An irreversible stage in which cellular and tissue injury is 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 mechanisms include baroreceptor reflexes, release of catecholamines and anti-diuretic hormone, activation of the renin-angiotensin-aldersterone axis, and generalized sympathetic stimulation. The net effect is tachycardia, peripheral vasoconstriction, and renal fluid conservation; cutaneous vasoconstriction causes the characteristic “shocky” skin coolness and pallor (notably, septic shock can initially cause cutaneous vasodilation, so the patient may present with warm, flushed skin). Coronary and cerebral vessels are less sensitive to sympathetic signals and maintain relatively normal caliber, blood flow, and oxygen delivery. Thus, blood is shunted away from the skin to the vital organs such as the heart and the brain.
If the underlying causes are not corrected, shock passes imperceptibly to the progressive phase, which as noted is characterized by widespread tissue hypoxia. In the setting of persistent oxygen deficit, intracellular aerobic respiration is replaced by anaerobic glycolysis with excessive production of lactic acid. The resultant metabolic lactic acidosis lowers the tissue pH, which blunts the vasomotor response; arterioles dilate, and blood begins to pool in the microcirculation. Peripheral pooling not only worsens the cardiac output but also puts endothelial cells at risk for the development of anoxic injury with subsequent DIC. With widespread tissue hypoxia, vital organs are affected and begin to fail.
In the absence of appropriate intervention, or in severe cases, the process eventually enters an irreversible stage. Widespread cell injury is reflected in lysosomal enzyme leakage, further aggravating the shock state. Myocardial contractile function worsens, in part because of increased NO synthesis. The ischemic bowel may allow intestinal flora to enter the circulation, and thus bacteremic shock may be superimposed. Commonly, further progression to renal failure occurs as a consequence of ischemic injury of the kidney (Chapter 14), and despite the best therapeutic interventions, the downward spiral frequently culminates in death.
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MORPHOLOGYThecellularandtissueeffectsofshockareessentiallythoseofhypoxicinjury(Chapter2)andarecausedbyacombinationofhypoperfusion andmicrovascular thrombosis. Althoughanyorgancanbeaffected,thebrain,heart,kidneys,adrenals,andgastrointestinaltractaremostcommonlyinvolved.Fibrin thrombi canforminanytissuebuttypicallyaremostreadilyvisualizedinkidneyglomeruli.Adrenal cortical cell lipid depletion isakintothatseeninallformsofstressandreflectsincreaseduseofstoredlipidsforsteroidsynthesis.Whereasthelungsareresistanttohypoxicinjuryinhypovolemicshockoccurringafterhemorrhage,sepsisortraumacanprecipitatediffusealveolardamage(Chapter13),leadingtoso-called“shock lung.” Exceptforneuronalandcardiomyocyteloss,affectedtissuescanrecovercompletelyifthepatientsurvives.