Shock PDF

Shock  INTRODUCTION Shock is hypoperfusion to tssues The end results are: 1. hypotension, 2. impaired tssue perfusion 3. cellular hypoxia.  Although the hypoxic and metabolic efects of hypoperfusion initally cause only reversible cellular injury, persistence of shock eventually cause...

Shock  INTRODUCTION Shock is hypoperfusion to tssues The end results are: 1. hypotension, 2. impaired tssue perfusion 3. cellular hypoxia.  Although the hypoxic and metabolic efects of hypoperfusion initally cause only reversible cellular injury, persistence of shock eventually causes irreversible tssue injury and can culminate in the death of the patent  TYPES OF SHOCK: 1. Cardiogenic 2. Hypovolemic 3. Septc Type of Shock Clinical Examples Principal Mechanisms Cardiogenic Myocardial infarcton Failure of myocardial pump resultng Ventricular rupture from intrinsic myocardial damage, Arrhythmia extrinsic pressure, or obstructon to Cardiac tamponade outflow Pulmonary embolism Hypovolemic Hemorrhage Inadequate blood or plasma volume Fluid loss (e.g., vomitng, diarrhea, burns, or trauma) Septc Overwhelming microbial infectons Peripheral vasodilaton and pooling of Endotoxic shock blood; endothelial actvaton/injury; Gram-positve septcemia leukocyte-induced damage; Fungal sepsis disseminated intravascular Superantgens (e.g. toxic shock coagulaton; actvaton of cytokine syndrome) cascades  Other types of shock Less common, (neurogenic shock), may occur as a result of loss of vascular tone and peripheral pooling of blood. Occurs in 1. anesthetc accident 2. or a spinal cord injury  Anaphylactc shock represents systemic vasodilaton and increased vascular permeability caused by an immunoglobulin E hypersensitvity reacton  Pathogenesis of Septc Shock  25% to 50% mortality rate, Most cases of septc shock are caused by endotoxin-producing gram-negatve bacilli hence the term endotoxic shock. Endotoxins are bacterial wall lipopolysaccharides (LPS)  Free LPS ataches to a circulatng LPS- binding protein, the complex then binds to a specifc receptor (CD14) on monocytes, macrophages, and neutrophils. results in profound actvaton and producton of potent cytokines such as IL-1 and TNF  Both TNF and IL-1 act on endothelial cells (and other cell types) to produce additonal cytokines (e.g., IL-6 and IL-8) and induce adhesion molecules  cytokine now at high levels, result in 1. Systemic vasodilaton (hypotension) 2. Diminished myocardial contractlity 3. Widespread endothelial injury and actvaton, causing systemic leukocyte adhesion and difuse alveolar capillary damage in the lung 4. Actvaton of the coagulaton system, culminatng in disseminated intravascular coagulaton (DIC)  The hypoperfusion resultng from the combined efects of widespread vasodilaton, myocardial pump failure, and DIC causes multorgan system failure that afects the liver, kidneys, and central nervous system, others  Unless the underlying infecton (and LPS overload) is rapidly brought under control, the patent usually dies. Sudan airways Stages of Shock  Shock is a progressive disorder that if uncorrected leads to death.  An inital nonprogressive stage during which refex compensatory mechanisms are actvated and perfusion of vital organs is maintained  A progressive stage characterized by tssue hypoperfusion and onset of worsening circulatory and metabolic imbalances  An irreversible stage that sets in afer the body has incurred cellular and tssue injury so severe that even if the hemodynamic defects are corrected, survival is not possible In the early, nonprogressive phase of shock, various neurohumoral mechanisms help maintain cardiac output and blood pressure. These include baroreceptor refexes, release of catecholamines, actvaton of the renin-angiotensin axis, antdiuretc hormone release, and generalized sympathetc stmulaton. The net efect is tachycardia, peripheral vasoconstricton, and renal conservaton of fuid.).  Cutaneous vasoconstricton is responsible for the characteristc coolness and pallor of skin in shock although septc shock may initally cause cutaneous vasodilaton and thus present with warm, fushed skin  In the progressive stage of shock, If the underlying causes are not corrected, shock passes imperceptbly to the progressive phase, during which there is widespread tssue hypoxia. In the setng of persistent oxygen defcit, intracellular aerobic respiraton is replaced by anaerobic glycolysis, with excessive producton of lactc acid  The resultant metabolic lactc acidosis lowers the tssue pH and blunts the vasomotor response; arterioles dilate, and blood begins to pool in the microcirculaton.  Peripheral pooling not only worsens the cardiac output but also puts endothelial cells at risk of developing anoxic injury with subsequent DIC. With widespread tssue hypoxia, vital organs are afected and begin to fail. In the irreversible stage of shock, Unless there is interventon, the process eventually enters an irreversible stage. Widespread cell injury is refected in : lysosomal enzyme leakage, further aggravatng the shock state. Myocardial contractle functon worsens, in part because of nitric oxide synthesis.  If ischemic bowel allows intestnal fora to enter the circulaton, endotoxic shock may also be superimposed. complete renal shutdown due to ischemic acute tubular necrosis death. Morphology  The cellular and tssue changes induced by shock are essentally those of hypoxic injury due to some combinaton of hypoperfusion and microvascular thrombosis. shock is characterized by failure of many organ systems, the cellular changes may appear in any tssue. they are partcularly evident in 1. the brain, 2. heart, 3. kidneys, 4. adrenal glands, 5. and gastrointestnal tract. Fibrin thrombi may be identfed in virtually any tssue, although they are usually most readily visualized in kidney glomeruli.  The kidneys typically reveal acute tubular necrosis oliguria, anuria, and electrolyte disturbances  The gastrointestnal tract may mainfest focal mucosal hemorrhage and necrosis..  The lungs are rarely afected in pure hypovolemic shock, because they are somewhat resistant to hypoxic injury. However, when shock is caused by bacterial sepsis or trauma, changes of difuse alveolar damage may develop, the so-called shock lung. Clinical Course  In hypovolemic and cardiogenic shock, the patent presents with: hypotension; a weak, rapid pulse; tachypnea; and cool, clammy, cyanotc skin. In septc shock, however, the skin may be warm and fushed as a result of peripheral vasodilaton.