Mechanism of Action
The mechanisms of spinal and epidural anes-thesia remain speculative. The principal site ofaction for neuraxial blockade is believed to be the nerve root. Local anesthetic is injected into CSF (spinal anesthesia) or the epidural space (epidural and caudal anesthesia) and bathes the nerve root in the subarachnoid space or epidural space, respec-tively. Direct injection of local anesthetic into CSF for spinal anesthesia allows a relatively small dose and volume of local anesthetic to achieve dense sen-sory and motor blockade. In contrast, the same local anesthetic concentration is achieved within nerve roots only with much larger volumes and quanti-ties of local anesthetic molecules during epidural and caudal anesthesia. Moreover, the injection site (level) for epidural anesthesia must generally be close to the nerve roots that must be anesthetized. Blockade of neural transmission (conduction) in the posterior nerve root fibers interrupts somatic and visceral sensation, whereas blockade of ante-rior nerve root fibers prevents efferent motor and autonomic outflow. Local anesthetics may also have actions on structures within the spinal cord during epidural and spinal anesthesia.
By interrupting the afferent transmission of painful stimuli and abolishing the efferent impulses respon-sible for skeletal muscle tone, neuraxial blocks can provide excellent operating conditions. Sensory blockade interrupts both somatic and visceral pain-ful stimuli. The mechanism of action of local anes-thetic agents is discussed. The effect of local anesthetics on nerve fibers varies according to the size and characteristics of the nerve fiber, whether it is myelinated, the length of nerve that is bathed by the local anesthetic, and the concentra-tion of the local anesthetic. Spinal nerve roots con-tain varying mixtures of these fiber types. Smaller and myelinated fibers are generally more easily blocked than larger and unmyelinated ones. The size and character of the fiber types, and the fact that the concentration of local anesthetic decreases with increasing distance from the level of injection, explains the phenomenon of differential blockadeduring neuraxial anesthesia. Differential block-ade typically results in sympathetic blockade(judged by temperature sensitivity) that may be two segments or more cephalad than the sensory block (pain, light touch), which, in turn, is usually several segments more cephalad than the motor blockade.
Interruption of efferent autonomic transmis-sion at the spinal nerve roots during neuraxialblocks produces sympathetic blockade. Sympathetic outflow from the spinal cord may be described as thoracolumbar, whereas parasympathetic outflow is craniosacral. Sympathetic preganglionic nerve fibers (small, myelinated B fibers) exit the spinal cord with the spinal nerves from T1–L2 and may course many levels up or down the sympathetic chain before synapsing with a postganglionic cell in a sympathetic ganglion. In contrast, parasympa-thetic preganglionic fibers exit the spinal cord with the cranial and sacral nerves. Neuraxial anesthesia does not block the vagus nerve (tenth cranial nerve). The physiological responses of neuraxial blockade therefore result from decreased sympathetic tone and/or unopposed parasympathetic tone.
Neuraxial blocks produce variable decreases in blood pressure that may be accompaniedby a decrease in heart rate. These effects are gener-ally proportional to the dermatomal level and extent of sympathectomy. Vasomotor tone is primarily determined by sympathetic fibers arising from T5– L1, innervating arterial and venous smooth muscle. Blocking these nerves causes vasodilation of the venous capacitance vessels and pooling of blood in the viscera and lower extremities, thereby decreas-ing the effective circulating blood volume and venous return to the heart. Arterial vasodilation may also decrease systemic vascular resistance. The effects of arterial vasodilation may be minimized by compensatory vasoconstriction above the level of the block, particularly when the extent of sensory anesthesia is limited to the lower thoracic derma-tomes. A high sympathetic block not only prevents compensatory vasoconstriction, but may also block the sympathetic cardiac accelerator fibers that arise at T1–T4. Profound hypotension may result from arterial dilation and venous pooling combined with bradycardia (and possibly also milder degrees of decreased contractility). These effects are exagger-ated if venous pooling is further augmented by a head-up position or the weight of a gravid uterus. Unopposed vagal tone may explain the sudden car-diac arrest sometimes seen with spinal anesthesia.Deleterious cardiovascular effects should be anticipated and steps undertaken to minimizethe degree of hypotension. However, volume load-ing with 10–20 mL/kg of intravenous fluid in a healthy patient before initiation of the block has been shown repeatedly to fail to prevent hypoten-sion (in the absence of preexisting hypovolemia). Left uterine displacement in the third trimester of pregnancy helps to minimize physical obstruction to venous return. Despite these efforts, hypotension may still occur and should be treated promptly. Autotransfusion may be accomplished by placing the patient in a head-down position. A bolus of intravenous fluid (5–10 mL/kg) may be helpful in patients who have adequate cardiac and renal function to be able to “handle” the fluid load after the block wears off. Excessive or symptomaticbradycardia should be treated with atropine, and hypotension should be treated with vasopressors. Direct α-adrenergic agonists (such as phenyleph-rine) primarily produce arteriolar constriction and may reflexively increase bradycardia, increasing systemic vascular resistance. The “mixed” agent ephedrine has direct and indirect β-adrenergic effects that increase heart rate and contractility and indirect effects that also produce vasoconstriction. Much like ephedrine, small doses of epinephrine (2–5 mcg boluses) are particularly useful in treating spinal anesthesia induced hypotension. If profound hypotension and/or bradycardia persist, vasopres-sor infusions may be required.
Alterations in pulmonary physiology are usually minimal with neuraxial blocks because the dia-phragm is innervated by the phrenic nerve, with fibers originating from C3–C5. Even with high tho-racic levels, tidal volume is unchanged; there is only a small decrease in vital capacity, which results from a loss of the abdominal muscles’ contribution to forced expiration.
Patients with severe chronic lung disease may rely upon accessory muscles of respiration (inter-costal and abdominal muscles) to actively inspire or exhale. High levels of neural blockade will impair these muscles. Similarly, effective coughing and clearing of secretions require these muscles for expi-ration. For these reasons, neuraxial blocks should be used with caution in patients with limited respi-ratory reserve. These deleterious effects need to be weighed against the advantages of avoiding airway instrumentation and positive-pressure ventilation. For surgical procedures above the umbilicus, a pure regional technique may not be the best choice in patients with severe lung disease. On the other hand, these patients may benefit from the effects of tho-racic epidural analgesia (with dilute local anesthetics and opioids) in the postoperative period, particu-larly following upper abdominal or thoracic surgery. Some evidence suggests that postoperative thoracic epidural analgesia in high-risk patients can improve pulmonary outcome by decreasing the incidence of pneumonia and respiratory failure, improving oxy-genation, and decreasing the duration of mechanical ventilatory support.
Sympathetic outflow originates at the T5–L1 level. Neuraxial block-induced sympathectomy allows vagal tone dominance and results in a small, con-tracted gut with active peristalsis. This can improve operative conditions during laparoscopy when used as an adjunct to general anesthesia. Postoperative epidural analgesia with local anesthetics and mini-mal systemic opioids hastens the return of gastroin-testinal function after open abdominal procedures.
Hepatic blood flow will decrease with reduc-tions in mean arterial pressure from any anesthetic technique, including neuraxial anesthesia.
Renal blood flow is maintained through autoregula-tion, and there is little effect of neuraxial anesthesia on renal function. Neuraxial anesthesia at the lum-bar and sacral levels blocks both sympathetic and parasympathetic control of bladder function. Loss of autonomic bladder control results in urinary reten-tion until the block wears off. If no urinary catheter is placed perioperatively, it is prudent to use the regional anesthetic of shortest duration sufficient for the surgical procedure and to administer the mini-mal safe volume of intravenous fluid. Patients with urinary retention should be checked for bladder dis-tention after neuraxial anesthesia.
Surgical trauma produces a systemic neuroendo-crine response via activation of somatic and vis-ceral afferent nerve fibers, in addition to a localized inflammatory response. This systemic response includes increased concentrations of adrenocortico-tropic hormone, cortisol, epinephrine, norepineph-rine, and vasopressin levels, as well as activation of the renin–angiotensin–aldosterone system. Clinical manifestations include intraoperative and postop-erative hypertension, tachycardia, hyperglycemia, protein catabolism, suppressed immune responses, and altered renal function. Neuraxial blockade can partially suppress (during major invasive surgery) or totally block (during lower extremity surgery) the neuroendocrine stress response. To maximize this blunting of the neuroendocrine stress response, neuraxial block should precede incision and con-tinue into the postoperative period.