Cardiovascular or circulatory shock refers to an acute condition where there is a generalized inadequacy of blood flow throughout the body. The patient appears pale, grey or cyanotic, with cold clammy skin, a weak rapid pulse and rapid shallow breathing. Urine output is reduced and blood pressure (BP) is generally low. Conscious patients may develop intense thirst. Cardiovascular shock may be caused by a reduced blood volume (hypovolaemic shock), profound vasodilatation (low-resistance shock), acute failure of the heart to maintain output (cardiogenic shock) or blockage of the cardiopulmonary circuit (e.g. pulmonary embolism).

Haemorrhagic Shock

Blood loss (haemorrhage) is the most common cause of hypovolaemic shock. Loss of up to ∼20% of total blood volume is unlikely to elicit shock in a fit person. If 20–30% of blood volume is lost, shock is normally induced and blood pressure may be depressed, although death is not common. Loss of 30–50% of volume, however, causes a profound reduction in BP and cardiac output (Figure 31a), with severe shock which may become irreversible or refractory (see below). Severity is related to amount and rate of blood loss – a very rapid loss of 30% can be fatal, whereas 50% over 24 h may be survived. Above 50% death is generally inevitable.

Immediate Compensation

The initial fall in BP is detected by the baroreceptors, and reduced blood flow activates peripheral chemoreceptors. These cause a reflex increase in sympathetic and decrease in parasympathetic drive, with a subsequent increase in heart rate, venoconstriction (which restores central venous pressure, CVP) and vasoconstriction of the splanchnic, cutaneous, renal and skeletal muscle circulations which helps restore BP. Vasoconstriction leads to pallor, reduced urine production and lactic acidosis. Increased sympathetic discharge also results in sweating, and characteristic clammy skin. Sympathetic vasoconstriction of the renal artery plus reduced renal artery pressure stimulates the renin–angiotensin system (see Chapter 29), and production of angiotensin II, a powerful vasoconstrictor. This has an important role in the recovery of BP and stimulates thirst. In more severe blood loss, reduction in atrial stretch receptor output stimulates production of vasopressin (antidiuretic hormone, ADH

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