Cardiac Arrest During Spinal Anesthesia
  Cardiac arrests during spinal anesthesia are described as “very rare,” “unusual,” and “unexpected,” but are actually relatively common. The two largest prospective studies designed to evaluate the incidence of complications during spinal anesthesia reported two arrests in 1881 patients and 26 arrests in 40,640 patients for an overall incidence of seven arrests for every 10,000 (0.07%) spinal anesthetics. The incidence of cardiac arrest with spinal anesthesia is also frequent compared with the rate of one cardiac arrest for every 10,000 cases (0.01%) recently reported for epidural anesthesia.
  The closed claims analysis by Caplan et al. reported 14 cardiac arrests with a mortality rate that exceeded 40% in healthy patients undergoing minor procedures. One-half of the patients who experienced cardiac arrest in the operating room during spinal anesthesia were, 30 years old.
  Because sedation is used for over 80% of patients who undergo spinal anesthesia, the potential role of sedation in these arrests must be considered. But it is now difficult to invoke hypoxemia as the primary cause of cardiac arrests during spinal anesthesia because they occur in the setting of oxygen saturation readings of 95–100% at the time of the arrests.
  Because a high degree of cardiac vagal activity can occur during spinal anesthesia, patients with strong resting vagal tone should be at increased risk for cardiac arrest during spinal anesthesia. The term “vagotonia” describes the clinical situation of resting bradycardia, atrio-ventricular block, or complete atrio-ventricular dissociation that is present in 7% of the population. Carpenter et al. reported that a baseline pulse of ˂ 60 bpm was associated with a fivefold increase in the odds of developing moderate bradycardia during spinal anesthesia.
  Typically, young patients have strong vagal tone, and they reported that ASA physical status I patients have a threefold increased risk for developing moderate bradycardia during spinal anesthesia. Current therapies with b-blockers or block height above T6 were also important risk factors for bradycardia. The patients who are ˂50 years old and patients with first-degree heart block are also at increased risk for moderate bradycardia during spinal anesthesia.
Risk Factors for Moderate Bradycardia (Pulse ˂50 bpm) During Spinal Anesthesia
Baseline heart rate ˂ 60 bpm
ASA physical status I (versus ASA physical status III or IV)
Use of beta-blocking drugs
Sensory level above T6
Age ˂50 yr
Prolonged PR interval
  The occurrence of bradycardia and cardiac arrest are directly or indirectly related to the blockade of sympathetic efferents during spinal anesthesia. For example, the level of sympathetic blockade during spinal anesthesia is often two to six levels higher than the sensory level, so a patient with a T4 sensory block may have completely blocked cardiac accelerator fibers that originate from T1 to T4. Blockade of these fibers can result in a variety of bradyarrhythmias.
  Baron et al. found that cardiac vagal tone is enhanced primarily through reduced venous return. The effect of spinal anesthesia on venous return can be profound. A reduction in the right atrial pressure of 36% after low spinal levels (below T4) and 53% after higher levels of blockade have been reported. With intravascular fluid losses, these effects are even more dramatic. For example, with removal of 10 mL of whole blood per kg of body weight in a study setting, the decrease in central venous pressure during spinal anesthesia averages 66%.
  These decreases in preload may initiate reflexes that cause severe bradycardia. Three such reflexes have been suggested.
The first involves the pacemaker stretch. The rate of firing of these cells within the myocardium is proportional to the degree of stretch. Decreased venous return results in decreased stretch and a slower heart rate.
The second reflex may be attributable to the firing of low-pressure baroreceptors in the right atrium and vena cava.
The third is a paradoxical Bezold-Jarisch reflex, in which mechanoreceptors in the left ventricle are stimulated and cause bradycardia.
  Decreases in preload can precipitate not only classic vagal symptoms, but also full cardiac arrest. Although one might assume that maintaining preload during spinal or epidural anesthesia is a uniform practice of anesthetists, the literature demonstrates otherwise.
  Moderate bradycardia during spinal anesthesia is defined as a heart rate of ˂ 50 bpm. Severe bradyarrhythmias have been reported with T4 levels of sympathetic blockade. In particular, spinal anesthesia has been associated with progression of first-degree heart block to second degree heart block and with the onset of sick sinus syndrome manifest after spinal anesthesia. Complete heart block and cardiac arrest may simply represent the most severe vagal-induced bradyarrhythmia associated with spinal anesthesia. The bradycardia during spinal anesthesia may help predict which patients are at risk for cardiac arrest during spinal anesthesia.
  The decreased incidence of cardiac arrest associated with epidural anesthesia compared with spinal anesthesia is a relatively new finding that has not been explained. One possibility is that the incremental dosing and slower onset of epidural anesthesia may allow time for compensatory mechanisms (e.g., upper body vasoconstriction) to compensate for the decrease in preload.
  Alternatively, the physiologic changes associated with pregnancy may help explain the small rate of cardiac arrest observed in these settings. Pregnancy is associated with changes in autonomic control and at-term heart rates of 90–95 bpm are typical. This may be attributable to decreased parasympathetic tone during pregnancy. If vagal predominance plays a key role in the cardiac arrests that occur during spinal or epidural anesthesia, then the weaker vagal tone associated with pregnancy may decrease this risk.
  Although multiple factors may lead to cardiac arrest during spinal anesthesia, a common mechanism is vagal predominance. More rigorous patient selection could decrease the risk of cardiac arrest during spinal anesthesia. For example, it may be appropriate to reconsider the use of spinal anesthesia for a patient with “vagotonia.” Similarly, it may be prudent to contemplate a different technique when significant blood loss or the use of vasodilators is anticipated.
  When an abrupt decrease in preload is suspected, placing the patient in the head down position and rapidly infusing IV fluids can be helpful. If this is not possible, or if it does not rapidly reverse vagal symptoms, the administration of atropine or a vasopressor may be appropriate. Anticipating an impending cardiac arrest can be difficult because a large preload deficit and the resulting increase in vagal tone may manifest initially as only bradycardia. Treating mild bradycardia (pulse ˂ 60 bpm) during spinal anesthesia may be appropriate especially if the patient has multiple risk factors as listed.
  Atropine may be recommended to treat bradycardia during spinal anesthesia because glycopyrrolate is ineffective in this setting. Treatment of bradycardia with atropine may decrease the morbidity of the arrests that occur during spinal anesthesia.
  Unfortunately, not all of the arrests that occur during spinal anesthesia are successfully treated, and fatal arrests still occur in healthy patients.
  “When the bradycardia is profound or a full cardiac arrest occurs after spinal anesthesia, the early administration of epinephrine can be critical”
  The vasodilation caused by spinal anesthesia can make cardiopulmonary resuscitation ineffective. Successful resuscitation requires a coronary perfusion pressure gradient of 15 to 20 mm Hg and during spinal anesthesia this may require epinephrine 0.01 to 0.1 mg/kg.
  Patients with risk factors for bradycardia or overt vagal symptoms during spinal anesthesia appear to be at increased risk for cardiac arrest during spinal anesthesia. In these patients preload should be a priority, and prophylactic preloading with a bolus of IV fluid should not be omitted before initiating spinal anesthesia.
  Additional fluid boluses, using vasopressors or repositioning the patient to augment venous return, may be appropriate.
  The stepwise escalation of treatment of bradycardia with atropine (0.4–0.6 mg), ephedrine (25–50 mg), and, if necessary, epinephrine (0.2– 0.3 mg) may be appropriate.
  For severe bradycardia or cardiac arrest, full resuscitation doses of epinephrine should be promptly administered at the earliest.
  John B. Pollard, MD., Cardiac Arrest During Spinal Anesthesia: Common Mechanisms and Strategies for Prevention. Anesth Analg 2001;92:252–6.
  1. Unexpected cardiac arrest in spinal anaesthesia. Acta Anaesth. Belg., 2006, 57, 365-370
  2. Cardiopulmonary arrest in spinal anesthesia. Rev. Bras. Anestesiol. vol.61 no.1 Campinas Jan./Feb. 2011.
  3. Cardiac arrest following spinal anaesthesia. Case report. Indian J. Anaesth. 2006; 50 (6) : 479 – 480.
  4. Unanticipated cardiac arrest under spinal anesthesia: An unavoidable mystery with review of current literature. Anesthesia: Essays and Researches: Year : 2014/Volume:8/Issue:1/Page : 99-102.
  5. Cardiac arrest after Caesarean section under subarachnoid block. British Journal of Anaesthesia 1996;77: 274–276.
  Pelvic wedge or Lateral table tilt at Caesarean Section is a Myth or Fact
  COMPRESSION of the inferior vena cava (IVC) during late pregnancy when parturients are in the supine position has been well recognized as a possible cause of supine hypotensive syndrome since the report of Howard et al. in 1953. Angiograph and magnetic resonance imaging (MRI) have directly demonstrated that IVC is almost completely compressed by the gravid uterus in the supine position and that IVC compression is reduced in the left-lateral position. Further, in the late 1960s, Bieniarz et al. energetically performed angiography and simultaneously measured brachial artery and femoral artery pressure of pregnant women, and advocated that, similar to the IVC, the abdominal aorta and its branches are compressed by the gravid uterus when parturients are in the supine position.
  Since then, compression of the abdominal aorta by the gravid uterus has been widely accepted among anesthesiologists and obstetricians, and both IVC compression and aortic compression together are referred to as aortocaval compression.
  Aortocaval compression can cause hemodynamic disturbances and uteroplacental hypoperfusion in parturients. Because the left-lateral position is impractical in clinical situations, a left-lateral tilt position is often promoted to reduce aortocaval compression by the pregnant uterus. The recommended tilt angle is reported to be 15° following spinal anesthesia for cesarean section and 30° during resuscitation in pregnant women, although these recommended angles remain controversial.
  Obste-tricians and anaesthetists have traditionally sought to reduce these disturbances by tilting the mother away from the supine position and in many centres it is routine practice for women to be placed immediately in a left tilted position following insertion of spinal anaesthesia for CS. The tilted position is a compromise between the need for easy surgical access and the avoidance of aortocaval compression, and there is no consensus on whether tilting the table improves maternal or neonatal outcome. Using wedges to tilt the mother may reduce aortocaval compression, but could also be associated with other complications such as reversible sciatic nerve compression neuropathy (Postaci 2006). Tilting and changing the position of the table may make the operation more difficult for the surgeon and could increase the chances of injury to the mother. It may also increase the time it takes to do the surgery and therefore increase the risk of sepsis and other complications for the mother. Venous embolism (most commonly air) can occur during any surgical procedure if the operative field is above the level of the heart. They occur frequently with the woman in the horizontal position during caesarean section (Fong 1991) and theoretically raising the level of the heart above the operative site could decrease the incidence of air entrainment. Some studies have shown that the use of a flexed 5º to 10º head-up tilt did not decrease the incidence of venous embolism (Karuparthy 1989) while others have shown a decrease in the rate of embolism (Robinson 1987). Whether all these air embolisms are clinically significant is still uncertain.
  What is the available evidence, the optimal positioning of the mother during a caesarean section improves out comes for both the mother and the baby?
  20º left lateral tilt versus horizontal position
  Maternal position did not influence the incidence of hypotension when comparing a 20° left lateral tilt versus a horizontal position. There were no changes in systolic and diastolic blood pressures when comparing a 20° left lateral tilt versus a horizontal position. One trial showed no statistical difference when comparing a 20° lateral tilt to the supine position five minutes after spinal anaesthesia for maternal pulse rate changes or five minute Apgar scores or cord blood pH less than 7.2 or in cord blood pH.
  Full left lateral tilt versus a 15º left lateral tilt
  Maternal position did not influence the incidence of hypotension when comparing a full lateral tilt versus a 15° tilt. There were no changes in systolic and diastolic blood pressures when comparing a full lateral tilt to a 15° tilt.
  Right lateral tilt versus horizontal position
  Maternal position did not influence the incidence of hypotension when comparing a right lateral tilt versus a horizontal position.
  Right lateral tilt versus left lateral tilt
  When a right lateral tilt was compared to a left lateral tilt the number of hypotensive events as higher in the right lateral tilt group. There was no statistical difference in the incidence of hypertensive events in this trial. There was a statistical difference in maternal blood gas pH values. There was a statistically significant difference in umbilical artery cord blood gas pH and in umbilical venous cordblood gas pH values when a left lateral tilt was compared to a right lateral tilt.
  Manual displacer versus 15° left lateral tilt
  When a manual displacer was compared with a 15° left lateral tilt it was found that the incidence of hypotensive events was lower in the manual displacer group and that there was a lower fall in mean systolic blood pressure in the manual displacer group.
  10º head down tilt versus horizontal position
  When a 10° head down tilt was compared with the horizontal position there was no difference in the incidence of hypotension or in changes in systolic blood pressure but there was a statistically significant difference in diastolic blood pressure. The mean diastolic pressure was lower in the head down tilt group.
  5º to 10º head up tilt versus horizontal position
  The incidence of air embolisms was not affected by a head up tilt versus a horizontal position.
  12 cm right pelvic wedge versus 12 cm right lumbar wedge
  There were fewer hypotensive events when using a 12 cm lumbar wedge compared to a 12 cm pelvic wedge. There was no statistical difference in cord blood pH value.
  What the Magnetic Resonance Imaging tells us?
  Magnetic resonance images of 10 singleton parturients at full term and 10 healthy nonpregnant women were obtained for measurement of the abdominal aorta and inferior vena cava volume between the L1–L2 disk and L3–L4 disk levels in both the supine and left-lateral tilt positions (15°, 30°, and 45°) maintained by insertion of a 1.5-m-long polyethylene foam placed under the right side of the parturient’s body.
  Aortic volume did not differ significantly between parturients and nonpregnant women in the supine position. Inferior vena cava volume in the supine position was significantly lower in parturients than in non pregnant women. Aortic volume in parturients did not differ among left lateral tilt positions. Inferior vena cava volume in the parturients was not increased at 15°, but was significantly increased at 30° and 45°.
  IN CONCLUSION, aortic volume in parturients did not differ among left-lateral tilt positions and did not differ from those in the non pregnant woman. The IVC volume in parturients was not increased at 15° compared with that in the supine position, whereas the corresponding values were significantly increased at 30° and 45°.
  1. Maternal position during caesarean section for preventing maternal and neonatal complications (Review). The Cochrane Collaboration and published in The Cochrane Library 2010, Issue 6.
  2. Effect of Lateral Tilt Angle on the Volume of the Abdominal Aorta and Inferior Vena Cava in Pregnant and Nonpregnant Women Determined by Magnetic Resonance Imaging.
The Journal of the American Society of Anesthesiologists February 2015, Vol.122, 286-293.
  1. Brock-Utne JG, Buley RJR, Downing JW, Cuerden C. Advantages of left over right lateral tilt for caesarean section. South African Medical Journal 1978;54(12):489-92.
  2. Cardiopulmonary arrest in spinal anesthesia. Rev. Bras. Anestesiol. vol.61 no.1 Campinas Jan./Feb. 2011.
  3. Cheesman K, Douglas JM, Massey S, Saran S, Murdoch A. The effect of head elevated ramped position during combined spinal epidural anaesthesia for elective cesarean delivery. International Journal of Obstetric Anesthesia 2011;20(Suppl 1):S9.
  4. Downing JW, Karuparthy VR, Husain FJ, Knape KG, Blanchard J, Solomon D, et al. Posture and the incidence of venous air embolism (VAE) during cesarean section (CS). Anesthesiology 1989;71:A910.
  5. Karuparthy VR, Downing JW, Husain FJ, Knape KG, Blanchard J, Solomon D, et al. Incidence of venous air embolism during cesarean section is unchanged by the use of a 5 to 10° head-up tilt. Anaesthesia & Analgesia 1989;69(5):620-3.
  6. Kundra P, Khanna S, Habeebullah S, Ravishankar M. Manual displacement of the uterus during caesarean section. Anaesthesia 2007;62(5):460-5.
  7. Lew TWK, Tay DHB, Thomas E. Venous air embolism during cesarean section: more common than previously thought. Obstetric Anesthesia 1993;77(3):448-52.
  8. Matorras R, Tacuri C, Anibal N, Gutierrez de Teran G, Cortes J. Lack of benefits of left tilt in emergent cesarean sections: a randomised study of cardiotocography, cord acid-base status and other parameters of the mother and the fetus. Journal of Perinatal Medicine 1998;26(4):284-92.
  9. Miyabe M, Sato S. The effect of head-down tilt position on arterial blood pressure after spinal anesthesia for cesarean delivery. Regional Anesthesia 1997;22(3):239-42.
  10. Rees SG, Thurlow JA, Gardner IC, Scrutton MJL, Kinsella SM. Maternal cardiovascular consequences of positioning after spinal anaesthesia for caesarean section: left 15° table tilt vs. left lateral. Anaesthesia 2002;57(1):15-20.
  11. Zheng L. Effect of blood pressure of cesarean section patients in different postures. Chinese Nursing Research 2001;15:325-6.
  12. Zhou ZQ, Shao Q, Zeng Q, Song J, Yang JJ. Lumbar wedge versus pelvic wedge in preventing hypotension following combined spinal epidural anaesthesia for caesarean delivery. Anaesthesia and Intensive Care 2008;36(6):835-9.
Norman M Kaplan, MD
  Preexisting hypertension is the most common medical reason for postponing surgery. Hypertension is well known to be a risk factor for cardiovascular catastrophe, a risk that logically extends into the perioperative period. In a case-control study of 76 patients who died of a cardiovascular cause within 30 days of elective surgery, a preoperative history of hypertension was four times more likely than among 76 matched controls.
  The issues regarding the perioperative management of the patient with hypertension are reviewed here.
  Sympathetic activation during the induction of anesthesia can cause the blood pressure to rise by 20 to 30 mmHg and the heart rate to increase by 15 to 20 beats per minute in normotensive individuals. These responses may be more pronounced in patients with untreated hypertension in whom the systolic blood pressure can increase by 90 mmHg and heart rate by 40 beats per minute.
  The mean arterial pressure tends to fall as the period of anesthesia progresses due to a variety of factors, including direct effects of the anesthetic, inhibition of the sympathetic nervous system, and loss of the baroreceptor reflex control of arterial pressure. These changes can result in episodes of intraoperative hypotension. Patients with preexisting hypertension are more likely to experience intraoperative blood pressure lability (either hypotension or hypertension), which may lead to myocardial ischemia.
  Blood pressure and heart rate slowly increase as patients recover from the effects of anesthesia during the immediate postoperative period. Hypertensive individuals in particular may experience significant increases in these parameters.
  Preexisting hypertension can induce a variety of cardiovascular responses that potentially increase the risk of surgery, including diastolic dysfunction from left ventricular hypertrophy, systolic dysfunction leading to congestive heart failure, renal impairment, and cerebrovascular and coronary occlusive disease. The level of risk is dependent upon the severity of hypertension
  However, much of the evidence for the impact of preoperative hypertension comes from uncontrolled studies performed before current (more effective) management was available. Furthermore, it is still unclear whether postponing surgery to achieve blood pressure control will lead to reduced cardiac risk. The ACC/AHA guidelines list uncontrolled hypertension as a "minor" risk factor for perioperative cardiovascular events .
  Severe hypertension
  An early study found that patients with untreated severe hypertension (mean systolic and diastolic pressure of 211 and 105 mmHg, respectively) had exaggerated hypotensive responses to the induction of anesthesia and marked hypertensive responses to noxious stimuli. Patients with well-controlled hypertension responded similarly to normotensive subjects. Other studies have found that a diastolic pressure over 110 mmHg immediately before surgery is associated with a number of complications including dysrhythmias, myocardial ischemia and infarction, neurologic complications, and renal failure.
  Mild to moderate hypertension
  Patients with less marked hypertension (diastolic pressure less than 110 mmHg) do not appear to be at increased operative risk. This was illustrated in a study of 676 operations involving a general anesthetic in patients over the age of 40. Subjects were divided into five groups:
Normotensive patients (group I, no medications; and group II on diuretics for non-hypertensive reasons) were significantly less likely to experience perioperative hypertension than patients normotensive on medication (group III), hypertensive despite treatment (group IV), and untreated hypertension (group V)
Patients with inadequately treated or untreated hypertension (groups IV and V) were no more likely to experience cardiac complications than normotensive patients not taking diuretics (group I).
Among patients with a history of hypertension (groups III, IV, and V), multivariate analysis identified only two independent risk factors for cardiac complications: the preoperative cardiac risk index score (which does not include hypertension) Table2; and marked reductions in intraoperative blood pressure (a decrease to less than 50 percent of preoperative levels or a decrease of 33 percent or more for more than 10 minutes).
  These results suggest that elective surgery in patients with hypertension does not need to be delayed as long as the diastolic blood pressure is less than 110 mmHg and intraoperative and postoperative blood pressures are carefully monitored to prevent hypertensive or hypotensive episodes. On the other hand, when hypertension has caused end-organ disease such as congestive heart failure and renal insufficiency, the probability of adverse cardiac outcomes in the perioperative period increases significantly.
  The impact of systolic hypertension on operative risk is less clear. One study of patients undergoing carotid endarterectomy found that a systolic pressure greater than 200 mmHg was associated with an increased risk of postoperative hypertension and neurologic deficits. Patients with isolated systolic hypertension are at increased risk for cardiovascular morbidity after coronary artery bypass surgery .
  Secondary hypertension
  The physical examination and simple laboratory tests can rule out some of the rare but important causes of hypertension. Further evaluation to exclude secondary hypertension is rarely warranted before necessary surgery. If pheochromocytoma is a serious possibility, surgery should be delayed to permit its exclusion. A loud abdominal bruit may suggest renal artery stenosis. A radial to femoral artery pulse delay suggests coarctation of the aorta, whereas hypokalemia in the absence of diuretic therapy raises the possibility of hyperaldosteronism.
  Oral antihypertensive medications should be continued up to the time of surgery. This recommendation is based upon the following observations:
With few exceptions, continuing antihypertensive medications is relatively safe.
Abruptly discontinuing some medications (eg, beta blockers, clonidine) may be associated with significant rebound hypertension.
There are risks associated with severe, uncontrolled hypertension.
  Table1: "Perioperative medication management"
Drug Day Before Surgery Day of Surgery During Surgery After Procedure
Beta-blockers Usual dose Usual dose on morning of surgery with sip of water) IV bolus or infusion (usually not required) Continue IV dose until medication can be taken PO
Calcium channel blockers Usual dose Usual dose on morning of surgery with sip of water IV bolus or infusion (usually not required) Continue IV dose until medication can be taken PO
ACE inhibitors Stop day before Do not take day of surgery IV formulations (usually not required) Continue IV dose until medication can be taken PO
Diuretics Stop day before IV beta-blockers/IV calcium channel blockers Restart when patient on oral liquids
Potassium supplements Stop day before; consider checking potassium level Restart when patient on oral liquids
Central-acting sympatholytics Usual dose Usual dose on morning of surgery with sip of water Transdermal clonidine/IV methyldopa Restart when patient on orals liquids
Peripheral sympatholytics Usual dose Usual dose on morning of surgery with sip of water Any IV formulation (usually not required) Restart when patient on oral liquids
Alpha-blockers Usual dose Usual dose on morning of surgery with sip of water Any IV formulation (usually not required) Restart when patient on oral liquids
Vasodilators Usual dose Usual dose on morning of surgery with sip of water IV formulation (usually not required) Continue IV dose until medication can betaken PO
  Safety of antihypertensive drugs preoperatively
  Most antihypertensive agents can be continued until the time of surgery, taken with small sips of water on the morning of surgery. For perioperative drug management for Patients with Hypertension See Table1.
  The following is a brief summary of recommendations for the various classes of antihypertensive drugs.
  Patients in whom chronic diuretic therapy has caused hypokalemia may have potentiation of the effects of muscle relaxants used during anesthesia, as well as predisposition to cardiac arrhythmias and paralytic ileus. Physicians should be aware of the potential perioperative risks associated with diuretics and pay close attention to volume and potassium replacement.
  Angiotensin converting enzyme inhibitors and angiotensin II receptor blockers
  Angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers can theoretically blunt the compensatory activation of the renin-angiotensin system during surgery and result in prolonged hypotension. One study of 150 vascular surgery patients found that the incidence of hypotension during anesthetic induction was significantly lower in patients who stopped taking captopril or enalapril the evening before surgery than in those who took the medication on the morning of surgery. A high incidence of severe hypotension in patients on an angiotensin II receptor blocker who underwent general anesthesia has also been reported.
  Although there are insufficient data upon which recommendations can be based, it seems reasonable to continue these drugs in patients who are taking them for the management of hypertension. On the other hand, it is also reasonable to withhold them on the morning of surgery in patients who are taking them for congestive heart failure in whom the baseline blood pressure is low, to avoid significant hypotension during the induction of anesthesia.
  Calcium channel blockers
  Patients receiving calcium channel blockers may have an increased incidence of postoperative bleeding, probably due to inhibition of platelet aggregation. The multiple benefits of these drugs probably outweigh the small risk of continued therapy.
  Withdrawal syndromes
  The centrally acting sympatholytic drugs (eg, clonidine, methyldopa, and guanfacine) and the beta blockers are associated with acute withdrawal syndromes that can lead to adverse perioperative events. These drugs should not be abruptly stopped perioperatively.
  Centrally acting sympatholytic drugs
  The primary clinical manifestation following abrupt cessation of clonidine therapy is acute, rebound hypertension above the pretreatment level. Rebound hypertension usually occurs after abrupt cessation of fairly large oral doses (eg, greater than 0.8 mg/day), but has also been noted with transdermal clonidine. Withdrawal symptoms have also been reported with methyldopa and guanfacine withdrawal but are less likely because of their slower onset of action.
  Beta blockers
  Beta blockers reduce intraoperative myocardial ischemia. Thus, in addition to a rise in blood pressure, beta blocker withdrawal in patients with underlying coronary disease can lead to accelerated angina, myocardial infarction, or sudden death.
  Furthermore, atenolol or bisoprolol given before surgery to patients with, or at high risk for, coronary heart disease (CHD) decreases mortality. Thus, it is recommended that patients with one or more risk factor for CHD be given beta blockers perioperatively.
  A history of hypertension preoperatively is the most important risk factor for postoperative hypertension. Other factors contributing to the development of hypertension were pain (35 percent), excitement on emergence from anesthesia (16 percent), and hypercarbia (15 percent). The type of surgery may influence the likelihood of developing postoperative hypertension.
  As illustrated in a study of 1844 patients, hypertension usually begins within 30 minutes of the completion of surgery and lasts approximately two hours. On the other hand, some patients with preexisting hypertension may experience normalization of blood pressure as a nonspecific response to surgery. This response can persist for months, usually followed by a gradual return to preoperative levels.
  Indications for therapy
  Any patient who experiences a marked rise in blood pressure following surgery should be treated immediately.
  The following approach can be used in other cases:
  Remedial causes of hypertension such as pain, agitation, hypercarbia, hypoxia, hypervolemia, and bladder distention should be excluded or treated.
  Patients on chronic antihypertensive therapy should resume their usual medications postoperatively as needed. Those who cannot take oral medications should be given a comparable alternative (see below).
  Therapy should be considered for patients with a sustained systolic blood pressure above 180 mmHg or diastolic blood pressure greater than 110 mmHg, once remedial causes have been excluded or treated.
  Choice of drugs
  A number of parenteral antihypertensive medications are available for patients who are unable to take oral medications postoperatively. These are the same drugs used to treat patients with hypertensive emergencies . (Table3) Without any data from controlled trials to indicate which is best, the experience of the surgeons, anesthesiologists, and internists who are caring for the patients should guide the choice.
  With the exception of beta blockers and clonidine, it is not necessary for patients receiving chronic antihypertensive therapy who are unable to resume oral medications to continue the same class of drugs postoperatively. Nevertheless, in many cases a comparable parenteral alternative is available.
Patients taking diuretics may be given parenteral furosemide or bumetanide.
Patients taking beta blockers may be given parenteral propranolol, labetalol, or esmolol.
Patients taking an ACE inhibitor may be given parenteral enalaprilat.
Patients taking centrally acting agents can be given a clonidine patch.
Patients taking calcium channel blockers can be given intravenous nicardipine.
  Patients with well-controlled hypertension preoperatively are less likely to experience intraoperative blood pressure lability and postoperative complications than patients with poorly controlled hypertension. The ideal circumstance is to normalize blood pressure (eg, to less than 140/90 mmHg) for several months prior to elective surgery. However, it is not necessary to postpone elective procedures in patients with a blood pressure below 170/110 mmHg.
  Elective surgery should be postponed in patients with blood pressures above 170/110 mmHg. Such patients who require urgent surgery should be treated with a parenteral drug acutely.
  Patients who are taking chronic antihypertensive medications should continue taking their medication until the time of surgery. The drug can be administered with a sip of water on the morning of surgery and resumed postoperatively as needed. Alternative parenteral agents can be prescribed for patients who are unable to resume oral medications.
  In particular, beta blockers and centrally acting agents such as clonidine should not be stopped acutely. If necessary, intravenous propranolol or labetalol can be administered to patients taking beta blockers or transdermal clonidine can be administered to patients taking clonidine.
  Remedial causes of postoperative hypertension such as pain, agitation, hypercarbia, hypoxia, hypervolemia, and bladder distention should be excluded or treated. Once this has been done, therapy should be considered for patients with a persistent systolic blood pressure above 180 mmHg or a diastolic blood pressure above 110 mmHg.
  Table2: Revised Goldman cardiac risk index (RCRI)
Six independent predictors of major cardiac complications*
High-risk type of surgery (includes any intraperitoneal, intrathoracic, or suprainguinal vascular procedures)
History of ischemic heart disease (history of MI or a positive exercise test, current complaint of chest pain considered to be secondary to myocardial ischemia, use of nitrate therapy, or ECG with pathological Q waves; do not count prior coronary revascularization procedure unless one of the other criteria for ischemic heart disease is present)
History of HF
History of cerebrovascular disease
Diabetes mellitus requiring treatment with insulin
Preoperative serum creatinine >2.0 mg/dL (177 mol/L)
Rate of cardiac death, nonfatal myocardial infarction, and nonfatal cardiac arrest according to the number of predictors
No risk factors - 0.4 percent (95% CI 0.1-0.8 percent)
One risk factor - 1.0 percent (95% CI 0.5-1.4 percent)
Two risk factors - 2.4 percent (95% CI 1.3-3.5 percent) ƒ
Three or more risk factors - 5.4 percent (95% CI 2.8-7.9 percent)
Rate of cardiac death & nonfatal MI, cardiac arrest or ventr.fibrillation, pulmonary edema, and/or complete heart block according to the No.of predictors and use nonuse or of beta blockers
No risk factors - 0.4 to 1.0 percent versus <1 percent with beta blockers ƒ
One to two risk factors - 2.2 to 6.6 percent versus 0.8 to 1.6 percent with beta blockers ƒ
Three or more risk factors - >9 percent versus >3 percent with beta blockers
  Table3: Parenteral drugs for treatment of hypertensive emergencies
Drug Dose Onset of action Duration of action Adverse effects Special indications
Sodium nitroprusside 0.25-10μg/kg/min as IV infusion Immediate 1-2 min Nausea, vomiting, muscle twitching, sweating, thiocynate and cyanide intoxication Most hypertensive emergencies; caution with high intracranial pressure or azotemia
Nicardipine hydrochloride 5-15 mg/h IV 5-10 min 15-30 min, May exceed 4 h Tachycardia, headache, flushing, local phlebitis Most hypertensive emergencies except acute heart failure; caution with coronary ischemia
Clevidipine 1-2 mg/h IV with rapid titration to max of 16 mg/h 1-2 min 5-15 min Atrial fibrillation,nausea All hypertensive emergencies
Fenoldopam mesylate 0.1-0.3 μg/kg per min IV infusion <5 min 30 min Tachycardia,headache, nausea,flushing Most hypertensive emergencies; caution with glaucoma
Nitroglycerin 5-100 μg/min as IV infusion 2-5 min 5-10 min Headache, vomiting,methemoglobinemia,tolerance withprolonged use Coronary ischemia
Enalaprilat 1.25-5 mg every 6 h IV 15-30 min 6-12 h Precipitous fall in pressure in high rennin states; variable response Acute left ventricular failure; avoid in acute myocardial infarction
Hydralazine hydrochloride 10-20 mg IV
10-40 mg IM
10-20 min
20-30 min IM
1-4 h IV
4-6 h IM
Tachycardia,flushing, headache,vomiting, aggravation of angina Eclampsia
Andrenergic inhibitors
Labetalol hydrochloride 20-80 mg IV bolus every 10 min
0.5-2.0 mg/min IV infusion
5-10 min 3-6 h Vomiting, scalp tingling, bronchoconstriction, dizziness, nausea, heart block, orthostatic hypotension Most hypertensive emergencies except acute heart failure
Esmolol hydrochlorideΔ 250-500 μg/kg/min by infusion; may repeat bolus after 5 min or increase infusion to 300 μg/min 1-2 min 10-30 min Hypotension, nausea, asthma, first-degree heart block, HF Aortic dissection, perioperative
Hydralazine hydrochloride 10-20 mg IV
10-40 mg IM
10-20 min
20-30 min IM
1-4 h IV
4-6 h IM
Tachycardia,flushing, headache,vomiting, aggravation of angina Eclampsia
Phentolamine 5-15 mg IV bolus 1-2 min 10-30 min Tachycardia, flushing, headache Catecholamine excess
  1. Perioperative management of hypertension. Norman M Kaplan, MD.
  2. ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery. Circulation. 2007; 116: e418-e500
  3. Perioperative hypertension management. Vasc Health Risk Manag. 2008 Jun; 4(3): 615–627.