The early postoperative course for most patients undergoing cardiac surgery with use of cardiopulmonary bypass (CPB) is characterized by a typical pattern of pathophysiologic derangements that benefits from standardized management.1 CPB is associated with a systemic inflammatory response that causes systemic vasodilatation and a capillary leak, which, along with hemodilution from a crystalloid prime, leads to total body volume overload. Use of CPB causes a dilutional and functional coagulopathy, and cardioplegic arrest may cause transient myocardial depression. Intraoperative monitoring to assess filling pressures and transesophageal echocardiography (TEE) are used to direct hemodynamic management and fluid administration upon termination of CPB. Anesthetic techniques and early extubation protocols should be designed to achieve “fast‐track” recovery of most patients (Table 8.1).2 The pathophysiology noted after off‐pump surgery is slightly different in that patients are not subjected to the insults of CPB and cardioplegic arrest. This chapter will summarize the basic clinical features of the post‐CPB patient and will then present scenarios commonly seen in the early postoperative period. It will then discuss aspects of postoperative care unique to various types of cardiac surgery, including off‐pump and catheter‐based procedures. The subsequent chapters will describe in greater detail the assessment and management of the major concerns of the postoperative period: mediastinal bleeding and respiratory, cardiovascular, renal, and metabolic problems.
Fentanyl 5–10 μg/kg, then 0.3–5 μg/kg/h Inhalational agents + low‐dose opiates, then propofol or dexmedetomidine Remifentanil 1 μg/kg for induction, then 0.05–2 μg/kg/min
Midazolam 2.5–5 mg before bypass Propofol 25–75 μg/kg/min (2–10 mg/kg/h) after bypass Dexmedetomidine 1 mg/kg over 10 minutes followed by a continuous infusion of 0.2–1.5 μg/kg/h
Withdrawal of autologous blood before starting bypass Consider retrograde autologous priming to maintain higher hematocrit Echo imaging for aortic atherosclerosis Maintain blood glucose <180 mg/dL Warm to slightly less than 37 °C before terminating bypass
Antegrade/retrograde blood cardioplegia with terminal “hot shot”
ε‐aminocaproic acid 5 g at skin incision and in pump prime, and 1 g/h infusion Tranexamic acid 10 mg/kg, then 1 mg/kg/h
Minimize fluid administration
Amiodarone 150 mg IV over 30 minutes, then continue as an infusion in the ICU for 24 hours Methylprednisolone 1 g before bypass, then dexamethasone 4 mg q6h × 4 doses
Intensive Care Unit
Morphine as small boluses or an infusion of 0.01–0.02 mg/kg/h depending on ageKetorolac 15–30 mg IV after extubation × 72 hours Acetaminophen 650 mg IV
Propofol 25 μg/kg/min Dexmedetomidine 1 mg/kg over 10 minutes followed by a continuous infusion of 0.2–1.5 μg/kg/h (if not started in the OR)
Metoprolol by POD #1 (AF prophylaxis) Magnesium sulfate 2 g on POD #1 (AF prophylaxis) Consider amiodarone for AF prophylaxis
I. Basic Features of the Early Postoperative Period
Following most cardiac procedures, patients arrive in the intensive care unit (ICU) fully anesthetized and sedated, requiring mechanical ventilation for several hours. Considerations during transfer to the ICU and a discussion of ICU monitoring techniques are presented in Chapter 7.3 Adequate pharmacologic sedation and pain control are essential at this time and during the weaning process from the ventilator, which generally should be started once standard criteria are met (Table 10.3, page 475). Early extubation is usually defined as withdrawal of mechanical ventilation within six hours of surgery, and many protocols are designed to achieve “ultra‐fast” extubation within a few hours.
Extubation can be accomplished at the conclusion of surgery following both on‐ and off‐pump surgery.4,5 After extubation, the blood pressure may be higher due to increased sympathetic tone and less vasodilation from sedatives (i.e. propofol, dexmedetomidine, and morphine). Right ventricular (RV) function may be improved when positive‐pressure ventilation is not required. However, it is important to provide adequate analgesia at this time without producing respiratory depression, generally using nonsteroidal anti‐inflammatory drugs (NSAIDs), intravenous (IV) acetaminophen, or low doses of narcotics.
Ventricular function is commonly compromised for several hours following operations on CPB with cardioplegic arrest.6 Inotropic medications may be required for postcardiotomy hemodynamic support during this time as the heart recovers from the insult imposed by ischemia and reperfusion. Furthermore, diastolic function is impaired with reduced compliance. Therefore, volume administration to achieve satisfactory preload will require higher filling pressures than noted preoperatively.
Urine output may be copious because of hemodilution during surgery. However, even though the patient is total body fluid overloaded, fluid administration is usually necessary to maintain intravascular volume to optimize hemodynamic status. Hypokalemia associated with excellent urine output must be monitored and treated. Renal function is generally a good marker of hemodynamic function, although it is subject to numerous variables. Consequently, an initial good urine output may be noted despite poor cardiac function, but a low urine output is of more concern.
Hyperglycemia is commonly noted, even in nondiabetic patients, and the blood sugar should be maintained at <180 mg/dL using intravenous insulin protocols (see Appendix 6).
Patients may have mediastinal bleeding as a result of surgical issues or a coagulopathy, and careful monitoring of chest tube drainage is essential. Blood or blood product transfusions may be indicated for profound anemia or ongoing bleeding.
Postoperative care requires an integration of a myriad of hemodynamic measurements and laboratory tests to ensure a swift and uneventful recovery from surgery. Use of a comprehensive handwritten or computerized flowsheet is essential in evaluating the patient’s course in the ICU.
Warming from hypothermia to 37 °C
Hypothermia (<36 °C) upon admission to the ICU has been associated with adverse outcomes.7 Therefore, it is imperative that adequate rewarming be performed prior to termination of CPB, since the temperature at that time correlates best with core temperature at the time of arrival in the ICU.8 Hypothermia upon arrival to the ICU must be actively treated since it may:
Predispose to atrial and ventricular arrhythmias and lower the ventricular fibrillation threshold
Produce peripheral vasoconstriction, increasing the systemic vascular resistance (SVR). This will elevate filling pressures, masking hypovolemia, increase afterload, raising myocardial oxygen demand, and often cause hypertension, potentially increasing mediastinal bleeding.
Precipitate shivering, which increases peripheral O2 consumption and CO2 production
Produce platelet dysfunction and a generalized impairment of the coagulation cascade
Prolong the duration of action of anesthetic drugs and prolong the time to extubation9
Increase the risk of wound infection, possibly related to immunosuppression
CPB for most nonaortic surgery is usually accompanied by mild systemic hypothermia to 33–35 °C and is terminated after the patient has been rewarmed to a core body temperature of at least 36.5 °C. Although it is common practice to warm patients to 37 °C before terminating bypass, this may require higher arterial inflow temperatures and may be associated with impairment in neurocognitive function.10 The brain temperature is several degrees warmer than the nasopharyngeal temperature during rewarming, suggesting that temperatures measured at other sites may underestimate the degree of cerebral hyperthermia. Even the rectum and bladder, two commonly monitored sites considered to represent the core temperature, are in an “intermediate compartment” where the temperature is close, but not identical, to core temperature. Thus, although hypothermia has potential adverse effects, aggressive “overwarming” during CPB may also prove detrimental.
Despite adequate core rewarming on pump, progressive hypothermia may ensue in the post‐pump period when the chest is still open and hemostasis is being achieved (so‐called temperature afterdrop). This results from insufficient rewarming of peripheral tissues that leaves a significant temperature gradient between the core temperature and the periphery. Thus, heat is subsequently redistributed to the periphery, resulting in a gradual reduction in core temperature. Heat loss is further exacerbated by continued intraoperative heat loss from exposure to cool ambient temperatures in the operating room, poor peripheral perfusion, administration of cold blood products or room‐temperature fluids, and anesthetic‐induced inhibition of normal thermoregulatory control.
Prevention of temperature afterdrop can be achieved by prolonging the warming phase on CPB, warming the periphery, warming blood products before administration, or using pharmacologic vasodilation. Increasing the ambient air temperature to a tolerable level for the surgeon is helpful, especially in patients undergoing off‐pump surgery. In these patients, the use of the Kimberly‐Clark temperature‐management system11 or a cutaneous forced‐air warming device, such as the Bair Hugger (3M), is helpful in avoiding hypothermia (Figure 8.1). These devices are also very helpful in preventing temperature afterdrop when deep hypothermic circulatory arrest (DHCA) is used, but they cannot actively warm the patient or reduce redistribution of heat.12 Sodium nitroprusside has been successful in reducing postbypass afterdrop because it produces peripheral vasodilation and improves peripheral perfusion. However, this benefit is usually noticed only in patients cooled to less than 32 °C.12,13
In the ICU, most patients are peripherally vasoconstricted as a compensatory mechanism to provide core warming. Pharmacologic vasodilation with medications such as nitroprusside, clevidipine, or propofol may facilitate the redistribution of core heat to peripheral tissues and improve tissue perfusion, but at the same time they may delay central warming because peripheral vasodilation augments heat loss. Forced‐air warming systems, radiant warming systems, and resistive heating blankets all appear to be effective in treating postoperative hypothermia, although forced‐air systems appear to be most comfortable for the patient.14 Other measures, such as heating intravenous fluids or using heated humidifiers in the ventilator circuit, are of some benefit in preventing progressive hypothermia, but generally they do not contribute to warming.
Shivering is associated with hypothermia and increases oxygen consumption and patient discomfort. Control of shivering is important in the postoperative period and is best controlled with meperidine (25 mg IV), which has specific antishivering properties related to several possible mechanisms.15 Dexmedetomidine is also effective in controlling shivering.16
Occasionally a patient will rapidly rewarm to 37 °C and then “overwarm” to higher temperatures due to resetting of the central thermoregulating system. Narcotics tend to increase the core temperature required for sweating and may contribute to this problem.17 Since warming may lead to profound peripheral vasodilation and hypotension, gradual vasodilation with nitroprusside or clevidipine and concomitant volume infusion can minimize this problem (see postoperative scenarios II.A and II.B, pages 376–380.
Numerous factors may predispose to mediastinal bleeding following CPB. These include residual heparin effect, thrombocytopenia and platelet dysfunction, clotting factor depletion, fibrinolysis, technical issues during surgery, hypothermia, and postoperative hypertension.18,19
Antifibrinolytic medications, including ε‐aminocaproic acid and tranexamic acid, are recommended for all cardiac surgical procedures to reduce intraoperative bleeding. These medications not only inhibit fibrinolysis but, to varying degrees, also preserve platelet function.20
A universal definition of perioperative bleeding was proposed by an expert panel in 2014.21 This took into consideration the amount of bleeding over 12 hours, the administration of transfusions, and the need for exploration, but did not define a specific amount of bleeding for which interventions were indicated. As anticipated, the more significant the degree of bleeding, the greater the risk of low cardiac output syndrome, inotrope use, acute kidney injury, and mortality.22Generally, an arbitrary bleeding rate of >200 mL/h is of concern, since it may contribute to hemodynamic problems and trigger blood and blood product transfusions.23
Careful monitoring of the extent of postoperative bleeding dictates the aggressiveness with which bleeding should be treated. Many patients with “nonsurgical” causes will drain about 100–200 mL/h for several hours before bleeding eventually tapers. Unless that produces anemia with a hematocrit <22–24% or there is evidence of hemodynamic compromise or end‐organ dysfunction, transfusion should not be necessary. A faster rate of bleeding without evidence of diminution requires systematic evaluation and treatment, often prompting re‐exploration, as described in Chapter 9.
Thromboelastography is helpful in delineating the specific coagulation defect that needs to be addressed and may improve clinical outcomes.24 Routine coagulation studies (INR, PTT, fibrinogen, platelet count) should also be analyzed. Even though they tend to be abnormal in patients with coagulopathic bleeding, they may also be abnormal in patients with ongoing surgical bleeding. Thus, abnormal coagulation studies should not delay exploration for significant bleeding. Persistent bleeding with normal coagulation studies tends to be more surgical in nature.
Recognition of the early signs of cardiac tamponade and the importance of prompt mediastinal exploration for severe bleeding or tamponade are critical to improving patient outcomes.25
Ventilatory support, emergence from anesthesia, weaning, and extubation (see Chapter 10)
Following off‐pump or uneventful on‐pump surgery, some groups prefer to extubate patients in the OR or upon arrival in the ICU.4,5 This can be accomplished using short‐acting narcotics, such as remifentanil, low doses of another narcotics, such as sufentanil 0.15 μg/kg/h, or primarily inhalational agents.26 Sevoflurane rather than isoflurane may be used as an inhalational agent to allow for early awakening and extubation in the OR or soon after arrival in the ICU.27Alternative approaches to achieve early extubation include high thoracic epidural analgesia or spinal (intrathecal) analgesia with bupivacaine, fentanyl, or morphine with clonidine, often combined with remifentanil.28–31 Neuromuscular blockers that have a short duration of action and do not require renal or hepatic elimination, such as cisatracurium or rocuronium, are best in this regard.
Careful monitoring of the patient’s mental status and respiratory drive is imperative after extubation as the patient is still in an early phase of recovery from anesthesia. Just prior to and after extubation, analgesia should be provided to minimize splinting and improve inspiratory effort, but narcotics must be used with caution as they depress the respiratory drive. NSAIDs are usually helpful and might reduce narcotic requirements.32,33 Ketorolac is a COX‐1 inhibitor that inhibits platelet aggregation, so in addition to providing analgesia, it also been shown to improve graft patency and reduce mortality after CABG.34,35 Ibuprofen given with a proton‐pump inhibitor has also been effective and devoid of major side effects.36 However, NSAIDs must be used with caution in patients with ongoing bleeding or chronic kidney disease. Intravenous acetaminophen might also be beneficial, although a randomized trial failed to show a reduction in opioid use.37 Acetaminophen combined with propofol or dexmedetomidine has been shown to reduce the incidence of delirium.38
Most groups select anesthetic agents to allow for early extubation within 6–8 hours of arrival in the ICU. Thus, fentanyl or sufentanil are used for narcotic‐based balanced anesthesia. Patients will remain anesthetized and sedated upon arrival in the ICU and will require mechanical ventilation for a short period of time. Propofol or dexmedetomidine will provide sedation as the narcotic effects dissipate, the latter generally being associated with shorter intubation times.39 The initial fraction of inspired oxygen (FiO2) of 1.0 is gradually weaned to below 0.5 as long as the PaO2 remains above 80 torr or the arterial oxygen saturation (SaO2) exceeds 95%. The respiratory rate or tidal volume of the mechanical ventilator is adjusted to accommodate the increased CO2 production that occurs with warming, awakening, and shivering. Use of a low tidal volume (6 mL/kg rather than 10 mL/kg) has been shown to be beneficial in patients with ARDS, and a study in cardiac surgery patients found a trend towards earlier extubation, with fewer patients requiring reintubation with this ventilatory strategy.40
Early extubation is feasible in most patients, conditional upon their mental status, gas exchange, and hemodynamic performance.
Virtually all patients have some compromise of pulmonary function after surgery related to a median sternotomy, entrance into the pleural cavity, and noncardiogenic pulmonary edema from the capillary leak caused by a systemic inflammatory response and fluid overload from crystalloid hemodilution. These issues are more prominent in patients undergoing prolonged complex operations with long bypass runs, who often receive multiple blood products as well. Superimposing these insults on preexisting heart failure or underlying lung disease, such as COPD, will predictably result in suboptimal oxygenation and ventilatory issues after surgery that might require a longer period of intubation.
Even so, as long as certain criteria are met, there is no reason to exclude a patient based upon age, comorbidities, cardiac disease, or the extent of surgery from a protocol of early extubation. Even if it takes a few hours longer to extubate a patient, the benefits of an early extubation strategy usually translate into a quicker recovery from surgery.41–43 The longer the patient remains intubated receiving sedation, the greater the risk of delirium.44
Once criteria for weaning are satisfied (see Table 10.3, page 475), propofol is weaned off, neuromuscular blocking agents are allowed to wear off, low‐dose narcotics or nonopioids may be given for analgesia (note that propofol is not an analgesic), and hypertension is controlled with nonsedating antihypertensive medications. If extubation criteria are met, the patient is extubated. Propofol‐based regimens allow for earlier extubation than fentanyl‐based regimens,45 but as noted, dexmedetomidine allows for earlier extubation than propofol because it has less sedative and respiratory depressant effects, and can “take the edge off” because of its anxiolytic properties.39 As such, it is also extremely useful when a patient exhibits agitation and dyssynchronous breathing while still on the ventilator.
Despite the desirability of early extubation, there are patients in whom it is ill‐advised to “rush to extubate” (Table 10.2, page 472).41–43,46,47
Preoperative factors predictive of prolonged postoperative ventilation are often cardiac in origin, including poor left ventricular (LV) function with congestive heart failure, cardiogenic shock, or pulmonary edema, especially if an intra‐aortic balloon pump (IABP) is required for hemodynamic support. Other risk factors include need for urgent or emergent surgery, reoperations, and the presence of significant comorbidities, including severe COPD, marked obesity, peripheral vascular disease, and chronic kidney disease. In these cases, use of sufentanil or fentanyl is advisable, rather than shorter‐acting medications. It is reasonable to use narcotics for the control of hypertension.
Postoperative clinical issues that may necessitate prolonged ventilation include hemodynamic instability requiring multiple inotropes and/or IABP dependence, low cardiac output syndrome, depressed level of consciousness or a stroke, ongoing mediastinal bleeding, oliguria from renal failure, and especially poor oxygenation or poor respiratory mechanics. In these patients, propofol can provide adequate sedation for several days and may be converted to other sedatives, such as fentanyl, if prolonged intubation is required. Careful review of the patient’s chest x‐ray, ECG, arterial blood gases, hemodynamic parameters, and renal function should allow for identification of problems that need to be addressed. Issues related to the management of hypoxia and acute respiratory failure are discussed in detail in Chapter 10.
Analgesia and sedation
An essential element of postoperative care is the provision of adequate analgesia without inducing too much sedation that may contribute to delirium or respiratory depression.48,49 Pain control reduces the sympathetic response, reducing the risk of myocardial ischemia and arrhythmias, and improves the patient‘s respiratory efforts, overall mental status, mobilization, and physical rehabilitation after surgery. Pain is especially prominent with coughing and deep breathing as well as with movement. “Cough pillows” to brace the chest wall are very helpful in reducing splinting. Pain often improves following removal of chest tubes.
Parasternal intercostal blocks or subcutaneous local anesthetic infusions of bupivacaine 0.5% 4 mL/h (ON‐Q Pain Relief System, Avanos) initiated at the time of surgery can ameliorate chest wall pain and decrease opioid requirements.50,51 This is especially beneficial when patients are extubated in the operating room.
While the patient remains intubated, there may be some residual analgesic effects of the intraoperative narcotics, but propofol is not an analgesic, and additional analgesic medications may be required around the time of extubation. Dexmedetomidine is beneficial in this regard since it has both sedative and analgesic properties. Use of narcotics is appropriate in patients in whom prolonged ventilation is anticipated. However, if extubation is considered imminent, a variety of analgesic regimens may be able to reduce or eliminate opioid requirements around the time of extubation. These include use of an NSAID, such as ketorolac 30 mg IV, and IV acetaminophen. A multimodal approach using a combination of dexamethasone, gabapentin, ibuprofen, and acetaminophen has been shown to provide superior analgesia to opiates with less nausea after surgery through a median sternotomy incision.52
After extubation, adequate analgesia can be provided by a variety of medications and via different routes.
Use of nonopioid analgesia is always preferable and may provide adequate pain relief in most patients. IV ketorolac (15–30 mg) for 72 hours or IV acetaminophen can often bridge the patient to oral analgesics within a few days. Gabapentin 300 mg up to three times a day is usually recommended to treat nerve pain, but it is often helpful in providing analgesia early after surgery. Tramadol 50–100 mg every 4–6 hours may also be considered.
Patient‐controlled analgesia (PCA) IV pumps using a variety of opioids provide excellent analgesia.53,54 One study found that use of morphine (1 mg bolus and 0.3 mg/h infusion), fentanyl (10 μg bolus and 1 μg/kg/h infusion), or remifentanil (0.5 mg/kg bolus and 0.05 μg/kg/min infusion) started after the completion of surgery for 24 hours provided comparable analgesia, but fewer side effects were noted with use of remifentanil.54
Thoracic epidural or intrathecal analgesia with narcotics and bupivacaine are beneficial in reducing pain, expediting extubation, and improving pulmonary function, especially in patients with COPD and obesity.28–30,55,56
Small bolus doses of IV narcotics or a continuous infusion of narcotics (such as morphine sulfate 0.02 mg/kg/h for patients under age 65 and 0.01 mg/kg/h for patients over age 65) may be considered to provide analgesia while minimizing respiratory depression.
On occasion, persistent pain refractory to the above regimens, especially in opioid tolerant patients, may require use of IV hydromorphone (Dilaudid) 1–2 mg q2–3h, which runs the risk of respiratory depression, or a fentanyl patch (25–50 μg/h patch every 72 hours).
If the patient does not tolerate the weaning process, often becoming agitated with the weaning of propofol, substitution of dexmedetomidine can provide anxiolysis, analgesia, sympatholysis, and mild sedation to expedite a more tolerable weaning process from the ventilator.57 It can be continued after the patient is extubated.
If delayed extubation is anticipated, propofol remains an excellent choice for several days and may be converted to IV fentanyl for longer‐term sedation.58 It should be noted that the offset of action of propofol depends on the duration of use, the depth of sedation, and body habitus. One study showed that, with light sedation for up to 24 hours, emergence occurs in only 13 minutes, but in heavily sedated patients it may take up to 25 hours!59 Although use of dexmedetomidine has only been recommended for 24 hours, several studies have found it to be comparable to or better than propofol or midazolam for long‐term sedation.60,61
Hemodynamic support during a period of transient myocardial depression (see Chapter 11)1,6,62
Myocardial function following a period of cardioplegic arrest may be transiently depressed from ischemia/reperfusion injury and will often benefit from low‐dose inotropic support for several hours. Systolic dysfunction may also be accompanied by diastolic dysfunction due to impaired ventricular compliance from cardioplegic arrest and myocardial edema. The reduction in ejection fraction (EF) is about 10–15% in patients with relatively normal LV function, but it may be even greater in those with preexisting LV dysfunction. Additionally, hypothermia and elevated levels of catecholamines lead to an increase in SVR and systemic hypertension, which increase afterload and can further depress myocardial performance. Factors influencing the need for inotropic support include the extent of preoperative LV dysfunction, a recent infarction or ongoing ischemia at the time of surgery, and the duration of aortic cross‐clamping. In patients sustaining a perioperative infarction, the period of myocardial depression tends to last somewhat longer, and may require more prolonged support.
Serial assessments of filling pressures, cardiac output and cardiac index (CI), and SVR allow for the appropriate selection of fluids, inotropes, and/or vasodilators to optimize preload, afterload, and contractility to provide hemodynamic support during this period of temporary myocardial depression. The objective is to maintain a cardiac index above 2.2 L/min/m2 with a stable blood pressure (systolic 100–130 mm Hg or a mean pressure of 70–80 mm Hg). Adequate tissue oxygenation is the primary goal of hemodynamic management and can be assessed by measuring the mixed venous O2 saturation (SvO2) from the pulmonary artery port of the Swan‐Ganz catheter (normal >65%).
Traditionally, the Swan‐Ganz catheter has been used to monitor filling pressures, assess the cardiac output, and measure the SvO2. Numerous studies have documented an imprecise correlation of measured filling pressures with intravascular volume and fluid responsiveness and have questioned the benefits of this catheter.63 In most low‐risk patients, not using a Swan‐Ganz catheter has not influenced outcomes; in fact, some have found its use prolongs the duration of ventilation with no impact on outcomes even in high‐risk patients.64 One study found not only poor correlation between echocardiography and a Swan‐Ganz catheter or FloTrac device in the assessment of hemodynamics, but also little correlation between the latter two devices!65 Nonetheless, numerous studies have suggested that a “goal‐directed” hemodynamic approach to optimize fluid status and cardiac output may reduce complications, facilitate recovery, and shorten the hospital length of stay, although a mortality benefit may not be evident.66,67 A survey reported that most centers are still using a Swan‐Ganz catheter as a matter of routine because of a perceived benefit in postoperative management.68
The initial intervention to augment cardiac output is fluid administration. The filling pressures do tend to underestimate volume status, because of impaired ventricular compliance. Furthermore, the response to volume may differ, depending on whether the heart is hypertrophied with a “pressure overload” condition, as noted with hypertension or aortic stenosis (AS), or is somewhat dilated from a “volume overload” condition, as noted with long‐standing aortic or mitral regurgitation. Observation of trends in filling pressures is essential when making clinical decisions about fluid administration.
Atrial or atrioventricular (AV) pacing at a rate of 80–90 beats/min is commonly required at the conclusion of surgery to achieve optimal hemodynamics, especially in hypertrophied hearts. Pacing is frequently required in patients taking β‐blockers before surgery. A slow heart rate may reduce myocardial oxygen demand but will compromise cardiac output. In a well‐revascularized heart, raising the heart rate to augment cardiac output is indicated and generally well tolerated. Ventricular pacing to increase heart rate will always produce inferior hemodynamic performance to atrial pacing, so atrial pacing wires should be placed in virtually all patients with preoperative sinus rhythm.
Inotropes should be selected based on an understanding of their hemodynamic benefits and potential complications (see pages 535–548). If a marginal cardiac output is present after adequate fluid status has been achieved, inotropic support is initiated and should improve the cardiac output to acceptable levels. When the thermodilution cardiac output appears inconsistent with the patient’s clinical course, a mixed venous oxygen saturation reflects the adequacy of tissue oxygenation. This indirectly correlates with cardiac output, since it is also influenced by arterial oxygen saturation. If a satisfactory cardiac output still cannot be achieved or begins to deteriorate, additional inotropes, an IABP, or rarely an assist device may be necessary. However, in most patients, cardiac function improves to baseline within a few hours and inotropes can be usually weaned off within 12 hours of surgery. In patients with preexisting severe ventricular dysfunction or acute perioperative cardiac insults (ischemia, infarction, prolonged cross‐clamp time), it may take somewhat longer.
Monitoring of serial hematocrits is important to ensure the adequacy of tissue oxygen delivery. The hematocrit may be influenced by hemodilution or mediastinal bleeding and should generally be maintained at a level greater than 22%. In elderly or critically ill patients, especially those with a low cardiac output state, hypotension, tachycardia, low mixed venous oxygen saturation, evidence of ischemia, metabolic acidosis, or hypoxemia, transfusion to a higher level should be considered, weighing the potential risks and benefits of transfusion.69
Fluid administration to maintain filling pressures in the presence of a capillary leak and vasodilation (see Chapter 12)
Following CPB, the patient will be total body salt and water overloaded and should theoretically be diuresed. However, numerous factors may contribute to inadequate preload that may compromise hemodynamic performance.
Mediastinal bleeding or bleeding from leg incisions from vein harvesting.
A capillary leak from the CPB‐induced systemic inflammatory response which contributes to interstitial edema.
Peripheral vasodilatation from medications (propofol, narcotics, antihypertensive medications), and rewarming. Note that peripheral vasoconstriction that is present when the patient is hypothermic or in a low flow state will mask intravascular hypovolemia despite adequate left‐heart filling pressures.
Impaired systolic function due to transient myocardial depression that requires increased preload to maintain stroke volume.
Fluid administration is necessary in most patients to maintain adequate preload and cardiac output. Crystalloid and colloid infusions are used to maintain intravascular volume, although this usually occurs at the expense of expansion of the interstitial space. After the capillary leak has ceased and hemodynamics have stabilized, the patient may be aggressively diuresed to eliminate the excessive salt and water administered during surgery and the early postoperative period. Scenario B in the next few pages addresses issues related to fluid resuscitation in the vasodilated patient.
Electrolytes and acid–base balance
Monitoring of serum potassium (KCl) is essential in the early postoperative period. Potassium levels may be elevated from cardioplegia solutions delivered for myocardial protection, but most patients with normal renal function and preserved myocardial function will make large quantities of urine during the first few hours after CPB, often resulting in hypokalemia. To minimize the risk of developing arrhythmias, potassium levels should be checked every four hours and KCL replaced as necessary.
Magnesium levels are usually lower due to hemodilution on CPB and should be replenished because of potential benefits in reducing postoperative arrhythmias.70
Metabolic acidosis may result from the use of epinephrine, but may be an ominous sign of inadequate tissue perfusion, especially in the vasoconstricted patient. In several studies that evaluated central venous oxygen saturations (ScvO2), an elevated lactate level was found to be a sensitive sign of inadequate perfusion, with levels >4 mmol/L that cleared slowly, even with a normal ScvO2, correlating with a higher rate of complications.71,72 In fact, complications were also found to be common in patients with lactate levels of 2–4 mmol/L and a ScvO2 <70%, despite normal mean arterial pressures, CVP, and urine output, and may be a marker of global tissue hypoxia from “occult hypoperfusion”.73 Metabolic acidosis generally resolves with improvement in hemodynamic parameters. Use of sodium bicarbonate may be considered for profound acidosis because of its adverse effects on cardiac function, but it only acts as a “bandaid” until the cause of the acidosis is corrected (see pages 715–716 in Chapter 12).
Strict management of hyperglycemia has been shown to reduce the incidence of sternal wound infection and surgical mortality.74,75 Factors that contribute to hyperglycemia are insulin resistance, endogenous catecholamine release on pump, and use of epinephrine post‐pump for hemodynamic support. A hyperglycemia protocol should be utilized to determine the appropriate amount of insulin to be given to maintain blood glucose <180 mg/dL (see Appendix 6).
II. Management of Common Postoperative Scenarios
There are several typical hemodynamic scenarios that are noted during the early phase of recovery from open‐heart surgery. An understanding of these patterns allows for therapeutic maneuvers to be undertaken in anticipation of hemodynamic changes, rather than as reactions to problems once they have occurred.
Vasoconstriction from hypothermia with hypertension and borderline cardiac output
The patient arriving in the ICU with a temperature below 35–36 °C will vasoconstrict in an attempt to increase core body temperature. The elevation in SVR may produce hypertension at a time when cardiac function is still somewhat depressed from surgery. These patients should be managed by a combination of fluid replacement to reach a pulmonary artery diastolic (PAD) pressure or pulmonary capillary wedge pressure (PCWP) around 15–20 mm Hg, pharmacologic vasodilation to maintain a systolic pressure of 100–120 mm Hg (mean pressure 70–80 mm Hg), and inotropic support if the cardiac index remains <2.0 L/min/m2. Warming methods noted above should also be employed. Among the commonly used vasodilators, clevidipine is a short‐acting calcium channel blocker that reduces SVR and is usually the drug of first choice.76 Nitroprusside is preferable to intravenous nitroglycerin (IV NTG) in reducing SVR, but it is a very powerful drug which requires careful monitoring. IV NTG is useful in patients with potential ischemia, but it tends to lower preload and reduce cardiac output to a greater degree while producing less systemic vasodilation than the other drugs. Nicardipine is a longer‐acting calcium channel blocker that can also be considered.
The use of arterial vasodilators is beneficial in the vasoconstricted patient in that they:
Reduce afterload, improving myocardial metabolism and LV function
Improve peripheral tissue perfusion and redistribute heat to the periphery
Facilitate gentle and adequate fluid administration
Vasodilators will reduce the SVR and blood pressure, and left‐sided filling pressures will fall modestly, requiring the simultaneous infusion of fluids to maintain cardiac output. The optimal left‐sided filling pressures depend on the state of myocardial contractility and compliance. Preload (generally the PA diastolic pressure) should generally not be raised above 20 mm Hg, because of the deleterious effects of elevated wall tension on myocardial metabolism and function. However, if preload is allowed to fall too low, the patient may become hypovolemic and hypotensive when normothermia is achieved. The general principle is to “optimize preload → reduce afterload → restore preload”.
If the patient has a marginal cardiac index (<2.0 L/min/m2), has adequate filling pressures, yet is somewhat hypertensive, a low dose of a vasodilator can be initiated. If the patient is already on inotropic support, it is imperative to assess the cardiac index before modifying the therapeutic approach. Despite the temptation to do so, stopping an inotropic medication in a hypertensive patient without first ensuring that a satisfactory cardiac output is present can be very dangerous. Some patients with very marginal cardiac function maintain a satisfactory blood pressure by intense vasoconstriction from enhanced sympathetic tone. Loss of this compensatory mechanism may result in rapid deterioration from loss of perfusion pressure.
Vasodilation and hypotension during the rewarming phase
Vasodilation reduces filling pressures and, in the hypovolemic patient, may produce hypotension and often a decrease in cardiac output despite good cardiac function. There are several reasons why a patient may vasodilate during the early postoperative period.
Medications used for analgesia and anxiolysis are vasodilators (narcotics, propofol, midazolam). Recent use of ACE inhibitors or angiotensin receptor blockers (ARBs) tends to cause hypotension during and after bypass.
Intravenous NTG used in the OR or in the ICU to control blood pressure, minimize ischemia, or prevent radial artery spasm will lower preload and cardiac output as well as blood pressure. To counteract these problems, significant fluid administration is frequently required. Unless active ischemia is present, IV NTG is best avoided during the rewarming phase to reduce fluid requirements.
Resolution of hypothermia leads to peripheral vasodilation, which is accentuated in patients who warm to higher than 37 °C.
Improvement in cardiac output often leads to relaxation of peripheral vasoconstriction.
A vasoplegic state of refractory hypotension may develop despite the presence of an adequate cardiac output. This may be a consequence of a systemic inflammatory response (although it has been noted after off‐pump surgery as well) and may be related to vasodilation induced by nitric oxide.
Transfusion reactions or anaphylactic reactions to medications will cause vasodilation.
Sepsis is very uncommon immediately after surgery but should be considered in the differential diagnosis.
To avoid hypotension, fluids must be given to maintain filling pressures. The quandary is whether crystalloid or colloid should be selected and how much should be given. If the basic reason for hypovolemia is a capillary leak syndrome, the use of colloid could be detrimental, because its oncotic elements may pass into the interstitial tissues, exacerbating tissue edema and compromising organ function. However, if vasodilation of the peripheral and splanchnic beds is the major problem, then colloids should be preferable, because they will augment the intravascular volume to a greater extent than crystalloids. Generally, if filling pressures are not elevated, the amount of extravascular lung water will not be influenced significantly whether colloid or crystalloid is infused.77 Volume resuscitation is usually required during the initial six hours after arrival in the ICU, following which most mechanisms for vasodilation are no longer present and the capillary leak begins to abate.
It is generally best to start with a 500 mL bolus of lactated Ringer’s, rather than normal saline. The latter may contribute to a hyperchloremic acidosis and worsen acute kidney injury.78,79 If there is a minimal increase in filling pressures, a colloid such as 5% albumin may be chosen because more volume is retained in the intravascular space. Hetastarch compounds increase the intravascular volume more effectively than crystalloid and for longer than 5% albumin, but they have fallen out of favor as they may contribute to a coagulopathy or renal dysfunction. If given, tetrastarches should be used and the total infusion volume limited to 1500–1750 mL (20 mL/kg) per 24 hours.80 If the patient’s hematocrit is low (<22%), a packed red cell transfusion is the most appropriate means of increasing intravascular volume. If the patient is bleeding, use of blood component transfusions may be indicated as well. It must always be remembered that any volume, but more so colloids and blood products than crystalloids, will also lower the hematocrit from hemodilution.
There is often a tendency to administer a tremendous amount of fluid during the period of vasodilation in order to maintain filling pressures and systemic blood pressure. Although most patients with satisfactory cardiac function will simultaneously produce a copious amount of urine, many patients will not. One should resist the temptation to “flood” the patient with fluid, because excessive fluid administration (>2 L within six hours) will exacerbate interstitial pulmonary edema and delay extubation, and may contribute to cerebral or bowel edema. It will also produce significant hemodilution, often necessitating blood transfusions for anemia, and will reduce the levels of clotting factors, possibly increasing mediastinal bleeding and necessitating plasma or platelet administration. Preload should be increased only as necessary to maintain satisfactory cardiac output and tissue perfusion.
The response to fluid administration is not always predictable and depends on the compliance of the left atrium and ventricle, the degree of “capillary leak”, and the intensity of peripheral vasoconstriction.
An increase in preload with repeated fluid challenges will generally raise the cardiac output and blood pressure to satisfactory levels. Less volume is required in noncompliant hearts, usually those with LV hypertrophy. Peripheral vasoconstriction tends to relax as the cardiac output improves and the patient warms. As this occurs, filling pressures tend to fall and some additional volume may be necessary. If cardiac function and filling pressures are adequate, yet the blood pressure remains marginal, use of an α‐agent (phenylephrine or norepinephrine) to support the blood pressure can limit the amount of fluid that needs to be given. If these drugs cannot maintain a satisfactory blood pressure with adequate filling pressures, yet the cardiac output is satisfactory, a “vasoplegic syndrome” may be present. This generally responds to vasopressin 0.01–0.1 units/min.81 This syndrome may be attributable to leukocyte activation and release of proinflammatory mediators caused by the systemic inflammatory response to CPB, although it has been described after off‐pump surgery as well. If vasoplegia persists, methylene blue 2 mg/kg IV followed by 0.5–1 mg/kg/h may be beneficial.82
Failure of filling pressures to rise with volume infusions may be noted in patients with highly compliant, volume‐overloaded hearts (such as mitral regurgitation), in whom the cardiac output improves before the filling pressures are noted to increase. Thus, further fluid therapy can be guided by the cardiac output. Consideration must always be given to possible sources of blood loss, including accumulation in the chest cavity not drained by chest tubes.
In other patients, filling pressures may not rise due to persistent vasodilation and the capillary leak of fluid into the interstitial space rather than retention in the intravascular space. This is particularly common in very sick patients with a long duration of CPB. Sometimes it seems virtually impossible to maintain filling pressures and cardiac output despite a tremendous amount of fluid administration, yet, on occasion, this may be necessary. One often has to accept the adverse consequences of excessive total body water to improve hemodynamics. Use of drugs to provide inotropic support and produce an increase in systemic resistance may reduce the amount of fluid administered.
If filling pressures do rise with fluid administration, but the blood pressure and cardiac output remain marginal, RV and LV distention may ensue, increasing myocardial oxygen demand and decreasing coronary blood flow. At this point, further fluid administration is contraindicated, and inotropic support must be initiated. An echocardiographic assessment may be necessary to rule out tamponade or assess for unsuspected additional pathology (ventricular septal defect, valvular pathology). A chest x‐ray may demonstrate a tension pneumothorax.
The following is a general guideline to hemodynamic management during the rewarming phase.
If the blood pressure is marginal, push the PAD pressure or PCWP to 18–20 mm Hg (often up to 25 mm Hg in hypertrophied hearts) using crystalloid and then colloid. Once this level is reached and the patient remains hypotensive, if the urine volume begins to match the infused volume, or if more than 2000 mL of fluid has been administered and filling pressures are not rising, consider the following:
If CI >2.2 L/min/m2, use phenylephrine (pure α), or if unsuccessful, vasopressin for a potential “vasoplegic” state
If CI is 1.8–2.2 L/min/m2, use norepinephrine (α and β)
If CI <1.8 L/min/m2, use an inotrope, then norepinephrine to support the blood pressure
Note: use of an α‐agent may not be able to minimize a capillary leak, but it does counteract vasodilation. This may decrease the volume requirement and improve SVR and blood pressure with little effect on myocardial function.
Copious urine output and falling filling pressures. Some patients will make large quantities of urine, resulting in a reduction in filling pressures, blood pressure, and cardiac output. Several factors should be considered when determining why this might be occurring.
Did the patient receive mannitol or furosemide in the OR because of a low urine output or hyperkalemia? Urine output is no longer a direct reflection of myocardial function when a diuretic has been administered. Excessive urine output often necessitates a significant amount of fluid administration to maintain filling pressures and confounds the selection of the appropriate fluid to administer (crystalloid vs. colloid).
Is the patient hyperglycemic and developing an osmotic diuresis? A hyperglycemia protocol should be used routinely to maintain blood glucose below 180 mg/dL (see Appendix 6).
Does the patient have normal LV function and the kidneys are simply mobilizing excessive interstitial fluid from hemodilution on pump? This beneficial effect is often seen in healthy patients with a short CPB run and reflects excellent cardiac output and renal function that should lead to a rapid postoperative recovery. However, copious urine output can be problematic when it lowers filling pressures, blood pressure, and cardiac output.
Any contributing factors or medications causing the diuresis should be addressed.
Crystalloid and colloid should be administered to keep the fluid balance modestly negative during this phase of spontaneous diuresis. The temptation should be resisted to administer too much colloid, because this can produce hemodilution and progressive anemia despite the negative fluid balance and can dilute clotting factors, potentially contributing to mediastinal bleeding. Use of an α‐agent or vasopressin may maintain filling pressures and decrease the volume requirement in some of these patients.
Low cardiac output syndrome with impaired left ventricular function
Isolated LV dysfunction requiring postcardiotomy inotropic support may be noted in patients with active ischemia at the time of surgery, preexisting LV dysfunction, a remote or recent myocardial infarction, or advanced valvular heart disease. It may also result from intraoperative problems, such as a prolonged period of cardioplegic arrest, inadequate myocardial protection, incomplete revascularization, or compromised graft flow. Poor RV or LV function often reflects reversible myocardial stunning rather than perioperative ischemia and infarction. Both are managed in similar fashion, but the suspicion of ongoing ischemia by ECG may require reevaluation and potential treatment in the cardiac cath lab.83–86
Appropriate measures should be taken at the conclusion of surgery to assess and optimize a patient’s hemodynamic status before arrival in the ICU, including pacing, optimal preload, inotropic support, and use of an IABP, if indicated. It is critical that the surgeon, along with the anesthesiologist, establish a “game plan” for how the patient should be managed in the ICU. Assessment of cardiac function by direct visualization and TEE allows for correlation with hemodynamic parameters obtained with the Swan‐Ganz catheter to establish an individualized therapeutic approach. Decisions on desired filling pressures, inotropic selection, plans for maintaining or weaning inotropes, and ventilatory requirements must be communicated to those caring for the patient in the ICU on a minute‐by‐minute basis. Careful monitoring and continuous reevaluation in the ICU are essential to identify whether the patient is recovering as desired or requires further evaluation and intervention.
In addition to careful examination and standard monitoring of critically ill patients, echocardiography in the ICU is very beneficial in clarifying potential problems. A typical scenario that may benefit from echo evaluation is the patient with a low cardiac output on substantial doses of inotropes, borderline and labile blood pressure, elevated filling pressures (often ascribed to volume infusions), worsening oxygenation, and bleeding that is ongoing or has tapered. In such a situation, an echo is indicated to assess whether there are factors other than LV dysfunction that may be causing the low cardiac output syndrome. Conditions such as circumferential or regional cardiac tamponade, severe diastolic dysfunction, RV dysfunction, regurgitant valvular lesions, or septal shunting may be identified. The most likely alternative cause of the scenario noted is cardiac tamponade, which, fortunately, is the most remediable. If a transthoracic echo does not provide adequate acoustic windows, a transesophageal study can easily be performed, especially in the intubated patient.87
A comprehensive discussion of the management of the low cardiac output syndrome is provided starting on page 521 in Chapter 11.
Normal left ventricular function but low cardiac output: diastolic dysfunction
A disturbing postoperative scenario is that of a low cardiac output syndrome associated with normal or elevated left‐heart filling pressures yet preserved LV function. This scenario is noted most commonly in small women with systemic hypertension who have small, hypertrophied LVs. A variant of this problem is seen in patients with AS and hyperdynamic hearts that manifest near cavity obliteration.88
The problem of severe diastolic dysfunction is characterized by reduced ventricular compliance exacerbated by myocardial edema from ischemia/reperfusion injury. Contributing factors to the low cardiac output are lack of AV synchrony with impaired ventricular filling, occasionally impaired RV function, and perhaps excessive use of inotropic agents.
The hemodynamic data derived from the Swan‐Ganz catheter typically show elevated filling pressures and a low cardiac output, suggestive of LV dysfunction. Thus, a typical therapeutic response would be to ensure AV conduction, administer some volume, and initiate inotropic support. However, this may lead to little improvement in cardiac output, even higher filling pressures leading to pulmonary congestion, a reduction in renal blood flow (often exacerbated by systemic venous hypertension), and progressive oliguria. The use of inotropes may also produce a significant sinus tachycardia that is detrimental to myocardial metabolism and recovery.
Transesophageal echocardiography (TEE) has been invaluable in the assessment and management of this problem. TEE will usually confirm a hypertrophic, stiff LV with hyperdynamic systolic function and signs of diastolic dysfunction. Fluid should be administered to raise the PAD pressure to about 20–25 mm Hg. This will increase the LV end‐diastolic volume, which tends to be lower than would be suggested by pressure measurements because of poor LV compliance. Lusitropic drugs that relax the LV should be substituted for catecholamines that have strong β‐adrenergic inotropic and chronotropic properties. Dobutamine or milrinone may be beneficial in this regard and can support RV function as well.
Other considerations include use of low‐dose calcium channel blockers or β‐blockers to improve diastolic relaxation, although it is conceptually difficult to start these when the cardiac output is compromised. Aggressive diuresis to reduce interstitial edema while providing colloid (salt‐poor albumin) to maintain intravascular volume may also improve diastolic relaxation. If the patient can survive the first few days of low output syndrome without end‐organ dysfunction, a gradual improvement in cardiac output generally results.
Low cardiac output states from right ventricular dysfunction
The problem of a marginal cardiac output and blood pressure with preserved LV function may also be noted in patients with markedly impaired RV function. This may result from RV infarction and prior RV dysfunction from pulmonary hypertension (PH) of any cause, most commonly mitral valve disease. Intraoperative issues include surgical correction of severe TR with preexisting RV dysfunction, poor intraoperative protection of the RV, especially with RV hypertrophy in patients with PH, and use of multiple blood products. Inadequate pulmonary blood flow compromises oxygenation, and RV dilatation and distention can then cause septal shift, compromising LV filling.
RV function can be improved by moderate volume infusions, maintenance of a satisfactory systemic perfusion pressure, and measures to improve RV contractility and reduce RV afterload. These include normalizing arterial blood gases with correction of acidosis, use of appropriate inotropes (usually milrinone or dobutamine), and initiation of a pulmonary vasodilator (inhaled nitric oxide, epoprostenol [Flolan], iloprost or milrinone).89–91 If these steps are insufficient, consideration should be given to use of an RV assist device or extracorporeal membrane oxygenation (ECMO).
The management of RV dysfunction is discussed in more detail on pages 530–534.
III. Postoperative Considerations Following Commonly Performed Procedures92
On‐pump coronary artery bypass grafting (CABG)
Even with relatively normal preoperative LV function, most centers use a low‐dose inotrope to support myocardial function at the termination of bypass and for several hours in the ICU during the early phase of transient myocardial dysfunction. The initial first‐line drug is usually epinephrine or dobutamine. Epinephrine (1–2 μg/min) is the preferred inotrope and usually produces less tachycardia than the other drugs. If there is an inadequate response to one of these catecholamines, milrinone is of great benefit in improving cardiac output. It is a positive inotrope that produces systemic vasodilation that frequently requires the addition of norepinephrine to support systemic resistance. When hemodynamic performance remains very marginal, placement of an IABP should be considered. In contrast to the catecholamines, the IABP can reduce myocardial oxygen demand and improve coronary perfusion. Inotropic support beyond 6–12 hours may be necessary if the patient has sustained a perioperative infarction or has a severely “stunned” myocardium that exhibits a prolonged period of dysfunction in the absence of infarction. A persistent low output state despite optimal pharmacologic therapy and an IABP may require placement of an assist device.
While the patient is intubated, propofol is an effective vasodilator to mitigate hypertension, but the blood pressure tends to creep upwards as the level of sedation is weaned. At this point, if the patient is otherwise hemodynamically stable, it is advisable to start a vasodilator which reduces SVR, such as clevidipine or nitroprusside, rather than give additional sedation or narcotics to control hypertension, in order to minimize respiratory depression. IV NTG may be used, especially if there is evidence of ischemia, but it will lower preload and cardiac output. Short‐acting antihypertensives are preferable, because, as the patient warms, hypertension will start to resolve as peripheral vasoconstriction abates.
Although patients who are β‐blocked preoperatively frequently require pacing at the conclusion of bypass, tachycardia may be present in those who are not well β‐blocked, especially in young, anxious patients. Although the potential causes of a tachycardia always need to be assessed, the combination of hypertension and tachycardia with a supranormal cardiac output can be managed by β‐blockers (esmolol or intermittent doses of IV metoprolol). Patients with a hyperdynamic left ventricle may develop progressive tachycardia when vasodilators are used to control hypertension. This should be managed by allowing the blood pressure to drift up to 140 mm Hg systolic and then using a β‐blocker to control both the tachycardia and the hypertension.
Atrial and ventricular pacing wires should be placed in all patients undergoing CABG. If the patient has sinus bradycardia or a junctional rhythm, atrial pacing at 90 beats/min should be used to ensure optimal LV filling and improve the cardiac output. If there is normal AV conduction, it is always preferable to use atrial pacing rather than AV sequential pacing, since the latter involves pacing of the right atrium (RA) and right ventricle (RV), which will produce ventricular dyssynchrony. If second‐ or third‐degree heart block is present, pacing in the DVI or DDD mode is appropriate. In patients with moderate–severe LV dysfunction, biventricular pacing (RA–BiV) using an extra set of leads will provide a superior cardiac output to standard RA–RV pacing.93,94 If the patient has a slow ventricular response to atrial fibrillation (AF), VVI pacing should be initiated. Atrial pacing wires are probably not necessary in patients with long‐standing AF, but many of these patients will be in sinus rhythm at the conclusion of surgery and for a few days afterwards, and, if bradycardic, they might benefit from atrial pacing.
A common practice is to initiate antiarrhythmic therapy with lidocaine in the OR to suppress ventricular arrhythmias, although there is little documented evidence of benefit.95 It is given at the time of removal of the aortic cross‐clamp and then continued on a prophylactic basis until the following morning. Alternatively, prophylactic amiodarone may be used to reduce the incidence of postoperative AF, especially in elderly patients, and it can also provide benefits in controlling ventricular ectopy. A common approach is to give the initial load intravenously during surgery, although protocols of preoperative oral loading or a postoperative IV load may be just as effective in reducing the incidence of postoperative AF.96
Atrial fibrillation is noted in about 25% of patients following CABG. It may be related to poor atrial preservation during surgery or to withdrawal of β‐blockers. Most centers initiate a β‐blocker by the first postoperative morning (usually metoprolol 25–50 mg bid) because of the overwhelming evidence that β‐blockers reduce the incidence of AF.97 Magnesium sulfate has been shown in several studies to reduce the incidence of AF as well as the occurrence of ventricular arrhythmias.70,98 Administration of 2 g at the termination of CPB and on the first postoperative morning can be recommended. Amiodarone may be used alone or in addition to β‐blockers for AF prophylaxis, the latter being perhaps the best approach.97,99 A detailed discussion of the prevention and management of AF is presented on pages 620–632.
Close attention must be paid to the postoperative ECG. Evidence of ischemia may represent incomplete revascularization, poor myocardial protection, or impaired myocardial perfusion due to anastomotic stenosis, acute graft occlusion, or coronary spasm (Figure 8.2).100 Regardless of the etiology, IV NTG (starting at 0.25 μg/kg/min) is usually indicated. Calcium channel blockers (nifedipine 30 mg SL or diltiazem 0.25 mg/kg IV over two minutes, then 5–15 mg/h IV) are useful if coronary spasm is suspected. These medications may resolve ischemic changes or minimize infarct size if necrosis is already under way. Placement of an IABP should also be considered. If a problem with a bypass graft is suspected as the cause of the ischemia, emergency angiography followed by percutaneous coronary intervention or re‐exploration may be indicated.83–86 Coronary spasm can be so refractory as to cause cardiogenic shock that can only be treated by emergency ECMO.101
ST elevation noted in multiple ECG leads is often consistent with acute pericarditis, although computerized interpretation of these ECGs often indicates “acute infarction” (Figure 8.3
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