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Postoperative Pain Management for the Cardiac Patient
Chapter 33
Postoperative Pain Management for the Cardiac Patient Mark A. Chaney, MD
Key Points 1. Inadequate postoperative analgesia and/or an uninhibited perioperative surgical stress response has the potential to initiate pathophysiologic changes in all major organ systems, which may lead to substantial postoperative morbidity. Adequate postoperative analgesia prevents unnecessary patient discomfort, may decrease morbidity, hospital lengths of stay, and thus may decrease costs. 2. Pain after cardiac surgery may be intense and originates from many sources, including the incision (sternotomy or thoracotomy), intraoperative tissue retraction and dissection, vascular cannulation sites, vein-harvesting sites, and chest tubes. Achieving optimal pain relief after cardiac surgery is often difficult, yet it may be attained through a wide variety of techniques, including local anesthetic infiltration, nerve blocks, intravenous agents, intrathecal techniques, and epidural techniques. 3. Traditionally, analgesia after cardiac surgery has been obtained with intravenous opioids (specifically morphine). However, intravenous opioid use is associated with definite detrimental side effects and longer-acting opioids such as morphine may delay tracheal extubation during the immediate postoperative period via excessive sedation and/or respiratory depression. Thus in the current era of early extubation (eg, fast-tracking), cardiac anesthesiologists are exploring unique options for the control of postoperative pain in patients after cardiac surgery. 4. Although patient-controlled analgesia is a well-established technique and offers potential unique benefits, whether it truly offers significant clinical advantages (compared with traditional nurse-administered analgesic techniques) to patients immediately after cardiac surgery remains to be determined. 5. Administration of intrathecal morphine to patients initiates reliable postoperative analgesia after cardiac surgery. Intrathecal opioids or local anesthetics cannot reliably attenuate the perioperative stress response associated with cardiac surgery that persists during the immediate postoperative period. Although intrathecal local anesthetics (not opioids) may induce perioperative thoracic cardiac sympathectomy, the hemodynamic changes associated with total spinal anesthesia make the technique unpalatable in patients with cardiac disease. 6. Administration of thoracic epidural opioids or local anesthetics to patients initiates reliable postoperative analgesia after cardiac surgery. The quality of analgesia obtained with thoracic epidural anesthetic techniques is sufficient to allow cardiac surgery to be performed in “awake” patients. 7. Use of intrathecal and epidural techniques in patients undergoing cardiac surgery remains extremely controversial. Concerns regard the risk of hematoma formations.
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8. The last decade has seen a resurgence of nerve blocks (including catheter-based techniques) in patients undergoing cardiac surgery. Recent clinical studies using intercostal, intrapleural, and paravertebral blocks indicate that these techniques may have unique clinical advantages, even when compared with traditional intrathecal and epidural techniques. The emergence of liposomal bupivacaine, which has the potential to provide clinical analgesia for 96 hours after a single injection, may revolutionize the use of single-shot nerve blocks for patients undergoing cardiac surgery. 9. As a general rule, avoiding intense, single-modality therapy for the treatment of acute postoperative pain is best. The administration of two analgesic agents that act by different mechanisms (multimodal or balanced analgesia) provides superior analgesic efficacy with equivalent or reduced adverse effects.
Adequate postoperative analgesia prevents unnecessary patient discomfort, may decrease morbidity, may decrease postoperative hospital lengths of stay, and thus may decrease costs. Because postoperative pain management has been deemed important, the American Society of Anesthesiologists has published practice guidelines regarding this topic. Furthermore, in recognition of the need for improved pain management, the Joint Commission has developed standards for the assessment and management of pain in accredited hospitals and other health care settings. Patient satisfaction (no doubt linked to adequacy of postoperative analgesia) has become an essential element that influences clinical activity of not only anesthesiologists but all health care professionals. Achieving optimal pain relief after cardiac surgery is often difficult. Pain may be associated with many interventions, including sternotomy, thoracotomy, leg vein harvesting, pericardiotomy, and/or chest tube insertion, among other interventions. Inadequate analgesia and/or an uninhibited stress response during the postoperative period may increase morbidity by causing adverse hemodynamic, metabolic, immunologic, and hemostatic alterations. Aggressive control of postoperative pain, associated with an attenuated stress response, may decrease morbidity and mortality in high-risk patients after noncardiac surgery and may also decrease morbidity and mortality in patients after cardiac surgery. Adequate postoperative analgesia may be attained via a wide variety of techniques (Box 33.1). Traditionally, analgesia after cardiac surgery has been obtained with intravenous opioids (specifically morphine). However, intravenous opioid use is associated with definite detrimental side effects (eg, nausea and vomiting, pruritus, urinary retention, respiratory depression), and longer-acting opioids such as morphine may delay tracheal extubation during the immediate
BOX 33.1
Techniques Available for Postoperative Analgesia
Local anesthetic infiltration Nerve blocks Opioids Nonsteroidal antiinflammatory agents α-Adrenergic agents Intrathecal techniques Epidural techniques Multimodal analgesia
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PAIN AND CARDIAC SURGERY Surgical or traumatic injury initiates changes in the peripheral and central nervous systems that must be addressed therapeutically to promote postoperative analgesia and, it is hoped, positively influence clinical outcomes (Box 33.2). The physical processes of incision, traction, and cutting of tissues stimulate free nerve endings and a wide variety of specific nociceptors. Receptor activation and activity are further modified by the local release of chemical mediators of inflammation and sympathetic amines released via the perioperative surgical stress response. The perioperative surgical stress response peaks during the immediate postoperative period and exerts major effects on many physiologic processes. The potential clinical benefits of attenuating the perioperative surgical stress response (above and beyond simply attaining adequate clinical analgesia) have received significant attention during the 2000s and remain fairly controversial. However, inadequate postoperative analgesia and/or an uninhibited perioperative surgical stress response clearly has the potential to initiate pathophysiologic changes in all major organ systems, including the cardiovascular, pulmonary, gastrointestinal, renal, endocrine, immunologic, and/or central nervous systems, all of which may lead to substantial postoperative morbidity. Pain after cardiac surgery may be intense, and it originates from many sources, including the incision (eg, sternotomy, thoracotomy), intraoperative tissue retraction and dissection, vascular cannulation sites, vein-harvesting sites, and chest tubes, among other sources. Patients in whom an internal mammary artery is surgically exposed and used as a bypass graft may have substantially more postoperative pain.
BOX 33.2
Pain and Cardiac Surgery
Originates from many sources Most commonly originates from the chest wall Preoperative expectations influence postoperative satisfaction Quality of postoperative analgesia may influence morbidity
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postoperative period via excessive sedation and/or respiratory depression. Thus in the current era of early extubation (fast-tracking), cardiac anesthesiologists are exploring unique options other than traditional intravenous opioids for the control of postoperative pain in patients after cardiac surgery. The last decade has witnessed increased use of smaller incisions by cardiac surgeons, prompting clinical investigations into the use of intercostal, intrapleural, and paravertebral blocks (with and without catheters), and the emergence of long-acting liposomal bupivacaine may revolutionize the use of these techniques. No single technique is clearly superior; each possesses distinct advantages and disadvantages. It is becoming increasingly clear that a multimodal approach and/or a combined analgesic regimen (using a variety of techniques) is the best way to approach postoperative pain in all patients after surgery to maximize analgesia and minimize side effects. When addressing postoperative analgesia in cardiac surgical patients, the choice of technique (or techniques) should be made only after a thorough analysis of the risk-benefit ratio of each technique in the specific patient in whom analgesia is desired.
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Persistent pain after cardiac surgery, although rare, can be problematic. The cause of persistent pain after sternotomy is multifactorial, yet tissue destruction, intercostal nerve trauma, scar formation, rib fractures, sternal infection, stainless-steel wire sutures, and/or costochondral separation may all play roles. Such chronic pain is often localized to the arms, shoulders, or legs. Postoperative brachial plexus neuropathies also may occur and have been attributed to rib fracture fragments, internal mammary artery dissection, suboptimal positioning of the patient during surgery, and/or central venous catheter placement. Postoperative neuralgia of the saphenous nerve has also been reported after harvesting of saphenous veins for coronary artery bypass grafting (CABG). Younger patients appear to be at greater risk for the development of chronic, long-lasting pain. The correlation of severity of acute postoperative pain and the development of chronic pain syndromes has been suggested (patients requiring more postoperative analgesics may be more likely to develop chronic pain), yet this link is still vague. Patient satisfaction with quality of postoperative analgesia is as much related to the comparison between anticipated and experienced pain as it is to the actual level of pain experienced. Satisfaction is related to a situation that is better than predicted, dissatisfaction to one that is worse than expected. Patients undergoing cardiac surgery remain concerned regarding the adequacy of postoperative pain relief and preoperatively tend to expect a greater amount of postoperative pain than that which is actually experienced. Because of these unique preoperative expectations, patients after cardiac surgery who postoperatively receive only moderate analgesia will likely still be satisfied with their pain control. Thus patients may experience pain of moderate intensity after cardiac surgery yet still express very high satisfaction levels.
POTENTIAL CLINICAL BENEFITS OF ADEQUATE POSTOPERATIVE ANALGESIA
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Inadequate analgesia (coupled with an uninhibited stress response) during the postoperative period may lead to many adverse hemodynamic (tachycardia, hypertension, vasoconstriction), metabolic (increased catabolism), immunologic (impaired immune response), and hemostatic (platelet activation) alterations. In patients undergoing cardiac surgery, perioperative myocardial ischemia is most commonly observed during the immediate postoperative period and appears to be related to outcome. Intraoperatively, initiation of cardiopulmonary bypass (CPB) causes substantial increases in stress response hormones (eg, norepinephrine, epinephrine) that persist into the immediate postoperative period and may contribute to myocardial ischemia observed during this time. Furthermore, postoperative myocardial ischemia may be aggravated by cardiac sympathetic nerve activation, which disrupts the balance between coronary blood flow and myocardial oxygen demand. Thus during the pivotal immediate postoperative period after cardiac surgery, adequate analgesia coupled with stressresponse attenuation may potentially decrease morbidity and enhance health-related quality of life.
LOCAL ANESTHETIC INFILTRATION Pain after cardiac surgery is often related to median sternotomy, peaking during the first 2 postoperative days. Because of problems associated with traditional intravenous opioid analgesia and with the nonsteroidal antiinflammatory drugs (NSAIDs) and cyclooxygenase (COX) inhibitors, alternative methods of achieving postoperative 824
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analgesia in cardiac surgical patients have been sought. One such alternative method that may hold promise is the continuous infusion of a local anesthetic. Clinical investigations have revealed the potential benefits of using a continuous infusion of a local anesthetic in patients after cardiac surgery. Patients undergoing elective CABG via median sternotomy were randomized to either ropivacaine or placebo groups. At the end of the surgery but before wound closure, bilateral intercostal nerve injections from T1 to T12 were performed using 20 mL of either 0.2% ropivacaine or normal saline. After sternal reapproximation with wires, two catheters with multiple side openings were placed anterior to the sternum (Fig. 33.1). These catheters were connected to a pressurized elastomeric pump containing a flow regulator, which allowed for the delivery of 0.2% ropivacaine or normal saline at approximately 4 mL/h. The postoperative pain management was via intravenous patient-controlled anesthesia (PCA) morphine (for 72 hours). The sternal catheters were removed after 48 hours. Total mean PCA morphine consumption during the immediate postoperative period (72 hours) was significantly decreased in the ropivacaine group (47.3 vs 78.7 mg, respectively; P = .038). Mean overall pain scores (scale ranging from 0 for no pain to 10 for maximum pain imaginable) were also significantly decreased in the ropivacaine group (1.6 vs 2.6, respectively; P = .005). Most interestingly, patients receiving ropivacaine had a mean hospital length of stay of 5.2 ± 1.3 days compared with 8.2 ± 7.9 days for patients receiving normal saline, a difference that was statistically significant (P = .001). No difference was observed in wound infections or wound healing between
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Fig. 33.1 Intraoperative placement of the pressurized elastomeric pump and catheters. (From Dowling R, Thielmeier K, Ghaly A, et al. Improved pain control after cardiac surgery: results of a randomized, double-blind, clinical trial. J Thorac Cardiovasc Surg. 2003;126:1271–1278.)
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the two groups during hospitalization or after hospital discharge. No complications related to placement of the sternal wound catheters or performance of the intercostal nerve blocks were encountered. The authors concluded that their analgesic technique significantly improves postoperative pain control while decreasing the amount of opioid analgesia required in patients subjected to standard median sternotomy.
NERVE BLOCKS With the increasing popularity of minimally invasive cardiac surgery, which uses nonsternotomy incisions (minithoracotomy), the use of nerve blocks for the management of postoperative pain has increased. Thoracotomy incisions (transverse anterolateral minithoracotomy, vertical anterolateral minithoracotomy), because of costal cartilage tissue trauma to ribs, muscles, or peripheral nerves, may induce more intense postoperative pain than that resulting from median sternotomy. Adequate analgesia after thoracotomy incisions is important because pain is a key component in the alteration of lung function after this type of incision. Uncontrolled pain causes a reduction in respiratory mechanics, reduced mobility, and increases in hormonal and metabolic activity. Perioperative deterioration in respiratory mechanics may lead to pulmonary complications and hypoxemia, which may in turn lead to myocardial ischemia or infarction, cerebrovascular accidents, thromboembolism, delayed wound healing, increased morbidity, and prolonged hospital stay. Various analgesic techniques have been developed to treat postoperative thoracotomy pain. The most commonly used techniques include intercostal nerve block, intrapleural administration of a local anesthetic, and thoracic paravertebral block. Intrathecal techniques and epidural techniques are also effective in controlling postthoracotomy pain. Intercostal nerve block has been extensively used for analgesia after thoracic surgery and can be performed either intraoperatively or postoperatively. It usually provides sufficient analgesia lasting approximately 6 to 12 hours (depending on the amount and type of local anesthetic used) and may need to be repeated if additional analgesia is required. Local anesthetics may be administered as a single injection under direct vision before chest closure, as a single preoperative percutaneous injection, as multiple percutaneous serial injections, or via an indwelling intercostal catheter. Blockade of intercostal nerves interrupts C-fiber afferent transmission of impulses to the spinal cord. A continuous intercostal catheter allows frequent dosing or infusions of local anesthetic agents and avoids multiple needle injections. Various clinical studies have confirmed the analgesic efficacy of this technique, and the technique compares favorably with thoracic epidural analgesic techniques. A major concern associated with intercostal nerve block is the potentially high amount of local anesthetic systemic absorption. However, multiple clinical studies involving patients undergoing thoracic surgery have documented safe blood levels with standard techniques. Clinical investigations involving patients undergoing thoracic surgery indicate that intercostal nerve blockade by intermittent or continuous infusion of bupivacaine (0.25% to 0.5%) or ropivacaine (0.5% to 0.75%) through indwelling intercostal catheters is an effective method for supplementing systemic intravenous opioid analgesia for postthoracotomy pain. Intrapleural administration of local anesthetics initiates analgesia via mechanisms that remain incompletely understood. However, the mechanism of action of extrapleural analgesia seems to depend primarily on diffusion of the local anesthetic into the paravertebral region. Local anesthetics then affect not only the ventral nerve root but also afferent fibers of the posterior primary ramus. Posterior ligaments of the posterior primary ramus innervate posterior spinal muscles and skin and are traumatized during posterolateral thoracotomy. Intrapleural administration of a local anesthetic 826
Esophagus
Descending aorta Sympathetic chain
Right lung
A
Transverse process
Thoracic duct
Superior costotransverse ligament
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Neck of rib Interpleural space Extrapleural compartment Subendothoracic compartment Intercostal nerve Posterior primary rami
Endothoracic fascia Pleura Visceral Parietal
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Interpleural space
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Fig. 33.2 Anatomy of the thoracic paravertebral space (A) and sagittal section through the thoracic paravertebral space showing a needle that has been advanced above the transverse process (B). (From Karmakar MK. Thoracic paravertebral block. Anesthesiology. 2001;95:771–780.)
to this region through a catheter inserted in the extrapleural space creates an analgesic region in the skin. The depth and width of this region depend on the diffusion of the local anesthetic in the extrapleural space. Thoracic paravertebral block involves the injection of a local anesthetic adjacent to the thoracic vertebrae close to where the spinal nerves emerge from the intervertebral foramina (Fig. 33.2). Thoracic paravertebral block, compared with thoracic epidural analgesic techniques, appears to provide equivalent analgesia, is technically easier, and may harbor less risk. Several different techniques exist for successful thoracic paravertebral block. The classic technique, most commonly used, involves eliciting loss of resistance. Injection of a local anesthetic results in ipsilateral somatic and sympathetic nerve blockade in multiple contiguous thoracic dermatomes above and below the site of injection, together with the possible suppression of the neuroendocrine stress response to surgery. These blocks may be effective in alleviating acute and chronic pain of unilateral origin from the chest. Continuous thoracic paravertebral infusion of a local anesthetic via a catheter placed under direct vision at thoracotomy is also a safe, simple, and an effective method of providing analgesia after thoracotomy. It is usually used in conjunction with adjunct intravenous opioid or other analgesics to provide optimal relief after thoracotomy. For a wide variety of reasons, including the increased use of small thoracic incisions by cardiac surgeons, the last decade has seen a resurgence of nerve blocks (usually catheter-based techniques) in patients undergoing cardiac surgery. Specifically, recent clinical studies using intercostal catheters, intrapleural catheters, and paravertebral blockade indicate that these techniques may have unique advantages, even when compared with traditional intrathecal and epidural techniques. Lastly, the emergence of liposomal bupivacaine, which has the potential to provide clinical analgesia for 96 hours after a single injection, may revolutionize the use of single-shot nerve blocks for thoracic and cardiac surgeries.
OPIOIDS The classic pharmacologic effect of opioids is analgesia, and these drugs have traditionally been the initial choice when a potent postoperative analgesic is required. Two anatomically distinct sites exist for opioid receptor–mediated analgesia: supraspinal and spinal. Systemically administered opioids produce analgesia at both sites. Supraspinally, the µ1 receptor is primarily involved in analgesia, whereas the µ2 receptor is the receptor predominantly involved in the spinal modulation of nociceptive processing. κ Receptors are important in mediating spinal and supraspinal analgesia as well. 827
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Subserous
Endo- fascia Pleura Azygos thoracic Visceral vein fascia Parietal
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δ Ligands may have a modulatory rather than a primary analgesic role. All three types of opioid receptors (µ, κ, and δ) have been demonstrated in peripheral terminals of sensory nerves. Activation of these receptors seems to require an inflammatory reaction because locally applied opioids do not produce analgesia in healthy tissue. The inflammatory process also may activate previously inactive opioid receptors. Morphine is the prototype opioid agonist with which all opioids are compared and is perhaps the most popular analgesic used in patients after cardiac surgery. Many semisynthetic derivatives are made by simple modifications of the morphine molecule. Morphine is poorly lipid-soluble and binds approximately 35% to plasma proteins, particularly albumin. Morphine is primarily metabolized in the liver, principally by conjugation to water-soluble glucuronides. The liver is the predominant site for morphine biotransformation, although extrahepatic metabolism also occurs in the kidney, brain, and possibly the gut. Extrahepatic clearance accounts for approximately 30% of the total body clearance. The terminal elimination half-life of morphine is 2 to 3 hours. In patients with liver cirrhosis, morphine pharmacokinetic actions are variable, probably reflecting the variability of liver disease in patients. Morphine’s terminal elimination half-life in patients with renal disease is comparable with that of patients without renal disease. Although morphine is perhaps the most popular intravenous analgesic used in patients after cardiac surgery, other synthetically derived opioids have been developed and may be used as well. These include fentanyl, alfentanil, sufentanil, and remifentanil. Transdermal delivery of fentanyl has also been investigated extensively. This modality is simple, noninvasive, and allows continuous release of fentanyl into the systemic circulation. However, the steady release of fentanyl in such a manner does not allow flexibility in dose adjustment, which may result in inadequate treatment of postoperative pain during rapidly changing intensity. Thus intravenous opioids are often necessary to supplement analgesia when transdermal fentanyl is used to manage acute postoperative pain. Alfentanil is approximately 5 to 10 times less potent than fentanyl. The drug acts rapidly; its peak effect is reached within minutes after intravenous administration. Its duration of action after bolus administration is also shorter than fentanyl. Alfentanil is highly lipid-soluble (approximately 100 times more lipid-soluble than morphine) and rapidly crosses the blood-brain barrier. Alfentanil pharmacokinetics is minimally affected by renal disease, and hepatic extraction is more a function of intrinsic hepatic enzyme capacity and protein binding than liver blood flow. The performance of a patient-demand, target-controlled alfentanil infusion system has compared favorably with traditional morphine PCA in patients after cardiac surgery. Morphine PCA versus alfentanil PCA for postoperative analgesia after undergoing elective cardiac surgery was evaluated in a nonblinded fashion. All patients received a similar standardized intraoperative anesthetic technique and were extubated during the immediate postoperative period. Overall median visual analogue pain scores were significantly lower in patients receiving alfentanil, yet both alfentanil and morphine delivered high-quality postoperative analgesia (Fig. 33.3). Although the clinical impression of these investigators was that alfentanil patients were less sedated in the immediate postoperative period, this clinical observation was not substantiated after statistical analysis of sedation scores. The two groups did not differ with respect to overall sedation scores, frequency of nausea and vomiting, hemodynamic instability, myocardial ischemia, or hypoxemia during the immediate postoperative period. Sufentanil is approximately 10 times more potent than fentanyl. The drug is extremely lipid-soluble and is highly bound to plasma proteins. Because of its high potency, conventional clinical doses of sufentanil result in plasma concentrations that rapidly decline to less than the sensitivity of most assayed methods, making it difficult to 828
60 Patients (%)
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Alfentanil PCA Morphine PCA 47%
40 30%
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35%
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14%
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2% 4%
0 Excellent
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Poor
Fig. 33.3 Overall patient satisfaction with postoperative analgesia. Ninety-one percent of patients using alfentanil rated their postoperative analgesia as excellent or good, whereas 82% of patients using morphine rated their postoperative analgesia similarly (differences not statistically significant). PCA, Patient-controlled analgesia. (From Checketts MR, Gilhooly CJ, Kenny GN. Patient-maintained analgesia with target-controlled alfentanil infusion after cardiac surgery: a comparison with morphine PCA. Br J Anaesth. 1998;80:748–751.)
determine accurate pharmacokinetic parameters. However, sufentanil pharmacokinetic actions appear not to be altered in patients with renal disease. Because hepatic sufentanil clearance approaches liver blood flow, the drug’s pharmacokinetic properties are expected to change with hepatic disease yet the clinical relevance remains undetermined. Sufentanil undergoes substantial (approximately 60%) first-pass uptake in the lungs. Remifentanil has a very fast onset and an ultrashort duration of action; it is unique in that it is readily susceptible to rapid hydrolysis by nonspecific esterases in the blood and tissues. The drug is moderately lipophilic and is half as potent as fentanyl when blood concentrations causing equivalent analgesia are compared. Remifentanil has an elimination half-life of 10 to 20 minutes, and the time required for a 50% reduction in blood concentration after discontinuation of an infusion that has attained a steady state is approximately 3 minutes and does not increase with the duration of infusion. Available evidence suggests that neither the pharmacokinetics nor the pharmacodynamics of remifentanil are significantly altered in patients with severe hepatic or renal disease. These properties should confer ease of titration to changing analgesic conditions. However, the quick offset of action, although desirable, may result in inadequate postoperative analgesia. Because of the rapid offset of analgesic effect of remifentanil, the continued requirement for postoperative analgesia needs to be considered before the remifentanil are discontinued. A transition must be made from remifentanil to some other longer-acting analgesic agent for the initiation of substantial postoperative analgesia. Although the transition to postoperative pain management can be made using a remifentanil infusion alone, this appears to be associated with a high incidence of adverse respiratory effects. The use of a remifentanil infusion to provide postoperative analgesia was evaluated during recovery from total intravenous anesthesia with remifentanil and propofol from a wide variety of noncardiac surgeries (eg, abdominal, spine, joint replacement, thoracic). This multiinstitutional study had a detailed protocol that specified doses and method of administration of all anesthetic drugs. Total intraoperative intravenous anesthesia consisted of midazolam (premedication only), remifentanil, propofol, and vecuronium. Propofol was stopped immediately before intraoperative extubation, 829
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and the remifentanil infusion was continued for postoperative analgesia. During the immediate postoperative period, intravenous morphine was administered during tapering of remifentanil infusion. Adverse respiratory events that included oxygen saturation via pulse oximetry less than 90%, respiratory rate less than 12 per minute, and apnea, affected 45 patients (29%; two required naloxone). Apnea occurred in 11 patients (7% treated with mask ventilation and downward titration of remifentanil infusion; one required naloxone). The administration of a bolus of remifentanil preceded the onset of adverse respiratory events in 19 of 45 cases and in 9 of 11 cases of apnea. These data suggest that remifentanil boluses plus an infusion are particularly likely to produce clinically significant adverse respiratory events. This open, dose-ranging study concluded that, although remifentanil certainly initiates analgesia, its use in the immediate postoperative period may pose dangers. Additional studies are needed to investigate the transition from remifentanil to longer-lasting analgesics and to refine strategies that minimize respiratory depression while optimizing pain control. The administration of a potent, rapid-acting opioid such as remifentanil by continuous infusion for postoperative analgesia must be performed with meticulous attention to detail and constant vigilance. Extreme caution should be exercised in the postoperative administration of bolus doses of remifentanil because substantial respiratory depression (including apnea) may develop. Furthermore, the remifentanil infusion should be inserted into the intravenous line as close as possible to the patient to minimize dead space, and the rate of the main intravenous infusion should be controlled at a rate that is high enough to flush remifentanil from the tubing continuously. A more dilute remifentanil solution that runs at greater rates (on a volume-per-time basis) helps minimize the effect of variations in flow rate of the main intravenous tubing on delivery of remifentanil to the patient. Remifentanil also may possess detrimental cardiovascular effects via bradycardia and decreases in systemic vascular resistance, leading to decreased cardiac output and hypotension. Such changes may occur during clinically used doses for cardiac surgery (0.1 to 1.0 µg/kg/min), inducing significant cardiovascular disturbances that are potentially deleterious to patients with cardiac disease.
PATIENT-CONTROLLED ANALGESIA When intravenous opioids are used for controlling postoperative pain, PCA technology is generally used. Essentials in the successful use of PCA technology include loading the patient with intravenous opioids to the point of patient comfort before initiating PCA, ensuring that the patient wants to control analgesic treatment, using an appropriate PCA dose and lockout interval, and considering the use of a basal rate infusion. Focused guidance of PCA dosing by a dedicated acute pain service, compared with surgeon-directed PCA, may result in more effective analgesia with fewer adverse effects.
NONSTEROIDAL ANTIINFLAMMATORY AGENTS NSAIDs, in contrast with the opioids’ central nervous system mechanism of action, primarily exert their analgesic, antipyretic, and antiinflammatory effects peripherally by interfering with prostaglandin synthesis after tissue injury. NSAIDs inhibit COX, the enzyme responsible for the conversion of arachidonic acid to prostaglandin. Combining NSAIDs with traditional intravenous opioids may allow a patient to 830
Phospholipase A 2 Arachidonic acid COX–1 “Constitutive”
COX–2 “Inducible”
Prostaglandins
Prostaglandins
Gastric protection Hemostasis Renal function
Pain Inflammation Fever
Fig. 33.4 Cyclooxygenase (COX) Pathways. Molecular studies distinguishing between COX-1 and COX-2 enzymes have led to the exciting hypothesis that the therapeutic and adverse effects of the nonspecific inhibitors (nonsteroidal antiinflammatory drugs) could be uncoupled. (From Gajraj NM. Cyclooxygenase-2 inhibitors. Anesth Analg. 2003;96:1720–1738.)
achieve an adequate level of analgesia with fewer side effects than if a similar level of analgesia was obtained with intravenous opioids alone. Unlike opioids, which preferentially reduce spontaneous postoperative pain, NSAIDs have comparable efficacy for both spontaneous and movement-evoked pain, the latter of which may be more important in causing postoperative physiologic impairment. Concerns regarding NSAID side effects, including alterations in the gastric mucosal barrier, renal tubular function, and inhibition of platelet aggregation, have likely made clinicians reluctant to use NSAIDs in patients undergoing cardiac surgery. NSAIDs are not a homogenous group and vary considerably in analgesic efficacy as a result of differences in pharmacodynamic and pharmacokinetic parameters. NSAIDs are nonspecific inhibitors of COX, which is the rate-limiting enzyme involved in the synthesis of prostaglandins. COX-1 is ubiquitously and constitutively expressed and has a homeostatic role in platelet aggregation, gastrointestinal mucosal integrity, and renal function, whereas COX-2 is inducible and primarily expressed at the sites of injury (and in the kidney and brain) and mediates pain and inflammation. NSAIDs are nonspecific inhibitors of both forms of COX yet vary in their ratio of COX-1 to COX-2 inhibition. Molecular studies distinguishing between constitutive COX-1 and inflammation-inducible COX-2 enzymes have led to the exciting hypothesis that the therapeutic and adverse effects of NSAIDs could be uncoupled (Fig. 33.4). Subsequently, clinicians have witnessed the growing use of COX-2 inhibitors in the perioperative period after noncardiac surgery. The primary advantage of COX-2 inhibitors, compared with NSAIDs, is their lack of effect on platelet function and bleeding.
ALPHA2-ADRENERGIC AGONISTS The α2-adrenergic agonists provide analgesia, sedation, and sympatholysis. The potential perioperative analgesic benefits of α2 agonists when administered to patients undergoing cardiac surgery were demonstrated 30 years ago. Most of the clinical investigations regarding perioperative use of this class of drugs remain focused on exploiting the sedative effects and beneficial cardiovascular effects (decreasing 831
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Membrane phospholipid
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hypertension and tachycardia) associated with their use. α2-Adrenergic agonists have been used perioperatively in patients undergoing cardiac surgery. However, the focus of such clinical investigations has been on the intraoperative period and the potential for enhanced postoperative hemodynamic stability, potentially leading to reduced postoperative myocardial ischemia (but not specifically to enhance postoperative analgesia). Taken together, these clinical investigations indicate that perioperative administration of α2-adrenergic agonists to patients undergoing cardiac surgery decreases intraoperative anesthetic requirements, may enhance perioperative hemodynamic stability, and may decrease perioperative myocardial ischemia. The potential ability of this class of drugs to initiate reliable postoperative analgesia awaits definitive investigation.
INTRATHECAL AND EPIDURAL TECHNIQUES Numerous clinical investigations clearly indicate that intrathecal and/or epidural techniques (using opioids and/or local anesthetics) initiate reliable postoperative analgesia in patients after cardiac surgery (Boxes 33.3 and 33.4). Additional potential advantages of using intrathecal and/or epidural techniques in patients undergoing cardiac surgery include stress-response attenuation and thoracic cardiac sympathectomy.
BOX 33.3
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Intrathecal Techniques
Advantages • Simple, reliable analgesia • Stress-response attenuation • Less hematoma risk than epidural techniques Disadvantages • No cardiac sympathectomy • Hematoma risk increased • Side effects of intrathecal opioids
BOX 33.4
Epidural Techniques
Advantages • Reliable analgesia • Stress-response attenuation • Cardiac sympathectomy Disadvantages • Labor-intensive • Hematoma formation risk increased • Side effects of epidural opioids
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Most clinical investigators have used intrathecal morphine in hopes of providing prolonged postoperative analgesia. Some clinical investigators have used intrathecal fentanyl, sufentanil, and/or local anesthetics for intraoperative anesthesia and analgesia (with stress-response attenuation) and/or thoracic cardiac sympathectomy. An anonymous survey of members of the Society of Cardiovascular Anesthesiologists published in 2001 indicated that almost 8% of practicing anesthesiologists incorporate intrathecal techniques into their anesthetic management of adults undergoing cardiac surgery. Of these anesthesiologists, 75% practice in the United States, 72% perform the intrathecal injection before the induction of anesthesia, 97% use morphine, 13% use fentanyl, 2% use sufentanil, 10% use lidocaine, and 3% use tetracaine. The mid-1990s saw the emergence of fast-track cardiac surgery, with the goal being tracheal extubation in the immediate postoperative period. Some clinical investigators have revealed that certain combinations of intraoperative anesthetic techniques coupled with appropriate doses of intrathecal morphine will allow tracheal extubation after cardiac surgery within the immediate postoperative period to coexist with enhanced analgesia. Many clinical investigations involving the use of intrathecal analgesic techniques in patients undergoing cardiac surgery indicate that the administration of intrathecal morphine to patients before CPB initiates reliable postoperative analgesia after cardiac surgery. Intrathecal opioids or local anesthetics cannot reliably attenuate the perioperative stress response associated with CPB that persists during the immediate postoperative period. A recently published metaanalysis of randomized, controlled trials (25 randomized trials, 1106 patients) concluded that spinal analgesia does not improve clinically relevant outcomes in patients undergoing cardiac surgery.
Postoperative Pain Management for the Cardiac Patient
Intrathecal Techniques
Epidural Techniques Since this initial impressive display of potential benefits (eg, reliable postoperative analgesia, stress-response attenuation, facilitation of early tracheal extubation), other clinical investigators have subsequently applied thoracic epidural anesthesia (TEA) to patients undergoing cardiac surgery. Most clinical investigators have used thoracic epidural local anesthetics in hopes of providing perioperative stress-response attenuation and/or perioperative thoracic cardiac sympathectomy. Some clinical investigators have used thoracic epidural opioids to provide intraoperative and/or postoperative analgesia. An anonymous survey of members of the Society of Cardiovascular Anesthesiologists published in 2001 indicated that 7% of practicing anesthesiologists incorporate thoracic epidural techniques into their anesthetic management of adults undergoing cardiac surgery. Of these anesthesiologists, 58% practice in the United States. Many clinical investigations have proved that TEA with local anesthetics significantly attenuates the perioperative stress response in patients undergoing cardiac surgery. Patients randomized to receive intermittent boluses of thoracic epidural bupivacaine intraoperatively, followed by continuous infusion postoperatively, exhibited significantly decreased blood levels of norepinephrine and epinephrine perioperatively when compared with patients similarly managed without thoracic epidural catheters. The February 2011 issue of Anesthesiology highlights the controversial nature of this topic as two clinical studies with opposite conclusions were published. These authors concluded, “Given the potentially devastating complications of epidural hematoma after insertion of an epidural catheter, it is questionable whether this procedure should be applied routinely in cardiac surgical patients who require full heparinization.” These two clinical studies were accompanied by an editorial that stated that “we 833
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continue to try and show that regional anesthesia and analgesia can substantially alter surgical outcomes without success … perhaps it is time to move away from trying to prove that anesthetic interventions will reduce morbidity or mortality and to focus on tangible benefits to patients or their families.” Despite enhanced postoperative analgesia offered via TEA techniques, such analgesia does not appear to decrease the incidence of persistent pain after cardiac surgery. Persistent pain, defined as pain still present 2 or more months after surgery, was similar in the two cohorts (reported in almost 30% of patients). The quality of analgesia obtained with TEA techniques is sufficient to allow cardiac surgery to be performed in awake patients without general endotracheal anesthesia. The initial report of awake cardiac surgery was published in the Annals of Thoracic Surgery in 2000. Since these initial small clinical reports appeared, larger series of patients have been published, demonstrating that awake cardiac surgery is feasible and safe. In 2003, the first case report of awake cardiac surgery requiring CPB was published. In this astonishing case report from Austria, a 70-year-old man with aortic stenosis underwent aortic valve replacement with the assistance of normothermic CPB (total time: 123 minutes; cross-clamp time: 82 minutes) solely via TEA. Verbal communication with the patient was possible on demand throughout the CPB surgery. The patient did well and experienced an unremarkable postoperative course.
Risk for Hematoma Formation
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Intrathecal or epidural instrumentation entails risk, the most feared complication being epidural hematoma formation. The estimated incidence of hematoma formation is approximately 1 : 220,000 after intrathecal instrumentation. Hematoma formation is more common (approximately 1 : 150,000) after epidural instrumentation because larger needles are used, catheters are inserted, and the venous plexus in the epidural space is prominent. Furthermore, hematoma formation does not exclusively occur during epidural catheter insertion; almost one half of all cases develop after catheter removal. Risk is increased when intrathecal or epidural instrumentation is performed before systemic heparinization, and hematoma formation has occurred in patients when diagnostic or therapeutic lumbar puncture has been followed by systemic heparinization. When lumbar puncture is followed by systemic heparinization, concurrent use of aspirin, difficult or traumatic instrumentation, and the administration of intravenous heparin within 1 hour of instrumentation increase the risk for hematoma formation. However, by observing certain precautions, intrathecal or epidural instrumentation can be safely performed in patients who will subsequently receive intravenous heparin. By delaying surgery 24 hours in the event of a traumatic tap, by delaying heparinization 60 minutes after catheter insertion, and by maintaining tight perioperative control of anticoagulation, more than 4000 intrathecal or epidural catheterizations were safely performed in patients undergoing peripheral vascular surgery who received intravenous heparin after catheter insertion. However, the magnitude of anticoagulation in these two studies (activated partial thromboplastin time of approximately 100 seconds and activated coagulation time approximately twice the baseline value) involving patients undergoing peripheral vascular surgery was substantially less than the degree of anticoagulation required in patients subjected to CPB. Most clinical studies investigating the use of intrathecal or epidural anesthesia and analgesia techniques in patients undergoing cardiac surgery include precautions to decrease the risk for hematoma formation. Some used the technique only after the demonstration of laboratory evidence of normal coagulation parameters, delayed surgery 24 hours in the event of traumatic tap, or required that the time from 834
MULTIMODAL ANALGESIA The possibility of synergism among analgesic drugs is a concept that is nearly a century old. Although subsequent research has demonstrated the difference between additivity and synergy, the fundamental strategy behind such combinations (multimodal or balanced analgesia) remains unchanged—enhanced analgesia with the minimization of adverse physiologic effects. The use of analgesic combinations during the postoperative period, specifically the combination of traditional intravenous opioids with other analgesics (eg, NSAIDs, COX-2 inhibitors, ketamine), has been proven clinically effective in noncardiac patients for decades.
Postoperative Pain Management for the Cardiac Patient
instrumentation to systemic heparinization exceed 60 minutes. Although most clinicians investigating the use of epidural anesthesia and analgesia techniques in patients undergoing cardiac surgery insert the catheters the day before scheduled surgery, investigators have performed instrumentation on the same day of surgery. Institutional practice (same-day admit surgery) may eliminate the option of epidural catheter insertion on the day before scheduled surgery. An alternative is to perform epidural instrumentation postoperatively (before or after tracheal extubation) after laboratory evidence demonstrates normal coagulation parameters. The use of regional anesthetic techniques in patients undergoing cardiac surgery remains extremely controversial, prompting numerous editorials by recognized experts in the field of cardiac anesthesia. One of the primary reasons such controversy exists (and likely will continue for some time) is that the numerous clinical investigations regarding this topic are suboptimally designed and use a wide array of disparate techniques, preventing clinically useful conclusions on which all can agree.
SUGGESTED READINGS Allen MS, Halgren L, Nichols FC, et al. A randomized controlled trial of bupivacaine through intercostal catheters for pain management after thoracotomy. Ann Thorac Surg. 2009;88:903. American Society of Anesthesiologists Task Force on Acute Pain Management. Practice guidelines for acute pain management in the perioperative setting: an updated report by the American Society of Anesthesiologists Task Force on Acute Pain Management. Anesthesiology. 2012;116:248. Bettex DA, Schmidlin D, Chassot PG, et al. Intrathecal sufentanil-morphine shortens the duration of intubation and improves analgesia in fast-track cardiac surgery. Can J Anaesth. 2002;49:711. Bignami E, Landoni G, Biondi-Zoccai GGL, et al. Epidural analgesia improves outcome in cardiac surgery: a meta-analysis of randomized controlled trials. J Cardiothorac Vasc Anesth. 2010;24:586. Blaudszun G, Lysakowski C, Elia N, et al. Effect of perioperative systemic α2 agonists on postoperative morphine consumption and pain intensity; systematic review and meta-analysis of randomized controlled trials. Anesthesiology. 2012;116:1312. Goldstein S, Dean D, Kim SJ, et al. A survey of spinal and epidural techniques in adult cardiac surgery. J Cardiothorac Vasc Anesth. 2001;15:158. Hansdottir V, Philip J, Olsen MF, et al. Thoracic epidural versus intravenous patient-controlled analgesia after cardiac surgery. Anesthesiology. 2006;104:142. Lena P, Balarac N, Lena D, et al. Fast-track anesthesia with remifentanil and spinal analgesia for cardiac surgery: the effect on pain control and quality of recovery. J Cardiothorac Vasc Anesth. 2008;22:536. Lynch JJ, Mauermann WJ, Pulido JN, et al. Use of paravertebral blockade to facilitate early extubation after minimally invasive cardiac surgery. Semin Cardiothorac Vasc Anesth. 2010;14:47. Mazzeffi M, Khelemsky Y. Poststernotomy pain: a clinical review. J Cardiothorac Vasc Anesth. 2011;25:1163. Metz S, Schwann N, Hassanein W, et al. Intrathecal morphine for off-pump coronary artery bypass grafting. J Cardiothorac Vasc Anesth. 2004;18:451. Monaco F, Biselli C, Landoni G, et al. Thoracic epidural anesthesia improves early outcome in patients undergoing cardiac surgery for mitral regurgitation: a propensity-matched study. J Cardiothorac Vasc Anesth. 2013;27:1301.
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Myles PS, Bain C. Underutilization of paravertebral block in thoracic surgery. J Cardiothorac Vasc Anesth. 2006;20:635. Ried M, Schilling C, Potzger T, et al. Prospective, comparative study of the On-Q painbuster postoperative pain relief system and thoracic epidural analgesia after thoracic surgery. J Cardiothorac Vasc Anesth. 2014;28:973. Royse C. Epidurals for cardiac surgery; can we substantially reduce surgical morbidity or should we focus on quality of recovery? Anesthesiology. 2011;114:232. Royse C, Royse A, Soeding P, et al. Prospective randomized trial of high thoracic epidural analgesia for coronary artery bypass surgery. Ann Thorac Surg. 2003;75:93. Viscusi ER, Candiotti KA, Onel E, et al. The pharmacokinetics and pharmacodynamics of liposome bupivacaine administered via a single epidural injection to healthy volunteers. Reg Anesth Pain Med. 2012;37:616. White PF, Rawal S, Latham P, et al. Use of a continuous local anesthetic infusion for pain management after median sternotomy. Anesthesiology. 2003;99:918. Zangrillo A, Bignami E, Biondi-Zuccai GGL, et al. Spinal analgesia in cardiac surgery: a meta-analysis of randomized controlled trials. J Cardiothorac Vasc Anesth. 2009;23:813.
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Postoperative Pain Management for the Cardiac Patient Mark A. Chaney, MD
Key Points 1. Inadequate postoperative analgesia and/or an uninhibited perioperative surgical stress response has the potential to initiate pathophysiologic changes in all major organ systems, which may lead to substantial postoperative morbidity. Adequate postoperative analgesia prevents unnecessary patient discomfort, may decrease morbidity, hospital lengths of stay, and thus may decrease costs. 2. Pain after cardiac surgery may be intense and originates from many sources, including the incision (sternotomy or thoracotomy), intraoperative tissue retraction and dissection, vascular cannulation sites, vein-harvesting sites, and chest tubes. Achieving optimal pain relief after cardiac surgery is often difficult, yet it may be attained through a wide variety of techniques, including local anesthetic infiltration, nerve blocks, intravenous agents, intrathecal techniques, and epidural techniques. 3. Traditionally, analgesia after cardiac surgery has been obtained with intravenous opioids (specifically morphine). However, intravenous opioid use is associated with definite detrimental side effects and longer-acting opioids such as morphine may delay tracheal extubation during the immediate postoperative period via excessive sedation and/or respiratory depression. Thus in the current era of early extubation (eg, fast-tracking), cardiac anesthesiologists are exploring unique options for the control of postoperative pain in patients after cardiac surgery. 4. Although patient-controlled analgesia is a well-established technique and offers potential unique benefits, whether it truly offers significant clinical advantages (compared with traditional nurse-administered analgesic techniques) to patients immediately after cardiac surgery remains to be determined. 5. Administration of intrathecal morphine to patients initiates reliable postoperative analgesia after cardiac surgery. Intrathecal opioids or local anesthetics cannot reliably attenuate the perioperative stress response associated with cardiac surgery that persists during the immediate postoperative period. Although intrathecal local anesthetics (not opioids) may induce perioperative thoracic cardiac sympathectomy, the hemodynamic changes associated with total spinal anesthesia make the technique unpalatable in patients with cardiac disease. 6. Administration of thoracic epidural opioids or local anesthetics to patients initiates reliable postoperative analgesia after cardiac surgery. The quality of analgesia obtained with thoracic epidural anesthetic techniques is sufficient to allow cardiac surgery to be performed in “awake” patients. 7. Use of intrathecal and epidural techniques in patients undergoing cardiac surgery remains extremely controversial. Concerns regard the risk of hematoma formations.
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8. The last decade has seen a resurgence of nerve blocks (including catheter-based techniques) in patients undergoing cardiac surgery. Recent clinical studies using intercostal, intrapleural, and paravertebral blocks indicate that these techniques may have unique clinical advantages, even when compared with traditional intrathecal and epidural techniques. The emergence of liposomal bupivacaine, which has the potential to provide clinical analgesia for 96 hours after a single injection, may revolutionize the use of single-shot nerve blocks for patients undergoing cardiac surgery. 9. As a general rule, avoiding intense, single-modality therapy for the treatment of acute postoperative pain is best. The administration of two analgesic agents that act by different mechanisms (multimodal or balanced analgesia) provides superior analgesic efficacy with equivalent or reduced adverse effects.
Adequate postoperative analgesia prevents unnecessary patient discomfort, may decrease morbidity, may decrease postoperative hospital lengths of stay, and thus may decrease costs. Because postoperative pain management has been deemed important, the American Society of Anesthesiologists has published practice guidelines regarding this topic. Furthermore, in recognition of the need for improved pain management, the Joint Commission has developed standards for the assessment and management of pain in accredited hospitals and other health care settings. Patient satisfaction (no doubt linked to adequacy of postoperative analgesia) has become an essential element that influences clinical activity of not only anesthesiologists but all health care professionals. Achieving optimal pain relief after cardiac surgery is often difficult. Pain may be associated with many interventions, including sternotomy, thoracotomy, leg vein harvesting, pericardiotomy, and/or chest tube insertion, among other interventions. Inadequate analgesia and/or an uninhibited stress response during the postoperative period may increase morbidity by causing adverse hemodynamic, metabolic, immunologic, and hemostatic alterations. Aggressive control of postoperative pain, associated with an attenuated stress response, may decrease morbidity and mortality in high-risk patients after noncardiac surgery and may also decrease morbidity and mortality in patients after cardiac surgery. Adequate postoperative analgesia may be attained via a wide variety of techniques (Box 33.1). Traditionally, analgesia after cardiac surgery has been obtained with intravenous opioids (specifically morphine). However, intravenous opioid use is associated with definite detrimental side effects (eg, nausea and vomiting, pruritus, urinary retention, respiratory depression), and longer-acting opioids such as morphine may delay tracheal extubation during the immediate
BOX 33.1
Techniques Available for Postoperative Analgesia
Local anesthetic infiltration Nerve blocks Opioids Nonsteroidal antiinflammatory agents α-Adrenergic agents Intrathecal techniques Epidural techniques Multimodal analgesia
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PAIN AND CARDIAC SURGERY Surgical or traumatic injury initiates changes in the peripheral and central nervous systems that must be addressed therapeutically to promote postoperative analgesia and, it is hoped, positively influence clinical outcomes (Box 33.2). The physical processes of incision, traction, and cutting of tissues stimulate free nerve endings and a wide variety of specific nociceptors. Receptor activation and activity are further modified by the local release of chemical mediators of inflammation and sympathetic amines released via the perioperative surgical stress response. The perioperative surgical stress response peaks during the immediate postoperative period and exerts major effects on many physiologic processes. The potential clinical benefits of attenuating the perioperative surgical stress response (above and beyond simply attaining adequate clinical analgesia) have received significant attention during the 2000s and remain fairly controversial. However, inadequate postoperative analgesia and/or an uninhibited perioperative surgical stress response clearly has the potential to initiate pathophysiologic changes in all major organ systems, including the cardiovascular, pulmonary, gastrointestinal, renal, endocrine, immunologic, and/or central nervous systems, all of which may lead to substantial postoperative morbidity. Pain after cardiac surgery may be intense, and it originates from many sources, including the incision (eg, sternotomy, thoracotomy), intraoperative tissue retraction and dissection, vascular cannulation sites, vein-harvesting sites, and chest tubes, among other sources. Patients in whom an internal mammary artery is surgically exposed and used as a bypass graft may have substantially more postoperative pain.
BOX 33.2
Pain and Cardiac Surgery
Originates from many sources Most commonly originates from the chest wall Preoperative expectations influence postoperative satisfaction Quality of postoperative analgesia may influence morbidity
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postoperative period via excessive sedation and/or respiratory depression. Thus in the current era of early extubation (fast-tracking), cardiac anesthesiologists are exploring unique options other than traditional intravenous opioids for the control of postoperative pain in patients after cardiac surgery. The last decade has witnessed increased use of smaller incisions by cardiac surgeons, prompting clinical investigations into the use of intercostal, intrapleural, and paravertebral blocks (with and without catheters), and the emergence of long-acting liposomal bupivacaine may revolutionize the use of these techniques. No single technique is clearly superior; each possesses distinct advantages and disadvantages. It is becoming increasingly clear that a multimodal approach and/or a combined analgesic regimen (using a variety of techniques) is the best way to approach postoperative pain in all patients after surgery to maximize analgesia and minimize side effects. When addressing postoperative analgesia in cardiac surgical patients, the choice of technique (or techniques) should be made only after a thorough analysis of the risk-benefit ratio of each technique in the specific patient in whom analgesia is desired.
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Persistent pain after cardiac surgery, although rare, can be problematic. The cause of persistent pain after sternotomy is multifactorial, yet tissue destruction, intercostal nerve trauma, scar formation, rib fractures, sternal infection, stainless-steel wire sutures, and/or costochondral separation may all play roles. Such chronic pain is often localized to the arms, shoulders, or legs. Postoperative brachial plexus neuropathies also may occur and have been attributed to rib fracture fragments, internal mammary artery dissection, suboptimal positioning of the patient during surgery, and/or central venous catheter placement. Postoperative neuralgia of the saphenous nerve has also been reported after harvesting of saphenous veins for coronary artery bypass grafting (CABG). Younger patients appear to be at greater risk for the development of chronic, long-lasting pain. The correlation of severity of acute postoperative pain and the development of chronic pain syndromes has been suggested (patients requiring more postoperative analgesics may be more likely to develop chronic pain), yet this link is still vague. Patient satisfaction with quality of postoperative analgesia is as much related to the comparison between anticipated and experienced pain as it is to the actual level of pain experienced. Satisfaction is related to a situation that is better than predicted, dissatisfaction to one that is worse than expected. Patients undergoing cardiac surgery remain concerned regarding the adequacy of postoperative pain relief and preoperatively tend to expect a greater amount of postoperative pain than that which is actually experienced. Because of these unique preoperative expectations, patients after cardiac surgery who postoperatively receive only moderate analgesia will likely still be satisfied with their pain control. Thus patients may experience pain of moderate intensity after cardiac surgery yet still express very high satisfaction levels.
POTENTIAL CLINICAL BENEFITS OF ADEQUATE POSTOPERATIVE ANALGESIA
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Inadequate analgesia (coupled with an uninhibited stress response) during the postoperative period may lead to many adverse hemodynamic (tachycardia, hypertension, vasoconstriction), metabolic (increased catabolism), immunologic (impaired immune response), and hemostatic (platelet activation) alterations. In patients undergoing cardiac surgery, perioperative myocardial ischemia is most commonly observed during the immediate postoperative period and appears to be related to outcome. Intraoperatively, initiation of cardiopulmonary bypass (CPB) causes substantial increases in stress response hormones (eg, norepinephrine, epinephrine) that persist into the immediate postoperative period and may contribute to myocardial ischemia observed during this time. Furthermore, postoperative myocardial ischemia may be aggravated by cardiac sympathetic nerve activation, which disrupts the balance between coronary blood flow and myocardial oxygen demand. Thus during the pivotal immediate postoperative period after cardiac surgery, adequate analgesia coupled with stressresponse attenuation may potentially decrease morbidity and enhance health-related quality of life.
LOCAL ANESTHETIC INFILTRATION Pain after cardiac surgery is often related to median sternotomy, peaking during the first 2 postoperative days. Because of problems associated with traditional intravenous opioid analgesia and with the nonsteroidal antiinflammatory drugs (NSAIDs) and cyclooxygenase (COX) inhibitors, alternative methods of achieving postoperative 824
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analgesia in cardiac surgical patients have been sought. One such alternative method that may hold promise is the continuous infusion of a local anesthetic. Clinical investigations have revealed the potential benefits of using a continuous infusion of a local anesthetic in patients after cardiac surgery. Patients undergoing elective CABG via median sternotomy were randomized to either ropivacaine or placebo groups. At the end of the surgery but before wound closure, bilateral intercostal nerve injections from T1 to T12 were performed using 20 mL of either 0.2% ropivacaine or normal saline. After sternal reapproximation with wires, two catheters with multiple side openings were placed anterior to the sternum (Fig. 33.1). These catheters were connected to a pressurized elastomeric pump containing a flow regulator, which allowed for the delivery of 0.2% ropivacaine or normal saline at approximately 4 mL/h. The postoperative pain management was via intravenous patient-controlled anesthesia (PCA) morphine (for 72 hours). The sternal catheters were removed after 48 hours. Total mean PCA morphine consumption during the immediate postoperative period (72 hours) was significantly decreased in the ropivacaine group (47.3 vs 78.7 mg, respectively; P = .038). Mean overall pain scores (scale ranging from 0 for no pain to 10 for maximum pain imaginable) were also significantly decreased in the ropivacaine group (1.6 vs 2.6, respectively; P = .005). Most interestingly, patients receiving ropivacaine had a mean hospital length of stay of 5.2 ± 1.3 days compared with 8.2 ± 7.9 days for patients receiving normal saline, a difference that was statistically significant (P = .001). No difference was observed in wound infections or wound healing between
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Fig. 33.1 Intraoperative placement of the pressurized elastomeric pump and catheters. (From Dowling R, Thielmeier K, Ghaly A, et al. Improved pain control after cardiac surgery: results of a randomized, double-blind, clinical trial. J Thorac Cardiovasc Surg. 2003;126:1271–1278.)
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the two groups during hospitalization or after hospital discharge. No complications related to placement of the sternal wound catheters or performance of the intercostal nerve blocks were encountered. The authors concluded that their analgesic technique significantly improves postoperative pain control while decreasing the amount of opioid analgesia required in patients subjected to standard median sternotomy.
NERVE BLOCKS With the increasing popularity of minimally invasive cardiac surgery, which uses nonsternotomy incisions (minithoracotomy), the use of nerve blocks for the management of postoperative pain has increased. Thoracotomy incisions (transverse anterolateral minithoracotomy, vertical anterolateral minithoracotomy), because of costal cartilage tissue trauma to ribs, muscles, or peripheral nerves, may induce more intense postoperative pain than that resulting from median sternotomy. Adequate analgesia after thoracotomy incisions is important because pain is a key component in the alteration of lung function after this type of incision. Uncontrolled pain causes a reduction in respiratory mechanics, reduced mobility, and increases in hormonal and metabolic activity. Perioperative deterioration in respiratory mechanics may lead to pulmonary complications and hypoxemia, which may in turn lead to myocardial ischemia or infarction, cerebrovascular accidents, thromboembolism, delayed wound healing, increased morbidity, and prolonged hospital stay. Various analgesic techniques have been developed to treat postoperative thoracotomy pain. The most commonly used techniques include intercostal nerve block, intrapleural administration of a local anesthetic, and thoracic paravertebral block. Intrathecal techniques and epidural techniques are also effective in controlling postthoracotomy pain. Intercostal nerve block has been extensively used for analgesia after thoracic surgery and can be performed either intraoperatively or postoperatively. It usually provides sufficient analgesia lasting approximately 6 to 12 hours (depending on the amount and type of local anesthetic used) and may need to be repeated if additional analgesia is required. Local anesthetics may be administered as a single injection under direct vision before chest closure, as a single preoperative percutaneous injection, as multiple percutaneous serial injections, or via an indwelling intercostal catheter. Blockade of intercostal nerves interrupts C-fiber afferent transmission of impulses to the spinal cord. A continuous intercostal catheter allows frequent dosing or infusions of local anesthetic agents and avoids multiple needle injections. Various clinical studies have confirmed the analgesic efficacy of this technique, and the technique compares favorably with thoracic epidural analgesic techniques. A major concern associated with intercostal nerve block is the potentially high amount of local anesthetic systemic absorption. However, multiple clinical studies involving patients undergoing thoracic surgery have documented safe blood levels with standard techniques. Clinical investigations involving patients undergoing thoracic surgery indicate that intercostal nerve blockade by intermittent or continuous infusion of bupivacaine (0.25% to 0.5%) or ropivacaine (0.5% to 0.75%) through indwelling intercostal catheters is an effective method for supplementing systemic intravenous opioid analgesia for postthoracotomy pain. Intrapleural administration of local anesthetics initiates analgesia via mechanisms that remain incompletely understood. However, the mechanism of action of extrapleural analgesia seems to depend primarily on diffusion of the local anesthetic into the paravertebral region. Local anesthetics then affect not only the ventral nerve root but also afferent fibers of the posterior primary ramus. Posterior ligaments of the posterior primary ramus innervate posterior spinal muscles and skin and are traumatized during posterolateral thoracotomy. Intrapleural administration of a local anesthetic 826
Esophagus
Descending aorta Sympathetic chain
Right lung
A
Transverse process
Thoracic duct
Superior costotransverse ligament
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Neck of rib Interpleural space Extrapleural compartment Subendothoracic compartment Intercostal nerve Posterior primary rami
Endothoracic fascia Pleura Visceral Parietal
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Fig. 33.2 Anatomy of the thoracic paravertebral space (A) and sagittal section through the thoracic paravertebral space showing a needle that has been advanced above the transverse process (B). (From Karmakar MK. Thoracic paravertebral block. Anesthesiology. 2001;95:771–780.)
to this region through a catheter inserted in the extrapleural space creates an analgesic region in the skin. The depth and width of this region depend on the diffusion of the local anesthetic in the extrapleural space. Thoracic paravertebral block involves the injection of a local anesthetic adjacent to the thoracic vertebrae close to where the spinal nerves emerge from the intervertebral foramina (Fig. 33.2). Thoracic paravertebral block, compared with thoracic epidural analgesic techniques, appears to provide equivalent analgesia, is technically easier, and may harbor less risk. Several different techniques exist for successful thoracic paravertebral block. The classic technique, most commonly used, involves eliciting loss of resistance. Injection of a local anesthetic results in ipsilateral somatic and sympathetic nerve blockade in multiple contiguous thoracic dermatomes above and below the site of injection, together with the possible suppression of the neuroendocrine stress response to surgery. These blocks may be effective in alleviating acute and chronic pain of unilateral origin from the chest. Continuous thoracic paravertebral infusion of a local anesthetic via a catheter placed under direct vision at thoracotomy is also a safe, simple, and an effective method of providing analgesia after thoracotomy. It is usually used in conjunction with adjunct intravenous opioid or other analgesics to provide optimal relief after thoracotomy. For a wide variety of reasons, including the increased use of small thoracic incisions by cardiac surgeons, the last decade has seen a resurgence of nerve blocks (usually catheter-based techniques) in patients undergoing cardiac surgery. Specifically, recent clinical studies using intercostal catheters, intrapleural catheters, and paravertebral blockade indicate that these techniques may have unique advantages, even when compared with traditional intrathecal and epidural techniques. Lastly, the emergence of liposomal bupivacaine, which has the potential to provide clinical analgesia for 96 hours after a single injection, may revolutionize the use of single-shot nerve blocks for thoracic and cardiac surgeries.
OPIOIDS The classic pharmacologic effect of opioids is analgesia, and these drugs have traditionally been the initial choice when a potent postoperative analgesic is required. Two anatomically distinct sites exist for opioid receptor–mediated analgesia: supraspinal and spinal. Systemically administered opioids produce analgesia at both sites. Supraspinally, the µ1 receptor is primarily involved in analgesia, whereas the µ2 receptor is the receptor predominantly involved in the spinal modulation of nociceptive processing. κ Receptors are important in mediating spinal and supraspinal analgesia as well. 827
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Subserous
Endo- fascia Pleura Azygos thoracic Visceral vein fascia Parietal
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δ Ligands may have a modulatory rather than a primary analgesic role. All three types of opioid receptors (µ, κ, and δ) have been demonstrated in peripheral terminals of sensory nerves. Activation of these receptors seems to require an inflammatory reaction because locally applied opioids do not produce analgesia in healthy tissue. The inflammatory process also may activate previously inactive opioid receptors. Morphine is the prototype opioid agonist with which all opioids are compared and is perhaps the most popular analgesic used in patients after cardiac surgery. Many semisynthetic derivatives are made by simple modifications of the morphine molecule. Morphine is poorly lipid-soluble and binds approximately 35% to plasma proteins, particularly albumin. Morphine is primarily metabolized in the liver, principally by conjugation to water-soluble glucuronides. The liver is the predominant site for morphine biotransformation, although extrahepatic metabolism also occurs in the kidney, brain, and possibly the gut. Extrahepatic clearance accounts for approximately 30% of the total body clearance. The terminal elimination half-life of morphine is 2 to 3 hours. In patients with liver cirrhosis, morphine pharmacokinetic actions are variable, probably reflecting the variability of liver disease in patients. Morphine’s terminal elimination half-life in patients with renal disease is comparable with that of patients without renal disease. Although morphine is perhaps the most popular intravenous analgesic used in patients after cardiac surgery, other synthetically derived opioids have been developed and may be used as well. These include fentanyl, alfentanil, sufentanil, and remifentanil. Transdermal delivery of fentanyl has also been investigated extensively. This modality is simple, noninvasive, and allows continuous release of fentanyl into the systemic circulation. However, the steady release of fentanyl in such a manner does not allow flexibility in dose adjustment, which may result in inadequate treatment of postoperative pain during rapidly changing intensity. Thus intravenous opioids are often necessary to supplement analgesia when transdermal fentanyl is used to manage acute postoperative pain. Alfentanil is approximately 5 to 10 times less potent than fentanyl. The drug acts rapidly; its peak effect is reached within minutes after intravenous administration. Its duration of action after bolus administration is also shorter than fentanyl. Alfentanil is highly lipid-soluble (approximately 100 times more lipid-soluble than morphine) and rapidly crosses the blood-brain barrier. Alfentanil pharmacokinetics is minimally affected by renal disease, and hepatic extraction is more a function of intrinsic hepatic enzyme capacity and protein binding than liver blood flow. The performance of a patient-demand, target-controlled alfentanil infusion system has compared favorably with traditional morphine PCA in patients after cardiac surgery. Morphine PCA versus alfentanil PCA for postoperative analgesia after undergoing elective cardiac surgery was evaluated in a nonblinded fashion. All patients received a similar standardized intraoperative anesthetic technique and were extubated during the immediate postoperative period. Overall median visual analogue pain scores were significantly lower in patients receiving alfentanil, yet both alfentanil and morphine delivered high-quality postoperative analgesia (Fig. 33.3). Although the clinical impression of these investigators was that alfentanil patients were less sedated in the immediate postoperative period, this clinical observation was not substantiated after statistical analysis of sedation scores. The two groups did not differ with respect to overall sedation scores, frequency of nausea and vomiting, hemodynamic instability, myocardial ischemia, or hypoxemia during the immediate postoperative period. Sufentanil is approximately 10 times more potent than fentanyl. The drug is extremely lipid-soluble and is highly bound to plasma proteins. Because of its high potency, conventional clinical doses of sufentanil result in plasma concentrations that rapidly decline to less than the sensitivity of most assayed methods, making it difficult to 828
60 Patients (%)
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Alfentanil PCA Morphine PCA 47%
40 30%
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35%
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2% 4%
0 Excellent
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Fig. 33.3 Overall patient satisfaction with postoperative analgesia. Ninety-one percent of patients using alfentanil rated their postoperative analgesia as excellent or good, whereas 82% of patients using morphine rated their postoperative analgesia similarly (differences not statistically significant). PCA, Patient-controlled analgesia. (From Checketts MR, Gilhooly CJ, Kenny GN. Patient-maintained analgesia with target-controlled alfentanil infusion after cardiac surgery: a comparison with morphine PCA. Br J Anaesth. 1998;80:748–751.)
determine accurate pharmacokinetic parameters. However, sufentanil pharmacokinetic actions appear not to be altered in patients with renal disease. Because hepatic sufentanil clearance approaches liver blood flow, the drug’s pharmacokinetic properties are expected to change with hepatic disease yet the clinical relevance remains undetermined. Sufentanil undergoes substantial (approximately 60%) first-pass uptake in the lungs. Remifentanil has a very fast onset and an ultrashort duration of action; it is unique in that it is readily susceptible to rapid hydrolysis by nonspecific esterases in the blood and tissues. The drug is moderately lipophilic and is half as potent as fentanyl when blood concentrations causing equivalent analgesia are compared. Remifentanil has an elimination half-life of 10 to 20 minutes, and the time required for a 50% reduction in blood concentration after discontinuation of an infusion that has attained a steady state is approximately 3 minutes and does not increase with the duration of infusion. Available evidence suggests that neither the pharmacokinetics nor the pharmacodynamics of remifentanil are significantly altered in patients with severe hepatic or renal disease. These properties should confer ease of titration to changing analgesic conditions. However, the quick offset of action, although desirable, may result in inadequate postoperative analgesia. Because of the rapid offset of analgesic effect of remifentanil, the continued requirement for postoperative analgesia needs to be considered before the remifentanil are discontinued. A transition must be made from remifentanil to some other longer-acting analgesic agent for the initiation of substantial postoperative analgesia. Although the transition to postoperative pain management can be made using a remifentanil infusion alone, this appears to be associated with a high incidence of adverse respiratory effects. The use of a remifentanil infusion to provide postoperative analgesia was evaluated during recovery from total intravenous anesthesia with remifentanil and propofol from a wide variety of noncardiac surgeries (eg, abdominal, spine, joint replacement, thoracic). This multiinstitutional study had a detailed protocol that specified doses and method of administration of all anesthetic drugs. Total intraoperative intravenous anesthesia consisted of midazolam (premedication only), remifentanil, propofol, and vecuronium. Propofol was stopped immediately before intraoperative extubation, 829
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and the remifentanil infusion was continued for postoperative analgesia. During the immediate postoperative period, intravenous morphine was administered during tapering of remifentanil infusion. Adverse respiratory events that included oxygen saturation via pulse oximetry less than 90%, respiratory rate less than 12 per minute, and apnea, affected 45 patients (29%; two required naloxone). Apnea occurred in 11 patients (7% treated with mask ventilation and downward titration of remifentanil infusion; one required naloxone). The administration of a bolus of remifentanil preceded the onset of adverse respiratory events in 19 of 45 cases and in 9 of 11 cases of apnea. These data suggest that remifentanil boluses plus an infusion are particularly likely to produce clinically significant adverse respiratory events. This open, dose-ranging study concluded that, although remifentanil certainly initiates analgesia, its use in the immediate postoperative period may pose dangers. Additional studies are needed to investigate the transition from remifentanil to longer-lasting analgesics and to refine strategies that minimize respiratory depression while optimizing pain control. The administration of a potent, rapid-acting opioid such as remifentanil by continuous infusion for postoperative analgesia must be performed with meticulous attention to detail and constant vigilance. Extreme caution should be exercised in the postoperative administration of bolus doses of remifentanil because substantial respiratory depression (including apnea) may develop. Furthermore, the remifentanil infusion should be inserted into the intravenous line as close as possible to the patient to minimize dead space, and the rate of the main intravenous infusion should be controlled at a rate that is high enough to flush remifentanil from the tubing continuously. A more dilute remifentanil solution that runs at greater rates (on a volume-per-time basis) helps minimize the effect of variations in flow rate of the main intravenous tubing on delivery of remifentanil to the patient. Remifentanil also may possess detrimental cardiovascular effects via bradycardia and decreases in systemic vascular resistance, leading to decreased cardiac output and hypotension. Such changes may occur during clinically used doses for cardiac surgery (0.1 to 1.0 µg/kg/min), inducing significant cardiovascular disturbances that are potentially deleterious to patients with cardiac disease.
PATIENT-CONTROLLED ANALGESIA When intravenous opioids are used for controlling postoperative pain, PCA technology is generally used. Essentials in the successful use of PCA technology include loading the patient with intravenous opioids to the point of patient comfort before initiating PCA, ensuring that the patient wants to control analgesic treatment, using an appropriate PCA dose and lockout interval, and considering the use of a basal rate infusion. Focused guidance of PCA dosing by a dedicated acute pain service, compared with surgeon-directed PCA, may result in more effective analgesia with fewer adverse effects.
NONSTEROIDAL ANTIINFLAMMATORY AGENTS NSAIDs, in contrast with the opioids’ central nervous system mechanism of action, primarily exert their analgesic, antipyretic, and antiinflammatory effects peripherally by interfering with prostaglandin synthesis after tissue injury. NSAIDs inhibit COX, the enzyme responsible for the conversion of arachidonic acid to prostaglandin. Combining NSAIDs with traditional intravenous opioids may allow a patient to 830
Phospholipase A 2 Arachidonic acid COX–1 “Constitutive”
COX–2 “Inducible”
Prostaglandins
Prostaglandins
Gastric protection Hemostasis Renal function
Pain Inflammation Fever
Fig. 33.4 Cyclooxygenase (COX) Pathways. Molecular studies distinguishing between COX-1 and COX-2 enzymes have led to the exciting hypothesis that the therapeutic and adverse effects of the nonspecific inhibitors (nonsteroidal antiinflammatory drugs) could be uncoupled. (From Gajraj NM. Cyclooxygenase-2 inhibitors. Anesth Analg. 2003;96:1720–1738.)
achieve an adequate level of analgesia with fewer side effects than if a similar level of analgesia was obtained with intravenous opioids alone. Unlike opioids, which preferentially reduce spontaneous postoperative pain, NSAIDs have comparable efficacy for both spontaneous and movement-evoked pain, the latter of which may be more important in causing postoperative physiologic impairment. Concerns regarding NSAID side effects, including alterations in the gastric mucosal barrier, renal tubular function, and inhibition of platelet aggregation, have likely made clinicians reluctant to use NSAIDs in patients undergoing cardiac surgery. NSAIDs are not a homogenous group and vary considerably in analgesic efficacy as a result of differences in pharmacodynamic and pharmacokinetic parameters. NSAIDs are nonspecific inhibitors of COX, which is the rate-limiting enzyme involved in the synthesis of prostaglandins. COX-1 is ubiquitously and constitutively expressed and has a homeostatic role in platelet aggregation, gastrointestinal mucosal integrity, and renal function, whereas COX-2 is inducible and primarily expressed at the sites of injury (and in the kidney and brain) and mediates pain and inflammation. NSAIDs are nonspecific inhibitors of both forms of COX yet vary in their ratio of COX-1 to COX-2 inhibition. Molecular studies distinguishing between constitutive COX-1 and inflammation-inducible COX-2 enzymes have led to the exciting hypothesis that the therapeutic and adverse effects of NSAIDs could be uncoupled (Fig. 33.4). Subsequently, clinicians have witnessed the growing use of COX-2 inhibitors in the perioperative period after noncardiac surgery. The primary advantage of COX-2 inhibitors, compared with NSAIDs, is their lack of effect on platelet function and bleeding.
ALPHA2-ADRENERGIC AGONISTS The α2-adrenergic agonists provide analgesia, sedation, and sympatholysis. The potential perioperative analgesic benefits of α2 agonists when administered to patients undergoing cardiac surgery were demonstrated 30 years ago. Most of the clinical investigations regarding perioperative use of this class of drugs remain focused on exploiting the sedative effects and beneficial cardiovascular effects (decreasing 831
Postoperative Pain Management for the Cardiac Patient
Membrane phospholipid
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hypertension and tachycardia) associated with their use. α2-Adrenergic agonists have been used perioperatively in patients undergoing cardiac surgery. However, the focus of such clinical investigations has been on the intraoperative period and the potential for enhanced postoperative hemodynamic stability, potentially leading to reduced postoperative myocardial ischemia (but not specifically to enhance postoperative analgesia). Taken together, these clinical investigations indicate that perioperative administration of α2-adrenergic agonists to patients undergoing cardiac surgery decreases intraoperative anesthetic requirements, may enhance perioperative hemodynamic stability, and may decrease perioperative myocardial ischemia. The potential ability of this class of drugs to initiate reliable postoperative analgesia awaits definitive investigation.
INTRATHECAL AND EPIDURAL TECHNIQUES Numerous clinical investigations clearly indicate that intrathecal and/or epidural techniques (using opioids and/or local anesthetics) initiate reliable postoperative analgesia in patients after cardiac surgery (Boxes 33.3 and 33.4). Additional potential advantages of using intrathecal and/or epidural techniques in patients undergoing cardiac surgery include stress-response attenuation and thoracic cardiac sympathectomy.
BOX 33.3
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Intrathecal Techniques
Advantages • Simple, reliable analgesia • Stress-response attenuation • Less hematoma risk than epidural techniques Disadvantages • No cardiac sympathectomy • Hematoma risk increased • Side effects of intrathecal opioids
BOX 33.4
Epidural Techniques
Advantages • Reliable analgesia • Stress-response attenuation • Cardiac sympathectomy Disadvantages • Labor-intensive • Hematoma formation risk increased • Side effects of epidural opioids
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Most clinical investigators have used intrathecal morphine in hopes of providing prolonged postoperative analgesia. Some clinical investigators have used intrathecal fentanyl, sufentanil, and/or local anesthetics for intraoperative anesthesia and analgesia (with stress-response attenuation) and/or thoracic cardiac sympathectomy. An anonymous survey of members of the Society of Cardiovascular Anesthesiologists published in 2001 indicated that almost 8% of practicing anesthesiologists incorporate intrathecal techniques into their anesthetic management of adults undergoing cardiac surgery. Of these anesthesiologists, 75% practice in the United States, 72% perform the intrathecal injection before the induction of anesthesia, 97% use morphine, 13% use fentanyl, 2% use sufentanil, 10% use lidocaine, and 3% use tetracaine. The mid-1990s saw the emergence of fast-track cardiac surgery, with the goal being tracheal extubation in the immediate postoperative period. Some clinical investigators have revealed that certain combinations of intraoperative anesthetic techniques coupled with appropriate doses of intrathecal morphine will allow tracheal extubation after cardiac surgery within the immediate postoperative period to coexist with enhanced analgesia. Many clinical investigations involving the use of intrathecal analgesic techniques in patients undergoing cardiac surgery indicate that the administration of intrathecal morphine to patients before CPB initiates reliable postoperative analgesia after cardiac surgery. Intrathecal opioids or local anesthetics cannot reliably attenuate the perioperative stress response associated with CPB that persists during the immediate postoperative period. A recently published metaanalysis of randomized, controlled trials (25 randomized trials, 1106 patients) concluded that spinal analgesia does not improve clinically relevant outcomes in patients undergoing cardiac surgery.
Postoperative Pain Management for the Cardiac Patient
Intrathecal Techniques
Epidural Techniques Since this initial impressive display of potential benefits (eg, reliable postoperative analgesia, stress-response attenuation, facilitation of early tracheal extubation), other clinical investigators have subsequently applied thoracic epidural anesthesia (TEA) to patients undergoing cardiac surgery. Most clinical investigators have used thoracic epidural local anesthetics in hopes of providing perioperative stress-response attenuation and/or perioperative thoracic cardiac sympathectomy. Some clinical investigators have used thoracic epidural opioids to provide intraoperative and/or postoperative analgesia. An anonymous survey of members of the Society of Cardiovascular Anesthesiologists published in 2001 indicated that 7% of practicing anesthesiologists incorporate thoracic epidural techniques into their anesthetic management of adults undergoing cardiac surgery. Of these anesthesiologists, 58% practice in the United States. Many clinical investigations have proved that TEA with local anesthetics significantly attenuates the perioperative stress response in patients undergoing cardiac surgery. Patients randomized to receive intermittent boluses of thoracic epidural bupivacaine intraoperatively, followed by continuous infusion postoperatively, exhibited significantly decreased blood levels of norepinephrine and epinephrine perioperatively when compared with patients similarly managed without thoracic epidural catheters. The February 2011 issue of Anesthesiology highlights the controversial nature of this topic as two clinical studies with opposite conclusions were published. These authors concluded, “Given the potentially devastating complications of epidural hematoma after insertion of an epidural catheter, it is questionable whether this procedure should be applied routinely in cardiac surgical patients who require full heparinization.” These two clinical studies were accompanied by an editorial that stated that “we 833
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continue to try and show that regional anesthesia and analgesia can substantially alter surgical outcomes without success … perhaps it is time to move away from trying to prove that anesthetic interventions will reduce morbidity or mortality and to focus on tangible benefits to patients or their families.” Despite enhanced postoperative analgesia offered via TEA techniques, such analgesia does not appear to decrease the incidence of persistent pain after cardiac surgery. Persistent pain, defined as pain still present 2 or more months after surgery, was similar in the two cohorts (reported in almost 30% of patients). The quality of analgesia obtained with TEA techniques is sufficient to allow cardiac surgery to be performed in awake patients without general endotracheal anesthesia. The initial report of awake cardiac surgery was published in the Annals of Thoracic Surgery in 2000. Since these initial small clinical reports appeared, larger series of patients have been published, demonstrating that awake cardiac surgery is feasible and safe. In 2003, the first case report of awake cardiac surgery requiring CPB was published. In this astonishing case report from Austria, a 70-year-old man with aortic stenosis underwent aortic valve replacement with the assistance of normothermic CPB (total time: 123 minutes; cross-clamp time: 82 minutes) solely via TEA. Verbal communication with the patient was possible on demand throughout the CPB surgery. The patient did well and experienced an unremarkable postoperative course.
Risk for Hematoma Formation
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Intrathecal or epidural instrumentation entails risk, the most feared complication being epidural hematoma formation. The estimated incidence of hematoma formation is approximately 1 : 220,000 after intrathecal instrumentation. Hematoma formation is more common (approximately 1 : 150,000) after epidural instrumentation because larger needles are used, catheters are inserted, and the venous plexus in the epidural space is prominent. Furthermore, hematoma formation does not exclusively occur during epidural catheter insertion; almost one half of all cases develop after catheter removal. Risk is increased when intrathecal or epidural instrumentation is performed before systemic heparinization, and hematoma formation has occurred in patients when diagnostic or therapeutic lumbar puncture has been followed by systemic heparinization. When lumbar puncture is followed by systemic heparinization, concurrent use of aspirin, difficult or traumatic instrumentation, and the administration of intravenous heparin within 1 hour of instrumentation increase the risk for hematoma formation. However, by observing certain precautions, intrathecal or epidural instrumentation can be safely performed in patients who will subsequently receive intravenous heparin. By delaying surgery 24 hours in the event of a traumatic tap, by delaying heparinization 60 minutes after catheter insertion, and by maintaining tight perioperative control of anticoagulation, more than 4000 intrathecal or epidural catheterizations were safely performed in patients undergoing peripheral vascular surgery who received intravenous heparin after catheter insertion. However, the magnitude of anticoagulation in these two studies (activated partial thromboplastin time of approximately 100 seconds and activated coagulation time approximately twice the baseline value) involving patients undergoing peripheral vascular surgery was substantially less than the degree of anticoagulation required in patients subjected to CPB. Most clinical studies investigating the use of intrathecal or epidural anesthesia and analgesia techniques in patients undergoing cardiac surgery include precautions to decrease the risk for hematoma formation. Some used the technique only after the demonstration of laboratory evidence of normal coagulation parameters, delayed surgery 24 hours in the event of traumatic tap, or required that the time from 834
MULTIMODAL ANALGESIA The possibility of synergism among analgesic drugs is a concept that is nearly a century old. Although subsequent research has demonstrated the difference between additivity and synergy, the fundamental strategy behind such combinations (multimodal or balanced analgesia) remains unchanged—enhanced analgesia with the minimization of adverse physiologic effects. The use of analgesic combinations during the postoperative period, specifically the combination of traditional intravenous opioids with other analgesics (eg, NSAIDs, COX-2 inhibitors, ketamine), has been proven clinically effective in noncardiac patients for decades.
Postoperative Pain Management for the Cardiac Patient
instrumentation to systemic heparinization exceed 60 minutes. Although most clinicians investigating the use of epidural anesthesia and analgesia techniques in patients undergoing cardiac surgery insert the catheters the day before scheduled surgery, investigators have performed instrumentation on the same day of surgery. Institutional practice (same-day admit surgery) may eliminate the option of epidural catheter insertion on the day before scheduled surgery. An alternative is to perform epidural instrumentation postoperatively (before or after tracheal extubation) after laboratory evidence demonstrates normal coagulation parameters. The use of regional anesthetic techniques in patients undergoing cardiac surgery remains extremely controversial, prompting numerous editorials by recognized experts in the field of cardiac anesthesia. One of the primary reasons such controversy exists (and likely will continue for some time) is that the numerous clinical investigations regarding this topic are suboptimally designed and use a wide array of disparate techniques, preventing clinically useful conclusions on which all can agree.
SUGGESTED READINGS Allen MS, Halgren L, Nichols FC, et al. A randomized controlled trial of bupivacaine through intercostal catheters for pain management after thoracotomy. Ann Thorac Surg. 2009;88:903. American Society of Anesthesiologists Task Force on Acute Pain Management. Practice guidelines for acute pain management in the perioperative setting: an updated report by the American Society of Anesthesiologists Task Force on Acute Pain Management. Anesthesiology. 2012;116:248. Bettex DA, Schmidlin D, Chassot PG, et al. Intrathecal sufentanil-morphine shortens the duration of intubation and improves analgesia in fast-track cardiac surgery. Can J Anaesth. 2002;49:711. Bignami E, Landoni G, Biondi-Zoccai GGL, et al. Epidural analgesia improves outcome in cardiac surgery: a meta-analysis of randomized controlled trials. J Cardiothorac Vasc Anesth. 2010;24:586. Blaudszun G, Lysakowski C, Elia N, et al. Effect of perioperative systemic α2 agonists on postoperative morphine consumption and pain intensity; systematic review and meta-analysis of randomized controlled trials. Anesthesiology. 2012;116:1312. Goldstein S, Dean D, Kim SJ, et al. A survey of spinal and epidural techniques in adult cardiac surgery. J Cardiothorac Vasc Anesth. 2001;15:158. Hansdottir V, Philip J, Olsen MF, et al. Thoracic epidural versus intravenous patient-controlled analgesia after cardiac surgery. Anesthesiology. 2006;104:142. Lena P, Balarac N, Lena D, et al. Fast-track anesthesia with remifentanil and spinal analgesia for cardiac surgery: the effect on pain control and quality of recovery. J Cardiothorac Vasc Anesth. 2008;22:536. Lynch JJ, Mauermann WJ, Pulido JN, et al. Use of paravertebral blockade to facilitate early extubation after minimally invasive cardiac surgery. Semin Cardiothorac Vasc Anesth. 2010;14:47. Mazzeffi M, Khelemsky Y. Poststernotomy pain: a clinical review. J Cardiothorac Vasc Anesth. 2011;25:1163. Metz S, Schwann N, Hassanein W, et al. Intrathecal morphine for off-pump coronary artery bypass grafting. J Cardiothorac Vasc Anesth. 2004;18:451. Monaco F, Biselli C, Landoni G, et al. Thoracic epidural anesthesia improves early outcome in patients undergoing cardiac surgery for mitral regurgitation: a propensity-matched study. J Cardiothorac Vasc Anesth. 2013;27:1301.
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Myles PS, Bain C. Underutilization of paravertebral block in thoracic surgery. J Cardiothorac Vasc Anesth. 2006;20:635. Ried M, Schilling C, Potzger T, et al. Prospective, comparative study of the On-Q painbuster postoperative pain relief system and thoracic epidural analgesia after thoracic surgery. J Cardiothorac Vasc Anesth. 2014;28:973. Royse C. Epidurals for cardiac surgery; can we substantially reduce surgical morbidity or should we focus on quality of recovery? Anesthesiology. 2011;114:232. Royse C, Royse A, Soeding P, et al. Prospective randomized trial of high thoracic epidural analgesia for coronary artery bypass surgery. Ann Thorac Surg. 2003;75:93. Viscusi ER, Candiotti KA, Onel E, et al. The pharmacokinetics and pharmacodynamics of liposome bupivacaine administered via a single epidural injection to healthy volunteers. Reg Anesth Pain Med. 2012;37:616. White PF, Rawal S, Latham P, et al. Use of a continuous local anesthetic infusion for pain management after median sternotomy. Anesthesiology. 2003;99:918. Zangrillo A, Bignami E, Biondi-Zuccai GGL, et al. Spinal analgesia in cardiac surgery: a meta-analysis of randomized controlled trials. J Cardiothorac Vasc Anesth. 2009;23:813.
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