Shock

Shock

1. SHOCK DR. VAMSHIKRISHNA MD (H)

2. Definition: Shock is a life-threatening clinical syndrome of cardiovascular collapse characterized by: AN INADEQUATE PERFUSION OF CELLS AND TISSUES (HYPOPERFUSION). ” AN ACUTE REDUCTION OF EFFECTIVE CIRCULATING BLOOD VOLUME (HYPOTENSION). IF UNCOMPENSATED IMPAIRED CELLULAR METABOLISM AND DEATH

3. Classification according to etiology: Simple etiologic classification of shock syndrome divides it into following 3 major types and a few other variants.

4. HYPOVOLAEMIC SHOCK This form of shock results from inadequate circulatory blood volume by various etiologic factors that may be Either from the loss of red cell mass and plasma due to haemorrhage, or From the loss of plasma volume alone.

5. FORMS OF HYPOVOLAEMIC SHOCK:

6. PATHOGENESIS OF HYPOVOLAEMIC SHOCK: The major effects in this are due to Decreased cardiac output and Low intracardiac pressure. HYPOVOLAEMIA DECREASED VENOUS RETURN DECREASED PRELOAD DECREASED CARDIAC OUTPUT HYPOPERFUSION AND TISSUE HYPOXIA ORGAN DYSFUNCTION MULTIORGAN FAILURE/ DEATH

7. CLINICAL FEATURES The severity of clinical features depends upon degree of blood volume lost; accordingly haemorrhagic shock is divided into 4 types: i ) < 1000 ml: Compensated ii) 1000-1500 ml: Mild iii) 1500-2000 ml: Moderate iv) >2000 ml: Severe

8. Major clinical features are Increased heart rate (Tachycardia), Low blood pressure (Hypotension), Low urinary output ( Oliguria to anuria ) and Alteration in mental state (Agitated to confused to lethargic).

9. CARDIOGENIC SHOCK Acute circulatory failure with sudden fall in cardiac output from acute diseases of the heart without actual reduction of blood volume ( normovolaemia ) is called as CARDIOGENIC SHOCK. Mortality rate is very high in cardiogenic shock if not treated early.

10. Etiology: i ) Deficient emptying e.g . a) Myocardial infarction. b) Cardiomyopathies. c) Rupture of the heart, ventricle or papillary muscle. c) Cardiac arrhythmias. ii) Deficient filling e.g. a) Cardiac tamponade from haemopericardium iii) Obstruction to the outflow e.g. a) Pulmonary embolism b) Ball valve thrombus c) Tension pneumothorax d) Dissecting aortic aneurysm

11. Rupture of papillary muscle

12. Ball valve thrombus Aortic aneurysms

13. Pathophysiology: ORGAN DYSFUNCTION MULTIORGAN FAILURE/ DEATH

14. Cardiogenic shock results from a severe left ventricular dysfunction from various causes such as acute myocardial infarction. The resultant decreased cardiac output has its effects in the form of decreased tissue perfusion and movement of fluid from pulmonary vascular bed into pulmonary interstitial space initially ( interstitial pulmonary oedema) and later into alveolar spaces ( alveolar pulmonary oedema)

15. SEPTIC SHOCK Septic shock  is a serious condition that occurs when a body-wide infection leads to dangerously low blood pressure. Severe bacterial infections or septicaemia induce septic shock. It may be the result of Gram-negative septicaemia ( endotoxic shock) which is more common, or less often from Gram-positive septicaemia ( exotoxic shock).

16. ETIOLOGY: GRAM-NEGATIVE SEPTICAEMIA (ENDOTOXIC SHOCK) e.g. Infection with E. coli, Proteus, Klebsiella , Pseudomonas II) GRAM-POSITIVE SEPTICEMIA (EXOTOXIC SHOCK) e.g. Infection with Streptococci, Pneumococci

17. PATHOGENESIS OF SEPTIC SHOCK Septic shock results most often from Gram-negative bacteria entering the body from genitourinary tract, alimentary tract, respiratory tract or skin, and less often from Gram-positive bacteria. In septic shock, there is immune system activation and severe systemic inflammatory response to infection as follows: i ) Activation of Macrophage-Monocytes ii) Activation of other inflammatory responses

18. I) ACTIVATION OF MACROPHAGE-MONOCYTES: LYSIS OF GRAM-NEGATIVE BACTERIA RELEASE OF ENDOTOXIN, A LIPOPOLYSACCHARIDE (LPS), INTO CIRCULATION IT BINDS TO LIPOPOLYSACCHARIDE BINDING PROTEIN (LBP). THE COMPLEX OF LPS-LBP BINDS TO CD14 MOLECULE ON THE SURFACE OF THE MONOCYTE/MACROPHAGES THEY RELEASE CYTOKINES TNF- α AND IL-1.

19. LIPOPOLYSACCHARIDE (LPS ) LIPOPOLYSACCHARIDE BINDING PROTEIN (LBP) COMPLEX OF LPS-LBP CD14 MOLECULE MACROPHAGE TNF- α AND IL-1 GRAM NEGATIVE BACTERIA TNF- α AND IL-1.

20. CAUSE VASCULAR INJURY.

21. II) ACTIVATION OF OTHER INFLAMMATORY RESPONSES: MICROBIAL INFECTION ACTIVATES OTHER INFLAMMATORY CASCADES A) ACTIVATION OF COMPLEMENT PATHWAY: End-products C5a and C3a induce microemboli and endothelial damage. B) ACTIVATION OF MAST CELLS: Histamine is released which increases capillary permeability. C) ACTIVATION OF COAGULATION SYSTEM: Enhances development of thrombi D) ACTIVATION OF KININ SYSTEM: Released bradykinin causes vasodilatation and increased capillary permeability

22. The net result of above mechanisms is: REDUCED BLOOD FLOW PRODUCES HYPOTENSION, INADEQUATE PERFUSION OF CELLS AND TISSUES, FINALLY LEADING TO ORGAN DYSFUNCTION. VASODILATATION AND INCREASED VASCULAR PERMEABILITY IN SEPTIC SHOCK. PROFOUND PERIPHERAL VASODILATATION AND POOLING OF BLOOD CAUSES HYPERDYNAMIC CIRCULATION IN SEPTIC SHOCK, IN CONTRAST TO HYPOVOLAEMIC AND CARDIOGENIC SHOCK. MULTIORGAN FAILURE/ DEATH

23. ACTIVATION OF COAGULATION SYSTEM: ENHANCES DEVELOPMENT OF THROMBI DIC (DISSEMINATED INTRAVASCULAR COAGULATION)

24. 4. OTHER TYPES i ) Traumatic shock a) Severe injuries b) Surgery with marked blood loss c) Obstetrical trauma ii) Neurogenic shock High cervical spinal cord injury. Accidental high spinal anesthesia. Severe head injury. iii) Hypoadrenal shock Administration of high doses of Glucocorticoids Secondary adrenal insufficiency (e.g. in tuberculosis, metastatic disease, bilateral adrenal haemorrhage, idiopathic adrenal atrophy)

25. STAGES OF SHOCK

26. S hock has been divided arbitrarily into 3 stages.

27. 1. COMPENSATED SHOCK (NON-PROGRESSIVE , INITIAL, REVERSIBLE ) . In the early stage of shock, an attempt is made to maintain adequate cerebral and coronary blood supply by redistribution of blood so that the vital organs ( brain and heart) are adequately perfused and oxygenated. BY ACTIVATION OF VARIOUS NEUROHORMONAL MECHANISMS VITAL ORGANS ARE PERFUSED WIDESPREAD VASOCONSTRICTION B. FLUID CONSERVATION BY THE KIDNEY. C . STIMULATION OF ADRENAL MEDULLA

28. A ) WIDESPREAD VASOCONSTRICTION REDUCED BLOOD FLOW (HYPOTENSION) AND TISSUE ANOXIA ACTIVATION OF BARORECEPTORS, CHEMORECEPTORS, CATECHOLAMINES, RENIN, AND ANGIOTENSIN-II VASOCONSTRICTION OF VESSELS OF THE SKIN AND ABDOMINAL VISCERA INCREASED PERIPHERAL RESISTANCE, INCREASED HEART RATE (TACHYCARDIA) AND INCREASED BLOOD PRESSURE (COOL AND PALE SKIN) NOTE: IN SEPTIC SHOCK, THERE IS INITIAL VASODILATATION FOLLOWED BY VASOCONSTRICTION VITAL ORGANS ARE PERFUSED

29. B) FLUID CONSERVATION BY THE KIDNEY REDUCED BLOOD FLOW (HYPOTENSION) a. Release of ALDOSTERONE (by activation of RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM.) b. Release of ADH c. Reduced Glomerular F iltration Rate ( GFR) due to arteriolar constriction. d. Shifting of tissue fluids into the plasma due to lowered capillary hydrostatic pressure (hypotension). Na+, WATER RETENTION, STABILISES BLOOD PRESSURE RENAL REABSORPTION OF WATER DECREASED URINE PRODUCTION INCREASED PLASMA VOLUME

30. C) STIMULATION OF ADRENAL MEDULLA LOW CARDIAC OUTPUT STIMULATION OF ADRENAL MEDULLA RELEASE OF CATECHOLAMINES (EPINEPHRINE AND NON EPINEPHRINE) INCREASED HEART RATE (TACHYCARDIA) INCREASED CARDIAC OUTPUT.

31. **** AT THIS STAGE NORMAL COMPENSATORY MECHANISMS EVENTUALLY CAUSE FULL RECOVERY WITHOUT HELP FROM OUTSIDE THERAPY.

32. 2. PROGRESSIVE DECOMPENSATED SHOCK With compensated shock, the body is able to take measures to maintain blood pressure, however as shock worsens, the body becomes unable to keep up. At this point, perfusion of vital organs is no longer maintained.  THIS IS AGGRAVATED BY PRE-EXISTING CARDIOVASCULAR AND LUNG DISEASE

33. E FFECTS I) PULMONARY HYPOPERFUSION II) TISSUE ISCHAEMIA TACHYPNOEA ADULT RESPIRATORY DISTRESS SYNDROME (ARDS). Impaired tissue perfusion causes switch from aerobic to anaerobic glycolysis resulting in metabolic lactic acidosis. ISCHAEMIA

34. *** CLINICALLY, AT THIS STAGE THE PATIENT DEVELOPS CONFUSION AND WORSENING OF RENAL FUNCTION .

35. 3. IRREVERSIBLE DECOMPENSATED SHOCK IF NO RECOVERY TAKES PLACE (due to widespread cell injury) INSPITE OF COMPENSATORY MECHANISMS, THERAPY AND CONTROL OF ETIOLOGIC AGENT DECOMPENSATED OR IRREVERSIBLE SHOCK IT LEADS TO

36. CAUSES FOR DECOMPENSATED OR IRREVERSIBLE SHOCK. I) PROGRESSIVE VASODILATATION II) INCREASED VASCULAR PERMEABILITY III) MYOCARDIAL DEPRESSANT FACTOR (MDF) IV) WORSENING PULMONARY HYPOPERFUSION V) ANOXIC DAMAGE TO HEART, KIDNEY AND BRAIN VI) HYPERCOAGULABILITY OF BLOOD DUE TO ANOXIA WHICH DAMAGES THE CAPILLARY AND VENULAR WALL ANOXIC TISSUES RELEASES PROINFLAMMATORY MEDIATORS WHICH CAUSE INCREASED VASCULAR PERMEABILITY IT IS RELEASED DUE TO REDUCED BLOOD FLOW TO MYOCARDIUM WHICH RESULTS IN FURTHER DEPRESSION OF CARDIAC FUNCTION ATP DEPLETION CAUSES LACTIC ACIDOSIS LEADING ISCHAEMIC CELL DEATH TISSUE DAMAGE IN SHOCK ACTIVATES COAGULATION CASCADE LEADING TO MICROTHROMBI FORMATION