Anatomy and physiology of spinal and epidural anesthesia

Anatomy and Physiology of Spinal and Epidural Anesthesia Thomas M. Halaszynski and Maximilian W. B. Hartmannsgruber

NESTHESIOLOGISTS who are comfort. able with spinal and epidural techniques appreciate that both have inherent advantages. Each can and should be used, with the choice being based on maximal benefit Io the individual patient. Those who try to compare spinal (SA) and epidural anesthesia (EA) as major regional anesthetic techniques must first come to the realization that there are significant differences between them. Differences can be best understood with a sound knowledge of the physiology and anatomy of the vertebral column along with its contents. This understanding is essential to the safe and successful performance of neural blockade.

A

HISTORY

In 1884, an ophthalmologist named Carl Koller introduced the use of cocaine to achieve topical anesthesia of the cornea and conjunctiva; thus, Koller is attributed with the introduction of regional anesthesia (RA) into clinical practice. ~ Subsequent to the report by Koller, cocaine was injected intervertebrally in dogs by Corning, a neurologist, in 1885. 2 Corning's goal to treat chronic pain inadvertently resulted in the performance of the first documented spinal anesthetic. In 1899, August Bier 3 performed lumbar punctures using the techniques described by Quincke, 4 injecting cocaine intrathecally to provide anesthesia for surgical procedures. Reports of SA, using cocaine, resulted in numerous studies using this technique to provide anesthesia. Tuffier5 from France and Matas 6 in New Orleans, LA, provided the description of cocaine SA that resulted in the first representation of this technique in the United States. The new-found technique of SA with the use

From the Department of Anesthesiology, Yale School of Medicine, New Haven, CT. Address reprint requests to Maximilian W. B. Hartmannsgruber, MD, Department of Anesthesiology, Yale University School of Medicine, 333 Cedar St, TMP-3, New Haven, CT 06510. Copyright 9 1998 by W.B. Saunders Company 0277-0326/98/1701-000558. 00/0

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of cocaine was unpopular due to the undesirable side effects, resulting in its limited use. With the development of synthetically produced procaine in 1904 by Einhorn, there was renewed enthusiasm and popularity for operative S A . 7 Although Dogliotti is credited with popularizing segmental EA for surgery, it was Cathelin from France who is recognized as performing the first caudal epidural anesthetic in 1901. 8,9 The lumbar approach to the epidural space was further described by Pages in 1921. l~ Adaptation of the Tuohy subarachnoid needle in 1945 sustained interest in techniques of neural blockade and played a major role in improvement of epidural blockade for surgical anesthesia. H Lumbar epidural anesthesia (EA), by the continuous catheter technique, was used extensively in obstetrical applications, as well as surgical operations and those situations requiring sustained postoperative pain control.22 With the development of lidocaine in 1948, detailed information on the site of action of epidural blockade, and the spread of analgesia, helped to rationalize support for this technique. 13 Increased enthusiasm for the use of epidural blockade resulted in widespread use during the 1960s, especially for pain relief in obstetrics. Spinal anesthesia and EA continue to be among the most popular techniques of RA for obstetrics, surgery, and postoperative analgesia. Increased understanding, gained through controlled clinical studies of local anesthetics and their dosage, advantage of segmental blockade, and reduced toxicity, has permitted the persistence and further development of both SA and EA. Epidemiologic studies by Dripps and Vandam TM have clearly demonstrated the safety profile for clinical application of neural blockade. A persistent and even accelerated popularity of RA also can be attributed to detailed pharmacokinetic studies of local anesthetic drugs administered by single injection, repeated injection, and infusion. Studies comparing blood concentrations of local anesthetics have allowed for determination of toxicity ratios of local anesthetics clinically used in both spinal and epidural blockade. The intro-

Seminars in Anesthesia, Periaperative Medicine and Pain, Vol 17, No 1 (March), 1998: pp 24-37

SPINAL AND EPIDURAL ANESTHESIA duction of amide local anesthetics, concurrently with detailed studies of the neurologic and cardiorespiratory effects of neural blockade, provided important information that has increased the safety profile of these techniques. ANATOMY Most standard anatomy textbooks do not describe what the tip of the anesthesiologist's needle encounters. This section on anatomy will describe what the tip of a needle (both spinal and epidural) will encounter whenever neuraxial anesthesia is performed.

Bony Structures of the Vertebral Column The vertebral column comprises seven cervical, 12 thoracic, and five lumbar vertebrae. Extension of the vertebral column consists of the sacrum and coccyx. The coccyx is affixed to the distal end of the five fused sacral vertebrae, and its tip is an easily palpable anatomical landmark; this can be useful when attempting to define in obese patients the midline of the vertebral column, especially in combination with the prominent spinal process of C7. Posterior to the vertebral bodies are bony arches that form the spinal canal. The spinal canal extends from the foramen magnum to the sacral hiatus. The vertebral column is lordotic in the cervical and lumbar segments (curved away from the needle) and kyphotic in the thoracic and sacral segments. This is influential in the spread of neuraxi.al local anesthetics (Fig 1). The vertebrae increase in size and shape from the cervical segments to the lumbar region. This aspect needs to be considered when placing a regional anesthetic needle, depending on the level at which it is to enter the spinal canal. The dimensional differences are related to the role of the vertebrae, in which smaller cervical areas function less with weight bearing, while the greatest amount of weight is supported by larger lumbar vertebrae. The bony arches, which are dorsai to the vertebral bodies, consist of two pedicles anteriorly and two laminae posteriorly. These bony arches are separated by ligamentous tissue. The tip of the needle penetrates the ligamentous tissue, permitting access to contents of the spinal canal necessary for neuraxial blockade. The bony arches and the laminae of each, which unite to form the spinous process, serve as a bony guide for

25 directing or redirecting the needle tip to the spinal canal. An awareness of varying degrees of angulation of spinous processes, dependent on the vertebral segment, provides further direction for successful access to the spinal canal. Spinal processes are nearly horizontal in lumbar, lower thoracic, and cervical vertebrae. Spinal processes of the upper and midthoracic regions have a degree of angulation that is more caudad in direction. The regional anesthetic needle will have marked differences in the angle required to gain access to the spinal canal, between spinal processes, at various segments. This influence is most conspicuous between the vertebrae of T3 to T7, which require the maximum range of angulation from the horizontal plane. Stability and elasticity of the vertebrae are achieved by several spinal ligaments. The ligaments that connect the vertebrae posteriorly include the supraspinous ligament, interspinous ligament, and ligamentum flavum (Fig 2). These ligaments are denser and larger in the lumbar region of the vertebral column. In the experienced hand, the tip of the needle can be adjusted, depending on which of the ligaments are encountered on the path to the spinal canal due to changes in resistance to passage. After the needle tip has passed through the skin and subcutaneous tissue, the supraspinous ligament, a fibrous band, is encountered by the tip of the needle. The supraspinous ligament usually offers minimal resistance to passage in most patients. In contrast, this ligament may be calcified in the elderly such that a small-gauge needle cannot penetrate and requires the assistance of a larger, introducer needle. The spinal processes are connected by the interspinous ligament. As the needle tip merges into the interspinous ligament, increasing resistance is encountered due to increased fiber density. As depicted in Fig 2, this tissue layer can occasionally confuse even the experienced anesthesiologist, because an undetected deviation of the needle tip from midline can result in loss of resistance similar to the loss of resistance felt when entering the true epidural space. This potential confusion is due to lateral penetration of the interspinous ligament rather than penetration of the ligamentum flavum. The ligamentum flavum, or "yellow ligament," offers the most resistance to needle penetration. Once entered, this tissue layer embraces the needle shaft so firmly

26

HALASZYNSKI AND HARTMANNSGRUBER

Fig 1. Anatomy of cervical, thoracic, and lumbar segments of the vertebral column. Relationship between cervical and lumbar segments (curve anteriorly) versus thoracic and sacral segments (curve posteriorly). Reprinted with permission?9

that tapping the needle hub will lead to a characteristic vibration. Once the needle tip has reached the ligamentum ftavum, an unnoticed deviation from midline is unlikely because the spinal canal is so close. When loss of resistance or a " p o p " is felt, the needle tip is in the epidural or subarachnoid space, respectively. In contrast to the midline approach, the paramedian technique will usually first encounter the ligamentum flavum. The paramedian approach is often used in patients with significant calcification of ligaments and those patients that pose difficulties to assuming optimum positioning. Optimum positioning is defined as arching of the back, which results in flexion of the vertebrae and widening of the interspinous space. In morbidly obese patients, a needle with an unnoticed deviation from midline out of the interspinous ligament into paravertebral planes is more likely. Therefore, a paramedian approach offers the ad-

vantage that once "ligamentous resistance" is encountered, the needle tip is typically in the ligamentum flavum; with subsequent loss of resistance, the epidural or subarachnoid space is entered. THE SPINAL CANAL

The spinal canal is occupied by the spinal cord, which begins at the level of the foramen magnum and extends to the first or second lumbar vertebra. It is continuous with the medulla oblongata above and ends below as the conus medullaris, from which the cauda equina (collection of segmental nerve fibers) and the filum terminale continue to the coccyx. At birth, the spinal cord ends at the third lumbar vertebra before rising to the more cephalad adult level. The cauda equina is suspended in spinal fluid, allowing sufficient mobility to deviate from the needle tip, which enters the subarachnoid space. The spinal cord could

SPINAL AND EPIDURAL ANESTHESIA

27

1

lagmm~ntum rims.am

'2 ~ i n o u s 3

S~raspinous

Fig 2. General relationships of vertebral ligaments. Reprinted with permission.29

be pierced by a needle that enters the spinal canal at levels cephalad to L1; this leads to greater popularity of the lumbar approach to neuraxial blockade. As the tip of the needle enters the spinal c a n a l and approaches the spinal cord or cauda equina, the following structures are sequentially encountered (Fig 3): the epidural space, the dura mater, the subdural space, the arachnoid mater, and the subarachnoid space containing cerebrospinal fluid and the spinal cord (the spinal cord is c o v -

ered by the pia mater). First, the needle enters the epidural space. The posterior epidural space is located between the dura mater anteriorly, the ligamentum flavum posteriolaterally, and the connective tissue of the laminea of the vertebrae laterally. The thin, narrow anterior epidural space is situated between the posterior longitudinal ligament and the anterior spinal dura (Fig 4). The epidural space extends from the base of the skull to the sacrococcygeal ligament of the sacral hiatus. It is filled with fatty tissue, loose connec-

28

HALASZYNSKI AND HARTMANNSGRUBER Spinal Cord

A

Tenth Thoracic Spinal Gar~glion

/

Dura Mater

Pia Mater Overlying /-,-.SPinal Cord

Dora Mater Opened Out

/

Conus Meduilari8

First Lumbar 3orsat Nerve Root

Filum Terminale _ Ii'lter nuiTi

Gauda Equma

five tissue, lymphatics, arteries, a rich venous plexus, 15 and segmental nerve roots traversing the lateral boundaries. Most neuraxial blockades are performed in the mid-lumbar region, where the needle anatomically has the deepest epidural space (L2; approximately 5 to 6 mm cross-section). In contrast, the narrowest region is located around C5 (approximately 1.0 to 1.5 mm), with the intermediate region at T6 (approximately 2.5 to 3 ram). The shape of the dorsal epidural space

Fig 3. The spinal cord, cauda equina, connective tissue covering, and related structures of the vertebral column. Reprinted with permission? ~

is triangular in cross-section. With the midline approach, the needle finds the greatest distance from the dura mater in a horizontal plane. In clinical practice, however, much greater importance is not the anatomical dimension, but the angle in which the tip of the needle penetrates through the ligamentum flavum into the epidural space. In the lumbar region, when a steeper needle angulation and/or a paramedian approach is used, the dimension within the epidural space

SPINAL A N D EPIDURAL ANESTHESIA

29

B

Ventral R

SPinal Ne

e Matter)

Dorsal Ro and Gangl

Rami Communlcar

SymPathetic Gang F~amen

Fig 3.

(Cant'd}.

may go beyond 5 to 6 ram, and occasionally the needle may even completely miss the dura mater laterally. This is of clinical importance when attempting to access the subarachnoid space with a spinal needle inserted through an epidural needle

(dual technique). Therefore, the success rate of the dual technique increases with a midline approach (Fig 5A). The longitudinal shape of the dorsal epidural space simulates a sawtooth contour. This pattern results in a narrower epidural

VERTE~AL BODY

INOID SPACE

AN1 SPIN~

ORD

PARAVE NE

~OOT GANGLION gER

POS SPiN

SPACE

LIGAMENTUM FLAVUM Fig 4. Crosssection of the spinal cord identifying the epidural spaces (anterior and posterior), subdural space, and subarachnoid space. Reprinted with permission.31

30

HALASZYNSKI ANDHARTMANNSGRUBER L i[aavm entum Fg um

~i~ '~_~--~'--~ 1 Dura Lamina

2

3

Epidural Ligamentum Fa l vum

Space

Fig 5. (A) Lateral (paramedian approach) angulation of a needle results in an oblique penetration of the ligamentum flavum. The dural cuff region is rich in spinal nerves and vessels. It also has a narrow epidural space and thin dura. (B) "Saw tooth" shape of the epidural space due to attachments of the ligamentum flavum. Notice the needle angulation necessary to penetrate the ligamentum flavum. (I) Needle contact with lamina of the inferior spinous process (X and Y). (2 and 3) Needle is angled superiorly at the level of subcutaneous tissues. Withdraw of the needle from the fibrous ligaments is necessary prior to changing angulation of the needle. (3) Penetration of the ligamentum flavum for successful access to the centroneuroaxis. Reprinted with permission?~

space at the caudal portion of the upper lamina and a wider space near the rostral segment of the lower lamina of each interspace (Fig 5B). 16 The epidural space has no direct communication with the cerebrospinal fluid (CSF); medications injected into this space enter the subarachnoid space only by diffusion. Large epidural veins, which contain no valves, drain into the azygos vein, perivertebral venous plexus, and intracranial veins. Thus, drugs or air inadvertently injected into an epidural vessel have a direct path to the systemic circulation. After penetration into and through the posterior epidural space, the needle tip next encounters the three protective coverings of the spinal cord and cauda equina. The outermost meningeal layer, the dura mater, is comprised of longitudinally organized fibers that extend down the verte-

bral column as a fibroelastic tube and terminate at the inferior border of $2. For subarachnoid placement of local anesthetics, the dura mater provides the characteristic " p o p , " which usually indicates that the subarachnoid space has been entered. Between the dura and arachnoid mater, immediately subdurally, there is a potential space that contains lymph and capillaries. In rare cases (0.1% to 0.2%), the needle tip and deposition of drugs may open this subdural space. 17 This may result in either a total spinal when epidural doses of drugs are administered or may be one of the potential causes of a failed spinal. This potential cavity extends to the nerve roots and ganglia, with communication to the cranial cavity, but once again, has no direct accessibility to the CSF. Directly adjacent to the dura mater is the arachnoid mater, a nonvascular connective tissue cov-

SPINAL AND EPIDURAL ANESTHESIA ering, which is the middle meningeal membrane. With the dura mater, this meningeal layer also extends to the inferior border of the $2 vertebra. After passing through the arachnoid mater, the needle tip enters the subarachnoid space. This space contains the CSF and is confined to the area between the pia and arachnoid mater. The pia mater is a fragile vascular membrane, closely attached to the spinal cord, the cauda equina, and the spinal nerve roots. The spinal cord and spinal nerve roots are bathed in CSF. As the spinal nerve roots penetrate beyond spinal dura and enter the epidural space, they retain all three meningeal layers. The subarachnoid space continues along both nerve roots (dorsal and ventral), ending at the dorsal root ganglia. Deeper penetration of the needle tip at the level of the cauda equina disperses the segmental nerves, which are covered by pia mater and leaves the subarachnoid space to enter into the anterior dura. At the spinal cord level, deeper penetration of the needle tip will encounter the pia mater before injuring the spinal cord.

SURFACE ANATOMY Successful neural blockade begins with knowledge of the surface anatomy (Fig 6). The midlumbar region is the level at which the majority of neuraxial blockades are performed. A line drawn between the superior portion of the two iliac crests most commonly passes through this midlumbar region at the level of the spinal process of L4. The interspinous space below is L45. This space, the space above (L3-4), and the interspinous space at L2-3 are the most common sites chosen for needle placement. Confirming the location of the interspaces at L2-3 and L3-4 can be additionally made by identification of the first lumbar vertebra via a line drawn through the inferior border of the outer end of the fight and left 12th ribs. As previously noted, the spinal cord in adults ends at the lower border of L1. A line drawn between each of the posterior superior iliac spines crosses at the approximate level of $2, corresponding to the termination of the dural sac in adults. The inferior angle of the scapula corresponds to the seventh thoracic vertebra, the root of each spine of the scapulae corresponds to T3, and C7 (one of the most important midline landmarks) corresponds to the vertebra prominens.

31

C7

I

birte T3

gte T7

lOcm ~e LI spect }st L4

~uperior S2

Fig 6. Landmarks and surface anatomy for centroneuraxis blockade. Reprinted with permission?~

For a paramedian approach to the spinal canal in the lumbar area, assuming the patient is in the lateral decubitus position, we recommend drawing a vertical line through one spinal process. On this line, the needle entry point should be at least 2 cm (approximately two finger-breadths) lateral from the midline. This is in contrast to the midline approach, in which the needle entry point is immediately cranial to the lower spinal process (Fig 7). An entry point this far from midline is suggested because the tip of the needle should not contact the spinal process of the upper or lower vertebra, but rather the lamina of the vertebra through which the vertical line has been drawn. Contacting the lamina of the vertebra means that the needle should be withdrawn 5 to 8 m m and a steeper, more cephalad angle attempted until the needle tip walks over the superior rim of the lamina of the lower vertebra. The novice will be amazed at the steep angle required to walk the needle tip over the rim. The hub of the needle is frequently less than 1 cm away from the skin on entering the epidural or subarachnoid space. The needle direction should aim toward

32

HALASZYNSKI AND HARTMANNSGRUBER LUMBAR EPIDURAL (b) Patasp~ncus

(a) Midline

.:

J

~(b) THORACIC EPIDURAL (a) Midline

(b) ParaspJnous

an imaginary point deep to the spinal process of the next higher vertebra in a cephalo-medialanterior direction. For the thoracic paramedian approach, variation of the needle direction toward an imaginary point in a cephalo-medialanterior direction of the interspinous space above the next higher spinous process is required. For example, if the needle entry site is on a line inferior to the spinous process of T7, an imaginary point deep to the interspinous space of T5T6 is the directional path chosen for the needle. PHYSIOLOGY Spinal neural blockade is defined as subarachnoid injection of a local anesthetic agent into the CSF, producing a temporary interruption of nerve transmission. Spinal anesthesia is effective with small amounts of drug, producing exceedingly reliable surgical anesthesia. Systemic absorption and plasma concentrations of local anesthetics are so low with this technique that physiologic effects on various organ systems can

Fig 7. Relationship of needle insertion site for midline and paramedian approach to the vertebral column at thoracic and lumbar segments. Upper panel: Lumbar epidural. (a) Midline. Note insertion closer to the superior spinous process and with a slight upward angulation; (b) Paraspinous (paramedian). Note insertion beside caudad edge of "inferior" spinous process, with 45 degree angulation to long axis of spine below. Lower panel: Thoracic epidural. (a) Midline. Note extreme angulation required in mid thoracic region. Therefore, a paraspinous approach may be easier; (b) paraspinoas. Note needle insertion next to caudad tip of the spinous process above interspace of intended level of entry through ligamentum flavum. Upward angulafion is 55 degrees to long axis of spine below and inward angulafion is 10 to 15 degrees. Reprinted with permission?~

be excluded. Therefore, physiologic responses after subarachnoid blockade originate from actions of the anesthetic agents on the nerve fibers contained within the subarachnoid space. Immediately following injection of an anesthetic into the CSF, there is a rapid decrease in concentration, as well as uptake into local tissues, as it spreads away from the injection site. The location of the highest concentration of the anesthetic in the CSF is dependent on (1) the site of injection, (2) the baricity of the injected solution, (3) the position of the patient until fixation of local anesthetics (approximately 20 minutes), (4) the volume of the drug in relation to the volume of the CSF, (5) the speed of injection, and (6) the concentration of the anesthetic solution. Following subarachnoid injection, local anesthetics have been found to be most highly concentrated in the lateral and posterior columns. Intermediate concentrations are found in ventral roots, with the lowest in dorsal root ganglia and gray matter of the anterior horn. The dorsal roots

SPINAL AND EPIDURAL ANESTHESIA are the primary targeted area when SA is performed. The dorsal roots contain small-diameter nerve fibers carrying preganglionic autonomic fibers, temperature, dull pain, and touch fibers. Large-diameter fibers, centrally embedded in the nerve bundle, carry motor ability and proprioceptive senses. The majority of the physiologic effects of SA, and essentially all the cardiovascular effects, are mediated by preganglionic sympathetic blockade. Sympathetic nervous system fibers are more peripherally located in the nerve roots than are the ~sensory fibers. The level of sympathetic fiber blockade is produced at two or more dermatomes higher than the sensory blockade. These conclusions are clinically confirmed by the loss of cold sensation and an increase in skin temperature (thermography). These methods are not sufficiently quantitative to determine complete sympathetic denervation, and recent evidence indicates that it is difficult to achieve a complete sympathetic block during EA or SA using standard clinical doses of local anesthetic agents. Spinal anesthesia using tetracaine has been reported to produce a decrease in plasma catecholamine concentrations, which has not been demonstrated for EA; it was assumed in the past that SA results in a more complete sympathetic blockade than EA. However, in a recent cross-over study in young healthy volunteers subjected to a cold stimulation test, both techniques resulted in equal but not complete attenuation of the sympathetic response.18 The "tourniquet pain" problem is further evidence that the degree of sympathetic blockade is not complete and that different local anesthetics, or supplements to local anesthetics, attenuate this sympathetic response by different means. The degree of sympathectomy occurs at a graded intensity, depending on the local anesthetic used, despite adequate sensory or motor blockade. Smaller volumes and lower concentrations of local anesthetic agents, as well as local anesthetics that have been mixed with glucose (hyperbaric mixture), have been shown to increase the chance for early tourniquet pain. When glucose was added to 3 mL of 0.5% bupivacaine, the incidence of tourniquet pain at similar sensory levels was 37%, compared with 13% when the same volume of plain isobaric bupivacaine was used.19 Concepion et al20 found that 15 mg of bupiva-

33 caine and 15 mg of tetracaine were associated with a statistically significant difference in the incidence of tourniquet pain (25% and 60%, respectively). One explanation for the prolonged tourniquet tolerance with bupivacaine is that tetracaine offers less prolonged blockade of C fibers. 21 Therefore, our recommendation regarding surgeries performed using SA in which a tourniquet is to be applied is the use of a large volume of isobaric bupivacaine. In a 70-kg man, we usually administer 3 mL of isobaric 0.5% bupivacaine. With this large volume of a local anesthetic agent, an alteration of hemodynamic response should be anticipated, and neosynephfine or ephedrine and fluids should be readily available.

Cardiovascular System Effects The systemic cardiovascular changes to subarachnoid injections of local anesthetic agents, as mentioned above, are not from direct effects on the cardiovascular system. The cardiovascular response varies considerably from patient to patient and is dependent on the extent of spread and resultant preganglionic sympathetic denervation. The resultant reduction in blood pressure is one of the hallmarks of SA. The clinician appreciates this reduction in systolic blood pressure as the first objective signal of local anesthetic deposition in the subarachnoid space. Spinal anesthesia decreases afterload due to arterial and arteriolar vasodilation (decreases preload by venous pooling), thereby reducing the stress within the walls of the ventricle during contraction and leading to increased perfusion of affected tissues and organs. Peripheral vascular resistance, in the absence of vasopressors, is decreased with SA to the magnitude of 10% to 30%. With a lower level of SA, a decrease in blood pressure may not be seen due to compensatory vasoconstriction in sympathetically nonblocked areas. Vasodilatation in the areas of sympathetic blockade is not maximal and has been shown to be augmented by hypercarbia, acidosis, hypoxia, barbiturates, opioids, and other vasodilating drugs. The capillary bed is profoundly affected by SA. The volume of blood in capillary tissues is increased after subarachnoid blockade, resulting in a greater than normal percentage of the total blood volume in these peripheral sites. Tetracaine, versus general anesthesia, has been shown to double

34 the mean leg blood flow; this blood flow has remained elevated for up to 2 hours postoperatively. 22

Heart Rate Effects Although the heart rate may not change after subarachnoid injection of local anesthetic agents, most frequently a decreased heart rate is observed. Pronounced decreases in heart rate can be seen when cardiac output and mean arterial blood pressure are markedly decreased as a result of a high spinal level. This bradycardia is often preceded by nausea, both of which can be treated by prompt intravenous administration of atropine. The bradycardia is caused by blockade of preganglionic cardiac accelerator fibers and decreased filling of the heart due to increased venous capacitance. Cardiac accelerator fibers arise from the first four thoracic spinal segments. A marked decrease in heart rate usually is seen when the sensory level reaches T4. The Trendelenburg position should be used with caution, favoring a neutral, supine, position when a level T4 spinal is obtained and bradycardia along with hypotension result. This is due to the concern that the segmental level may rise even higher than T4 with the Trendelenburg position, if the local anesthetic has not yet become fixed. A reversed Trendelenburg position also should be avoided in this circumstance, as it would further decrease cerebral perfusion. This bradycardia and hypotension should be treated with atropine, vasopressors, and intravenous hydration. Baroreceptors in the great veins and the right atrium dominate over carotid sinus reflexes. This is felt to be the reason why tachycardia does not result from high SA.

Cardiac Output In the first 15 minutes following subarachnoid blockade, the cardiac output may increase from 5% to 15% secondary to afterload reduction. However, the predominant response to spinal blockade is a reduction of cardiac output due to decreased venous return to the heart. This reduction in cardiac output is dependent on the level of sympathetic denervation. Cardiac output is depressed more with high levels of SA and with the reverse Trendelenburg position. A 36% and 21% reduction in cardiac output has been described with a T6 to T3 sensory level of SA when

HALASZYNSKI AND HARTMANNSGRUBER patients are placed in a 30- to 49-degree headup position compared with a horizontal supine position. The reduction in cardiac output probably effects all organs equally. With clinical levels of SA, there is no significant change in either distribution of cardiac output or in absolute levels of blood flow in various tissues and organs. 23

Coronary Blood Flow Spinal anesthesia decreases blood supply to the myocardium, but to a greater extent, SA decreases the myocardial metabolic and oxygen requirements. Spinal anesthesia with local anesthetics has a pharmacologic effect similar to nitroglycerin. In rats, the threshold of myocardial ischemia recently has been shown to be increased significantly after intrathecal bupivacaine, an effect equivalent to that of propranolol. 24 In the patient with severe coronary artery disease, care must be taken in the transition phase after surgery. Regression of the sensory level below the incision site can lead to increased pain, an increased heart rate, increased afterload, and preload. The net effect may be deleterious for coronary perfusion. Monitoring in an intensive care or postanesthesia care unit is important in this patient subgroup until the effects of SA have completely resolved. The resulting physiologic changes, due to resolution of spinal blockade, may be deleterious for a heart with stenotic coronary blood flowY

Hypotension Hypotension is the most common side effect of SA. It is primarily due to blockade of preganglionic sympathetic fibers that transmit motor impulses to the smooth muscle of the peripheral vasculature. The degree of decrease in the blood pressure is proportional to the number of sympathetic fibers blocked. A decrease in peripheral vascular resistance precedes the decrease in cardiac output. The magnitude of hypotension, for clinical purposes, is indicative of the relative role played by changes in peripheral vascular resistance and by changes in cardiac output. Relatively minor degrees of arterial hypotension primarily stem from changes in peripheral vascular resistance, whereas a systolic blood pressure below 90 m m Hg has a stronger component due to a reduction in cardiac output. 23 Historically, hypotension has been viewed as a

SPINAL AND EPIDURAL ANESTHESIA complication; however, it is increasingly recognized that this hypotension can result in decreased oozing and less blood loss at the operative site. The duration of sympathetic denervation usually outlasts surgical time. The time necessary for the sympathetic block to resolve completely is dependent on the volume and lipid solubility of the local anesthetic used and whether epinephrine was added to the local anesthetic solution. Once levels of sensory blockade have regressed below L2, hypotension can no longer be attributed to a sympathetic blockade caused by local anesthetics.

Respiratory System Effects Sensory blockade below the level of T10 does not impair respiratory function. However, upper abdominal procedures often require a sensory dermatomal blockade higher than T1, resulting in blockade of motor fibers to expiratory, abdominal, and intercostal muscles. In normal, healthy patients, high thoracic levels of SA have little effect on resting ventilatory mechanics. This is because the diaphragm can compensate for decreases in ventilation resulting from intercostal muscle paralysis. This compensatory mechanism is aided by a concurrent paralysis of abdominal muscles, thereby allowing the diaphragm to descend with less resistance. It is the expiratory ability (especially forced expiration) that is most affected by high sensory spinal blockade. However, there is no increase in the frequency to develop wheezing in asthmatic patients as a result of the sympathectomy produced by SA. In theory, by decreasing systemic catecholamines, the bronchodilating effects of the sympathetic nervous system can be removed. The most frequent culprit to induce bronchospasm is manipulation of the airway, which may be avoided by neuraxial techniques. Gas diffusion under SA is essentially unchanged. There is no significant effect on arterial oxygen content or oxygen saturation. Arterial Pc02 levels actually may be slightly decreased in the unsedated patient, again indicating little effect of SA on alveolar ventilation. Minor hyperventilation and decreased carbon dioxide production, as documented with SA, may be the reason. Increases in Pc02 during SA are due most frequently to concomitant administration of narcotics and/or sedatives. Complete phrenic nerve paralysis, with resultant respiratory arrest, is rare during SA, even

35 with very high (cervical and cranial) levels of sensory anesthesia. This is due to relative resistance to the effects of local anesthetics by the phrenic nerve compared with the smaller sensory fibers. Local anesthetic concentrations used during SA rarely reach concentrations sufficient to block phrenic nerve fibers. A more frequent reason for respiratory arrest, during high spinal blockade, is the reduction in cardiac output and hypotension, resulting in hypoperfusion of the respiratory center in the brain stem. Therefore, treatment of respiratory arrest during SA requires the maintenance o f venous return to the heart to provide an adequate cardiac output. 23

Renal System Effects Under clinical conditions, a sympathetic denervation resulting from SA has little effect on renal blood flow, when the blood pressure remains within normal values. Normal renal blood flow decreases when the mean arterial blood pressure decreases below 80 m m Hg. Mean arterial blood pressure below 100 m m Hg has been shown to decrease glomerular filtration, resulting in a proportionally decreased urine production. However, there usually is prompt return to normal levels of renal blood flow as the effects of SA begin to wane. This return of normal renal blood flow occurs without an increase in blood urea nitrogen. If hypotension has been severe or prolonged, this may not occur.

Gastrointestinal System Effects Sympathetic denervation, produced by local anesthetics during SA, causes contraction of the stomach, jejunum, ileum, and colon, and relaxation of sphincters due to the unopposed action of the parasympathetic nervous system. Intraluminal pressures are increased. Splanchnic blood flow is increased by approximately 20% during SA. Return of normal intestinal activity (balance between sympathetic and parasympathetic) has been shown to be significantly more rapid following SA compared with general anesthesia. A relatively frequent complication of neuraxial anesthesia, nausea and vomiting, is caused by hypoperfusion of the brain stem. This is due to a low cardiac output state that results from a sympathectomy and decreased cardiac accelerator activity. Prompt restoration of the blood pressure is the most effective treatment. As men-

36 tioned above, additional factors contributing to nausea and v o m i t i n g are increased gastric motility and increased intestinal tone.

Effects on the Hematologic System Although there is no direct effect o f the local anesthetics used during S A on coagulation and the fibrinolytic system, S A decreases b l o o d loss (probably due to its effect on m e a n arterial b l o o d pressure). In addition, S A reduces the incidence of deep venous thrombosis up to 10% to 20% in patients for total hip replacement. 26 The incidence o f p u l m o n a r y e m b o l i s m has been shown to be d e c r e a s e d with the use o f SA. This m a y be due to d e c r e a s e d venous stasis as a result o f doubling o f the m e a n leg b l o o d flow with S A c o m p a r e d with only a 36% increase in m e a n leg blood flow during general anesthesia. Earlier ambulation also m a y partially explain the reduction in serious p o s t o p e r a t i v e h e m a t o l o g i c c o m p l i c a tions.

Comparison of the Physiologic Factors of Epidural Versus Spinal Anesthesia A l t h o u g h S A and E A have m a n y p h y s i o l o g i c effects in c o m m o n , subtle differences do exist. S o m e o f the fundamental differences in p h y s i o l ogy b e t w e e n S A and E A are the h e m o d y n a m i c and organ effects o f EA, due not only to s y m p a thetic denervation, but also in part to circulating concentrations o f local anesthetics. B l o o d levels of local anesthetics, resulting from epidural techniques, can lead to both systemic and central nervous system effects. The addition o f epinephrine to epidural solutions o f local anesthetics can increase the cardiac output and p o s s i b l y decrease peripheral vascular resistance due to beta-adrenergic stimulation. A major difference b e t w e e n E A and S A is the extent of the sensory to m o t o r level o f blockade. W h e n a high level o f S A is c o m p a r e d with a high level of EA, the m o t o r to sensory level o f b l o c k a d e is a p p r o x i m a t e l y two d e r m a t o m a l segments lower in the epidural group. 27 Clinically, this difference m a y b e c o m e important in patients with decreased p u l m o n a r y reserve as p u l m o n a r y function is altered with increasing p u l m o n a r y m u s c l e paralysis. These same sensory to m o t o r zone differential effects with epidural local anesthetic solutions, seen especially with m o r e dilute concentrations o f local anesthetics (for e x a m p l e ,

HALASZYNSKI AND HARTMANNSGRUBER 1/16% to 1/32% bupivacaine), p l a y an important role in the m a n a g e m e n t o f acute pain and labor pain. A higher concentration o f local anesthetic solutions and the addition o f epinephrine increase the intensity o f m o t o r b l o c k a d e for EA. W i t h the exception o f etidocaine, c o m p l e t e m o t o r paralysis is unlikely, even with use o f high concentrations o f local anesthetics during EA. Injection o f 15 m L of normal saline into an epidural catheter will achieve partial reversal o f (now undesired) m u s c l e b l o c k a d e within 5 minutes without a decrease in sensory blockade. This effect is most likely e x p l a i n e d b y a washout effect. 28

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