In general terms shock is a clinical state in which target organ–tissue perfusion is inadequate to supply vital sub¬strates and remove the metabolic waste. Inadequate cellular oxygenation leads to marked generalized impairment of cellular function and multiorgan failure.
The heart tries to contract more vigorously in the face of this catastrophic event; the renin–angiotensin–aldosterone system is activated and causes severe vasoconstriction in an attempt to increase blood pressure (see Fig. 1 in the chapter Angiotensin-Converting Enzyme Inhibitors/ Angiotensin Receptor Blockers), but over time the hyper-contractility of the heart ceases. This occurs because there is utilization of glucose over fatty acids, loss of Krebs cycle intermediates, and depletion of substrate required for ATP production.
Figure 1 illustrates the pathophysiology of shock. Because forward flow of blood is severely retarded, blood returned to the heart from veins of the body and from the lungs cannot be accommodated in a heart that is already full of blood. Blood then backs up into the venous circulation of the neck and in the lungs. This pressure of blood returning to the heart is referred to as an increased filling pressure (Fig. 1). It is easy to visualize that the shock state may occur if there is no filling pressure as would occur in severe dehydration or severe blood loss (i.e., the tank has no gas).

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