Compensated shock Progressive decompensated shock Irreversible decompensated shock Pathophysiology 1 Compensated nonprogressive initial reversible shock In the early stage of shock an attempt is made to maintain adequate cerebral and coronary blood supply by ID: 997803
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1. Stages of shock
2. Stages of shockCompensated shockProgressive decompensated shockIrreversible decompensated shock
3. Pathophysiology1. 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: Activation of various neurohormonal mechanisms causing widespread vasoconstriction.Fluid conservation by the kidney.Condition causing shock is treated adequately and normal circulation is re-established by the compensatory mechanism- Compensated or reversible shock
4. Hypotension and tissue anoxiaActivation of neural and humoral factors e.g. baroreceptors, chemoreceptors, catecholamines, renin, and angiotensin-II, ADHWidespread vasoconstriction (Skin and abd viscera)Peripheral resistense & heart rateBlood pressure
5. septic shockInitial – vasodilatation followed by vasoconstriction In severe septic shock- elevated level of thromboxone A2 (potent vasoconstrictor) augment the cardiac output along with other sympathetic mechanism.Effects in compensated shock - 1.Cold and clammy skin in initial stage- cutaneous vasoconstriction2. Tachycardia
6. ii) Fluid conservation by kidneyRelease of Aldosterone by the hypoxic kidney by activation of RAAS.Release of ADH due to decreased effective circulating blood volumeReduced GFR due to arteriolar constrictionShifting of tissue fluid into the plasma due to lowered capillary hydrostatic pressureiii) Stimulation of adrenal medulla In response to low CO adrenal medulla is stimulated to release excess of catecholamines which inc. heart rate and try to increase CO.
7. 2. Progressive decompensated shockIf 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 glycolysisExcessive production of lactic acidMetabolic lactic acidosis tissue pHIneffective vasomotor responseVasodilation & peripheral pooling of blood
8. 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
9. 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 vasodilatationAnoxia 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.
10. 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 factorProgressive 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.
11. 4. Worsening pulmonary hypoperfusionFurther pulmonary hypoperfusion causes respiratory distress due to pulmonary oedema, tachypnoea and ARDS.5. Anoxic damage to heart, kidney and brainProgressive 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.
12. 6. Hypercoagulability of bloodTissue 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.
13. Mechanisms and effects of three stages of shock