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The preoperative evaluation and anesthetic management of common cardiovascular diseases are discussed in Chapter 21. The same principles apply whether these patients are undergoing cardiac or noncardiac surgery. An important distinction is that patients undergoing cardiac procedures will by definition have advanced disease. 
Establishing the adequacy of the patient’s preoperative cardiac function should be based on exercise (activity) tolerance, measurements of myocardial contractility such as ejection fraction, severity and location of coronary stenoses, ventricular wall motion abnormalities, cardiac end-diastolic pressures, cardiac output, and valvular areas and gradients. Fortunately, unlike noncardiac surgery, cardiac surgery improves cardiac function in the majority of patients, and these patients have usually been extensively evaluated before being offered surgical repair. The anesthetic preoperative evaluation should also include a focus on pulmonary, neurological, and kidney function, as preoperative impairment of these organ systems predisposes patients to myriad postoperative complications.
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1. Preinduction Period
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The prospect of heart surgery is frightening, and relatively “heavy” premedication was often given in the past (see Chapter 21). Benzodiazepine sedative-hypnotics (diazepam, 5–10 mg orally), alone or in combination with an opioid (morphine, 5–10 mg intramuscularly or hydromorphone, 1–2 mg intramuscularly), were often used. However, in current practice most patients receive no sedative-hypnotic premedication until their arrival on the surgical unit, at which time many will receive small doses of intravenous midazolam. Longer acting premedicant agents (eg, lorazepam) are avoided by most practitioners to permit fast-tracking of patients through their recovery.
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The best practitioners of cardiac anesthesia formulate a simple anesthetic plan that includes adequate preparations for contingencies. In an emergency one cannot wait for an assistant to search for drugs and equipment. Preparation, organization, and attention to detail permit one to deal more efficiently with unexpected intraoperative problems. The anesthesia machine, monitors, infusion pumps, and blood warmer should all be checked before the patient arrives. Drugs—including anesthetic and vasoactive agents—should be immediately available. Many clinicians prepare one vasoconstrictor and one vasodilator infusion before the start of the procedure.
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Cardiac surgery is sometimes associated with large and rapid blood loss, and with the need for multiple drug infusions. Ideally, two large-bore (16-gauge or larger) intravenous catheters should be placed. One of these should be in a large central vein, usually an internal or external jugular or subclavian vein. Central venous cannulations may be accomplished while the patient is awake but sedated or after induction of anesthesia. Studies show no benefit from placing either central venous or pulmonary arterial catheters in awake (versus anesthetized) patients undergoing cardiovascular surgery.
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Drug infusions should ideally be given into a central catheter, preferably directly into the catheter or into the injection port closest to the catheter (to minimize dead space). Multilumen central venous catheters and multilumen pulmonary artery catheter introducer sheaths allow for multiple drug infusions with simultaneous measurement of vascular pressures. One intravenous port should be solely for drug infusions; drug and fluid boluses should be administered through another site.
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Blood should be immediately available for transfusion if the patient has had previous cardiac surgery (a “redo”); when there has been a previous sternotomy, the right ventricle or coronary grafts may be adherent to the sternum and may be accidentally entered during the repeat sternotomy.
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A. Electrocardiography
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The electrocardiogram (ECG) is continuously monitored with two leads, usually leads II and V5. Baseline tracings of all leads may be recorded for future reference. Computerized ST-segment analysis and the use of TEE have greatly improved detection of ischemic episodes.
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B. Arterial Blood Pressure
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In addition to all basic monitoring, arterial cannulation is always performed either prior to or immediately after induction of anesthesia. Radial arterial catheters may occasionally give falsely low readings following sternal retraction as a result of compression of the subclavian artery between the clavicle and the first rib. They may also provide falsely low values early after CPB due to the opening of atrioventricular shunts in the hand during rewarming. The radial artery on the side of a previous brachial artery cutdown should be avoided, because its use is associated with a greater incidence of arterial thrombosis and wave distortion. Obviously, if a radial artery will be harvested for a coronary bypass conduit, it cannot be used as a site for arterial pressure monitoring. Other useful catheterization sites include the brachial, femoral, and axillary arteries. A backup manual or automatic blood pressure cuff should also be used.
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C. Central Venous and Pulmonary Artery Pressure
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Central venous pressure is not terribly useful for diagnosis of hypovolemia but has been customarily monitored in nearly all patients undergoing cardiac surgery. The pulmonary artery occlusion pressure provides a better measure of left ventricular filling pressure. Pulmonary artery catheterization has declined precipitously in nearly all circumstances except adult cardiac surgery due to lack of evidence of a positive effect on patient outcomes. In theory the decision about whether to use a pulmonary artery catheter should be based on the patient and the procedure; however, in most centers, it is the preferences of the anesthetic, surgical, and critical care teams that really matter. In many centers, either every or almost no cardiac surgery patient receives pulmonary artery catheterization. In general, pulmonary artery catheterization has been most often used in patients with compromised ventricular function, pulmonary hypertension, or those undergoing complicated procedures. The most useful data are pulmonary artery pressures, the pulmonary artery occlusion (“wedge”) pressure, and thermodilution cardiac outputs. Specialized catheters provide extra infusion ports, continuous measurements of mixed venous oxygen saturation and cardiac output, and the capability for right ventricular or atrioventricular sequential pacing. Given the risk associated with placing any pulmonary artery catheter, some clinicians opine that it makes sense to insert only those devices that offer these advanced capabilities. Intraoperatively and postoperatively, when pulmonary artery occlusion pressure measurements are not available, left ventricular filling pressures can be measured with a left atrial pressure line inserted by the surgeon during bypass.
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The right internal jugular vein is a preferred approach for intraoperative central venous cannulation, particularly when the line will be removed after a day or two. Catheters placed through the other sites, particularly on the left side, are more likely to kink following sternal retraction (as noted earlier) and are less likely to pass into the superior vena cava as those placed through the right internal jugular vein.
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Pulmonary artery catheters migrate distally during CPB and may spontaneously wedge without balloon inflation. Inflation of the balloon under these conditions can rupture a pulmonary artery causing lethal hemorrhage. Pulmonary artery catheters should be routinely retracted 2 to 3 cm during CPB and the balloon subsequently inflated slowly. If the catheter wedges with less than 1.5 mL of air in the balloon, it should be withdrawn farther.
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Once the patient is anesthetized, an indwelling urinary catheter is placed to monitor the hourly output. Bladder temperature is often monitored as a measure of core temperature but may not track core temperature well with reduced urinary flow. The sudden appearance of reddish urine may indicate excessive red cell hemolysis caused by CPB or a transfusion reaction.
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Multiple temperature monitors are usually placed once the patient is anesthetized. Bladder (or rectal), esophageal, and pulmonary artery (blood) temperatures are often simultaneously monitored. Because of the heterogeneity of readings during cooling and rewarming, bladder and rectal readings are generally taken to represent an average body temperature, whereas esophageal represents core temperature. Pulmonary artery temperature provides an accurate estimate of blood temperature, which should be the same as core temperature in the absence of active cooling or warming. Nasopharyngeal and tympanic probes may most closely approximate brain temperature. Myocardial temperature is often measured directly during instillation of cardioplegia.
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F. Laboratory Parameters
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Laboratory testing is mandatory during cardiac surgery. Blood gases, hemoglobin, potassium, ionized calcium, and glucose measurements should be immediately available. The activated clotting time (ACT) approximates the Lee–White clotting time and is used to monitor heparin anticoagulation and its reversal with protamine. Some centers routinely use thromboelastography (TEG) to identify causes of bleeding after CPB.
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One of the most important forms of intraoperative monitoring is inspection of the surgical field. Once the sternum is opened, lung expansion can be observed through the pleura. When the pericardium is opened, the heart (primarily the right ventricle) is visible; thus cardiac rhythm, volume, and contractility can often be judged visually. Blood loss and surgical maneuvers must be closely watched and related to changes in hemodynamics and rhythm.
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H. Transesophageal Echocardiography
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TEE provides valuable information about cardiac anatomy and function during surgery. Two-dimensional, multiplane TEE can detect regional and global ventricular abnormalities, chamber dimensions, valvular anatomy, and the presence of intracardiac air. TEE can also be helpful in confirming cannulation of the coronary sinus for cardioplegia. Multiple views should be obtained from the upper esophagus, mid-esophagus, and transgastric positions in the transverse, sagittal, and in-between planes (Figure 22–2). The two views most commonly used for monitoring during cardiac surgery are the four-chamber view (Figure 22–3) and the transgastric (short-axis) view (Figure 22–4). Three-dimensional echocardiography offers better visualization of complex anatomic features, particularly of cardiac valves. The following represent the most important applications of intraoperative TEE.
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1. Assessment of valvular function
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Valvular morphology can be assessed by multiplane and three-dimensional TEE. Pressure gradients, area and severity of stenosis, and severity of valvular regurgitation can be assessed by Doppler echocardiography and color-flow imaging (Figure 22–5). Colors are usually adjusted so that flow toward the probe is red and flow in the opposite direction is blue. TEE also can detect prosthetic valve dysfunction in the forms of obstruction, regurgitation, paravalvular leak, or vegetations from endocarditis. The TEE images in the upper mid-esophagus at 40° to 60° and 110° to 130° are useful for examining the aortic valve and ascending aorta (Figure 22–6). The diameter of the aortic valve annulus can be estimated accurately. Doppler flow across the aortic valve must be measured looking up from the deep transgastric view (Figure 22–7). The anatomic features of the mitral valve relevant to TEE are shown in Figure 22–8. The mitral valve is examined from the mid-esophageal position, looking at the mitral valve apparatus with and without color in the 0° through 180° views (Figure 22–9). TEE is an invaluable aid to guide and assess the completeness of mitral valve repair surgery. The commissural view (at about 60°) is particularly helpful because it cuts across many scallops of the mitral valve.
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2. Assessment of ventricular function
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Ventricular function can be assessed by global systolic function, estimated by means of ejection fraction (often calculated using Simpson’s method of disks) and left ventricular end-diastolic volume; diastolic function (ie, looking for abnormal relaxation and restrictive diastolic patterns by checking mitral flow velocity or by measuring movements of the mitral valve annulus using tissue Doppler techniques); and regional systolic function (by assessing wall motion and thickening abnormalities). Regional wall abnormalities from myocardial ischemia often appear before ECG changes. Regional wall motion abnormalities can be classified into three categories based on severity (Figure 22–10): hypokinesis (reduced wall motion), akinesis (no wall motion), and dyskinesis (paradoxical wall motion). The location of a regional wall motion abnormality can indicate which coronary artery is experiencing reduced flow. The left ventricular myocardium is supplied by three major arteries: the left anterior descending artery, the left circumflex artery, and the right coronary artery (Figure 22–11). The approximate areas of distribution of these arteries on echocardiographic views are shown in Figure 22–12. Increasingly it is recognized that areas classically presented as the distribution of the circumflex artery may receive blood flow from the right coronary artery or the left anterior descending artery. The ventricular short-axis mid view at the mid-papillary muscle level contains all three blood supplies from the major coronary arteries.
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3. Assessment of other cardiac structures and abnormalities
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In adults undergoing elective cardiac surgery we have used TEE to diagnose previously undetected congenital defects such as an atrial or ventricular septal defect; pericardial effusions and constrictive pericarditis; and cardiac tumors. Doppler color-flow imaging helps delineate abnormal intracardiac blood flows and shunts. TEE can assess the extent of myomectomy in patients with hypertrophic cardiomyopathy (idiopathic hypertrophic subaortic stenosis). Upper-, mid-, and lower-esophageal views are valuable in diagnosing aortic disease processes such as dissection, aneurysm, and atheroma (Figure 22–13). The extent of dissections in the ascending and descending aorta can be accurately defined; however, airway structures prevent complete visualization of the aortic arch with TEE. The presence of protruding atheroma in the ascending aorta increases the risk of postoperative stroke and should prompt the use of epiaortic scanning to identify an atheroma-free cannulation site or a change in surgical plans.
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4. Examination for residual air
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Air is introduced into the cardiac chambers during all “open” heart procedures, such as valve surgery. Residual amounts of air often remain in the left ventricular apex even after the best deairing maneuvers. TEE is helpful in defining the volume of residual air, to determine whether additional surgical maneuvers need to be undertaken to help avoid cerebral or coronary embolism.
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I. Electroencephalography
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Computer-processed electroencephalographic (EEG) recordings can be used to assess anesthetic depth during cardiac surgery, and either the processed or “raw” EEG can be used to ensure complete drug-induced electrical silence (for brain protection) prior to circulatory arrest. These recordings are generally not useful in detecting neurological insults during CPB. Progressive hypothermia (or progressively deepened anesthesia) is typically associated with EEG slowing, burst suppression, and, finally, an isoelectric recording. Most strokes during CPB are due to small emboli that are not likely to produce changes in the EEG. Artifacts from the CPB roller pump may be seen on the raw EEG (due to piezoelectric effects from compression of the pump tubing) but can usually be identified as such by computer processing.
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J. Transcranial or Carotid Doppler
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Transcranial Doppler (TCD) provides noninvasive measurements of blood flow velocity in the middle cerebral artery, which is insonated through the temporal bone. TCD and carotid Doppler are useful for detecting cerebral emboli. Increased numbers of emboli detected by TCD or carotid Doppler have been associated with an increased risk of postoperative neurobehavioral dysfunction.
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K. Near-Infrared Cerebral Oximetry (NIRS)
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Cerebral oximetry (see Chapter 6) is increasingly employed during cardiac surgery. A baseline value is established for each patient prior to preoxygenation. Decreased cerebral oxygen saturation may be seen when oxygen delivery is impaired secondary to decreased PaCO2 tension, anemia, decreased arterial oxygen saturation, and diminished cardiac output.
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Induction of Anesthesia
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Cardiac operations usually require general anesthesia, endotracheal intubation, and controlled ventilation. Some centers have used thoracic epidural anesthesia alone for minimally invasive surgery without CPB or combined thoracic epidural with light general endotracheal anesthesia for other forms of cardiac surgery. These techniques have never been popular in North America due to concerns about the risk of spinal hematomas following heparinization, the associated medical–legal consequences, and the limited evidence of an outcome benefit. Some centers use a single intrathecal opioid injection to provide postoperative analgesia.
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Induction of general anesthesia should be performed in a smooth, controlled (but not necessarily “slow”) fashion—often referred to as a “cardiac induction” when it is used for other types of surgery. The principles are discussed in Chapter 21. Selection of anesthetic agents is generally less important than the way they are used. Indeed, studies have failed to show differences in long-term outcome with various anesthetic techniques. Anesthetic dose requirements are variable. Severely compromised patients should be given anesthetic agents in incremental, small doses. Patient tolerance of inhaled anesthetics generally declines with declining ventricular function. Blood pressure and heart rate are continuously evaluated following unconsciousness, insertion of an oral airway, urinary catheterization, and tracheal intubation. A sudden increase in heart rate or blood pressure may indicate light anesthesia and the need for more anesthetic prior to the next challenge, whereas a decrease or no change suggests that the patient is ready for the subsequent stimulus. Reductions in blood pressure greater than 20% generally call for administration of a vasopressor (as described later). A series of challenges may be used to judge when anesthetic depth will allow intubation without a marked hypertensive response, while also avoiding hypotension from excessive anesthetic dosing.
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The period following intubation is often characterized by a gradual decrease in blood pressure resulting from the anesthetized state (often associated with vasodilation and decreased sympathetic tone) and a lack of surgical stimulation. Patients will usually respond to fluid boluses or a vasoconstrictor. Nevertheless, the administration of large amounts of intravenous fluids prior to the bypass may serve to accentuate the hemodilution associated with CPB (as described below). Small doses of phenylephrine (25–100 mcg), vasopressin (1–3 units), or ephedrine (5–10 mg) may be useful to avoid excessive hypotension. Following intubation and institution of controlled ventilation; arterial blood gases, hematocrit, serum potassium, and glucose concentrations are measured. The baseline ACT (normal <130 s) is best measured after skin incision.
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Choice of Anesthetic Agents
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Anesthetic techniques for cardiac surgery have evolved over the years. Successful techniques range from primarily inhalation anesthesia to high-dose opioid totally intravenous techniques. In recent years, total intravenous anesthesia with short-acting agents and combinations of intravenous and volatile agents have become most popular.
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A. “High-Dose” Opioid Anesthesia
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This technique was originally developed to circumvent the myocardial depression associated with older volatile anesthetics, particularly halothane. But pure high-dose opioid anesthesia (eg, fentanyl, 50–100 mcg/kg, or sufentanil, 15–25 mcg/kg) produces prolonged postoperative respiratory depression (12–24 h), is associated with an unacceptably high incidence of patient awareness (recall) during surgery, and often fails to control the hypertensive response to stimulation in many patients with preserved left ventricular function. Other undesirable effects include skeletal muscle rigidity during induction and prolonged postoperative ileus. Moreover, simultaneous administration of benzodiazepines with large doses of opioids can produce hypotension and myocardial depression. Patients anesthetized with sufentanil and other shorter acting agents generally regain consciousness and can be extubated sooner than those anesthetized with comparable doses of fentanyl.
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B. Total Intravenous Anesthesia (TIVA)
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The drive for cost containment in cardiac surgery was a major impetus for development of anesthesia techniques with short-acting agents. Although the drugs may be costlier, large economic benefits resulted from earlier extubation, decreased intensive care unit (ICU) stays, earlier ambulation, and earlier hospital discharge (“fast-track” management). One technique employs induction with propofol (0.5–1.5 mg/kg followed by 25–100 mcg/kg/min), and modest doses of fentanyl (total doses of 5–7 mcg/kg) or remifentanil (0–1 mcg/kg bolus followed by 0.25–1 mcg/kg/min). Target controlled infusion (TCI) employs software and hardware (computerized infusion pump) to deliver a drug and achieve a set concentration at the effect site based on pharmacokinetic modeling. For propofol, the clinician sets only the patient’s age and weight, and the desired blood concentration on the DiprifusorTM, a TCI device widely available in countries outside North America. During cardiac surgery, a target propofol concentration of 1.5 to 2 mcg/mL is often used. When remifentanil (rather than a longer persisting agent) is used during cardiac anesthesia one must anticipate the need for postoperative analgesia after its discontinuation.
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C. Mixed Intravenous/Inhalation Anesthesia
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Selection of anesthetic agents is oriented to hemodynamic stability as well as early extubation (1–6 h). Propofol (0.5–1.5 mg/kg) or etomidate (0.1–0.3 mg/kg) is often used for induction. Induction usually follows sedation with small doses of midazolam (0.05 mg/kg). Renewed interest in volatile agents came about following studies demonstrating the protective effects of volatile agents on ischemic myocardium and the utility of these agents for fast-track recovery of cardiac patients. Opioids are given in small doses together with a volatile agent (0.5–1.5 minimum alveolar concentration [MAC]) to maintain anesthesia and to blunt the sympathetic response to stimulation. The opioid may be given by intermittent bolus injections, by continuous infusion, or both (Table 22–1). To facilitate fast-track management, typical total doses of fentanyl and sufentanil generally do not exceed 15 and 5 mcg/kg, respectively, and some clinicians combine smaller doses of fentanyl or sufentanil with an analgesic dose of hydromorphone or morphine administered toward the end of CPB. Some clinicians also administer propofol in a low-dose infusion (25–50 mcg/kg/min) or TCI (1.5–2.0 mcg/mL) for maintenance. The major advantage of volatile agents or infusions of remifentanil or propofol is the ability to change the anesthetic concentration and depth rapidly. Isoflurane, sevoflurane, and desflurane are the most commonly used volatile anesthetics. Early laboratory reports of isoflurane inducing intracoronary steal have been overshadowed by later reports of myocardial protection. Isoflurane remains a commonly used volatile agent. Nitrous oxide is generally not used. Nitrous is particularly disadvantageous during the time interval between cannulation and decannulation, because of its tendency to expand any intravascular air bubbles that may form. Moreover, it cannot be given conveniently during CPB.
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The combination of ketamine with midazolam (or propofol) for induction and maintenance of anesthesia is a useful technique, particularly in frail patients with hemodynamic compromise. It is associated with stable hemodynamics, reliable amnesia and analgesia, minimal postoperative respiratory depression, and rare (if any) psychotomimetic side effects. For induction, ketamine, 1 to 2 mg/kg, with midazolam, 0.05 to 0.1 mg/kg, is given as a slow intravenous bolus. Anesthesia can then be maintained by infusion of ketamine, 1.3 to 1.5 mg/kg/h, and midazolam, 0.065 to 0.075 mg/kg/h, or more easily with an inhaled agent. Hypertension following intubation or surgical stimulation can be treated with propofol, opioids, β-blockers, or a volatile agent.
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Muscle relaxation is helpful for intubation, to facilitate sternal retraction, and to prevent patient movement and shivering. Unless airway difficulties are expected, intubation may be accomplished after administration of a nondepolarizing muscle relaxant. The choice of muscle relaxant in the past was often based on the desired hemodynamic response. Modern, shorter acting agents such as rocuronium, vecuronium, and cisatracurium are commonly used and have almost no hemodynamic side effects of their own. Vecuronium, however, has been reported to markedly enhance bradycardia associated with large doses of opioids, particularly sufentanil. Because of its vagolytic effects, pancuronium was often used in patients with marked bradycardia who were taking β-blocking agents, Succinylcholine remains appropriate for endotracheal intubation, particularly for rapid sequence induction. Judicious dosing, appropriate use of a peripheral nerve stimulator, and reversal (if needed) allow fast-tracking with any of these agents.
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Following induction and intubation, the anesthetic course is typically characterized by an initial period of minimal stimulation (skin preparation and draping) that is frequently associated with hypotension, followed by discrete periods of intense stimulation that can produce tachycardia and hypertension. These periods of stimulation include the skin incision, sternotomy and sternal retraction, opening the pericardium, and, sometimes, aortic dissection. The anesthetic agent should be adjusted appropriately in anticipation of these events.
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Accentuated vagal responses resulting in marked bradycardia and hypotension may occasionally be seen during sternal retraction or opening of the pericardium, perhaps more commonly in patients who have been taking β-adrenergic blocking agents or diltiazem.
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Myocardial ischemia in the prebypass period is not always associated with hemodynamic perturbations such as tachycardia, hypertension, or hypotension. Prophylactic infusion of nitroglycerin (1–2 mcg/kg/min) has been studied many times and continues to be used in some centers, but it has never been shown to reduce the incidence of ischemia or improve outcomes.
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Anticoagulation must be established before CPB to prevent acute disseminated intravascular coagulation and formation of clots in the CPB pump. In most centers the adequacy of anticoagulation will be confirmed by measuring the ACT. An ACT longer than 400 to 480 s is considered adequate. Heparin, 300 to 400 units/kg, is usually given before aortic cannulation. Some surgeons prefer to administer the heparin themselves directly into the right atrium. If heparin is administered by the anesthesiologist, it should be given through a reliable (usually central) intravenous line, and the ACT should be measured 3 to 5 min later. If the ACT is less than 400 s, additional heparin (100 units/kg) is given. Some drugs (eg, aprotinin) prolong the celite-activated ACT but not the kaolin-activated ACT; the kaolin-ACT should be used to assess adequacy of anticoagulation in these circumstances. Heparin concentration assays (see Reversal of Anticoagulation, later) measure heparin levels and not necessarily effect; these assays are therefore not reliable for measuring the degree of anticoagulation but can be used as an adjunct. A whole blood heparin concentration of 3 to 4 units/mL is usually sufficient for CPB. The high-dose thrombin time (HiTT) is not influenced by aprotinin but is more complicated to perform than a kaolin-ACT. HiTT cannot provide a preheparin control and does not provide an index for the adequacy of reversal with protamine (as discussed later).
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Resistance to heparin is occasionally encountered; many such patients have antithrombin III deficiency (acquired or congenital). Antithrombin III is a circulating serine protease that irreversibly binds and inactivates thrombin (as well as the activated forms of factors X, XI, XII, and XIII). When heparin complexes with antithrombin III, the anticoagulant activity of antithrombin III is enhanced 1000-fold. Patients with antithrombin III deficiency will achieve adequate heparin anticoagulation following infusion of antithrombin III (or fresh frozen plasma). Milder forms of heparin resistance can be managed by administration of a modestly larger than normal dose of heparin.
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Patients with a history of heparin-induced thrombocytopenia (HIT) require special consideration. These patients produce heparin-dependent (platelet factor 4) antibodies that agglutinate platelets and produce thrombocytopenia, sometimes associated with thromboembolism. If the history of HIT is remote and antibodies can no longer be demonstrated, heparin may safely be used for CPB. When significant antibody titers are detected, alternative anticoagulants including hirudin, bivalirudin, anacrod, and argatroban may be considered.
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Bleeding prophylaxis with antifibrinolytic agents may be initiated before or after anticoagulation. Some clinicians prefer to administer antifibrinolytic agents after heparinization to reduce the possible incidence of thrombotic complications; others fear that delayed administration may reduce antifibrinolytic efficacy. Antifibrinolytic therapy may be particularly useful for patients who are undergoing a repeat operation; who refuse blood products (such as Jehovah’s Witnesses); who are at high risk for postoperative bleeding because of recent administration of glycoprotein IIb/IIIa inhibitors (abciximab [RheoPro], eptifibatide [Integrilin], or tirofiban [Aggrastat]); who have preexisting coagulopathy; or who are undergoing long and complicated procedures. The antiplatelet effect of abciximab typically lasts 24 to 48 h; those of eptifibatide and tirofiban are 2 to 4 h and 4 to 8 h, respectively. The frequent combination of aspirin and the adenosine diphosphate receptor antagonist clopidogrel (Plavix) is also associated with excessive bleeding.
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The antifibrinolytic agents currently available, ε-aminocaproic acid and tranexamic acid, do not affect the ACT and only rarely induce allergic reactions. ε-Aminocaproic acid is usually administered as a 50 to 75 mg/kg loading dose followed by a 20 to 25 mg/kg/h maintenance infusion (some clinicians use a standard 5–10 g loading dose followed by 1 g/h). Tranexamic acid is often dosed at 10 mg/kg followed by 1 mg/kg/h, although pharmacokinetic studies suggest that larger doses may more reliably maintain effective blood concentrations. Intraoperative collection of platelet-rich plasma by pheresis prior to CPB is employed by some centers; reinfusion following bypass may decrease bleeding and reduce transfusion requirements.
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Placement of venous and arterial cannulas for CPB is a critical time. After heparinization, aortic cannulation is usually done first because of the hemodynamic problems sometimes associated with venous cannulation and to allow convenient and rapid transfusion from the pump oxygenator. The inflow cannula is most often placed in the ascending aorta. The small opening of most arterial cannulas produces a jet stream that, when not positioned properly, can cause aortic dissection or preferential flow of blood to the innominate artery. The systemic arterial pressure is customarily reduced to 90 to 100 mm Hg systolic during placement of the aortic cannula to reduce the likelihood of dissection. Air bubbles should be absent from the arterial cannula and inflow line, and adequacy of the connection between the arterial inflow line and the patient must be demonstrated before bypass is initiated. Failure to remove all air bubbles will result in air emboli, possibly into the coronary or cerebral circulations, whereas failure of the cannula tip to fully enter the aorta may result in aortic dissection. Some clinicians routinely hand compress the carotid arteries during aortic cannulation to decrease the likelihood of cerebral emboli, but the efficacy of this technique is doubtful.
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One or two venous cannulas are placed in the right atrium, usually through the right atrial appendage. One cannula is usually adequate for most coronary artery bypass and aortic valve operations. The single cannula used often has two portals (two-stage); when it is properly positioned, one opening is in the right atrium and the other is in the inferior vena cava.
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Separate cannulas in the superior and inferior venae cavae are used for other forms of open-heart procedures (other forms of valve surgery and congenital repairs). Hypotension from impaired ventricular filling may occur during manipulation of the venae cavae and the heart. Venous cannulation also frequently precipitates atrial or, less commonly, ventricular arrhythmias. Premature atrial contractions and transient bursts of a supraventricular tachycardia are common and need no treatment if they are not sustained. Sustained paroxysmal atrial tachycardia or atrial fibrillation frequently leads to hemodynamic deterioration, which may be treated pharmacologically, electrically, or by immediate initiation of bypass (provided that full anticoagulation has been confirmed). Malpositioning of the venous cannulas can interfere with venous return or impede venous drainage from the head and neck (superior vena cava syndrome). Upon initiation of CPB, the former is manifested as inadequate volume in the venous reservoir, whereas the latter produces engorgement of the head and neck.
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Once the cannulas are properly placed and secured, the ACT is acceptable, and the perfusionist is ready, CPB is initiated. The main CPB pump is started and with satisfactory arterial inflow the venous cannula(s) is unclamped. Establishing the adequacy of venous return to the pump reservoir is critical. Normally, the reservoir level rises and CPB pump flow is gradually increased. If venous return is poor, the level of blood in the reservoir will decline, potentially allowing air to enter the pump circuit. When the venous reservoir volume declines the cannulas should be checked for proper placement and for forgotten clamps, kinks, or an air lock. Under these circumstances, pump flow should be slowed until the problem is resolved. Adding volume (blood or colloid) to the reservoir may be necessary. With full CPB and unimpeded venous drainage, the heart should empty; failure to empty or progressive distention may result from malpositioning of the venous cannula or aortic regurgitation. In the rare case of severe aortic insufficiency that limits the extent of peripheral perfusion, immediate aortic cross-clamping (and cardioplegia) may be necessary.
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Systemic mean arterial pressure is closely monitored as pump flow is gradually increased to 2 to 2.5 L/min/m2. At the onset of CPB, systemic arterial pressure usually decreases abruptly. Initial mean systemic arterial (radial) pressures of 30 to 40 mm Hg are not unusual. This decrease is usually attributed to abrupt hemodilution, which reduces blood viscosity and effectively lowers SVR. It is often treated with increased flow and vasopressors.
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Persistent and excessive hypotension (<30 mm Hg) should prompt a search for unrecognized aortic dissection. If dissection is present, CPB must be temporarily stopped until a cannula can be placed distally in the “true” aortic lumen. Other possible causes for hypotension include inadequate pump flow from poor venous return or a pump malfunction, or pressure transducer error. Factitious hypertension has been reported when the right radial artery is used for monitoring and the aortic cannula is directed toward the innominate artery.
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The relationship between pump flow, SVR, and mean systemic arterial blood pressure may be conceptualized as follows:
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Mean arterial pressure = Pump flow · SVR
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Consequently, with a constant SVR, mean arterial pressure is proportional to pump flow. Similarly, at any given pump flow, mean arterial pressure is proportional to SVR. To maintain both adequate arterial pressures and blood flows one can manipulate pump flow and SVR. Most centers strive for blood flows of 2 to 2.5 L/min/m2 (50–60 mL/kg/min) and mean arterial pressures between 50 and 80 mm Hg in adults. Metabolic flow requirements decline with decreasing core body temperature. Evidence also suggests that during deep hypothermia (20–25°C), mean blood pressures as low as 30 mm Hg may still be consistent with adequate cerebral blood flow and cerebral oxygen delivery. Moderately decreased SVR can be increased with phenylephrine, vasopressin, or norepinephrine.
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Increased mean arterial pressures (>150 mm Hg) are deleterious and may promote aortic dissection or cerebral hemorrhage. Generally, when mean arterial pressure exceeds 100 mm Hg, hypertension is said to exist and is treated by decreasing pump flow or increasing the concentration of a volatile agent to the oxygenator inflow gas. If the hypertension is refractory to these maneuvers or if pump flow is already low, a vasodilator such as clevidipine, nicardipine, or nitroprusside is used.
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Additional monitoring during CPB includes the pump flow rate, venous reservoir level, arterial inflow line pressure (as noted earlier), blood (perfusate and venous) and myocardial temperatures, and in-line (arterial and venous) oxygen saturations. In-line pH, CO2 tension, and oxygen tension sensors are also available. Blood gas tensions and pH should be confirmed by direct measurements. In the absence of hypoxemia, low venous oxygen saturations (<70%), a progressive metabolic acidosis, or reduced urinary output may indicate inadequate flow rates.
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During bypass, arterial inflow line pressure is almost always greater than the systemic arterial pressure recorded from a radial artery or even an aortic catheter. The difference in pressure represents the pressure drop across the arterial filter, the arterial tubing, and the narrow opening of the aortic cannula. Nonetheless, monitoring this pressure is important for detecting problems with an arterial inflow line. Inflow pressures should remain below 300 mm Hg; higher pressures may indicate a clogged arterial filter, obstruction of the arterial tubing or cannula, or aortic dissection.
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Serial ACT, hematocrit, and potassium measurements are performed during CPB. Blood glucose should be checked even in patients without a history of diabetes. The ACT is measured immediately after bypass and then every 20 to 30 min thereafter. Cooling generally increases the half-life of heparin and prolongs its effect. Some centers calculate a heparin dose–response curve to guide calculation of heparin dosing and protamine reversal (Figure 22–14). The hematocrit is usually not allowed fall much below 22%. Red cell transfusions into the pump reservoir may be necessary. Marked increases in serum potassium concentrations (secondary to cardioplegia) are usually treated with a furosemide-induced diuresis.
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Hypothermia & Cardioplegia
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Moderate (26–32°C) or deep (20–25°C) hypothermia is used routinely for some procedures, particularly those involving the aortic root and great vessels. The lower the temperature, the longer the time required to achieve cooling and rewarming. Lower temperatures, however, permit lower CPB flows to be used safely. At a temperature of 20°C, flows as low as 1.2 L/min/m2 may be adequate.
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Hypothermia produces characteristic changes in the ECG including the Osborne wave, a positive deflection between the QRS and ST segments. Ventricular fibrillation often occurs as the heart is cooled below 28°C to 29°C. Cardioplegia should be established immediately, as fibrillation consumes high-energy phosphates at a greater rate than slower rhythms. Cardioplegia is achieved by cross-clamping the ascending aorta proximal to the aortic inflow cannula and (as previously described) infusing cardioplegia solution through a small catheter proximal to the cross-clamp or directly into the coronary ostia if the aorta is opened (eg, for aortic valve replacement). Many surgeons routinely employ retrograde cardioplegia via a catheter in the coronary sinus (see earlier discussion). During aortocoronary bypass grafting, cardioplegia solution may also be given through the graft when the surgeon elects to perform the distal anastomosis first.
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Ventilation of the lungs is discontinued when adequate pump flows are reached and the heart stops ejecting blood. Following institution of full CPB, ventricular ejection continues briefly until the left ventricular volume reaches a critically low level. Discontinuing ventilation prematurely when there is any remaining pulmonary blood flow acts as a right-to-left shunt that can promote hypoxemia. The importance of this mechanism depends on the relative ratio of remaining pulmonary blood flow to pump flow. At some centers, once ventilation is stopped, oxygen flow is continued in the anesthesia circuit with a small amount of continuous positive airway pressure (5 cm H2O) in the hope of preventing postoperative pulmonary dysfunction. Most centers either stop all gas flow or continue a low flow of oxygen (1–2 L/min) in the anesthesia circuit. Ventilation is resumed at the conclusion of CPB in anticipation of the heart beginning to eject blood.
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Management of Respiratory Gases
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There formerly was controversy about whether to use temperature-corrected (pH stat) or uncorrected (α-stat) arterial blood gas tensions during hypothermic CPB in adults. The controversy stemmed from the fact that the solubility of a gas increases and the neutral pH (ie, the pH at which concentrations of H+ and OH− ions are the same) of water increases with hypothermia. As a result of the former effect, although total CO2 content does not change (in a closed system), the partial pressure of CO2 will decrease as blood temperature drops. The problem is most significant for arterial CO2 tension because of its effect on arterial pH and cerebral blood flow. As the temperature decreases, the plasma bicarbonate concentration does not change, but the decreased arterial CO2 tension increases pH to what would be alkalotic values at normothermia. Blood with a CO2 tension of 40 mm Hg and a pH of 7.40 at 37°C, when cooled to 25°C, will have a CO2 tension of about 23 mm Hg and a pH of 7.60, yet will have an unchanged ratio of H+ to OH– ions.
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Normally—regardless of the patient’s temperature—blood samples are heated to 37°C in blood gas analyzers before gas tensions are measured. If a temperature-corrected reading is desired, a table or a program in the blood gas machine can be used to estimate what the gas tension and pH would have been if they had been measured at the patient’s temperature. The practice of temperature correcting gas tensions with the goal of maintaining a constant CO2 tension of 40 mm Hg and a constant pH of 7.40 during hypothermia is referred to as pH-stat management. During hypothermic CPB, pH-stat management, which may require adding CO2 to the oxygenator gas inflow, increases total blood CO2 content. Under these conditions, cerebral blood flow increases (due to increased CO2 tension relative to α-stat management) more than is required based on oxygen consumption. Increased cerebral blood flow is useful to increase uniformity of brain cooling prior to deep hypothermic circulatory arrest (more often used in children than adults). On the other hand, increased cerebral blood flow can also direct a greater fraction of atheromatous arterial emboli to the brain—a greater concern than uniformity of brain cooling during most cardiac surgery in adults.
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The use of uncorrected gas tensions during hypothermia—α-stat management—is the rule in adults and is common in children when circulatory arrest will not be used. The basis of this approach is that preservation of normal protein function depends on maintaining a constant state of intracellular electroneutrality (the balance of charges on proteins). At physiological pH, these charges are primarily located on the imidazole rings of histidine residues (referred to as α residues). Moreover, as temperature decreases, Kw—the dissociation constant for water—also decreases (pKw increases). Therefore, at lower temperatures, the electroneutrality of aqueous solutions, where [H+] = [OH−], corresponds to a lower [H+] (a higher pH). Hypothermic “alkalosis” thus does not necessarily reflect [OH–] > [H+] but rather an absolute decrease in both [H+] and [OH–]. Hypothermic CPB with α-stat management does not require addition of CO2 to the oxygenator: The total CO2 content of blood and the electroneutrality are unchanged. In contrast to pH-stat management, α-stat management appears to preserve cerebral autoregulation of blood flow. Despite the theoretical and observed differences, in most studies comparisons between the two techniques fail to reveal appreciable differences in patient outcomes except in children undergoing circulatory arrest.
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Hypothermia (<34°C) potentiates general anesthetic potency, but failure to give anesthetic agents, particularly during rewarming on CPB, may result in awareness and recall. With light anesthesia hypertension may be seen and, if muscle paralysis is also allowed to wear off, the patient may move. Consequently, additional doses of anesthetic agents may be necessary during CPB. Reduced concentrations of a volatile agent (eg, 0.5–0.75% isoflurane) via the oxygenator are frequently used. The volatile agent concentration may need to be reduced to a value that does not depress contractility immediately prior to termination of bypass if residual myocardial depression is apparent. Those relying on opioids and benzodiazepines for anesthesia during CPB may need to administer additional doses of these agents or commence a propofol infusion. Some clinicians routinely administer a benzodiazepine (eg, midazolam) when rewarming is initiated. Alternatively, a propofol, opioid, or ketamine–midazolam infusion may be continued throughout CPB. Sweating during rewarming is common and usually indicates a hypothalamic response to perfusion with warm blood (rather than “light” anesthesia). During rewarming, blood temperature should not exceed core temperature by more than 2°C.
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The incidence of neurobehavioral deficits after CPB varies widely, depending on how long after surgery the examination is performed and the criteria for diagnosis. In the first week after surgery the incidence may be as high as 80%. Fortunately, in most instances, these deficits are transient. Neurobehavioral deficits detectable 8 weeks or more (20–25%) after operation or strokes (2–6%) are less common. Factors that have been associated with neurological sequelae include increased numbers of cerebral emboli, combined intracardiac (valvular) and coronary procedures, advanced age, and preexisting cerebrovascular disease.
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During open-heart procedures, deairing of cardiac chambers, assumption of a head-down position, and venting before and during initial cardiac ejection are important in preventing gas emboli. Some centers fill the surgical field with CO2, a gas that if entrained and embolized will more rapidly be reabsorbed. TEE can detect residual air within the heart and the need for further deairing procedures. During coronary bypass procedures, minimizing the amount of aortic manipulation, the number of aortic clampings, and the number of graft sites on the surface of the aorta, and using sutureless proximal anastomotic devices may help reduce atheromatous emboli. Palpation of the aorta, TEE, and especially epiaortic echocardiography can help identify high-risk patients and guide management. Epiaortic echocardiography is the most sensitive and specific technique.
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The relative contributions of emboli versus cerebral hypoperfusion in causing neurological deficits remains unclear. The data are controversial and sparse that prophylactic drug infusions immediately before and during intracardiac (open ventricle) procedures will decrease the incidence and severity of neurological deficits. Prior to circulatory arrest with very deep hypothermia, some clinicians administer a corticosteroid (methylprednisolone, 30 mg/kg, or the equivalent dose of dexamethasone) and mannitol (0.5 g/kg). The head is also covered with ice bags (avoiding the eyes). Surface cooling delays rewarming and may also facilitate adequacy of brain cooling. A long list of drugs has been tested and has failed to improve cerebral outcomes after heart surgery. Human studies during cardiac surgery have not shown improved neurobehavioral outcomes with prophylactic administration of calcium channel blockers (nimodipine), N-methyl-D-aspartate (NMDA) antagonists (remacemide), free radical scavengers (pegorgotein), sedative-hypnotics (thiopental, propofol, or clomethiazole), or lazaroids (tirilazad).
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4. Termination of CPB
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Discontinuation of bypass is accomplished by a series of necessary procedures and conditions, the first of which is adequate rewarming. The surgeon’s decision about when to rewarm is important; adequate rewarming requires time, but rewarming too soon removes the protective effects of hypothermia. Rapid rewarming often results in large temperature gradients between well-perfused organs and peripheral vasoconstricted tissues; subsequent equilibration following separation from CPB decreases core temperature again. An excessive gradient between the infusate temperature and the patient’s core temperature can result in deleterious brain hyperthermia. Infusion of a vasodilator drug (eg, isoflurane) allows higher pump flows and will often speeds the rewarming process. Allowing some pulsatile flow (ventricular ejection) may also speed rewarming. Excessively rapid rewarming, however, can result in the formation of gas bubbles in the bloodstream as the solubility of gases rapidly decreases. If the heart fibrillates during rewarming, direct electrical defibrillation (5–10 J) may be necessary. Administration of lidocaine, 100 to 200 mg, and magnesium sulfate, 1 to 2 g, prior to removal of aortic cross-clamping is a common protocol and may decrease the likelihood of fibrillation. Many clinicians advocate a head-down position while intracardiac air is being evacuated to decrease the likelihood of cerebral emboli. Lung inflation facilitates expulsion of (left-sided) intracardiac air by compressing pulmonary vessels and returning blood into the left heart. TEE is useful in detecting residual intracardiac air. Initial reinflation of the lungs requires greater than normal airway pressure and should generally be done under direct visualization of the surgical field because excessive lung expansion can interfere with internal mammary artery grafts.
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General guidelines for separation from CPB include the following:
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The core body temperature should be at least 37°C.
A stable rhythm must be present. Pacing is often used and confers the benefit of a properly timed atrial systole. Persistence of atrioventricular block should prompt measurement of serum potassium concentration. If hyperkalemia is present, it can be treated with calcium, NaHCO3, furosemide, or glucose and insulin.
The heart rate must be adequate (generally 80–100 beats/min). Slow heart rates are generally treated by pacing. Many inotropic agents will also increase heart rate. Supraventricular tachycardias generally require cardioversion.
Laboratory values must be within acceptable limits. Significant acidosis (pH <7.20), hypocalcemia (ionized), and hyperkalemia (>5.5 mEq/L) should be treated; ideally the hematocrit should exceed 22%; however, a hematocrit <22% should not by itself trigger transfusion of red blood cells at this time. When CPB reservoir volume and flow are adequate, ultrafiltration may be used to increase the hematocrit.
Adequate ventilation with 100% oxygen must have been resumed.
All monitors should be rechecked for proper function and recalibrated if necessary.
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CPB should be discontinued as systemic arterial pressure, ventricular volumes and filling pressures, and cardiac function (on TEE) are assessed. Central aortic pressure may be measured directly and compared with the radial artery pressure and cuff pressure (if there is concern about radial artery hypotension). A reversal of the normal systolic pressure gradient, with aortic pressure being greater than radial pressure, is often seen immediately postbypass. This has been attributed to opening of arteriovenous connections in the hand as a consequence of rewarming. Central aortic root pressure can also be estimated by palpation by an experienced surgeon. Right ventricular volume and contractility can be estimated visually, whereas filling pressures are measured directly by central venous, pulmonary artery, or left atrial catheters. Cardiac output can be measured by thermodilution. TEE can define adequacy of end-diastolic volumes, right and left ventricular contractility, and valvular function.
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Weaning is typically accomplished by progressively clamping the venous return line (tubing). As the beating heart fills, ventricular ejection resumes. Pump flow is gradually decreased as arterial pressure rises. Once the venous line is completely occluded and systolic arterial pressure is judged to be adequate (>80–90 mm Hg), pump flow is stopped and the patient is evaluated. Some surgeons wean by clamping the venous line and then progressively “filling” the patient with arterial inflow.
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Most patients fall into one of four groups when coming off bypass (Table 22–2). Patients with good ventricular function are usually quick to develop good blood pressure and cardiac output and can be separated from CPB immediately. Hyperdynamic patients can also be rapidly weaned. These patients emerge from CPB with a very low SVR, demonstrating good contractility and adequate volume, but have low arterial pressure; their hematocrit is often reduced (<22%). Diuresis (off CPB) or red blood cell transfusions increase arterial blood pressure.
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Hypovolemic patients include those with normal ventricular function and those with varying degrees of impairment. Those with preserved myocardial function quickly respond to infusion of blood via the aortic cannula. Blood pressure and cardiac output rise with each bolus, and the increase becomes progressively more sustained. Most of these patients maintain good blood pressure and cardiac output with a left ventricular filling pressure below 10 to 15 mm Hg. Ventricular impairment should be suspected (when definitive diagnosis using TEE is not available) in hypovolemic patients whose filling pressures rise during volume infusion without appreciable changes in blood pressure or cardiac output or in those who require filling pressures above 10 to 15 mm Hg. Ventricular dysfunction is easily diagnosed by TEE.
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Patients with pump failure emerge from CPB with a sluggish, poorly contracting heart that progressively distends. In such cases, CPB may need to be reinstituted while inotropic therapy is initiated; alternatively, if the patient is less unstable, a positive inotrope (epinephrine, dopamine, dobutamine) can be administered while the patient is observed for improvement. If the patient does not respond to reasonable doses of one of these three agents, milrinone can be added. In patients with poor preoperative ventricular function milrinone may be administered as the first-line agent prior to separation from CPB. In the rare instance that SVR is increased, afterload reduction with nitroprusside or milrinone can be tried. The patient should be evaluated for unrecognized ischemia (kinked graft or coronary vasospasm), valvular dysfunction, shunting, or right ventricular failure (the distention is primarily right sided). TEE will facilitate the diagnosis in these cases.
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If drug therapies fail, intraaortic balloon pump (IABP) counterpulsation should be initiated while the heart is “rested” on CPB. The efficacy of IABP depends on proper timing of inflation and deflation of the balloon (Figure 22–15). The balloon should inflate just after the dicrotic notch is seen on the intraaortic pressure tracing to augment diastolic blood pressure and coronary flow after closure of the aortic valve. Inflation too early increases afterload and exacerbates aortic regurgitation, whereas late inflation reduces diastolic augmentation. Balloon deflation should be timed just prior to left ventricular ejection to decrease its afterload. Early deflation makes diastolic augmentation and afterload reduction less effective. Use of a left or right ventricular assist device (LVAD or RVAD, respectively) may be necessary for patients with refractory pump failure. If myocardial stunning is a major contributor or there are areas of hibernating myocardium, a delayed improvement in contractile function may allow complete weaning from all drugs and support devices only after 12 to 48 h of therapy. Ventricular assist devices can be used as a bridge to cardiac transplantation.
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Many clinicians believe that positive inotropes should not routinely be used in patients coming off CPB because positive inotropes increase myocardial oxygen demand. The routine use of calcium similarly may worsen ischemic injury and may contribute to coronary spasm (particularly in patients who were taking calcium channel blockers preoperatively). Nevertheless, there are centers that administer calcium salts or a positive inotrope (eg, dobutamine), or both, to every patient at the conclusion of CPB. Commonly used positive inotropes and vasopressors are listed in Table 22–3. Epinephrine, dopamine, and dobutamine are the most commonly used agents. Epinephrine is the most potent inotrope and is often effective in increasing both cardiac output and systemic blood pressure when others agents have failed. In lower doses, it has predominantly β-agonist activity. Dobutamine, unlike dopamine, does not increase filling pressures and may be associated with less tachycardia than dopamine; unfortunately, cardiac output often increases without significant changes in blood pressure. On the other hand, dopamine is sometimes more effective in increasing blood pressure than in increasing cardiac output. Interestingly, when infused to increase cardiac output to similar extents, epinephrine is associated with no more increase (and perhaps less) in heart rate than dobutamine. Inamrinone, enoximone, milrinone, and olprinone are selective phosphodiesterase inhibitors, and inotropes with arterial and venous dilator properties. Only inamrinone and milrinone are available in North America. In studies of patients with chronic heart failure inamrinone and milrinone, unlike other inotropes, did not appreciably increase myocardial oxygen consumption. The combination of an inodilator (usually milrinone) and a β-adrenergic agonist results in at least additive (and possibly synergistic) inotropic effects. Norepinephrine is useful for increasing SVR but may compromise splanchnic and renal blood flow at increased doses. Some clinicians use norepinephrine in combination with phosphodiesterase inhibitors to prevent excessive reductions in systemic arterial pressure. Arginine vasopressin may be used in patients with refractory hypotension, a low SVR, and resistance to norepinephrine. There are experimental reports in which doses of methylene blue or vitamin C have successfully counteracted vasodilation that could not be overcome with norepinephrine, vasopressin, or both. Inhaled nitric oxide and prostaglandin E1 (or even inhaled milrinone) may also be helpful for refractory pulmonary hypertension and right ventricular failure (Table 22–4); nitric oxide has the added advantage of not decreasing systemic arterial pressure. Studies have not confirmed outcome benefits to the use of thyroid hormone (T3) or glucose–insulin–potassium infusions for vasoactive/inotropic support after CPB.
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Following CPB, bleeding is controlled, bypass cannulas are removed, anticoagulation is reversed, and the chest is closed. Systolic arterial pressure is generally maintained at less than 140 mm Hg to minimize bleeding. Checking for bleeding, particularly from the posterior surface of the heart, requires lifting the heart, which can cause periods of precipitous hypotension. Some surgeons will need to be informed of the extent and duration of the hypotension; others have greater situational awareness. The atrial cannula(s) is removed before the aortic cannula in case the latter must be used to rapidly administer volume to the patient. Most patients need additional blood volume after termination of bypass. Administration of blood, colloids, and crystalloid is guided by observation of the left ventricle on TEE, filling pressures, and the postbypass hematocrit. A final hematocrit of 25% to 30% is desirable. Blood remaining in the CPB reservoir can be transfused via the aortic cannula, or it can be washed and processed by a cell-saver device and given intravenously. Frequent ventricular ectopy may reflect electrolyte disturbances or residual ischemia and usually should be treated with amiodarone; hypokalemia or hypomagnesemia should be corrected. Ventricular arrhythmias in this setting can rapidly deteriorate into ventricular tachycardia and fibrillation.
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Reversal of Anticoagulation
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Once hemostasis is judged acceptable and the patient continues to remain stable, heparin activity is reversed with protamine. Protamine is a highly positively charged protein that binds and effectively inactivates heparin (a highly negatively charged polysaccharide). Heparin–protamine complexes are then removed by the reticuloendothelial system. Protamine can be dosed in varying ways, but the results of all techniques should be checked for adequacy by repeating the ACT 3 to 5 min after completion of the protamine infusion. Additional incremental doses of protamine may be necessary.
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One dosing technique bases the protamine dose on the amount of heparin initially required to produce the desired ACT; the protamine is then given in a ratio of 1 to 1.3 mg of protamine per 100 units of heparin. A still simpler approach is to give adult patients a defined dose (eg, 3–4 mg/kg) then check for adequacy of reversal. Another approach calculates the protamine dose based on the heparin dose–response curve (Figure 22–14). Automated heparin–protamine titration assays effectively measure residual heparin concentration and can also be used to calculate the protamine dose. The justification for using this methodology is the observation that when protamine is given in excess it may have anticoagulant activity, although this has never been demonstrated in humans. This approach also assumes that administered protamine remains in circulation for a prolonged time (which has been proven false in studies of patients undergoing cardiac surgery). To accomplish the heparin:protamine titration, premeasured amounts of protamine are added in varying quantities to several wells, each containing a blood sample. The well whose protamine concentration best matches the heparin concentration will clot first. Clotting will be prolonged in wells containing either too much or too little protamine. The protamine dose can then be estimated by multiplying the concentration in the tube that clots first by the patient’s calculated blood volume. Supplemental protamine (50–100 mg) may be considered after administration of unwashed blood remaining in the pump reservoir after CPB because that blood contains heparin.
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Protamine administration can result in a number of adverse hemodynamic effects, some of which are immunological in origin. Protamine given slowly (5–10 min) usually has few effects; when given more rapidly it produces a fairly consistent vasodilation that is easily treated with blood from the pump oxygenator and small doses of phenylephrine. Catastrophic protamine reactions often include myocardial depression and marked pulmonary hypertension. Diabetic patients previously maintained on protamine-containing insulin (such as NPH) may be at increased risk for adverse reactions to protamine.
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Persistent bleeding often follows prolonged durations of bypass (>2 h) and in most instances has multiple causes. Inadequate surgical control of bleeding sites, incomplete reversal of heparin, thrombocytopenia, platelet dysfunction, hypothermia-induced coagulation defects, and undiagnosed preoperative hemostatic defects, or newly acquired factor deficiency or hypofibrinogenemia may be responsible. The absence (or loss) of clot formation may be noted in the surgical field. Normally, the ACT should return to baseline following administration of protamine; additional doses of protamine (25–50 mg) may be necessary. Reheparinization (heparin rebound) after apparent adequate reversal is poorly understood but often attributed to redistribution of peripherally bound heparin to the central compartment and to the exceedingly short persistence of protamine in blood. Hypothermia (<35°C) accentuates hemostatic defects and should be corrected. The administration of platelets and coagulation factors should be guided by additional coagulation studies, but empiric therapy may be necessary when such tests are not readily or promptly available as well as when treating massive transfusion. On the other hand, there can be abnormalities in multiple tests of coagulation whether or not there is bleeding, so the true diagnostic specificity and reliability of these tests is often overstated.
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If diffuse oozing continues despite adequate surgical hemostasis and the ACT is normal or the heparin–protamine titration assay shows no residual heparin, thrombocytopenia or platelet dysfunction is most likely. Comparison of a conventional ACT with an ACT measured in the presence of heparinase (an enzyme that cleaves and inactivates heparin) can confirm that no residual heparin requiring protamine reversal remains present when both tests provide the same result. Platelet defects are recognized complications of CPB, which may necessitate platelet transfusion. Significant depletion of coagulation factors, particularly factors V and VIII, during CPB is less commonly responsible for bleeding but should be treated with fresh frozen plasma; both the prothrombin time and partial thromboplastin time are usually prolonged in such instances. Hypofibrinogenemia (fibrinogen level <100 mg/dL or a prolonged thrombin time without residual heparin) should be treated with cryoprecipitate. Desmopressin (DDAVP), 0.3 mcg/kg (intravenously over 20 min), can increase the activity of factors VIII and XII and the von Willebrand factor by releasing them from the vascular endothelium. DDAVP may be effective in reversing qualitative platelet defects in some patients but is not recommended for routine use. Accelerated fibrinolysis may occasionally be encountered following CPB and should be treated with ε-aminocaproic acid or tranexamic acid if one or the other of these agents has not already being given; the diagnosis should be confirmed by elevated fibrin degradation products (≥32 mg/mL), or evidence of clot lysis on thromboelastography. Increasingly, factor VII concentrate or prothrombin complex concentrate are administered as a “last resort” in the setting of coagulopathic bleeding following cardiac surgery.
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Unless a continuous intravenous infusion technique is used, additional anesthetic agents are necessary following CPB; the choice may be determined by the hemodynamic response of the patient following CPB. We have found that most patients tolerate modest doses of volatile agents or propofol infusion. Patients with hypertension that is unresponsive to adequate anesthesia with opioids and either a volatile agent or propofol (or both) should receive a vasodilator such as nitroglycerin, nitroprusside, clevidipine, or nicardipine (Table 22–4). Fenoldopam may be used and has the added benefit of increasing renal blood flow, which might possibly improve kidney function in the early postoperative period.
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It is common for an opioid (morphine or hydromorphone) and either propofol or dexmedetomidine to be given to provide analgesia and sedation during transfer to the ICU and analgesia (after discontinuation of the propofol or dexmedetomidine) during emergence.
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Transporting patients with critical illness from the operating room to the ICU is a consistently nerve-wracking and occasionally hazardous process that is complicated by the possibilities of monitor failure, overdosage, or interruption of drug infusions, and hemodynamic instability en route. Portable monitoring equipment, infusion pumps, and a full oxygen cylinder with a self-inflating bag for ventilation should be readied prior to the end of the operation. Minimum monitoring during transportation includes the ECG, arterial blood pressure, and pulse oximetry. A spare endotracheal tube, laryngoscope, succinylcholine, and emergency resuscitation drugs should also accompany the patient. Upon arrival in the ICU, the patient should be attached to the ventilator, breath sounds should be checked, and an orderly transfer of monitors and infusions (one at a time) should follow. The handoff to the ICU staff should include a brief summary of the procedure, intraoperative problems, current drug therapy, and any expected difficulties. Many centers insist on a standard protocol for the “handoff,” and we strongly recommend this practice.
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6. Postoperative Period
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Depending on the patient, the type of surgery, and local practices, patients may be mechanically ventilated for 1 to 12 h postoperatively. Sedation may be maintained by a propofol or dexmedetomidine infusion. The emphasis in the first few postoperative hours should be on maintaining hemodynamic stability and monitoring for excessive postoperative bleeding. Chest tube drainage in the first 2 h of more than 250 to 300 mL/h (10 mL/kg/h)—in the absence of a hemostatic defect—is excessive and may require surgical reexploration. Subsequent drainage that exceeds 100 mL/h is also worrisome. Intrathoracic bleeding at a site not adequately drained may cause cardiac tamponade, requiring immediate reopening of the chest.
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Hypertension despite analgesia and sedation is a common postoperative problem and should generally be treated promptly so as not to exacerbate bleeding or myocardial ischemia. Nitroprusside, nitroglycerin, clevidipine, nicardipine, or esmolol is generally used. Fluid replacement may be guided by filling pressures, echocardiography, or by responses to treatment. Most patients present with relative hypovolemia for several hours following operation. Hypokalemia (from intraoperative diuretics) often develops and requires replacement. Postoperative hypomagnesemia should be expected in patients who receive no magnesium supplementation intraoperatively.
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Extubation should be considered only when muscle paralysis has worn off (or been reversed) and the patient is hemodynamically stable. Caution should be exercised in obese and elderly patients and those with underlying pulmonary disease. Cardiothoracic procedures are typically associated with marked decreases in functional residual capacity and postoperative diaphragmatic dysfunction.
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Off-Pump Coronary Artery Bypass Surgery
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The development of advanced epicardial stabilizing devices, such as the Octopus (Figure 22–16), facilitated coronary artery bypass grafting without the use of CPB, also known as off-pump coronary artery bypass (OPCAB). This type of retractor uses suction to stabilize and lift the anastomotic site rather than compress it down, which allows for greater hemodynamic stability. Full (CPB) dose heparinization is usually given and the CPB machine is usually immediately available if needed.
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Intravenous fluid loading together with intermittent or continuous infusion of a vasopressor may be necessary while the distal anastomoses are sewn. In contrast, a vasodilator may be required to reduce the systolic pressure to 90 to 100 mm Hg during partial clamping of the aorta for the proximal anastomosis. Intravenous nitroglycerin is often used because of its ability to ameliorate myocardial ischemia.
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Although OPCAB was initially proposed for “simple” one- or two-vessel bypass grafting in patients with good left ventricular function, it may be the sicker, older patients who benefit most from avoidance of CPB. The surgeon may use an intraluminal shunt to maintain coronary blood flow during sewing of distal anastomoses. Volatile anesthetic agents and morphine provide myocardial protection during prolonged periods of ischemia. Maintenance of anesthesia with a volatile agent may therefore be desirable. When the surgeon is skillful, long-term graft patency may be comparable to procedures done with CPB. Patients with extensive coronary disease, particularly those with poor target vessels, may not be good candidates. OPCAB may decrease the incidence of postoperative neurological complications and the need for transfusion relative to conventional coronary bypass with CPB.
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Cardiovascular function in infants and young children differs from that in adults. Stroke volume is relatively fixed, so that cardiac output is primarily dependent on heart rate. The immature hearts of neonates and infants often are less forgiving of pressure or volume overload. Furthermore, the functions of both ventricles are more interdependent, so that failure of one ventricle often precipitates failure of the other (biventricular heart failure). Transition of the neonate from the fetal to the adult circulation is discussed in Chapter 40.
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Preoperative Evaluation
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The potentially complex nature of congenital heart defects and their operative repair demand close communication among the anesthesiologist, perfusionist, and surgeon. In children, the focus should include the exact anatomic abnormality and its physiological consequences, whether there has been any previous palliation or correction, and whether there are any other congenital malformations. The hemodynamic significance of the lesion and the planned surgical correction must be clearly understood. Congestive heart failure and pulmonary infections should be treated. Prostaglandin E1 infusion (0.05–0.1 mcg/kg/min) is used preoperatively to prevent closure of the ductus arteriosus in infants dependent on ductal flow for survival. Congenital cardiac surgical emergencies are rare, chiefly correction of total anomalous pulmonary venous return or of excessive postoperative bleeding, or institution of extracorporeal membrane oxygenation (ECMO).
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Assessment of disease severity relies on both clinical and laboratory evaluation. Deterioration in infants may be manifested by increasing tachypnea, cyanosis, or sweating, particularly during feeding. Older children may complain of easy fatigability. In infants body weight is generally a good indication of disease severity, with the sickest children showing failure to thrive and reduced weight relative to expectations for age. Signs of congestive heart failure include failure to thrive, tachycardia, an S3 gallop, weak pulses, tachypnea, pulmonary rales, and hepatomegaly. Cyanosis may be noted, but hypoxemia is best assessed by measurements of arterial blood gases and the hematocrit. In the absence of iron deficiency, the degree of polycythemia is related to the severity and duration of hypoxemia. Clubbing of the fingers is frequent in children with cyanotic defects. The evaluation should also search for other congenital abnormalities, which are present in up to 30% of patients with congenital heart disease.
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The results of echocardiography, heart catheterization, electrocardiography, and chest radiography should be reviewed. Laboratory evaluation typically includes a complete blood count (with platelet count), coagulation studies, electrolytes, blood urea nitrogen, and serum creatinine. Measurements of ionized calcium and glucose are also useful in neonates and critically ill children.
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Fasting requirements vary according to the patient’s age and current guidelines. A preoperative intravenous infusion that provides maintenance fluid requirements should be used in patients susceptible to dehydration, in those with severe polycythemia, and when excessive delays occur prior to surgery.
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Premedication varies according to age and cardiac and pulmonary reserves. Atropine, 0.02 mg/kg intramuscularly (minimum dose, 0.15 mg), has by tradition been given to pediatric cardiac patients to counteract enhanced vagal tone. Neonates and infants younger than 6 months of age may receive no premedication or be given only atropine. Sedation is desirable in older patients, particularly those with cyanotic lesions (tetralogy of Fallot), as agitation and crying worsen right-to-left shunting. Patients older than 1 year may be given midazolam orally (0.5–0.6 mg/kg) or intramuscularly (0.08 mg/kg).
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Induction of Anesthesia
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A. Hemodynamic Anesthetic Goals
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1. Obstructive lesions
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Anesthetic management should strive to avoid hypovolemia, bradycardia, tachycardia, and myocardial depression. The optimal heart rate should be selected according to age; slow rates decrease cardiac output, whereas fast rates may impair ventricular filling. Mild cardiac depression may be desirable in some hyperdynamic patients, eg, those with coarctation of the aorta.
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A favorable ratio of pulmonary vascular resistance (PVR) to SVR should be maintained in the presence of shunting. Factors known to increase PVR, such as acidosis, hypercapnia, hypoxia, enhanced sympathetic tone, and high mean airway pressures, are to be avoided in patients with right-to-left shunting; hyperventilation (hypocapnia) with 100% oxygen is usually effective in lowering PVR. Systemic vasodilation also worsens right-to-left shunting and should be avoided; phenylephrine may be used to raise SVR. Inhaled nitric oxide has no effect on systemic arterial pressure. Conversely, patients with left-to-right shunting may benefit from systemic vasodilation and increases in PVR.
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Standard intraoperative monitors are generally used, but they may be first applied during the course of an inhaled induction in some patients. A large discrepancy between end-tidal and arterial CO2 tensions should be anticipated in patients with large right-to-left shunts because of increased dead space. Following induction, intraarterial and central venous pressure monitoring are employed for thoracotomies and all procedures employing CPB. We recommend sonographic guidance for these cannulations. A 22- or 24-gauge catheter is used to enter the radial artery; 24-gauge catheters may be more appropriate for small neonates and premature infants. A cutdown may be necessary in some instances. The internal jugular or subclavian vein is generally used for central venous cannulation; if this approach is unsuccessful, a right atrial catheter may be placed intraoperatively by the surgeon. TEE is invaluable for assessing the surgical repair following CPB. Ever smaller probes are yielding better resolution as the technology advances. Probes are currently available for patients as small as 3 kg. Intraoperative epicardial echocardiography is commonly used either in addition to or instead of TEE.
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Venous access is desirable but not always necessary for induction. Agitation and crying are particularly undesirable in patients with cyanotic lesions and can increase right-to-left shunting. Intravenous access can be established after induction but before intubation in most patients. Subsequently, at least two intravenous fluid infusion portals are required; one is typically via a central venous catheter. Caution is necessary to avoid even the smallest air bubbles. Shunting lesions allow the passage of venous air into the arterial circulation; paradoxical embolism can occur through the foramen ovale even in patients without obvious right-to-left shunting. Aspiration prior to each injection prevents dislodgment of any trapped air at stopcock injection ports.
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D. Route of Induction
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To a major extent, the effect of premedication and the presence of venous access determine the induction technique.
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Propofol (2–3 mg/kg), ketamine (1–2 mg/kg), fentanyl (25–50 mcg/kg), or sufentanil (5–15 mcg/kg) can be used for intravenous induction. A pure opioid technique may be suitable for critically ill patients when postoperative ventilation is planned. Intravenous agents’ onset of action may be more rapid in patients with right-to-left shunting; drug boluses should be given slowly to avoid transiently high arterial blood levels. In contrast, recirculation in patients with large left-to-right shunts dilutes arterial blood concentration and can delay the appearance of intravenous agents’ clinical effects.
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Ketamine, 4 to 10 mg/kg, is most commonly used, and onset of anesthesia is within 5 min. Coadministration with atropine helps prevent excessive secretions. Ketamine is a good choice for agitated and uncooperative patients as well as patients with decreased cardiac reserve. Its safety with cyanotic lesions (particularly in patients with tetralogy of Fallot) is well established. Ketamine does not appear to increase PVR in children.
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Sevoflurane is the most commonly used volatile agent. The technique is the same as for noncardiac surgery, except for greater concerns about avoiding excessive anesthetic doses. Sevoflurane is particularly suitable for patients with good cardiac reserve. Nitrous oxide is not often used other than to speed loss of consciousness with inhalation inductions. The uptake of inhalation agents may be slowed in patients with right-to-left shunts; in contrast, no significant effect on uptake is generally observed with left-to-right shunting. Intubation is facilitated by a nondepolarizing agent (rocuronium, 1.2 mg/kg, or vecuronium, 0.1 mg/kg) or, much less commonly, succinylcholine, 1.5 to 2 mg/kg.
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Maintenance Anesthesia
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Following induction, opioids or inhalation anesthetics are used for maintenance. Fentanyl and sufentanil are the most commonly used intravenous agents, and isoflurane and sevoflurane the most commonly used inhalation agents. Some clinicians choose the anesthetic according to the patient’s hemodynamic responses. Isoflurane and sevoflurane may be more suitable than halothane (the most commonly used inhaled agent in years past) for most patients; in equivalent anesthetic doses, halothane causes more myocardial depression, more slowing of the heart rate, but less vasodilation than sevoflurane or isoflurane. However, one can make a sound theoretical argument in favor of halothane over sevoflurane for patients with tetralogy of Fallot (and similarly obstructive lesions such as hypertrophic subaortic stenosis), where myocardial depression is much preferred over vasodilation.
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Cardiopulmonary Bypass
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The circuit and technique used are similar to those used for adults. Because the smallest circuit volume used is still about three times an infant’s blood volume, blood is used to prime the circuit for neonates and infants to prevent excessive hemodilution. CPB may be complicated by intracardiac and extracardiac shunts and a very compliant arterial system (in very young patients); both tend to lower mean arterial pressure (20–50 mm Hg) and can impair systemic perfusion. High flow rates (up to 200 mL/kg/min) may be necessary to ensure adequate perfusion in very young patients. As noted previously, some evidence suggests that pH-stat management during CPB may be associated with better neurological outcome in children who will undergo circulatory arrest. Weaning from CPB is generally not a problem in pediatric patients if the surgical repair is adequate; primary pump failure is unusual. Difficulty in weaning should prompt the surgeon to check the repair and search for undiagnosed and uncorrected lesions. Intraoperative echocardiography, together with measurement of the pressure and oxygen saturation within the various chambers, may reveal the problem. Inotropic support may be provided by any of the agents used for adults. Calcium salts are more often useful in critically ill young patients than in adults as children more often have impaired calcium homeostasis; ionized calcium measurements are invaluable in such cases. Close monitoring of glucose is required because both hyperglycemia and hypoglycemia may be observed. Dopamine and epinephrine are the most commonly used inotropes in pediatric patients. Addition of a phosphodiesterase inhibitor is also useful when PVR or SVR is increased. Hypocapnia, systemic alkalosis, and a high inspired oxygen concentration should also be used to decrease PVR in patients with pulmonary hypertension; additional pharmacological adjuncts may include prostaglandin E1 (0.05–0.1 mcg/kg/min) or prostacyclin (1–40 mcg/kg/min). Inhalation nitric oxide may also be helpful for refractory pulmonary hypertension.
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Children appear to have an intense inflammatory response during CPB that may be related to their blood being exposed to very large artificial surfaces relative to their size. Corticosteroids are often given to suppress this response. Many centers use modified ultrafiltration after weaning from CPB to partially correct the hemodilution but remove inflammatory vasoactive substances (cytokines); the technique takes blood from the aortic cannula and venous reservoir, passes it through an ultrafilter, and returns it to the right atrium.
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Surgical correction of complex congenital lesions often requires a period of complete circulatory arrest under deep hypothermia (deep hypothermic circulatory arrest; DHCA). Following institution of CPB, cooling is accomplished by a combination of surface cooling and a cold perfusate. At a core temperature of 15°C, up to 60 min of complete circulatory arrest may be safe. Ice packing around the head is used to delay rewarming and for surface cooling of the brain. Pharmacological brain protection is often attempted with methylprednisolone, 30 mg/kg, and mannitol, 0.5 g/kg. Following the repair, CPB flow is restarted and rewarming takes place.
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Because of the large priming volumes used (often 200–300% of the patient’s blood volume), hemostatic defects from dilution of clotting factors and platelets are commonly seen after CPB in infants; in addition to heparin reversal, administration of fresh frozen plasma and platelets is often necessary.
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Patients undergoing extensive or complicated procedures will generally remain intubated. Extubation may be considered for older, relatively healthy patients undergoing simple procedures such as closure of a patent ductus or atrial septal defect or repair of coarctation of the aorta.