Patients with coexisting systemic disease may be at a higher risk for specific perioperative complications related to surgery and anesthesia. Regional anesthesia is often thought of as being particularly beneficial in patients. However, the physiologic changes that occur with some regional anesthesia techniques must be understood and viewed within the context of an individual patient’s pathophysiology so that the technique used provides maximum patient benefit and reduces the risk of complications. This chapter focuses on the pathophysiology of systemic diseases frequently encountered by the regional anesthesiologist and discusses the interplay between common regional anesthesia techniques and patient disease.
Surgical patients with coexisting pulmonary impairment are at risk for intraoperative or postoperative pulmonary complications, regardless of anesthetic technique.1 A growing body of evidence suggests that regional anesthesia may be associated with improved pulmonary outcomes compared with general anesthesia.2,3,4,5,6 However, regional anesthetic blockade may carry risks in some patients. 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.
Epidural & Spinal Anesthesia
Most of the pulmonary effects of neuraxial anesthesia are due to motor block of the intercostal and abdominal musculature. If 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.7 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.8 Diaphragmatic paralysis (phrenic nerve block, C3–C5) in the absence of total spinal anesthesia does not occur with neuraxial blockade, since even a sensory block as high as C3 will only produce a motor block at approximately T1 through T3.7 Apnea following high neuraxial anesthesia is most likely precipitated by brainstem hypoperfusion as a result of hypotension and unlikely to be related to phrenic nerve blockade. Spontaneous respiration returns following adequate volume resuscitation and/or vasopressor therapy.
Apnea associated with a high spinal anesthetic is most often related to hypotension and hypoperfusion of the brainstem, rather than motor blockade of the nerve roots supplying the phrenic nerve (C3–5).
Supporting ventilation while maintaining the blood pressure with fluids and vasopressor therapy is the key resuscitative strategy.
With a high level of epidural or spinal anesthesia, the chest wall musculature and intercostal muscles may become impaired. This may even result in altered chest wall motion during spontaneous respiration. During high neuraxial anesthesia, the more compliant chest wall is retracted during inspiration ...