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Patients with coexisting severe systemic disease may be at a higher
risk for perioperative complications related to surgery and administration
of anesthesia. Regional anesthesia is often touted as beneficial in many
patients who have pulmonary, cardiac, renal, and other disease. However, the
physiologic changes that occur with various regional anesthesia techniques
must be understood and viewed within the context of an individual patient's
pathophysiology so that the technique benefits the patient fully and reduces
the risk of complications from the patient' disease. This chapter focuses on
the pathophysiology of several common systemic diseases frequently
encountered by the regional anesthesiologist and discusses the interplay
between common regional anesthesia techniques and patient disease.
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Surgical patients with coexisting pulmonary impairment are at risk for
intraoperative or postoperative pulmonary complications, regardless of
anesthetic technique.1 However, increasing evidence
suggests that regional anesthesia may be associated with improved pulmonary
outcomes compared with those associated with general anesthesia.2–4 A thorough understanding of respiratory physiology and the
implications of regional anesthetic techniques is crucial to the safe and
effective use of regional anesthesia in these patients.
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Epidural & Spinal Anesthesia
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Most of the pulmonary effects of neuraxial anesthesia are due to motor
block of the intercostal and abdominal musculature. If a significant
systemic uptake of local anesthetic occurs, some central and direct
myoneural respiratory depression can also be seen, although this plays a
minor role overall.5 Since neuraxial anesthesia produces a
“differential” blockade of motor, sensory, and autonomic fibers, the degree
to which respiratory function is impaired depends on the relative extent of
segmental motor blockade. Using dilute concentrations of epidural local
anesthetic may provide adequate sensory block as high as the cervical
levels, while sparing the motor function of the respiratory muscles in the
lower somatic segments.6 Achieving diaphragmatic paralysis
via a phrenic nerve (C3 through C5) block in the absence of a total spinal
anesthesia is difficult in practice, since even a sensory block as high as
C3 will only produce a motor block at approximately T1 through
T3.5 However, high neuraxial blocks may precipitate
hypotension sufficient to decrease blood flow to the respiratory center in
the medulla, leading to respiratory arrest.
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With higher levels of epidural or
spinal anesthesia, chest wall musculature, and in
particular the intercostal muscles, become segmentally weakened and
contribute less to the respiratory effort. This in turn, may eventually lead
to altered chest wall motion during spontaneous respiration. For instance,
some studies have suggested that during high neuraxial anesthesia, the more
compliant chest wall is retracted during inspiration and may actually
display paradoxical rib cage motion.7,8 Others, however,
have found that epidural blockade to sensory levels of T6 or even T1 do not
lead to rib cage constriction with inspiration and may in fact increase the
contribution that chest wall expansion makes to tidal
volume.9,10 This may be explained by an incomplete motor
block ...