Page 589 - ACCCN's Critical Care Nursing

566 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

Infection
(Bacterial, Inflammation Endothelial
viral, fungal, Coagulation Dysfunction Hypoperfusion Acute
Organ
or parasitic and Ischaemia Dysfunction
infection/ Fibrinolysis Microvascular
endotoxin) Thrombosis

FIGURE 21.3 Progression of SIRS-Sepsis-Shock-
MODS (Courtesy Eli Lilly and Company).

TABLE 21.1 Actions of the stress response 38

Response stage Neurohormonal response Actions
Alarm reaction Hypothalamus ● Impulses to sympathetic nervous system and adrenal medulla
Noradrenaline/adrenaline ● α-Adrenergic receptors: vasoconstriction or arterial wall smooth muscle
and viscera; rise in heart rate and contractility
● Increased hepatic glucose production
● β 2 -Adrenergic receptors: vasodilation to lungs and skeletal muscles
Resistance reaction Anterior pituitary/ ● Secretes adrenocorticotrophic hormone (ACTH)
corticotrophin-releasing factor
Anterior pituitary/thyroid-stimulating ● Stimulates T3 and T4 production, increasing use of glucose for adenosine
hormone (TSH) triphosphate (ATP) production
Human growth hormone (hGH) ● Increase in protein synthesis
● Increased mobilisation of fatty acids from adipose tissue for energy use
● Decreased rate of glucose utilisation
● Excessive secretion may result in ketosis and insulin resistance
ACTH ● Cortisol secretion by adrenal cortex
Kidney/renin release ● Angiotensin–aldosterone secretion
Angiotensin II ● Intense vasoconstriction of arterioles, renal retention of sodium and water,
with increased total peripheral resistance and arterial blood pressure
Aldosterone ● Sodium reabsorption and water retention with an increase in intravascular
volume, cardiac output and blood pressure
Exhaustion ● Progressive loss of homeostasis
● Cellular dysfunction

● reduces thrombin production when activated via sympathetic–adrenal–medullary axis, results in ongoing
thrombin–thrombomodulin complexes (anticoagu- production of glucocorticoid hormones and catechol-
17
lant action) amines. This response interferes with the regulation of
● inhibits thrombin-activatable fibrinolysis inhibitor cytokine-producing immune cells, leading to immune
and plasminogen activator inhibitor-1 (profibrino- dysfunction. Other compensatory mechanisms are insti-
lytic action). 33,34 gated in an attempt to maintain supply and perfusion to
organs. 15
APC is consumed in severe sepsis, and thrombomodulin
is unable to activate protein C, 33,34,37 promoting a pro- These homeostatic mechanisms are activated through
inflammatory, prothrombotic state. 34 positive or negative feedback systems to counteract stress.
When stress is extreme or prolonged, these normal
ENDOCRINE RESPONSE homeostatic mechanisms may be insufficient and a
Physiological changes are triggered as a normal patient may respond through a sequence of physiological
response to a stressor. In a critically ill patient, however, changes called the stress response. The stress response
chronic activation of the stress response, including occurs in three stages: the alarm reaction, the resistance
the hypothalamic–pituitary–adrenal axis and the reaction and exhaustion (see Table 21.1). 38