Shock

Presentation on Shock (Pathology). A brief explanation of types of shock with flow charts and diagrams.

1. SHOCK

2. We will learn :

3. Definition of shock What exactly happens in shock? Classification Pathogenesis Pathophysiology – Stages of shock Morphologic features Clinical features Complications

4. Definition of Shock Shock is a life threatening clinical syndrome, of cardiovascular collapse, characterised by- Hypotension Hypoperfusion

5. What is Hypotension? Acute reduction of circulatory blood volume. Decreased blood pressure.

6. What is Hypoperfusion ? It is the inadequate amount of blood that flows through the capillaries, which leads to decreased supply of oxygen and nutrients to the cells .

7. Classification of Shock on the basis of its cause: Hypovol ae mic Shock Cardiogenic Shock Septic Shock Other Types Inadequate circulatory blood volume Sudden fall in cardiac output from acute diseases of the heart Severe bacterial infection Anaphylactic Shock Severe reaction in response to an allergen

8. Other types of Shock Traumatic Shock Neurogenic Shock Hypoadrenal Shock Spinal cord injury Anesthetic Accidents Peripheral Vasodilatation Pooling of blood

9. What exactly does the word pathogenesis mean? The pathogenesis is the mechanism by which a disease is caused.

10. Pathogenesis of Shock

11. Effective circulating blood volume Venous return to heart Cardiac output Blood flow Supply of oxygen at cellular level Anoxia Inflammatory mediators Shock Heart Failure

12. HYPOVOLAEMIC SHOCK Occurs from - Inadequate circulating blood volume due to various causes. Major effects of hypovolaemic shock are due to - Cardiac Output C.O. Low Intracardiac pressue

13. Inadequate circulatory blood volume BLOOD LOSS DEHYDRATION Burns Excessive use of diuretics Vomiting Excessive Perspiration Bleeding from cuts, injuries Internal bleeding Increased Heart Rate Low Blood Pressure Low Urinary Output Alteration in mental state Diarrhoea

14. Compensatory Mechanisms HYPOVOLAEMIA HYPOTENSION REDISTRIBUTION OF BLOOD SUPPLY Fluid conservation ADH Aldosterone Renin - Angiotensin Blood Pressure Sympatheic Vasoconstriction Peripheral resistance Coronary and Cerebral vessels are spared due to sympathetic vasoconstriction

15. CARDIOGENIC SHOCK Inadequate circulation of blood due to primary failure of the ventricles

16. Decreased Cardiac Output Decreased Tissue Perfusion Decreased movement of fluid from Pulmonary vascular bed into pulmonary interstitial space Pulmonary interstial odema followed by Alveolar Pulmonary odema Myocardial Infarction Arrhythmia Cardiac Tamponade Pulmonary Embolism Failure of Myocardial Pump

17. Compensatory mechanisms Frank – Starling mechanism : Increased preload of dilatation enhancing cardiac contractility . 2. Myocardial structural change : Hypertrophy 3. Activation of neurohumoral system: a) Release of neurotransmitter : Nor epinephrine by adrenergic cardiac nerves which increases the heart rate & augments myocardial contractility b) Activation of renin-angiotensin-aldosteron system

18. Compensatory mechanisms to maintain Arterial pressure Perfusion of vital organs

19. Ana - against Phylaxis - protection

20. ANAPHYLACTIC SHOCK Anaphylaxis is an allergic reaction condition in which the C.O. and B.P. often decrease drastically. It results primarily from an Ag- Ab reaction that takes place immediately after an antigen to which the person is sensitive enters the circulation.

21. HISTAMINE CAUSES : Venous Dilatation Decreased V.R. Dilatation of Arterioles Decreased B.P. Increased Capillary Permeability Great Loss of fluid and protein into tissue spaces.

22. Anaphylaxis can occur in response to any allergen. Animal Dander : Material shed from the body of animals – Hair, Dry skin, Feathers

23. Hives or Urticaria are dark red, raised icthy bumps.

24. Septic shock is a serious medical condition caused by decreased tissue perfusion and oxygen delivery as a result of infection and sepsis, though the microbe may be systemic or localized to a particular site. Septic shock results from spread & expansion of initially localized infection to blood stream The mortality rate from septic shock is approximately 50% SEPTIC SHOCK

25. In septic shock, there is immune system activation and severe systemic inflammatory response to infection as follows: Activation of macrophage - monocytes . Activation of other inflammatory responses: Ulitimately – the net result of these mechanisms is vasodilation and increased vascular permeability.

26. Gram-negative bacteria enter the body from -

27. LYSIS OF GRAM –VE BACTERIA RELEASE OF ENDOTOXIN LPS LPS BINDS TO LBP LPS-LBP BINDS TO CD14 RECEPTOR ON MACROPHAGE THIS STIMULATES RELEASE OF CYTOKINES MOST IMPORTANT BEING TNF AND IL1

28. What are these cytokines? Cytokines : cyto - cell kinos - movement) are small cell- signaling protein molecules used extensively in intercellular communication.

29. Shock Hypoperfusion Hypoxic Cell Injury Activation of innate immunity Stimulation of Macrophages Release of inflammatory mediators Tumor Necrotic Factor - alpha Interleukin 1 Other cytokines

30. Toxic Shock Syndrome

31. Pathophysiology is the study of the changes of normal mechanical, physical, and biochemical functions, caused by a disease. Pathophysiology

32. Stages of Shock Progressive Stage Non Progressive Stage Irreversible Stage Reflex Compensatory Mechanisms Activated Perfusion of Vital Organs Maintained Tissue Hypoperfusion Onset of Worsening circulatory BV and metabolic imbalances-acidosis Severe cell and tissue injury Even if Haemodynamic effects are corrected Survival not possible

33. Brain - Hypoxic Encephalopathy Heart in shock - Focal Myocardial Necrosis Shock Lung – Acute Respiratory Distress Syndrome ARDS Shock Kidney – Acute Tubular Necrosis ATN Adrenals in Shock – Necrosis Liver in Shock – Necrosis Blood – Disseminated Intravascular Coagulation MORPHOLOGIC FEATURES

34. Shock Kidney – Acute Tubular Necrosis ATN

35. Normal Pathology KIDNEY Proteinaceous casts in tubules

36. Ischemic encephalopathy Normal Swollen brain, distended gyri , narrow sulci

37. Clinical features Very low BP Shallow and Sighing Respiration Subnormal Temperature Feeble and irregular pulse

38. Life Threatening Complications ARDS – Acute Respiratory Distress Syndrome DIC – Disseminated Intravascular Coagulation ARF – Acute Renal Failure Multiple Organ failure are due to hypoxic cell injury resulting in immuno -inflammatory responses and activation of various cascades

39. SOURCE Textbook of Pathology – Harsh Mohan Pathologic Basis of Disease – Robbins & Cotran Internet