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The physiologic effects of neuraxial blocks

The physiologic effects of neuraxial blocks are often misinterpreted as complications, which is highlighted by observers listing hypotension under complications of the techniques. Clear distinction should be made between the physiologic effects of an anesthetic technique and complications, which imply some harm to the patient.This distinction is important to determine the risk-benefit equation of the technique in question. Cardiovascular Effects The cardiovascular effects of neuraxial blocks are similar in some ways to the combined use of intravenous 1- and -adrenergic blockers: decreased heart rate and arterial blood pressure. The sympathectomy that accompanies the techniques depends on the height of the block, with the sympathectomy typically described as extending for two to six dermatomes above the sensory level with spinal anesthesia and at the same level with epidural anesthesia. This sympathectomy causes venous and arterial vasodilation, but because of the large amount of blood in the venous system (approximately 75% of the total volume of blood), the venodilation effect predominates as a result of the limited amount of smooth muscle in venules; in contrast, the vascular smooth muscle on the arterial side of the circulation retains a considerable degree of autonomous tone. After neuraxial blockinduced sympathectomy, if normal cardiac output is maintained, total peripheral resistance should decrease only 15% to 18% in normovolemic healthy patients, even with nearly total sympathectomy. In elderly patients with cardiac disease, systemic vascular resistance may decrease almost 25% after spinal anesthesia, whereas cardiac output decreases only 10%. The heart rate during a high neuraxial block typically decreases as a result of blockade of the cardioaccelerator fibers arising from T1 to T4. The heart rate may decrease because of a fall in right atrial filling, which decreases outflow from intrinsic chronotropic stretch receptors located in the right atrium and great veins. The clinical question of what level of decrease in arterial blood pressure after a neuraxial block is acceptable remains to be answered. It will probably remain speculative because conducting ethical human investigations designed to define a dose-response curve of decreased arterial blood pressure accompanying neuraxial blockade would be difficult. That dilemma notwithstanding, it appears that total-body oxygen consumption in patients undergoing spinal anesthesia correlates with the extent of spinal anesthesia, thus providing a margin of safety for organ perfusion unavailable with non-neuraxial techniques Some data are available to help determine the extent to which arterial blood pressure should be allowed to decrease Despite methodologic problems with the study, * Kety and colleagues [44] demonstrated that producing spinal anesthesia to the midthoracic levels with procaine, even in patients with essential hypertension, results in a decrease in mean arterial pressure of 26% (155 to 115 mm Hg) accompanied by only a 12% (52 to 46 mL/100 g/min) decrease in CBF.

When the level of spinal anesthesia was purposely increased to produce higher levels of block (T4) in normotensive and hypertensive patients, mean arterial pressure decreased by 32% (93 to 63 mm Hg) and 50% (158 to 79 mm Hg), respectively. Although CBF was unchanged in the normotensive group (45 to 46 mL/100 g/min), a 19% decrease occurred in the apparently untreated hypertensive patients (46.5to37.5 mL/100 g/min). When coronary artery blood flow and myocardial metabolism were determined in humans during spinal anesthesia to T4 in hypertensive and normotensive patients, decreases in coronary blood flow (153 to 74 mL/100 g/min) paralleled the decrease in mean arterial blood pressure (119 to 62 mm Hg), and the percent extraction of myocardial oxygen was unchanged (75% to 72%). Extraction of oxygen was unchanged because myocardial work, as expressed by myocardial use of oxygen, paralleled the decrease in mean arterial pressure and coronary blood flow (16 to 7.5 mL/100 g/min) These data support the observations by Stanley and coworkers but still do not provide a patient-by-patient indication of the organ most at risk for flow-related ischemia, suggesting that further research in this area is required. Human investigations are limited by cerebral and myocardial blood flow methodologies that were not limiting factors when Sivarajan and associates investigated organ blood flow by means of microspheres in rhesus monkeys during spinal anesthesia at the T10 and T1 levels. During the T10 block, there was no significant change in organ blood flow; during the T1 block, with a 22% decrease in mean arterial pressure, cerebral and myocardial blood flow was insignificantly altered. Prevention of decreases in mean arterial pressure of greater than 30% has some basis, but it is important to remember that these data were derived from severely hypertensive, presumably untreated patients. For normotensive and treated hypertensive patients, a wider undocumented margin of safety probably exists. After arterial blood pressure decreases to a level at which treatment is believed to be necessary, ephedrine, a mixed adrenergic agonist, provides more appropriate therapy for the noncardiac circulatory sequelae of neuraxial block than a pure -adrenergic agonist does , unless the patient has a specific and defined blood pressure requirement. That the decrease in arterial blood pressure after neuraxial block can be minimized by the administration of crystalloids intravenously is probably not a valid concept. Specifically, 250- to 2000-mL preblock hydration regimens appear to temporarily increase preload and cardiac output without consistently increasing arterial blood pressure or preventing hypotension.[20] Is there any indication that epidural and spinal anesthesia differ in their effect on arterial blood pressure? A common concept is that the decrease in arterial blood pressure is more gradual and of less magnitude with epidural than with spinal anesthesia of comparable levels. Despite this belief, it was shown that when tetracaine (10 mg) spinal anesthesia was compared with lidocaine (20 to 25 mL of a 1.5% solution) epidural anesthesia, there was a

larger decrease in arterial blood pressure, approximately 10%, with the epidural technique than with the spinal one. The proposed advantage of a slower onset of epidural blockade is often mitigated by anesthesiologists administering a decreased volume of local anesthetic with the initial epidural therapeutic dose; when the block height does not rise as rapidly as desired, additional epidural local anesthetic is administered, and a higher block than necessary may result. The extent to which arterial blood pressure decreases with either technique depends on multiple factors, including patient age and intravascular volume status. * Cerebral blood flow (CBF) was studied with nitrous oxide. Only global CBF was measured, and the patients studied were severely hypertensive (i.e., average mean arterial blood pressure of 155 mm Hg).

Respiratory Effects
Alterations in pulmonary variables in healthy patients during neuraxial block are usually of little clinical consequence. Tidal volume remains unchanged during high spinal anesthesia, and vital capacity decreases a small amount from 4.05 to 3.73 L. This decrease in vital capacity is a result of a decrease in expiratory reserve volume related to paralysis of the abdominal muscles necessary for forced exhalation rather than a decrease in phrenic or diaphragmatic function. This minimal impact on pulmonary function also holds for elderly patients undergoing lumbar and thoracic epidural anesthesia. Pulmonary function testing in cesarean section patients undergoing epidural anesthesia shows that using lidocaine provides larger decrements in peak expiratory pressure (abdominal musculaturedependent maneuver) than using bupivacaine does. The rare respiratory arrest associated with spinal anesthesia is also unrelated to phrenic or inspiratory dysfunction but rather to hypoperfusion of the respiratory centers in the brainstem. Supportive evidence for this concept is observed after resuscitation, when apnea almost always disappears as soon as pharmacologic and fluid therapies have restored cardiac output and blood pressure. This would not be the case if phrenic paralysis induced by high levels of local anesthetic was the cause of the apnea. There is experimental evidence from rabbits during epidural anesthesia that their response to hypoxia results in apnea, which is different from the response without neuraxial anesthesia. This finding may have implications for understanding some episodes of cardiovascular depression during neuraxial blockade in humans, although confirmation is needed. Conversely, in a canine model of hypoxia, epidural anesthesia and hypoxic

challenge result in the same outcome but with more normal acid-base function than in animals receiving general anesthesia alone. Neuraxial block should be used cautiously in respiratory cripples because of paralysis of the respiratory muscles. Except for severely compromised patients with respiratory failure, inspiratory muscle function during neuraxial blocks should be adequate to maintain ventilatory function. The physiologic consideration related to muscle paralysis with neuraxial block should focus on the expiratory muscles in these severely compromised patients because these muscles are important for effective coughing and clearing of intrapulmonary secretions.

Gastrointestinal Function
Another organ system affected during neuraxial blockade is the gastrointestinal tract. Nausea and vomiting may be associated with neuraxial block in up to 20% of patients and are primarily related to gastrointestinal hyperperistalsis caused by unopposed parasympathetic (vagal) activity. Atropine is effective in treating nausea associated with high (T5) subarachnoid anesthesia. This gastrointestinal hyperperistalsis has the advantage of providing excellent surgical conditions because of a contracted gut. An often-cited advantage of regional anesthesia in patients with compromised gastrointestinal function (e.g., hepatic dysfunction) is that less physiologic impairment is possible than with general anesthesia. Nevertheless, it appears that if intra-abdominal surgery is performed, the magnitude of the decrease in hepatic blood flow parallels the site of surgery rather than the anesthetic technique chosen. The decrease in hepatic blood flow during spinal anesthesia parallels the decrease in mean arterial blood pressure. When epidural analgesia is continued into the postoperative period, there may be a protective effect on the gastric mucosa because intramucosal pH is higher during postoperative epidural analgesia than during systemic analgesia.[59]

Renal Function
Renal function has a wide physiologic reserve. Despite predictable decreases in renal blood flow accompanying neuraxial blockade, the decrease is of little physiologic importance One aspect of genitourinary function that is of clinical importance is the belief that neuraxial blocks are a frequent cause of urinary retention, which delays discharge of outpatients and necessitates bladder catheterization in inpatients. Lower concentrations of local anesthetic are necessary for paralysis of bladder function than for paralysis of motor nerves to the lower extremities. However, some studies do not support this belief. For example, in orthopedic patients undergoing hip replacement, it was demonstrated that bladder catheterization was no more frequent after neuraxial (spinal or epidural) block than after general anesthesia and narcotic analgesics.

In any case, it is prudent to avoid administration of excessive volumes of crystalloid solutions intravenously to patients undergoing spinal anesthesia and to individualize the requirement for voiding before discharge in low-risk ambulatory surgery patients after shortacting spinal or epidural anesthetics are used.

Effects Specific to Epidural Anesthesia

The physiologic effects of epidural anesthesia are similar to those of spinal anesthesia, with the exception that local anesthetic blood levels reach concentrations sufficient enough to produce systemic effects on their own. Even intravenously administered lidocaine (resulting in blood levels similar to those after continuous epidural analgesia) can decrease postoperative narcotic requirements. When blood levels are excessive, adverse CNS and cardiovascular effects occur Millar 7th e