Hypotension and bradycardia during spinal anesthesia: Significance, prevention, and treatment

Hypotension and Bradycardia During Spinal Anesthesia: Significance, Prevention, and Treatment Joseph M. Neal, MD

Hypotension and bradycardia are common side effects of spinal anesthesia, and they represent normal physiologic responses to anesthetized spinal sympathetic nerve fibers. The primary physiologic alterations are decreased preload and cardiac volume, which combine with bradycardia to reduce arterial blood pressure and cardiac output. Mild hypotension or bradycardia may be treated with volume expansion, ephedrine, or atropine. However, severe and/or rapidly progressing bradycardia demands aggressive treatment with epinephrine, followed by cardiopulmonary resuscitation if appropriate. Although somewhat controversial, evidence given in favor of prophylactic volume loading or vasopressor administration is generally unsupportive. Not every episode of spinal hypotension or bradycardia is clinically significant, but the anesthesiologist’s vigilance is challenged to prevent mild aberrations from developing into major hemodynamic compromise. Controlling sensory block height, being alert to downward trends in heart rate and blood pressure, and reacting quickly and decisively to these changes are the key steps toward preventing catastrophe. Copyright © 2000 by W.B. Saunders Company

ypotension and bradycardia are common side effects of spinal anesthesia. When unrecognized or unH treated, they can lead to devastating complications. This article reviews the pathophysiology, significance, and associated risk factors for spinal hypotension and bradycardia. It then offers a practical approach to prevention and treatment. Although similar side effects occur with epidural anesthesia, the focus here is on spinal anesthesia. For a more detailed discussion of hypotension in both epidural and spinal anesthesia, the reader is referred to McCrae and Wildsmith’s classic review.1

Pathophysiology Reviewing circulatory physiology and spinal cord anatomy facilitates an understanding of spinal hypotension and bradycardia. These physiologic perturbations are ultimately the manifestations of anesthetized spinal sympathetic nerve fibers. It is important to note that as neural blockade extends to higher thoracic spinal cord levels, the ability to compensate for physiologic alterations is progressively impaired. As T5 through L1 spinal nerve fibers From the Department of Anesthesiology, Virginia Mason Medical Center, Seattle, WA. Reprints not available. Copyright © 2000 by W.B. Saunders Company 1084-208X/00/0404-0001$10.00/0 doi:10.1053/trap.2000.20600

are blocked, efferent input to the adrenal glands is attenuated, thereby limiting normal catecholamine response to hypotension and bradycardia. Sensory block above T4 eliminates compensatory upper extremity vasoconstriction, and further ascendance to T1 through T5 sympathetic (cardioaccelerator) fibers blocks reflex tachycardia and reduces myocardial contractility. Compensatory mechanisms are likely further impaired by autonomic imbalance, such as is found in diabetic and elderly patients.2 Figure 1 details the physiologic principles of blood pressure regulation, and Figure 2 illustrates spinal cord anatomy pertinent to the sympathetic autonomic nervous system. Hypotension Systemic blood pressure is dependent on cardiac output and systemic vascular resistance (SVR), the latter being the primary contributor to spinal hypotension.3 Local anesthetic–induced blockade of lumbar preganglionic sympathetic fibers decreases SVR, causing peripheral pooling of blood, which reduces venous return and preload. Diminished preload results in reduced stroke volume and cardiac output, leading to systemic hypotension (Fig 1). Other factors, such as aortocaval compression in the parturient, may exacerbate this condition. High thoracic blocks further contribute to hypotension by decreasing myocardial contractility. Spinal hypotension in elderly patients with cardiac disease deserves special consideration, because spinal anesthesia is frequently recommended for this population. Average T4 sensory block results in markedly decreased mean arterial pressure (⫺33% ⫾ 15%) consequent to a 26% reduction in SVR and a 10% reduction in cardiac output. Nevertheless, overall cardiac performance is minimally affected, assuming appropriate vasopressor and/or contractility support is rendered.3 Bradycardia Spinal bradycardia is partially the result of unopposed parasympathetic tone resulting from blockade of T1 through T5 cardioaccelerator sympathetic fibers (Fig 2), but it is primarily caused by decreased preload.4 Decreased preload contributes to bradycardia by activating a group of reflexes that respond to a stretch of intracardiac volume and/or pacemaker receptors. Rapid decrease in left ventricular volume has been speculated to cause se-

Fig 1. Overview of the physiology of systemic arterial pressure. (Reprinted by permission of the Mayo Foundation.23)

vere bradycardia and asystole via paradoxic activation of the Bezold-Jarisch reflex.2

Clinical Significance Because the aforementioned physiologic changes are associated with spinal anesthesia, bradycardia and hypotension are relatively common side effects, even if they are

not always clinically significant.4 Gradual heart rate reduction that stabilizes within 10% to 15% of baseline and is not associated with hypotension requires careful observance but may not require treatment. Similarly, 15% to 20% reduction of arterial blood pressure in healthy patients without pre-existing hypertension, coronary artery disease, or aortic stenosis is not necessarily associated with compromised end-organ blood flow. Indeed, im-

Image available in print only Fig 2. Contribution of spinal sympathetic nerve input to circulatory control. (Adapted and reprinted with permission.24)

proved coronary blood flow coupled with bradycardia and decreased contractility reduces myocardial oxygen demand, thereby partially offsetting reduction in coronary perfusion pressure that occurs secondary to decreased diastolic blood pressure (Fig 2). Normal autoregulatory parameters may serve as guidelines for acceptable essential organ perfusion pressures during spinal anesthesia in healthy patients.1 For instance, the lower limit of coronary blood flow autoregulation is a mean arterial pressure of 60 mm Hg, whereas for cerebral blood flow it is 50 mm Hg. Glomerular filtration rate is not significantly affected by spinal anesthesia.5 Thus, mild to moderate hypotension and bradycardia do not always require treatment, but their presence demands vigilance and rapid action should more serious hemodynamic compromise develop. A 1966 review reported that hypotension requiring treatment occurred in 38% of 11,574 patients undergoing spinal anesthesia.6 Thirty years later, the same institution reported a similar incidence (33%) when hypotension was defined as a systolic blood pressure below 90 mm Hg. Bradycardia (heart rate less than 50 beats/min) occurred in 13% of patients.4 Despite the frequency of these side effects, severe hypotension, bradycardia, and asystole are uncommon but not rare. When they do occur, serious morbidity and mortality may result, as noted by Caplan et al7 in their sentinel-event reporting of 14 cases of unexpected cardiac arrest during spinal anesthesia in healthy patients, 6 of whom died and an additional 7 of whom suffered severe neurologic injury. Of these patients, 8 presented with hypotension, and 11 had bradycardia or asystole as initial clues before cardiac arrest.

Associated Risk Factors Hypotension Carpenter et al4 prospectively studied risk factors for spinal anesthesia side effects in 952 patients. Peak sensory block height at or above T5 was the most predictive variable for developing hypotension (odds ratio 3.8) (Fig 3), and it directly correlated with the severity of hypotension (Fig 4). Other risk factors, in order of predictive strength, were age above 40 years, baseline systolic blood pressure below 120 mm Hg, combined spinal/general anesthesia, and lumbar puncture at or above the L2-L3 interspace. Hypotension occurred 28 ⫾ 34 minutes after subarachnoid injection, but there was a wide range of onset times, emphasizing the need for vigilance throughout the anesthetic course. Bradycardia The likelihood of bradycardia developing during a spinal anesthetic is increased in patients with baseline heart rates below 60 beats/min, in healthy American Society of Anesthesiologists class I patients as compared with those in classes III or IV, and in patients currently using ␤-adrenergic blockers. In contrast to the common perception that bradycardia is related to high sensory blockade, a spinal sensory level above T5 is a weak predictor of bradycardia (Fig 3) and does not correlate with the severity of bradycardia (Fig 5).4 Mean time to onset is 36 to 47 minutes, but like hypotension, there is a wide range of time between subarachnoid injection and onset of bradycardia.4,7 Caplan et al’s report7 of serious morbidity and

Image available in print only

Fig 3. The incidence of hypotension strongly correlates to peak sensory block height. The correlation with bradycardia is considerably weaker. (Reprinted with permission.4)

Image available in print only Fig 4. The magnitude of systolic blood pressure (SBP) change correlates in a linear fashion (R2 ⴝ 0.07) with peak sensory block height. (Reprinted with permission.4)

death in otherwise healthy patients identified 2 risk factors for severe bradycardia and asystole: sedation to the point of no spontaneous verbalization and delayed provision of aggressive ␣-receptor agonist intervention once asystole developed.7 However, precipitous bradycardia may also appear in stable, well-oxygenated, alert patients (Fig 6).2 Thus, spinal bradycardia may occur any time during a routine spinal anesthetic, regardless of sensory block height, hemodynamic stability, or patient level of consciousness.

Prevention Many predictors of hypotension and bradycardia, such as age, American Society of Anesthesiologists classification, or preoperative ␤-adrenergic receptor blockade, are beyond the anesthesiologist’s control. However, sensory block height is highly predictive of hypotension and mildly predictive of bradycardia. Anesthesiologists can variably affect block height by administering spinal anesthesia at or below the L3-L4 interspace,4 by using incre-

Image available in print only Fig 5. Minimum heart rate does not correlate with peak sensory block height in patients with spinal bradycardia. (Reprinted with permission.4)

Fig 6. Trended heart rate analysis. Subarachnoid block was administered at arrow. About 12 minutes later, after gradual slowing, the heart rate precipitously dropped to below 30 bpm. The patient quickly responded to rapid administration of atropine, ephedrine, and chest compressions. (Reprinted with permission.2)

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mental dosing with a continuous spinal technique,8 by positioning the patient to avoid cephalad spread of local anesthetic, or by using isobaric local anesthetic solutions and avoiding hyperbaric ones.9 Although unilateral spinal blockade minimally decreases the incidence of hypotension, it may be impractical because it requires that patients stay in the lateral decubitus position for 15 to 20 minutes after subarachnoid injection.10,11 Two other interventions—prophylactic volume loading and/or vasopressors— deserve expanded comment. Prophylactic Volume Loading Multiple studies of volume loading as an effective prophylaxis against spinal hypotension have failed to provide consensus. This failure is largely due to the various patient populations studied (surgical, obstetric, elderly); nonuniform definitions of hypotension; and confounding influences from prophylactic or treatment vasopressors. Most recent studies fail to show sustained and predictable blood pressure maintenance after prophylactic crystalloid administration. Blood pressure and cardiac indices transiently increase, but these effects are short-lived because crystalloid solutions remain intravascular for only a limited time. Alternatively, volume preloading with colloid solutions results in greater and longer-lasting volume expansion, but this approach requires larger volumes (1.0 L of 6% hydroxyethyl starch solution) to accomplish this effect and still fails to prevent hypotension in all patients.12 Even though elderly patients are perhaps less able to compensate for spinal hypotension, neither crystalloid nor colloid prehydration significantly altered the incidence of hypotension or ephedrine use when compared with no prehydration in a group of healthy elderly patients undergoing hip replacement.13 Furthermore, clinical reports of hypotension and bradycardia have not shown a link to volume preloading ranging from below 500 to 900 mL.4,7 Given the absence of consistent evidence supporting

the usefulness of prophylactic volume preloading, it is difficult to recommend this intervention for euvolemic patients undergoing spinal anesthesia. Moreover, in parturients there is little evidence that spinal hypotension leads to significant maternal or fetal morbidity when it is recognized early and treated appropriately.14 Similarly, prophylactic hydration does not ameliorate hypotension in the elderly. These questionable benefits must be weighed against the risks of volume expansion: the cost of colloid therapy, including its small risk of anaphylaxis; congestive heart failure in elderly or pregnant patients; and urinary retention in healthy outpatients. Prophylactic Vasopressors The use of prophylactic vasopressors, like volume loading, is controversial because of inherent difficulties associated with appropriate study design. Prophylactic 50 mg ephedrine given intramuscularly significantly reduced the incidence of hypotension in cesarean section patients who were given spinal anesthesia15 but not in those parturients who received epidural anesthesia.16 A recent study reported17 that the minimum effective intravenous ephedrine dose in parturients was 30 mg, yet hypotension still occurred in 35% of these patients, and 45% developed reactive hypertension. In another study,18 the incidence of hypotension was reduced after large-volume (1.0 L crystalloid ⫹ 0.5 L colloid) prehydration and small-dose (5 mg intravenous) ephedrine, but total ephedrine dose was comparable with a placebo dose. When compared with prophylactic fluid administration, prophylactic dihydroergotamine shifted the time course of hemodynamic changes later into the postsubarachnoid injection period, but neither intervention consistently prevented hypotension.19 Thus, as suggested by McCrae and Wildsmith,1 the most significant difficulties with prophylactic ephedrine are unreliable prevention of hypotension and unpredictable pharmacokinetics. Consequently, they rec-

ommend judicious vasopressor treatment of hypotension when it occurs rather than prophylaxis.

Treatment Hypotension Treatment of spinal hypotension is best directed toward reversal of underlying physiologic causation— decreased SVR, preload, and cardiac output. Simple maneuvers to supplement volume, such as fluid administration and use of the Trendelenberg position, are rapid and easy, even if only moderately effective. Elderly patients may not be able to sufficiently increase stroke volume in response to increasing preload and therefore often require vasopressors.3 Vasopressor management is predicated on the patient’s hemodynamic profile and the desired effect on heart rate or diastolic blood pressure. Ephedrine has mixed direct and indirect actions on ␣- and ␤-adrenergic receptors. It is the vasopressor of choice for spinal hypotension in the parturient because of its ability to maintain uteroplacental blood flow. Ephedrine is also the most appropriate choice for treating the noncardiac sequelae of spinal anesthesia, that is, increased arteriolar dilatation and venous capacitance.20 Ephedrine is the preferred treatment of hypotension in patients with relatively low heart rate. It restores systolic arterial pressure by increasing heart rate and cardiac output. However, it does not restore mean or diastolic arterial pressure. Phenylephrine, a strong ␣-receptor agonist with weak ␤-receptor effects, is best used in hypotensive, tachycardic patients. Phenylephrine decreases heart rate and restores systolic, mean, and diastolic arterial pressures, but it also decreases cardiac output.21 Epinephrine, a potent ␣- and ␤-adrenergic receptor agonist, augments arterial pressure by increasing cardiac output when given in low doses (0.1 ␮g/kg/min) to patients with central neuraxial blockade.22 Furthermore, it is the drug of choice for hypotension refractory to ephedrine or phenylephrine, particularly in the setting of severe bradycardia.7 Bradycardia and Asystole Mild to moderate bradycardia is treated with 0.4 to 1.0 mg of atropine given intravenously, repeated every 5 minutes, not to exceed 2 mg. Note that less than 0.1 mg atropine has been associated with paradoxic bradycardia. Epinephrine provides the intense ␣- and ␤-adrenergic stimulation required to overcome spinal anesthesia–induced sympathectomy. In the case of severe bradycardia, particularly if refractory or occurring after a precipitous decrease in heart rate, 5 to 20 ␮g epinephrine should be administered intravenously and the dose incrementally increased every minute until achievement of the desired effect. Should asystole ensue, 1 mg epinephrine should be administered without delay. Failure to achieve timely resuscitation after cardiac arrest in the setting of spinal anesthesia has been associated with delayed and inade-

quate dosing of epinephrine.7 In addition, raising the patient’s legs enhances preload, thereby interrupting those cardiac reflexes that are reacting to intracardiac hypovolemia.

Summary Hypotension and bradycardia are common sequelae of spinal anesthesia. They demand the anesthesiologist’s vigilance because of their propensity to suddenly and unpredictably cause major hemodynamic compromise. When this occurs, treatment is aimed toward reversal of those physiologic perturbations leading to impaired cardiac output—reduced SVR, reduced preload, bradycardia, and decreased myocardial contractility. Although high sensory block level, advanced age, and preoperative ␤-adrenergic blocker use are risk factors for spinal hypotension and bradycardia, they are not reliably predictive. Nor can prophylactic volume loading or vasopressors be relied on to prevent these side effects. Ultimately, it is the anesthesiologist’s understanding of the physiology of spinal anesthesia combined with intraoperative vigilance that best protects the patient from having an expected side effect develop into a major complication.

References 1. McCrae AF, Wildsmith JAW: Prevention and treatment of hypotension during central neural block. Br J Anaesth 70:672-680, 1993 2. Mackey DC, Carpenter RL, Thompson GE, et al: Bradycardia and asystole during spinal anesthesia: A report of three cases without morbidity. Anesthesiology 70:866-868, 1989 3. Rooke GA, Freund PR, Jacobson AF: Hemodynamic response and change in organ blood volume during spinal anesthesia in elderly men with cardiac disease. Anesth Analg 85:99-105, 1997 4. Carpenter RL, Caplan RA, Brown DL, et al: Incidence and risk factors for side effects of spinal anesthesia. Anesthesiology 76:906-916, 1992 5. Kennedy WF, Sawyer TK, Gerbershagen HU, et al: Simultaneous systematic cardiovascular and haemodynamic measurements during high spinal anaesthesia in normal man. Acta Anaesthesiol Scan 37:163-171, 1970 6. Moore DC, Bridenbaugh LD: Spinal (subarachnoid) block. A review of 11,574 cases. JAMA 195:907-912, 1966 7. Caplan RA, Ward RJ, Posner K, et al: Unexpected cardiac arrest during spinal anesthesia: A closed claims analysis of predisposing factors. Anesthesiology 68:5-11, 1988 8. Schnider TW, Mueller-Duysing S, Johr M, et al: Incremental dosing versus single-dose spinal anesthesia and hemodynamic stability. Anesth Analg 77:1174-1178, 1993 9. Wildsmith JAW, Rocco AG: Current concepts in spinal anesthesia. Reg Anesth 10:119-124, 1985 10. Sumi M, Sakura S, Koshizaki M, et al: The advantages of the lateral decubitus position after spinal anesthesia with hyperbaric tetracaine. Anesth Analg 87:879-884, 1998 11. Casati A, Fanelli G, Aldegheri G, et al: Frequency of hypotension during conventional or asymmetric hyperbaric spinal block. Reg Anesth Pain Med 24:214-219, 1999 12. Ueyama H, He YL, Tanigami H, et al: Effects of crystalloid and colloid preload on blood volume in the parturient undergoing spinal anesthesia for elective cesarean section. Anesthesiology 91:1571-1576, 1999 13. Buggy D, Higgins P, Moran C, et al: Prevention of spinal anesthesiainduced hypotension in the elderly: Comparison between preanesthetic administration of crystalloids, colloids, and no prehydration. Anesth Analg 84:106-110, 1997

14. Rout C, Rocke DA: Spinal hypotension associated with Cesarean section. Will preload ever work? Anesthesiology 91:1565-1567, 1999 (editorial) 15. Gutsche BB: Prophylactic ephedrine preceding spinal analgesia for Cesarean section. Anesthesiology 45:462-465, 1976 16. Rolbin SH, Cole AFD, Hew EM, et al: Prophylactic intramuscular ephedrine before epidural anesthesia for Caesarean section: Efficacy and actions on the foetus and newborn. Can Anaesth Soc J 29:148153, 1982 17. Kee WDN, Khaw KS, Lee BB, et al: A dose-response study of prophylactic intravenous ephedrine for the prevention of hypotension during spinal anesthesia for cesarean delivery. Anesth Analg 90:1390-1395, 2000 18. Vercauteren MP, Coppejans HC, Hoffmann VH, et al: Prevention of hypotension by a single 5-mg dose of ephedrine during small-dose spinal anesthesia in prehydrated cesarean delivery patients. Anesth Analg 90:324-327, 2000 19. Arndt JO, Bomer W, Krauth J, et al: Incidence and time course of cardiovascular side effects during spinal anesthesia after prophylactic administration of intravenous fluids or vasoconstrictors. Anesth Analg 87:347-354, 1998

20. Butterworth IV JF, Piccione W, Berrizbeitia LD, et al: Augmentation of venous return by adrenergic agonists during spinal anesthesia. Anesth Analg 65:612-616, 1986 21. Brooker RF, Butterworth IV JF, Kitzman DW, et al: Treatment of hypotension after hyperbaric tetracaine spinal anesthesia. A randomized, double-blind, cross-over comparison of phenylephrine and epinephrine. Anesthesiology 86:797-805, 1997 22. Sharrock NE, Bading B, Mineo R, et al: Deliberate hypotensive epidural anesthesia for patients with normal and low cardiac output. Anesth Analg 79:899-904, 1994 23. Mackey DC: Physiologic effects of regional block, in Brown DL (ed): Regional Anesthesia and Analgesia. Philadelphia, PA, Saunders, 1996, pp 397-422 24. Liu SS, Carpenter RL, Neal JM: Epidural anesthesia and analgesia. Their role in postoperative outcome. Anesthesiology 82:1474-1506, 1995 25. Batra M, Mulroy MF, Neal J: Spinal, epidural, and caudal anesthesia, in Miller RD, Tremper KK (eds): Atlas of Anesthesia. IV. Principles of Anesthetic Techniques and Anesthetic Emergencies. Philadelphia, PA, Current Medicine Inc, 1997, 4.1-4.19