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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 ...

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