Stages of shock Stages of shock 1 Compensated

Stages of shock

Stages of shock 1) Compensated shock 2) Progressive decompensated shock 3) Irreversible decompensated shock

PATHOPHYSIOLOGY 1. COMPENSATED (NON-PROGRESSIVE, INITIAL, REVERSIBLE) SHOCK: IN THE EARLY STAGE OF SHOCK, AN ATTEMPT IS MADE TO MAINTAIN ADEQUATE CEREBRAL AND CORONARY BLOOD SUPPLY BY: a) ACTIVATION OF VARIOUS NEUROHORMONAL MECHANISMS CAUSING WIDESPREAD VASOCONSTRICTION. b) FLUID CONSERVATION BY THE KIDNEY. Condition causing shock is treated adequately and normal circulation is reestablished by the compensatory mechanism- Compensated or reversible shock

HYPOTENSION AND TISSUE ANOXIA ACTIVATION OF NEURAL AND HUMORAL FACTORS E. G. BARORECEPTORS, CHEMORECEPTORS, CATECHOLAMINES, RENIN, AND ANGIOTENSIN-II, ADH WIDESPREAD VASOCONSTRICTION (SKIN AND ABD VISCERA) áPERIPHERAL RESISTENSE & HEART RATE á BLOOD PRESSURE

SEPTIC SHOCK • INITIAL – VASODILATATION FOLLOWED BY VASOCONSTRICTION • IN SEVERE SEPTIC SHOCK- ELEVATED LEVEL OF THROMBOXONE A 2 (POTENT VASOCONSTRICTOR) AUGMENT THE CARDIAC OUTPUT ALONG WITH OTHER SYMPATHETIC MECHANISM. Effects in compensated shock 1. Cold and clammy skin in initial stage- cutaneous vasoconstriction 2. Tachycardia

II) FLUID CONSERVATION BY KIDNEY q. RELEASE OF ALDOSTERONE BY THE HYPOXIC KIDNEY BY ACTIVATION OF RAAS. q. RELEASE OF ADH DUE TO DECREASED EFFECTIVE CIRCULATING BLOOD VOLUME q. REDUCED GFR DUE TO ARTERIOLAR CONSTRICTION q. SHIFTING OF TISSUE FLUID INTO THE PLASMA DUE TO LOWERED CAPILLARY HYDROSTATIC PRESSURE III) STIMULATION OF ADRENAL MEDULLA q IN RESPONSE TO LOW CO ADRENAL MEDULLA IS STIMULATED TO RELEASE EXCESS OF CATECHOLAMINES WHICH INC. HEART RATE AND TRY TO INCREASE CO.

2. Progressive decompensated shock If the underlying causes are not corrected, shock passes to the progressive phase, during which there is widespread tissue hypoxia. (shock+ stress/risk factors) 1. Tissue ischaemia Anaerobic glycolysis Excessive production of lactic acid Metabolic lactic acidosis tissue p. H Ineffective vasomotor response Vasodilation & peripheral pooling of blood

2. PULMONARY HYPOPERFUSION DECOMPENSATED SHOCK –WORSENS THE PUL. PERFUSION AND INC. VAS. PERMEABILITY-TACHYPNOEA AND ARDS. Effects in progressive decompensated shock – § decreased CO § Mental confusion § tachypnoea §Decreased urinary output

3. IRREVERSIBLE DECOMPENSATED SHOCK: WHEN THE SHOCK IS SO SEVERE THAT IN SPITE OF COMPENSATORY MECHANISMS AND DESPITE THERAPY AND CONTROL OF ETIOLOGIC AGENT, NO RECOVERY TAKES PLACE, IT IS CALLED DECOMPENSATED OR IRREVERSIBLE SHOCK. EFFECTS 1. PROGRESSIVE VASODILATATION ANOXIA DAMAGES CAPILLARY AND VENULAR WALL WHILE ARTERIOLES BECOME UNRESPONSIVE TO VASOCONSTRICTIONS AND BEGIN TO DILATE. VASODILATATION RESULTS IN PERIPHERAL POOLING OF BLOOD WHICH FURTHER DETERIORATES THE EFFECTIVE CIRCULATING BLOOD VOLUME.

2. INCREASED VASCULAR PERMEABILITY- ANOXIA DAMAGE TO TISSUE RELEASE PROINFLAMMATORY MEDIATORS WHICH CAUSE INCREASED VASCULAR PERMEABILITY. THIS RESULTS IN ESCAPE OF FLUID FROM CIRCULATION INTO INTERSTITIAL TISSUE THUS DETERIORATING THE EFFECTIVE CIRCULATING BLOOD VOLUME. 3. MYOCARDIAL DEPRESSANT FACTOR PROGRESSIVE FALL IN BP AND PERSISTENTLY REDUCED BLOOD FLOW TO MYOCARDIUM CAUSES CORONARY INSUFFICIENCY AND MYOCARDIAL ISCHAEMIA DUE TO RELEASE OF MYOCARDIAL DEPRESSANT FACTOR. THIS RESULTS IN FURTHER DEPRESSION OF CARDIAC FUNCTION, REDUCED C. O. AND DECREASED BLOOD FLOW.

4. WORSENING PULMONARY HYPOPERFUSION FURTHER PULMONARY HYPOPERFUSION CAUSES RESPIRATORY DISTRESS DUE TO PULMONARY OEDEMA, TACHYPNOEA AND ARDS. 5. ANOXIC DAMAGE TO HEART, KIDNEY AND BRAIN PROGRESSIVE TISSUE ANOXIA CAUSES SEVERE METABOLIC ACIDOSIS DUE TO ANAEROBIC GLYCOLYSIS. THERE IS RELEASE OF PROINFLAMMATORY CYTOKINES AND OTHER INFLAMMATORY MEDIATORS AND GENERATION OF FREE RADICALS. SINCE HIGHLY SPECIALIZED CELLS OF MYOCARDIUM, PROXIMAL TUBULAR CELLS OF KIDNEY AND NEURONS OF CNS ARE DEPENDENT SOLELY ON AEROBIC RESPIRATION FOR ATP GENERATION, THERE IS ISCHAEMIC CELL DEATH IN THESE TISSUE.

6. HYPERCOAGULABILITY OF BLOOD TISSUE DAMAGE IN SHOCK ACTIVATES COAGULATION CASCADE WITH RELEASE OF CLOT PROMOTING FACTOR, THROMBOPLASTIN AND RELEASE OF PLATELET AGGREGATOR, ADP, WHICH CONTRIBUTE TO SLOWING OF BLOOD STREAM AND VASCULAR THROMBOSIS. IN THIS WAY HYPERCOAGULABILITY OF BLOOD WITH CONSEQENT MICRO THROMBI IMPAIR THE BLOOD FLOW AND CAUSE FURTHER TISSUE NECROSIS. CLINICALLY AT THIS STAGE THE PT. HAS FEATURES OF COMA, WORSENED HEART FUNCTION AND PROGRESSIVE RENAL FAILURE DUE TO ACUTE TUBULAR NECROSIS.

MECHANISMS AND EFFECTS OF THREE STAGES OF SHOCK