The site of action of spinal and epidural anesthesia is not precisely known but can potentially occur at any or all points along the neural pathways extending from the site of drug administration to the interior of the spinal cord.
Differential neural block refers to the clinically important phenomenon in which nerve fibers subserving different functions display varying sensitivity to local anesthetic blockade.
Sympathetic nervous system nerve fibers appear to be blocked by the lowest concentration of local anesthetic followed in order by fibers responsible for pain, touch, and motor function.
Although the mechanism for differential block in spinal and epidural anesthesia is not known, it is clear that fiber diameter is not the only, nor perhaps even the most important, factor contributing to differential blockade.
During spinal and epidural anesthesia, differential block is manifested as a spatial separation in the modalities blocked. (Sympathetic block may extend two to six dermatomes higher than sensory block, which is two to three dermatomes higher than motor block.) This spatial separation is believed to result from a gradual decrease in local anesthetic concentration within the CSF as a function of distance from the site of injection.
An occasional patient has intact touch and proprioception at the surgical site despite adequate blockade of pain sensation.
Central neuraxial block produces sedation, potentiates the effects of sedative drugs, and markedly decreases the anesthetic requirements.
Cardiovascular Physiology. Understanding the homeostatic mechanisms responsible for control of blood pressure and heart rate is essential for understanding and treating the cardiovascular changes associated with spinal and epidural anesthesia (Fig 34-7).
Spinal Anesthesia. Blockade of sympathetic nervous system efferent fibers is the principal mechanism by which spinal anesthesia produces cardiovascular derangements.
The incidence of significant hypotension or bradycardia is generally related to the extent of sympathetic nervous system blockade, which in turn parallels block height.
Hypotension during spinal anesthesia is the result of arterial (decreased systemic vascular resistance) and venous (decrease preload responsible for decreased cardiac output) dilation. An intact renin–angiotensin system helps to offset the hypotensive effects of sympathetic block. (Caution should be exercised when administering central neuraxial block to patients taking antihypertensives that impair the angiotensin system.)
Heart rate slows significantly in 10% to 15% of patients (because of blockade of sympathetic cardioaccelerator fibers or diminished venous return and the associated decreased stretch of intracardiac stretch receptors). Patients with unexplained severe bradycardia and asystole during spinal and epidural anesthesia may require aggressive intervention with epinephrine.
Spinal anesthesia can also produce second- and third-degree heart block. Pre-existing first-degree heart block may be a risk factor for progression to higher grade heart block during spinal anesthesia.
Hemodynamic changes of high epidural anesthesia without epinephrine in the local anesthetic solution resemble the changes seen with spinal anesthesia, although the magnitude is usually less than that seen with comparable levels of spinal block.
When epinephrine is added to the local anesthetic solution, the resulting β2-mediated vasodilation leads to a greater decrease in blood pressure than occurs in the absence of epinephrine.
Spinal and epidural anesthesia to midthoracic levels have little effect on pulmonary function in patients without pre-existing disease. (Drugs used for sedation may have a greater effect.)
The adverse impact of high blocks on active exhalation suggests that caution should be exercised when using spinal or epidural anesthesia in patients with chronic obstructive pulmonary disease and those who rely on the accessory muscles of respiration to maintain adequate ventilation.
Patients with high spinal or epidural anesthesia may complain of dyspnea (loss of ability to feel the chest move while breathing, which is usually adequately treated by reassurance). A normal speaking voice suggests that ventilation is normal. (With an excessively high block, the patient will have a faint, gasping whisper.)
Gastrointestinal Physiology
Unopposed parasympathetic nervous system activity results in increased secretions, relaxation of sphincters, and constriction of the bowel.
Nausea is a common complication of spinal and epidural anesthesia. (The cause unknown but is often associated with blocks higher than T5, hypotension, and opioid administration).
Endocrine–Metabolic Physiology. Spinal anesthesia and epidural anesthesia inhibit many of the changes associated with the stress response to surgery (presumed to reflect blockade of afferent sensory information).