular permeability Sudden increase vascular bed capacitance not adequately filled by normal circulating blood volume Results in hypotension, hypoperfusion and cellular hypoxia

10. PATHOGENESIS OF SEPTIC SHOCK Mortality 25-50% & leading cause of mortality in intensive care units Sepsis increasing due to Improved life support systems for high risk patients Immunosuppression (HIV, chemotherapy, transplants etc.)

11. Septic shock results from spread and expansion of an initially localised infection into blood stream abscess, pneumonia, peritonitis Most (70%) due to gram negative bacilli hence endotoxic shock

12. Endotoxins are bacterial wall lipopolysaccharides (LPS) released when cell walls are degraded (e.g. Inflammation) LPS = toxic fatty acid (lipid) core & complex polysaccharide coat Fungi and gram positive bacteria have similar molecules

13. LPS binds to cell surface receptors and directly activate endothelial cells, leucocytes or initiate the cytokine cascade Effect on endothelial cells leads to down regulation of anti-coagulation mechanisms including ↓ synthesis of tissue factor pathway inhibitor (TFPI) and thrombomodulin Interacts with monocytes and macrophages to cause production of cytokines IL-1 and TNF and fatal shock

14. Activates monocytes and macrophages, neutrophils with effects intended to eliminate bacteria Monocytes etc. produce cytokines (TNF, IL-6 and chemokines TNF and IL-1 which act on endothelial cells to produce other cytokines and chemokines

15. LOW DOSE Lipopolysaccharide (LPS) Moderate infection causes augmentation of cytokine cascade, cytokine induced secondary effects (NO) Systemic effects of TNF and IL-1 (fever etc) and acute phase reactants occur

16. MODERATE DOSE LPs ↓ Endothelial production of thrombomodulin and TPPI predispose to thrombosis

17. High dose LPS Syndrome of septic shock supervenes Cytokines and injury effectors cause: Systemic vasodilation ↓ Myocardial contractility Widespread endothelial injury and activation to cause systemic leucocyte adhesion an pulmonary alveolar capillary damage (acute respiratory distress syndrome)

18. CLINICAL CORRELATIONS Activation of coagulation system and DIC Vasodilatation and pump failure and DIC cause multi-organ failure Liver CNS kidneys)

19. SUPERANTIGENS Group of bacterial proteins that cause syndromes similar to septic shock Toxic shock syndrome toxin-1 is produced by staphylococci and causes toxic shock syndrome Polyclonal T-lymphocyte activators that induce systemic inflammatory cytokine cascades and septic shock and diffuse rash

20. STAGES OF SHOCK Shock is a progressive disorder leading to death if uncorrected Unless massive (and fatal) evolution is through three phases

21. Stages of shock initial  nonprogressive phase reflex compensatory mechanisms are activated and perfusion of vital organs is maintained progressive stage   characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances, including acidosis irreversible stage sets in after the body has incurred cellular and tissue injury so severe that even if the hemodynamic defects are corrected, survival is not possible

22. Clinical Consequences manifestations of shock depend on the precipitating insult. Hypovolemic and cardiogenic shock - hypotension; a weak, rapid pulse; tachypnoea; and cool, clammy, cyanotic skin. septic shock - the skin may initially be warm and flushed because of peripheral vasodilation. cardiac, cerebral, and pulmonary changes secondary to shock worsen the problem.

23. prognosis varies with the origin of shock and its duration. greater than 90% of young, otherwise healthy patients with hypovolemic shock survive with appropriate management; septic shock, or cardiogenic shock associated with extensive myocardial infarction, can have substantially worse mortality rates, even with optimal care.