SYSTEMIC RESPONSES TO PAIN
Acute pain is typically associated with a neuroendo-crine stress response that is proportional to pain intensity. The pain pathways mediating the afferent limb of this response are discussed above. The efferent limb is mediated by the sympathetic nervous and endocrine systems. Sympathetic activation increases efferent sympathetic tone to all viscera and releases catecholamines from the adrenal medulla. The hormonal response results from increased sym-pathetic tone and from hypothalamically mediatedreflexes. Moderate to severe acute pain, regard-less of site, can affect the function of nearlyevery organ and may adversely affect perioperative morbidity and mortality.
Cardiovascular effects are often prominent and include hypertension,
tachycardia, enhanced myo-cardial irritability, and increased systemic vascular
resistance. Cardiac output increases in most normal patients but may decrease
in patients with compro-mised ventricular function. Because of the increase in
myocardial oxygen demand, pain can worsen or precipitate myocardial ischemia.
An increase in total body oxygen consumption
and carbon dioxide production necessitates a con-comitant increase in minute ventilation.
The lat-ter increases the work of breathing, particularly in patients with
underlying lung disease. Pain due to abdominal or thoracic incisions further
com-promises pulmonary function because of guard-ing (splinting). Decreased
movement of the chest wall reduces tidal volume and functional residual
Stress increases catabolic hormones
(catecholamines, cortisol, and glucagon) and decreases anabolic hor-mones
(insulin and testosterone). Patients develop a negative nitrogen balance,
carbohydrate intoler-ance, and increased lipolysis. The increase in cortisol,
renin, angiotensin, aldosterone, and antidiuretic hor-mone results in sodium
retention, water retention, and secondary expansion of the extracellular space.
Stress-mediated increases in platelet adhesiveness, reduced
fibrinolysis, and hypercoagulability have been reported.
The neuroendocrine stress response produces
leuko-cytosis and has been reported to depress the reticu-loendothelial system.
The latter predisposes patients to infection. Stress-related immunodepression
may also enhance tumor growth and metastasis.
Anxiety and sleep disturbances are common reac-tions to acute pain. With
prolonged duration of the pain, depression is not unusual. Some patients react
with frustration and anger that may be directed at family, friends, or the
The neuroendocrine stress response is
generally observed only in patients with severe recurring pain due to
peripheral (nociceptive) mechanisms and in patients with prominent central
mechanisms such as pain associated with paraplegia. It is attenuated
or absent in most patients with chronic pain. Sleep and affective disturbances,
particularly depression, are often prominent. Many patients also experience
significant changes in appetite (increase or decrease) and stresses on social