I. Basic Features of the Early Postoperative Period

1. Overview
   
   
   
   1. 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.
      
   2. 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.
      
   3. 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.
      
   4. 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.
      
   5. 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).
      
   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.
      
   7. 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.
   
   
2. Warming from hypothermia to 37 °C
   
   
   
   1. 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:
      
      
      
      1. Predispose to atrial and ventricular arrhythmias and lower the ventricular fibrillation threshold
         
      2. 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.
         
      3. Precipitate shivering, which increases peripheral O₂ consumption and CO₂ production
         
      4. Produce platelet dysfunction and a generalized impairment of the coagulation cascade
         
      5. Prolong the duration of action of anesthetic drugs and prolong the time to extubation⁹
         
      6. Increase the risk of wound infection, possibly related to immunosuppression
      
      
   2. 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.
      
   3. 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.
      
   4. 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
      
   5. 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.
      
   6. 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
      
   7. 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.
   
   
3. Control of mediastinal bleeding (see Chapter 9)
   
   
   
   1. 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
      
   2. 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
      
   3. 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.²² Generally, 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
      
   4. 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.
      
   5. 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.
      
   6. 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
   
   
4. Ventilatory support, emergence from anesthesia, weaning, and extubation (see Chapter 10)
   
   
   
   1. 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.
      
   2. 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
      
   3. 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
      
   4. Early extubation is feasible in most patients, conditional upon their mental status, gas exchange, and hemodynamic performance.
      
      
      
      1. 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.
         
      2. 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
         
      3. 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.
      
      
   5. 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}
      
      
      
      1. 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.
         
      2. 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.
   
   
5. Analgesia and sedation
   
   
   
   1. 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.
      
      
      
      1. 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.
         
      2. 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
         
      3. After extubation, adequate analgesia can be provided by a variety of medications and via different routes.
         
         
         
         1. 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.
            
         2. 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
            
         3. 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}
            
         4. 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.
            
         5. 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).
      
      
   2. Sedation
      
      
      
      1. 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.
         
      2. 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
   
   
6. Hemodynamic support during a period of transient myocardial depression (see Chapter 11)^1,6,62
   
   
   
   1. 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.
      
   2. 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%).
      
   3. 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
      
   4. 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.
      
   5. 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.
      
   6. 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.
      
   7. 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
   
   
7. Fluid administration to maintain filling pressures in the presence of a capillary leak and vasodilation (see Chapter 12)
   
   
   
   1. 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.
      
      
      
      1. Mediastinal bleeding or bleeding from leg incisions from vein harvesting.
         
      2. A capillary leak from the CPB‐induced systemic inflammatory response which contributes to interstitial edema.
         
      3. 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.
         
      4. Decreased ventricular compliance producing higher filling pressures at lower intravascular volumes.
         
      5. Impaired systolic function due to transient myocardial depression that requires increased preload to maintain stroke volume.
      
      
   2. 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.
   
   
8. Electrolytes and acid–base balance
   
   
   
   1. 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.
      
   2. Magnesium levels are usually lower due to hemodilution on CPB and should be replenished because of potential benefits in reducing postoperative arrhythmias.⁷⁰
      
   3. 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).
   
   
9. 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).