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Shock and Haemorrhage


Shock and Haemorrhage
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).


Shock and Haemorrhage

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) and adrenal production of adrenaline, both of which contribute to vasoconstriction. These initial mechanisms may prevent any significant fall in BP or cardiac output following moderate blood loss, even though the degree of shock may be serious. If BP falls below 50 mmHg the CNS ischaemic response is activated, with powerful sympathetic activation (Figure 31a).

Medium and long-term Mechanisms
The vasoconstriction and/or fall in BP decreases capillary hydro- static pressure, resulting in fluid movement from the interstitium back into the vasculature (see Chapter 21). This ‘internal transfusion’ may increase blood volume by 0.5 L and takes hours to develop. Increased glucose production by the liver may contribute by raising plasma and interstitial fluid osmolarity, thus drawing water from intracellular compartments. This process results in haemodilution, and patients with severe shock often present with a reduced haematocrit. Fluid volume is brought back to normal over days by increased fluid intake (thirst), decreased urine production (oliguria) due to renal vasoconstriction, increased Na+ reabsorption caused by the production of aldosterone (stimulated by angiotensin II) and a fall in atrial natriuretic peptide (ANP), and increased water reabsorption caused by vasopressin (Figure 31b). The liver replaces plasma proteins within a week, and haematocrit returns to normal within 6 weeks due to stimulation of erythropoiesis (Figure 31b; see Chapter 6).
Other responses to haemorrhage are increased ventilation due to reduced flow through chemoreceptors (carotid body) and/or acidosis; decreased blood coagulation time due to an increase in platelets and fibrinogen that occurs within minutes (see Chapter 7); and increased white cell (neutrophil) count after 2–5 h.
Complications and irreversible (refractory) shock
When blood loss exceeds 30%, cardiac output may temporarily improve before continuing to decline (progressive shock; Figure 31c). This is due to a vicious circle initiated by circulatory failure and tissue hypoxia/ischaemia, leading to acidosis, toxin release and eventually multiorgan failure, including depression of cardiac muscle function, acute respiratory distress syndrome (ARDS), renal failure, disseminated intravascular coagulation (DIC), hepatic failure and damage to intestinal mucosa. Increased vascular permeability further decreases blood volume due to fluid loss into the tissues, and vascular tone is depressed. These complications lead to further tissue damage, impairment of tissue perfusion and gas exchange (Figure 31d). Rapid treatment (e.g. transfusion) is essential; after 1 h (‘the golden hour’) mortality increases sharply if the patient is still in shock, as transfusion and vasoconstrictor drugs may then cause only a temporary respite before cardiac output falls irrevocably. This is called irreversible or refractory shock (Figure 31c), and is primarily related to irretrievable damage to the heart.

Other types of hypovolaemic shock
Severe burns result in a loss of plasma in exudate from damaged tissue. As red cells are not lost, there is haemoconcentration, which will increase blood viscosity. Treatment of burns-related shock therefore involves infusion of plasma rather than whole blood. Traumatic and surgical shock can occur after major injury or surgery. Although this is partly due to external blood loss, blood and plasma can also be lost into the tissues, and there may be dehydration. Other conditions include severe diarrhoea or vomiting and loss of Na+ (e.g. cholera) with a consequent reduction in blood volume even if water is given, unless electrolytes are replenished.

Low resistance shock
Unlike in hypovolaemic shock, patients with low-resistance shock may present with warm skin due to profound peripheral vasodilatation.
Septic shock is caused by a profound vasodilatation due to endotoxins released by infecting bacteria, partly via induction of inducible nitric oxide synthase (see Chapter 24). Capillary permeability and cardiac function may be impaired, with consequent loss of fluid to the tissues and depressed cardiac output.
Anaphylactic shock is a rapidly developing and life-threatening condition resulting from presentation of antigen to a sensitized individual (e.g. bee stings or peanut allergy). A severe allergic reaction may result, with release of large amounts of histamine. This causes profound vasodilatation, and increased microvasculature permeability, leading to protein and fluid loss to tissues (oedema). Rapid treatment with antihistamines and glucocorticoids is necessary, but immediate application of a vasoconstrictor (adrenaline) may be required to save the patient’s life.