Patient stress is probably a contributing factor in some cases of adverse patient outcome. Stress during induction of anesthesia
can increase circulating catecholamine concentration predisposing the heart to arrhythmias. Additionally, stress or anxiety
can lead to increased doses of anesthetic agents resulting in excessive anesthetic depth once the patient is anesthetized.
Premedication with a tranquilizer or sedative will help reduce anxiety and stress during the perioperative period.
Use of analgesics prior to surgery (preemptive analgesia) may also be beneficial. Opioids are commonly incorporated into premedication
protocols to facilitate sedation and analgesia. When opioids are used, anesthetic drug associated respiratory depression may
be enhanced, but adequate patient monitoring will facilitate early detection of significant respiratory depression and allow
Acute clinical pain typically arises from soft tissue trauma or inflammation, with the most common example being postoperative
surgical pain. Though it does not serve a protective function in the sense that physiologic pain does, acute pain does play
a biologically adaptive role by facilitating tissue repair and healing. This is achieved by hyper-sensitizing the injured
area (primary hyperalgesia) as well as the surrounding tissues (secondary hyperalgesia) to all types of stimuli, such that
contact with any external stimulus is avoided and the reparative process can proceed undisturbed. This realization is not,
however, a license to allow patients to suffer needlessly in the postoperative period or upon presentation in the emergency
room. By having an appreciation of the underlying functional basis of such pain the practitioner is able to initiate appropriate
pain management strategies while taking steps to optimize wound healing.
An important conceptual breakthrough in understanding pain physiology is the recognition that pain following most types of
noxious stimulation is usually protective and quite distinct from pain resulting from overt damage to tissues or nerves. It
plays an integral adaptive role as part of the body's normal defense mechanisms, warning of contact with potentially damaging
environmental insults and initiating behavioral and reflex avoidance strategies. It is also often referred to as nociceptive
pain because it is only elicited when intense noxious stimuli threaten to injure tissue. It is characterized by a high stimulus
threshold, is well localized and transient, and demonstrates a stimulus-response relationship similar to the other somatosensations.
This protective mechanism is facilitated by a highly specialized network of nociceptors and primary sensory neurons which
encode the intensity, duration and quality of noxious stimuli and, by virtue of their topographically organized projections
to the spinal cord, its location.
The physiologic component of pain is termed nociception, which is comprised of the processes of transduction, transmission
and modulation of neural signals generated in response to an external noxious stimulus. It is a physiologic process that,
when carried to completion, results in the conscious perception of pain. In its simplest form the pain pathway can be considered
as a three neuron chain, with the first order neuron originating in the periphery and projecting to the spinal cord, the second
order neuron ascending the spinal cord, and the third order neuron projecting to the cerebral cortex. On a more complex level,
the pathway involves a network of branches and communications with other sensory neurons and descending inhibitory neurons
from the midbrain that modulate afferent transmission of painful stimuli.
Descending Modulation of Pain
The descending modulatory system has been described as having four tiers. The final, and perhaps most important, site involved
in the descending modulation of nociceptive information is at the level of the spinal cord. Just as dorsal horn processing
is vital to the integration of ascending noxious input, its role in anti-nociception is equally crucial. Dense concentrations
of GABA, glycine, serotonin, norepinephrine and the endogenous opioid peptides (enkephalins, endorphins and dynorphins) have
been identified in dorsal horn neurons, and all produce inhibitory effects on nociceptive transmission. Specifically, the
spinal opioid system fine-tunes descending control mechanisms by acting both presynaptically, as well as postsynaptically.
Communication among dorsal horn neurons involves complex interactions, and it is now apparent that a single neuron may be
influenced by many neurotransmitters, that each neurotransmitter may have numerous actions in a given region, and that multiple
neurotransmitters may exist within a single neuron. Simply stated on a more global level, nociceptive processing is a three-neuron
chain with dual input at each level. Discriminative and affective aspects of pain are transmitted in related, and yet distinct
ascending pathways, with modifications made by both segmental and descending modulatory systems.