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540 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

tissues while other areas receive more blood flow than
TABLE 20.1 Shock types 5 needed, 4,7,10,13,14 is often referred to as distributive shock,
and is typical of the shock types that affect vasomotor
Shock type Main characteristic tone (e.g. septic, neurogenic and anaphylactic shock).
This maldistribution may leave some organ systems isch-
Hypovolaemic a reduction in circulating blood volume
through haemorrhage or dehydration aemic for long periods leading to persistent organ dys-
6
or plasma fluid loss function and failure. There is also evidence supporting
the presence of cytopathic hypoxia as a result of excessive
Cardiogenic pump failure (impaired cardiac
contractility) usually as result of nitric oxide and tumour necrosis factor-alpha (TNFα)
myocardial infarction production (cellular proinflammatory mediators), where
● obstructive a sub category of cardiogenic shock there is impaired mitochondrial (the powerhouse of the
shock characterised by blockage of cell) oxygen utilisation which leads to depleted stores of
circulation to the tissues by impedance adenosine tri-phosphate (ATP) 4,11,13,15,16 and interferes
of outflow or filling in the heart (e.g. 16
due to cardiac tamponade or with electron transport and metabolism (see Chapter
pulmonary emboli) 19). Nitric oxide is associated with vascular relaxation
and is a major contributor to alterations in microvascu-
Distributive shock a maldistribution of circulation from 17
sepsis, anaphylaxis or neurogenic injury lature and capillary leak in sepsis.
Organ systems have varying responses in shock and are
not measured directly. Often surrogate markers of global
of hormones such as antidiuretic hormone [ADH] and hypoperfusion are used to indicate the severity of
adrenocorticoid trophic hormone [ACTH] to target organs shock. 18–19 Lactate and acid–base disturbances, such as an
such as the kidney) and the cortex of the adrenal gland increase in strong ion gap, have been suggested as early
to respond and counter the developing effects of shock. markers of mitochondrial dysfunction and cellular hypo-
Concurrently direct feedback stimulates the sympathetic perfusion. 8,20 These ‘surrogate’ biochemical markers of
nervous system to act on blood vessel tone, particularly hypoperfusion (pH, serum lactate and standard base
the arterioles, and also target organs such as the adrenal excess) assess acidaemia and provide some insight into
gland and kidney to respond via the release of endoge- the degree of shock present. Lactate, a strong anion with
21
nous catecholamines (adrenaline and noradrenaline), normal production of 1500–4500 mmol/day, is a product
mineral and glucocorticoids (aldosterone, cortisol), and of carbohydrate metabolism. Increased levels are present
the renin–angiotensin–aldosterone system (RAAS). RAAS in tissue hypoxia, hypermetabolism, decreased lactate
activation results in synthesis of angiotensin II, a power- clearance, inhibition of pyruvate dehydrogenase and acti-
ful vasoconstrictor that further potentiates the reduction vation of inflammatory cells; all characteristics of devel-
in peripheral blood vessel capacity. oping shock (see Table 20.2). Increased lactate production
Collectively, these responses form a sympatho– is a warning sign of impending organ failure, as it is
endocrine–adrenal–axis that moderates the systemic indicative of anaerobic metabolism. Blood lactate levels
response to shock. The axis maintains circulation to the have been directly linked to deteriorating patient out-
vital organ system and combines with the inflammatory comes in shock. 21,22
response to limit local and systemic tissue damage and As the shock state deteriorates and the body fails to com-
ultimately confer a survival advantage. Combined pensate, organ systems begin to fail. This is complicated
responses include profound vasoconstriction, oligo- by a systemic inflammatory response (SIRS) which can
anuria (fluid retention), redirection of blood flow to vital be a direct cause of the shock state (see section on Dis-
organs, hyperglycaemia, immunomodulation and proco- tributive shock) or develop as a consequence of protracted
agulation. This universal response to impending shock shock. This results in ‘capillary leak’ or increased micro-
is particularly effective in compensating for loss of vascular permeability which leads to interstitial oedema
circulating blood volume, but may be counterproductive as a consequence of alterations to tissue endothelium.
when pump failure occurs or ‘uncoupled’ in distributive Many immune mediators including circulating cytokines,
shock states. oxygen free-radicals and activated neutrophils alter the
As adaptive responses fail, cardiac output becomes insuf- structure of the endothelial cells, creating space to allow
ficient to provide adequate organ perfusion despite larger intravascular molecules to cross into the extravas-
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increasing tissue oxygen consumption (see Chapters 9 cular space, with proteins and water moving from the
24
and 10). When oxygen is ‘supply dependent’, oxygen intravascular space into the interstitium. This response
delivery is decreased and, to compensate, increased mechanism improves the supply of nutrient-rich fluid to
extraction occurs to enable continued tissue consump- the site of local injury, however, systemically, fluid shifts
tion. However, when oxygen delivery falls below a critical lead to hypovolaemia, impaired organ function and
threshold, and extraction demand rises above the avail- development of acute organ injury such as acute lung
24
able blood oxygen levels, this compensation mechanism injury (ALI) and acute kidney injury (AKI). This devel-
fails and oxygen debt results. 6,11,12 oping organ injury is the precedent to organ failure (more
fully described in Chapter 21).
Hypoperfusion may also exist despite a relatively normal
cardiac output, and may not be immediately evident The next sections describe the general assessment and
6
clinically. This maldistribution of bloodflow to some management of shock, different classifications of shock