INTRODUCTION — Cardiopulmonary bypass (CPB) is a form of extracorporeal circulation in which the patient's blood is diverted from the heart and lungs and rerouted outside of the body. The normal physiologic functions of the heart and lungs, including circulation of blood, oxygenation, and ventilation, are temporarily taken over by the CPB machine. In most cases, the heart is also separated from the circulation via aortic cross-clamping, and cardioplegia solution is administered to protect the non-perfused myocardium. This allows the surgeon to operate on a nonbeating heart in a field largely devoid of blood, while other end organs remain adequately oxygenated and perfused.
This topic will discuss strategies for patients with conditions that affect management of CPB including presence of a previous sternotomy, aortic regurgitation, cerebrovascular disease, renal insufficiency, or certain hematologic conditions (eg, cold agglutinin disease, hemoglobinopathies such as sickle cell disease or thalassemia, inherited bleeding disorders, and factors limiting availability of blood products). Management of systemic anticoagulation for CPB in patients with heparin-induced thrombocytopenia is discussed in a separate topic (algorithm 1). (See "Management of heparin-induced thrombocytopenia (HIT) during cardiac or vascular surgery".)
Initiation and management of routine aspects of CPB are discussed in separate topics. (See "Initiation of cardiopulmonary bypass" and "Management of cardiopulmonary bypass".)
Some cardiac surgical procedures also require temporary interruption of cerebral and systemic blood flow (eg, repair of portions of the ascending aorta or aortic arch). Elective circulatory arrest is accomplished during a period of deep hypothermia after cooling with the aid of CPB. Anesthetic management of deep hypothermic circulatory arrest during CPB is discussed separately. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Cardiopulmonary bypass with deep hypothermic circulatory arrest'.)
PREVIOUS MEDIAN STERNOTOMY — An increasing number of patients who had a previous operation performed through a median sternotomy require a repeat or "redo," sternotomy for cardiac surgical access. Common examples include the need for additional revascularization (ie, redo coronary artery bypass grafting [CABG] surgery), re-replacement of a previously implanted bioprosthetic valve due to structural degeneration, and transplant or circulatory assist device placement for end-stage heart disease previously treated with cardiac surgery.
Anatomic distortion and scarring from the previous sternotomy and cardiac operations add risk of injury to the heart, great vessels, or internal mammary and aorto-coronary grafts during re-entry into the mediastinum. Although surgical approaches attempt to avoid vascular injury, the surgery, anesthesiology, and perfusion teams must be prepared to immediately manage the consequences if such injury occurs. Perioperative planning and decision-making involving these teams includes:
●Developing a preoperative understanding of the individual patient's anatomy and risks for injury during sternal re-entry
●Preparing for and implementing intraoperative strategies to avoid or mitigate vascular or myocardial injury
●Readiness for immediate management of complications such as hemorrhage or myocardial ischemia during sternal re-entry, including emergency initiation of CPB
Preoperative considerations — Certain aspects in the patient's history and findings noted on the chest radiograph and computed tomography (CT) scans are critically important for preoperative planning.
●Patient history – Details regarding the previous cardiac surgical procedure that are important to note include:
•For patients with previous CABG, the coronary vessels that were previously bypassed, particularly the anatomic location of patent grafts vulnerable to injury during sternal re-entry.
•For patients with a thoracic aortic graft or those who developed an aortic pseudoaneurysm, close proximity or adherence of any portion of the aorta and/or graft to the posterior surface of the sternum increases risk for rupture and exsanguination during sternal re-entry.
•For patients with previous open ablation for atrial fibrillation (eg, Maze procedure), difficulties with access via a mediastinal approach to the right atrium (RA), superior vena cava (SVC), or inferior vena cava (IVC) to accomplish venous cannulation should be anticipated.
●Chest radiograph and computed tomography scans – The relationship between the sternum and the ascending aorta, RA, or right ventricular (RV) free wall is noted on the preoperative chest radiograph lateral view. Scar adherence of these structures to the posterior table of the sternum may cause life-threatening hemorrhage if myocardial or vascular injury occurs during sternotomy. Many centers now obtain routine chest CT scans in patients undergoing redo sternotomy to assess specific anatomic risks for injury. CT angiography provides an even more detailed image of mediastinal cardiovascular anatomy and proximity of each structure to the back of the sternum. In addition, a CT scan provides important information regarding the location and patency of other vascular structures that may be considered to achieve vascular access (eg, internal jugular veins, innominate vein, or femoral veins). (See "Preoperative evaluation for anesthesia for cardiac surgery", section on 'Chest radiograph and computed tomography imaging'.)
The patency of coronary arterial grafts and their anatomic course within the mediastinum is assessed with preoperative coronary angiography. Notably, a patent left internal mammary to left anterior descending artery graft may be vulnerable to injury as it passes underneath the sternum.
●Planning the surgical procedure – In some cases, an alternative procedure that does not involve redo sternotomy may be considered. Examples include a minimally invasive CABG or valve procedure accomplished via thoracotomy incision(s), or a percutaneous approach for transcatheter cardiac valve replacement or repair. (See "Off-pump and minimally invasive direct coronary artery bypass graft surgery: Clinical use" and "Anesthesia for percutaneous cardiac valve interventions" and "Minimally invasive aortic and mitral valve surgery".)
However, repeat sternotomy is necessary for many cardiac surgical operations that cannot be accomplished via alternative techniques.
Intraoperative strategies — During preparations for sternotomy and initiation of CPB, strategies are employed by the anesthesiology, surgery, and perfusion teams to avoid or mitigate the potential for bleeding or myocardial ischemia due to injury or compression of the heart, great vessels, or coronary grafts.
●Anesthetic management strategies include:
•Applying transcutaneous defibrillator pads before surgical prepping and draping, and ensuring immediate availability (in the operating room) of an external defibrillator with pacing capability. Since it may not be possible for the surgeon to gain immediate direct access to the heart during redo sternotomy, these external defibrillator pads permit rapid treatment of ventricular tachycardia, ventricular fibrillation, or other hemodynamically unstable arrhythmias.
•Establishing intravascular (IV) access sufficient to treat rapid blood loss. When possible, IV access is on the patient's right side because injury to the left brachiocephalic vein during sternal re-entry will disrupt continuity of left-sided IV catheters to the central vasculature. Either left or right femoral venous access are valuable if such injury occurs.
•Ensuring immediate availability (in the operating room) of prechecked red blood cells (RBC) units, typically four units.
•Preparing vasopressor agents to treat hypotension and maintain hemodynamic stability until IV volume can be restored during massive hemorrhage. Inotropic agents are also prepared in case treatment of right or left ventricular failure becomes necessary.
•Preparing a precalculated IV heparin dose appropriate for the individual patient in case emergency initiation of CPB is necessary.
•Planning use of intraoperative transesophageal echocardiography (TEE) to:
-Detect distention of the RV. Risk of injury to the RV or venous structures during sternal re-entry is increased when the RV (or RA) is distended, or if central venous pressure (CVP) is elevated.
-Detect RV or left ventricular (LV) dysfunction as a consequence of myocardial ischemia, which can occur if previous coronary arterial grafts are injured during sternal sawing or compressed during surgical dissection to gain exposure to the heart and great vessels. Early detection of ischemia may prevent irreversible injury to coronary grafts and/or myocardium.
-Assist with placement of guidewires and cannulae during percutaneous arterial and venous cannulation if these are inserted before sternotomy for initiation of CPB, or to treat hemorrhage or myocardial ischemia.
-Visualize the presence of the guidewire in the lumen of the descending thoracic aorta during percutaneous aortic cannulation (with verification that the wire is in the true lumen in patients with aortic dissection).
-Direct the guidewire from the femoral vein through the intrahepatic IVC into the RA and then into the SVC during percutaneous femoral venous cannulation, while ensuring that placement in the atrial appendage or a patent foramen ovale is avoided. The venous catheter that will be used during CPB is then imaged as it enters the RA through the IVC , and its tip is positioned near the superior caval-atrial junction.
●Surgical management strategies include:
•Using a sagittal oscillating saw for sternotomy, which allows the anterior and posterior tables of the sternum to be opened sequentially. This allows more control compared with use of a traditional saw, thereby reducing risk of injury to underlying vascular structures.
•Using alternative approach to cannulation for CPB such as percutaneous cannulation of a peripheral artery (eg, femoral or right axillary artery) and percutaneous cannulation of a femoral vein. The right femoral vein is typically accessed because it provides the most direct and straight route to the RA. This approach allows immediate initiation of CPB in case injury to the RA, RV, aorta, a previous coronary graft, or other vascular or myocardial structure occurs during sternotomy [1]. In patients with extreme risk for hemorrhage or myocardial injury, percutaneous cannulation, initiation of CPB, and patient cooling may be accomplished before attempting to enter the sternum. This strategy allows for chamber decompression to decrease risk of RV injury during sternal re-entry.
In some cases, small bore catheters may be selected to establish femoral arterial and venous access before the surgical incision. Exchange over guidewires for larger bore cannulation allows access for initiation of CPB. The right femoral vein is typically selected for this technique since it provides a more direct path to the RA for a long venous cannulae, together with the left femoral artery.
If the surgical procedure involves the aortic arch, then arterial cannulation of the right axillary artery (or via a graft anastomosed to this artery) is typically selected. This site also allows selective antegrade cerebral perfusion when deep hypothermia and elective circulatory arrest are necessary to repair myocardial injury. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Deep hypothermia with selective antegrade cerebral perfusion'.)
•Deliberate cooling with deep hypothermia and elective circulatory arrest to allow repair of an RV injury. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Cooling and deep hypothermia'.)
●Perfusion management strategies include:
•Priming the CPB circuit prior to skin incision.
•Preparing a precalculated IV heparin dose for direct administration into the CPB circuit upon emergency initiation of CPB (in addition to the systemic dose administered by the anesthesiologist).
•Ensuring immediate availability of arterial and venous cannulae for percutaneous cannulation to initiate CPB.
•Ensuring immediate availability of RBCs to prime the CPB circuit in the event of massive hemorrhage.
•Preparing the CPB heater cooler unit in case immediate cooling or deep deliberate hypothermia becomes necessary.
•Preparing apparatus for salvaging shed blood.
Management of myocardial or vascular injury — Despite meticulous planning and preparation, injury to the RA, RV, a patent coronary graft, or entry into the aorta with uncontrolled hemorrhage occasionally occurs during redo sternotomy.
●Crystalloid is added into the venous reservoir of the CPB circuit as well as RBCs and fresh frozen plasma if hemorrhage is significant or ongoing. Transfusion through the venous or arterial cannula can be accomplished as soon as either or both cannulae have been inserted.
●If bleeding cannot be immediately controlled or if myocardial injury and ischemia are severe, a typical dose of IV heparin (300 to 400 units/kg) is administered to achieve systemic anticoagulation and additional heparin (usually 20,000 units to account for extravasation of some of the systemic dose) is administered into the CPB circuit, arterial and venous cannulae are inserted, and CPB is initiated as rapidly as possible. The cardiotomy suction can often collect sufficient shed blood from the mediastinum into the venous reservoir of the CPB circuit to allow maintenance of adequate bypass flow as insertion of the cannulae is completed (termed "sucker bypass").
Alternatively, shed blood collected into the reservoir via the cardiotomy sucker can be processed via the cell saver device then reinfused.
●Once CPB is initiated, if bleeding is ongoing and/or if the heart cannot be easily repaired, an option is to cool the patient to a deep hypothermic temperature (eg, 18°C) and establish elective circulatory arrest. Management of deep hypothermia, subsequent rewarming strategies (which extend the duration of CPB), and consequences of using this technique are described separately. (See "Anesthesia for aortic surgery requiring deep hypothermia".)
AORTIC REGURGITATION — The presence and severity of aortic regurgitation (AR) is typically documented in the preoperative workup, and confirmed by intraoperative transesophageal echocardiography (TEE) examination during the prebypass period (movie 1 and image 1 and image 2 and image 3). (See "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults", section on 'Diagnosis and evaluation' and "Acute aortic regurgitation in adults", section on 'Diagnosis'.)
Problems before and during CPB
Left ventricular distention — Rapid and severe left ventricular (LV) distention can lead to impairment of myocardial perfusion and consequent LV injury in addition to severe mitral regurgitation with severe, hydrostatic pulmonary edema. LV distention may occur before or after initiation of CPB and systemic cooling. Ventricular fibrillation will result in rapid LV distention because the LV is no longer ejecting the regurgitant volume.
Strategies to manage LV distention before CPB and after initiation of CPB until the aortic cross-clamp can be applied include:
●If ventricular fibrillation occurs, defibrillate immediately using internal paddles applied directly to the heart to deliver 10 to 20 joules of electricity. However, successful defibrillation is more likely to be successful defibrillation if the heart is empty (nondistended).
●If ventricular distention is noted after CPB has been initiated, shut off or temporarily reduce CPB flow rate to allow the surgeon to decompress the LV by manually emptying the LV by hand, and then defibrillate the heart before resuming CPB flow. Subsequently, arterial flow is carefully adjusted to avoid acute increases in aortic pressure while providing adequate systemic perfusion with sufficient venous drainage. Hypotension is treated primarily by increasing CPB flow rather than be administering vasopressors. If a vasopressor is necessary to increase mean arterial pressure, small incremental doses) to avoid acute increases in aortic pressure (ie, hypertension).
●If ventricular arrhythmias are noted (but not ventricular fibrillation), administer intravenous (IV) lidocaine and minimize surgical instrumentation and irritation of the heart until after administration of the aortic cross-clamp.
●If severe bradycardia is noted, then rapidly establish CPB.
●If a slow heart rate develops during cooling, use epicardial pacing to maintain heart rate (ie, preserve the number of LV ejections per minute).
●If ventricular distention occurs despite these measures to control heart rhythm and rate, insert an LV vent to decompress the LV. In patients with severe AR, some surgeons elect to decompress the LV chamber by inserting a vent via the right upper pulmonary vein before cooling begins. (See "Initiation of cardiopulmonary bypass", section on 'Left ventricular vent placement'.)
Detecting and guiding treatment of LV distention includes:
●TEE monitoring to:
•Detect LV distention using serial assessments of LV size, typically obtained using the transgastric short-axis view. Notably, in patients with baseline dilated cardiomyopathy, qualitative assessments to distinguish further LV dilation may be challenging.
•Note incomplete LV ejection during systole, and retrograde filling of the LV from the aorta during diastole.
•Note distention of the mitral annulus with mitral regurgitation occurring in both systole and diastole, an indication of severe LV dilation.
•Verify position of the LV vent after placement into the right upper pulmonary vein, across the mitral valve, and within the LV cavity but not against the LV apex (figure 1). If the vent tip is too close to the LV apex, a ventricular contraction could cause the LV vent cannula to rupture through the LV wall.
•Frequently assess the LV for distention since the LV vent cannula can become dislodged, obstructed, or unable to completely decompress the LV.
●Pulmonary artery catheter (PAC) monitoring to note increases in pulmonary artery pressure (PAP) as the LV dilates. A mean PAP ≥20 mmHg indicates LV distention. In some institutions, the same pressure transducer that is used to measure PAP is also used to monitor coronary sinus pressure during CPB. To ensure that increasing PAP is detected, the anesthesiologist can intermittently toggle the three-way stopcock on the pressure transducer between the PAP and coronary sinus pressure (image 4).
Provision of adequate cardioplegia
●Antegrade cardioplegia – Antegrade cardioplegic is typically administered into the aortic root after application of the ascending aortic cross-clamp (figure 1). However, if significant AR is present, the cardioplegia solution regurgitates retrograde into the LV cavity via the incompetent aortic valve rather than entering the coronary arteries. Typically, initial cardiac standstill may be achieved using brief antegrade cardioplegic solution delivery, then alternative strategies to effectively achieve cardioplegia delivery, provide adequate myocardial protection, and avoid LV distention are necessary, as described below. (See "Initiation of cardiopulmonary bypass", section on 'Aortic cross-clamping and antegrade cardioplegia administration'.)
●Retrograde cardioplegia – After brief initial administration of antegrade cardioplegia, intermittent low pressure retrograde cardioplegia is typically delivered. A balloon-tipped retrograde cardioplegia cannula is inserted through the wall of the right atrium with its tip positioned just within the opening of the coronary sinus. The final position of the retrograde cannula is confirmed with TEE using the midesophageal (ME) 4-chamber view, with the TEE probe retroflexed until the coronary sinus comes into view. Alternatively, the TEE ME bicaval view can be used (obtained with slight probe rotation until the coronary sinus comes into view).
Coronary sinus pressure must be monitored and maintained <40 mmHg during delivery of retrograde cardioplegia to avoid myocardial edema. It is important that the coronary sinus catheter not be inserted too far into the coronary sinus, so that venous branches from the right ventricle are not occluded by the catheter balloon and are adequately perfused with cardioplegia. (See "Initiation of cardiopulmonary bypass", section on 'Retrograde cardioplegia administration'.)
●Direct infusion of cardioplegia into left and right coronary ostia – An additional option often used to supplement antegrade and regrade cardioplegia is direct delivery of cardioplegia solution into the left and right coronary ostia openings in the ascending aorta or aortic root.
Problems during weaning from CPB — Patients with clinically significant chronic AR (mild-to-moderate or ≥2+ severity) often have preexisting eccentric LV hypertrophy and reduced systolic function. Thus, inotropic agents are often necessary during weaning from CPB and the early postoperative period. Patients with acute AR who had no time to adapt to the sudden increase in LV volume may suffer rapid and severe LV distention with consequent LV injury. Such patients are even more likely to require inotropic support during weaning from CPB than those with chronic AR. (See "Weaning from cardiopulmonary bypass" and "Intraoperative problems after cardiopulmonary bypass", section on 'Left ventricular systolic dysfunction'.)
CEREBROVASCULAR DISEASE — Cerebrovascular disease is common in patients undergoing cardiac surgery, and is a risk factor for stroke following coronary artery bypass grafting (CABG) surgery [2]. Preoperative medical management and surgical treatment options for patients with severe cerebrovascular disease who require CABG surgery are discussed in a separate topic. (See "Coronary artery bypass grafting in patients with cerebrovascular disease".)
Traditional methods that identify large vessel cerebrovascular disease (eg, carotid Doppler) may not identify patients at highest risk for suffering stroke or other neurologic complications during cardiac surgery with CPB. Using preoperative magnetic resonance imaging, one study noted large cerebral vessel disease in 25 percent of 346 patients scheduled for cardiac surgery, but small vessel disease was found in 35 percent [3]. Another study noted that cerebral autoregulation was impaired in patients with cerebral small vessel disease during CPB, but not in those with large vessel disease [3].
Since cerebrovascular disease is frequently associated with aortic atherosclerosis [4,5], transesophageal echocardiography (TEE) or epiaortic ultrasound imaging is often used to guide selection of sites for aortic cannulation, cardioplegia administration, aortic cross-clamping, or placement of the "side-biter," clamp to complete proximal anastomoses during CABG (image 5). Avoiding surgical manipulation of aortic areas with known calcification or atherosclerotic plaque may reduce risk for cerebral embolism and postoperative stroke. (See "Anesthesia for cardiac surgery: General principles", section on 'Prebypass transesophageal echocardiography'.)
We carefully avoid hyperthermia (body temperature >37°C) during and after CPB since hyperthermia may increase the risk or worsen the severity of brain injury sustained as a consequence of hypoperfusion or cerebral embolism in a patient with known cerebrovascular disease [6-8]. (See "Management of cardiopulmonary bypass", section on 'Temperature'.)
Management of other aspects of CPB including oxygenation, ventilation, pump flow, mixed venous oxygen saturation, maintenance of anticoagulation, anesthesia, and hemoglobin as well as control of blood glucose and electrolytes, does not differ from management for other patients undergoing cardiac surgical procedures. Although mean arterial pressure (MAP) is generally targeted between 50 and 80 mmHg (or ≥65 mmHg) (table 1), a slightly higher MAP is often maintained in patients with known cerebrovascular disease [9-13]. However, data regarding the optimal target for MAP during CPB are inconsistent, probably due to interindividual differences in cerebral autoregulation among patients with or without known cerebrovascular disease [14]. (See "Management of cardiopulmonary bypass".)
Several pharmacologic agents have been studied (eg, antiinflammatory drugs, barbiturates, propofol, lidocaine). However, no definitive evidence supports the efficacy of any of these to mitigate neurologic risk as a consequence of cardiac surgery [15,16].
RENAL INSUFFICIENCY OR FAILURE
Dialysis-dependent end-stage renal disease — Patients with dialysis-dependent end-stage renal disease typically undergo routine scheduled dialysis the day prior to elective scheduled cardiac surgery. For emergency surgery, or if additional fluid removal is needed, continuous ultrafiltration (CUF) with hemoconcentration can be accomplished during CPB. Zero-balance ultrafiltration can be used when toxin or drug removal is necessary [17-23].
Pre-existing renal insufficiency — Factors associated with increased risk for exacerbation of chronic renal insufficiency during cardiac surgery with CPB include [24]:
●Patient-associated risk factors – Obesity, advanced age, African American race, male sex, preexisting hypertension, active congestive heart failure, chronic kidney disease, pulmonary disease, insulin-dependent diabetes mellitus, and peripheral vascular disease.
●Surgery-associated factors – Prolonged aortic cross-clamp duration, generation of micro- and macroemboli, prolonged hypotension, low pump flow with inadequate oxygen delivery to the kidneys, and/or inflammatory or oxidative insult during CPB.
General considerations to avoid or minimize worsening renal function or other complications in patients with pre-existing renal insufficiency include the following:
●Reduce doses of tranexamic acid – We select epsilon-aminocaproic acid for antifibrinolytic prophylaxis during CPB, or we administer lower doses when tranexamic acid is used due to increased seizure risk associated with use tranexamic acid in patients with moderate to severe renal insufficiency [25]. (See "Blood management and anticoagulation for cardiopulmonary bypass", section on 'Antifibrinolytic administration'.)
●Maintain oxygen delivery with adequate pump flow – Although pump flow rates between 2.2 and 2.4 L/minute/m2 are adequate for most patients during CPB (table 1), some evidence suggests that renal perfusion is optimal for some patients at higher flow rates [26-31]. We monitor oxygen delivery to determine adequacy of CPB perfusion. In a randomized trial in 300 patients, the incidence of acute kidney injury (AKI) was lower with use of pump flows that maintained estimated oxygen delivery at a high threshold index (DO2i) >300 mL/minute/m2 (relative risk [RR] 0.48, 95% CI 0.30-0.77) compared with conventional pump flow rates [32]. DO2i estimates are estimates of real-time indexed oxygen delivery calculated using actual pump flow, hematocrit, and oxygen saturation. Retrospective studies have noted that risk of AKI increased in a stepwise fashion with increasing cumulative degree/duration of reduced oxygen delivery <300 mL/minute/m2 [33]. Similarly, increased risk for AKI has been noted with exposure to DO2i flow rates <270 mL/minute/m2 lasting ≥30 minutes [34].
●Avoid nephrotoxic fluids and drugs [35]:
•We avoid administration of hydroxyethyl starch solutions, which have been associated with AKI [24,36-38]. Also, risk of bleeding may be increased when hydroxyethyl starch is used in pump prime and/or intraoperative fluid therapy, compared with use of balanced salt solutions [38-40]. However, we do not consistently avoid administration of albumin-containing colloid, which may mitigate risk of hypoalbuminemia in this setting, which has been identified as a risk factor for AKI [41].
•We avoid administration of large volumes of normal saline, which may cause hyperchloremia that has been associated with increased mortality and risk of renal dysfunction after noncardiac surgery [24,42,43]. However, we do not avoid use of balanced salt solution such as lactated Ringer's, Normosol-R, or Plasma-Lyte A in the pump prime in patients with renal insufficiency (or end-stage renal disease) since the amount of potassium in these balanced salt solutions is unlikely to contribute to hyperkalemia.
•We avoid or minimize administration of potentially nephrotoxic pharmacologic agents. Examples include major classes of drugs that can contribute or worsen AKI such as aminoglycoside antibiotics, angiotensin-converting enzyme (ACE) inhibitors, and nonsteroidal antiinflammatory agents. Furthermore, we appropriately adjust dosing and timing for administration of drugs eliminated by the kidneys (eg, vancomycin, cephalosporins, tacrolimus, cyclosporin, gabapentin) when administration is necessary in patients with renal insufficiency.
●Avoid hyperthermia – We carefully avoid hyperthermia (body temperature >37°C) during and after CPB to avoid exacerbation of end-organ injury of the kidney and other vital organs [44-46]. In a multicenter study with 8407 patients, rewarming temperature greater than 37°C (hyperthermic perfusion) was associated with AKI (odds ratio [OR] 1.52; 95% CI, 1.09-1.97) [46]. (See "Management of cardiopulmonary bypass", section on 'Temperature'.)
Some centers use hemofiltration strategies to manage fluid overload in patients with renal insufficiency. In support of CUF, a 2006 meta-analysis noted reduction in transfusion [47], and subsequently published small randomized studies indicate the CUF effectively increases hematocrit [47-50]. However, routine use of CUF during CPB to avoid or treat anemia is controversial and has been associated with AKI after cardiac surgery particularly when higher CUF volumes (>35 mL/kg) are used [51,52].
Management of other aspects of CPB does not differ from management for other patients undergoing cardiac surgical procedures (eg, maintenance of oxygenation, ventilation, pump flow, mixed venous oxygen saturation, anticoagulation, control of blood glucose and electrolytes, and management of anemia and transfusion therapy). Notably, anemia with hemoglobin ≤7.5 g/dL (or hematocrit ≤22 percent) has been associated with AKI after cardiac surgery [24,53-59], but transfusion of red blood cells (RBCs) to avoid or treat anemia has also been associated with AKI [56,59,60]. (See "Management of cardiopulmonary bypass".)
Although several technical interventions (eg, miniaturized circuits) and pharmacologic agents (eg, steroids, statins, cyclosporine) that may reduce inflammation or ischemia-reperfusion injury have been studied, none were noted to be effective in reducing incidence or severity of postoperative AKI [13,36,61-65]. However, leukocyte filtration during transfusion of RBCs, as is standard practice in the United States and Europe, was shown to reduce the incidence of worsening postoperative renal function from 7.5 to 1.1 percent in a 2014 meta-analysis (OR 0.18, 95% CI 0.05-0.64; six trials; 374 cardiac surgical participants) [61]. (See "Intraoperative transfusion of blood products in adults", section on 'Filters'.)
HEMATOLOGIC CONCERNS
Cold agglutinin disease — Cold agglutinin disease is a form of autoimmune hemolytic anemia in which autoantibodies cause agglutination of red blood cells (RBCs) at cooler temperatures, causing clinical symptoms related to agglutination as well as hemolytic anemia. Individuals with circulating cold agglutinins often do not develop overt symptomatic disease and may be unaware of the presence of autoantibodies unless or until they are exposed to cold temperatures that enhance their binding to RBCs in settings such as CPB [66]. Cases of catastrophic hemolysis and organ failure have been described during cardiac surgery with hypothermic CPB [67]. (See "Cold agglutinin disease".)
●Preoperative diagnosis and optimization – Although cold agglutinin disease is present in 0.3 to 4 percent of cardiac surgical patients, routine preoperative screening is uncommon and not recommended [66,68]. Rather, clumping of RBCs due to cold agglutination is typically discovered in the laboratory, blood bank, or occasionally in the operating room [69]. Once the diagnosis is known or suspected, the management plan for CPB can be altered based on severity of agglutination and the thermal amplitude of the autoantibody (ie, the temperature below which the cold-reactive autoantibody binds to its antigen). In such cases, optimal management is determined after consultation with a hematologist or blood banking expert. However, in some cases, cold agglutinin disease is only suspected when agglutination is noticed during blood priming of the cardioplegia heat exchanger, or in the surgical field after cooling and application of the aortic cross-clamp.
In conjunction with careful planning to minimize cold exposure during surgery, additional preoperative strategies to reduce the autoantibody titer are used in selected patients with known cold agglutinin disease [70]. These include administration of glucocorticoids, rituximab, cyclophosphamide, chlorambucil, intravenous immunoglobulin (IVIG), or plasma exchange before CPB to reduce cold agglutinin antibody titers. Plasma exchange is particularly useful for patients with active hemolysis or high thermal amplitude, or for procedures that require deep hypothermia [70-73]. Plasma exchange and RBC transfusion may be indicated in patients with severe cold agglutinin disease if hemolysis is sufficient to cause anemia. Although antibody titers are ideally reduced below 1:64 prior to cardiac surgery, more complex pharmacological measures (such as IVIG or rituximab) or plasma exchange should rarely be needed. (See "Cold agglutinin disease", section on 'Plasmapheresis or IVIG as a temporizing measure' and "Cold agglutinin disease", section on 'Transfusions' and "Cold agglutinin disease", section on 'Therapies directed at the pathogenic process'.)
●Intraoperative management – If the diagnosis is known preoperatively, the patient's systemic blood temperature can be kept above the patient's thermal amplitude. Blood temperature is controlled during CPB using the heat exchanger, and all intravenous (IV) fluids are administered through a warmer, particularly those kept at cold storage temperatures (eg, packed RBCs from the blood bank). During periods before and after CPB, a whole-body patient warming device may be employed to minimize cold peripheries. If the thermal amplitude of the cold agglutinins is near body temperature, the heat exchanger should be used to maintain body temperature above the thermal amplitude during CPB. If cold agglutination is first discovered during CPB, the patient is immediately rewarmed and maintained at 36 to 37°C during and after CPB.
Furthermore, cardioplegia delivery is modified so that either continuous warm blood cardioplegia, or only intermittent cold crystalloid cardioplegia is administered, rather than cold (2 to 4°C) blood cardioplegia [74]. We typically keep the blood or crystalloid cardioplegia induction dose at a temperature above the thermal amplitude, or we flush the coronary arteries with warm crystalloid before switching to cold crystalloid cardioplegia. If necessary before cross-clamp removal (depending on the myocardial temperature), we also rewarm the myocardium with crystalloid [69,75-77]. Notably, if the thermal amplitude is higher than room temperature, then extracorporeal whole blood cannot be kept stagnant at room temperature during or after CPB.
If hypothermia during CPB is necessary to complete the planned cardiac surgical procedure such as ascending aortic surgery accomplished with deep hypothermia and elective circulatory arrest (see "Anesthesia for aortic surgery requiring deep hypothermia"), then surgery is usually postponed to allow time for detailed blood analysis (including screening for high fibrinogen and/or high white blood cell count), treatment of possible causes of agglutination, and careful planning for surgery [78]. For example, cold agglutination may be occurring due to an infectious process that can be treated or await its resolution (eg, Mycoplasma pneumoniae [primary atypical pneumonia] or Epstein-Barr virus [infectious mononucleosis]).
We use cell saver technology in these patients, although there are no data to guide such use patients with cold agglutinins. Theoretical concerns depend on the thermal amplitude for cold agglutination compared to room temperature. However, washing away plasma proteins and antibodies and use of the 40 micrometer filter should prevent reinfusion of aggregates. Furthermore, use of a blood warmer during reinfusion further mitigates any risk.
Hemoglobinopathies
Sickle cell disease and sickle cell trait — Sickle cell disease or trait is an autosomal recessive genetic hemoglobinopathy caused by the hemoglobin S variant (HbS or sickle hemoglobin). Sickled RBCs are prothrombotic and more prone to adhere to vascular endothelium, promoting sludging in the capillaries. The higher the percentage of HbS cells that sickle and the higher the percentage of all RBCs containing HbS, the greater the risk of hemolysis and/or vaso-occlusive crises [79]. (See "Overview of the management and prognosis of sickle cell disease".)
Whether the patient has overt sickle cell disease (genotypes HbSS, HbSC or HbSb0), or is an asymptomatic heterozygous carrier with sickle cell trait (HbAS), the goal during CPB (and throughout the perioperative period) is to avoid sickling RBCs with consequent hypercoagulability and risk of vaso-occlusion. We avoid dehydration, anemia, hypotension, and conditions that promote the deoxygenated state for HbS (eg, acidosis, low cardiac output, increased oxygen consumption due to hyperthermia, fever, shivering), which increase the likelihood of RBC sickling. (See "Pathophysiology of sickle cell disease".)
Management strategies for patients undergoing cardiac surgery with CPB include:
●Preoperative optimization – Multidisciplinary teams including hematology, anesthesiology, surgical, and perfusion team members consider disease severity, medications, baseline hemoglobin, transfusion history, prior surgical complications, and the planned procedure. A few centers test all preoperative patients with African ancestry for presence of any HbS trait or disease (qualitative Sickledex test), although presence of HbS is not limited to patients with African heritage. More complex hemoglobin electrophoresis (ie, complete phenotyping) is reserved for patients who test positive. (See "Diagnosis of sickle cell disorders", section on 'Laboratory methods'.)
During preparation for surgery, blood transfusions are employed if necessary to treat symptomatic anemia and/or multiorgan failure. Notably, allosensitization due to previous transfusions may cause difficulty with crossmatching blood. (See "Red blood cell transfusion in sickle cell disease: Indications and transfusion techniques" and "Transfusion in individuals with complex serologies on pretransfusion testing", section on 'Sickle cell disease'.)
For sickle cell anemia patients with circulating HbS >30 percent, we perform preoperative exchange transfusion to reduce the circulating HbS fraction, thereby promoting adequate perfusion and decreasing risk of intraoperative or postoperative vaso-occlusive crisis with organ failure [80-84]. Erythrocytapheresis is the preferred targeted method to electively remove HbS containing red cells, replacing them with normal HbA containing cells. (See "Red blood cell transfusion in sickle cell disease: Indications and transfusion techniques", section on 'Simple versus exchange transfusion'.)
●Intraoperative management – It is particularly important to achieve adequate hydration throughout the perioperative period, as discussed in detail separately. (See "Overview of the management and prognosis of sickle cell disease", section on 'Hydration'.)
For urgent procedures, if exchange transfusion was not possible in the preoperative period, and especially if HbS is >30 percent, the perfusionist can perform an effective exchange transfusion during initiation of CPB after discussion with the team. This is accomplished by supplementing the patient's blood volume with a mixture of packed RBCs, fresh frozen plasma, albumin, and crystalloid solution (typically Plasmalyte). An intraoperative alternative is to perform exchange transfusion using a disposable autotransfusion device with plasma capture for reinfusion [85].
During CPB, the perfusionist controls patient temperature, cardiac output (pump flow rate), and oxygenation. To maximize tissue oxygen delivery and minimize sludging during CPB, we suggest:
•Using a centrifugal CPB pump, rather than a roller pump, to decrease damage to red blood cells.
•Maintaining mean arterial pressure (MAP) >60 mmHg, by adjusting flow rate and attempting to minimize use of vasopressor support
•Maintaining higher than normal flow (ie, cardiac index ≥2.4 L/minute/m2). If necessary, vasodilators may be administered to avoid hypertension from increased flow rates.
•Maintaining higher than normal arterial oxygen tension (PaO2) sufficient to target a higher mixed venous oxygen saturation (SvO2 >80 percent), with continuous arterial and venous blood gas monitoring.
•Administering sodium bicarbonate as necessary to keep the pH at 7.40 to 7.45 (ie, prevent acidosis).
•Avoiding systemic hypothermia is reasonable, although this is controversial [86].
•Using cold crystalloid cardioplegia exclusively, or use this first before switching to warm blood cardioplegia. Avoid cold blood cardioplegia which may cause sludging and blockages in the coronary arteries [81,87].
•Avoiding excessive hemoconcentration.
•Avoiding cell saver use since the washing process may induce hemolysis or sickling of RBCs that contain HbS in patients with sickle cell disease or trait. However, evidence regarding safety for use of these devices in patients with sickle cell disease or trait is scant [81,88-91]. (See "Surgical blood conservation: Blood salvage".)
•Avoiding administration of sodium nitroprusside as in all patients prone to hemolysis, since free hemoglobin in the plasma can catalyze release of cyanide from sodium nitroprusside [92].
Thalassemia — Thalassemia is another autosomal recessive genetic hemoglobinopathy. Symptoms result from hemolysis of abnormal variant RBCs and the resultant anemia, iron overload, splenomegaly, and marrow hypertrophy [93]. Hypercoagulability may also be a concern. Severity of thalassemia is determined by the number of genes affected by mutations of the alpha and beta globin chains. The alpha thalassemia trait usually results in only mild anemia. Hemoglobin H disease is a form of alpha thalassemia in which moderately severe anemia develops due to reduced formation of alpha globin chains. With beta thalassemia, mutant alleles with a heterozygous or homozygous state determine the severity of disease: thalassemia minor (beta/beta+ or beta/beta0) is mostly asymptomatic; intermediate disease occurs with the beta+/beta+ or beta+/beta0 genotype; and severe disease occurs in patients with the beta0/beta0 genotype as they have no normal adult hemoglobin (HbA). (See "Pathophysiology of thalassemia" and "Diagnosis of thalassemia (adults and children)".)
Management strategies for patients undergoing cardiac surgery with CPB include:
●Preoperative optimization – Amelioration of the effects of anemia and hypoxia in the preoperative period is often necessary [94]. (See "Management of thalassemia", section on 'Surgery/anesthesia concerns'.)
Allogeneic transfusion may be necessary for patients with severe anemia (either in the preoperative period or during CPB) to treat the anemia and reduce the percentage of abnormal hemoglobin in favor of normal HbA. However, as with sickle cell disease, allosensitization due to previous transfusions may cause difficulty with crossmatching blood. (See "Pretransfusion testing for red blood cell transfusion".)
Thalassemia patients are also evaluated for organ involvement and dysfunction due to iron overload, particularly the heart, kidneys, and liver. (See "Pathophysiology of thalassemia", section on 'Iron overload' and "Pathophysiology of thalassemia", section on 'Organ damage'.)
●Management during CPB – The function and resilience of the abnormal variant erythrocytes determine susceptibility to hemolysis during CPB [93,95]. Management strategies to minimize hemolysis include:
•Use a centrifugal CPB pump, rather than a roller pump, to decrease the tendency for hemolysis [96].
•Monitor for delayed hemolytic transfusion reaction. Alloimmunization in individuals receiving regular transfusions leads to formation of alloantibodies that react with donor RBCs causing delayed hemolytic transfusion reactions. (See "Hemolytic transfusion reactions".)
•Monitor for hemolysis, which may be detected either by observing hemoglobinuria or by tracking lactate dehydrogenase or free hemoglobin levels in plasma. Risk for postoperative renal injury depends on the degree that intraoperative intravascular hemolysis with release of free hemoglobin occurs, and whether haptoglobin scavenging is overwhelmed [97]. Supplementing haptoglobin with plasma transfusion is an option, although efficacy of this therapeutic approach is unknown, and use of haptoglobin concentrates is experimental [98,99].
Inherited bleeding disorders — The more common inherited coagulation disorders, such as von Willebrand disease, hemophilia A and B, factor XI (11) deficiency, and fibrinogen disorders, are discussed in detail in separate topic reviews:
●Hemophilia A and B – (See "Treatment of bleeding and perioperative management in hemophilia A and B".)
●Von Willebrand disease – (See "Clinical presentation and diagnosis of von Willebrand disease".)
●Factor XI deficiency – (See "Factor XI (eleven) deficiency".)
●Fibrinogen disorders – (See "Disorders of fibrinogen".)
●Plasminogen activator inhibitor deficiency – (See "Thrombotic and hemorrhagic disorders due to abnormal fibrinolysis", section on 'PAI-1 deficiency'.)
Several other inherited coagulation disorders are associated with clinical bleeding, including inherited deficiencies of factors XIII (13), XI (11), X (10), VII (7), V (5), and II (2, prothrombin), as well as some rare, combined factor deficiencies. These rare (or recessively inherited) coagulation disorders inherited coagulation disorders are discussed separately. As in patients with other clinically symptomatic hematologic disorders scheduled for cardiac surgery, preoperative consultation with a hematologist is recommended. (See "Rare inherited coagulation disorders".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Management of cardiopulmonary bypass".)
SUMMARY AND RECOMMENDATIONS
●Previous sternotomy – Anatomic pathology and scarring increase risk for injury to the heart or great vessels. Risk management includes (see 'Previous median sternotomy' above):
•Understanding the patient's anatomy and risks for injury
•Implementing strategies to avoid injury
•Readiness for immediate management of complications (hemorrhage, myocardial ischemia), including emergency initiation of cardiopulmonary bypass (CPB)
●Aortic regurgitation – Aortic regurgitation may cause left ventricular (LV) distention and/or limit effective delivery of antegrade cardioplegia during CPB. Continuous monitoring of transesophageal echocardiography (TEE) views and pulmonary artery pressure can detect LV distention. Surgical technical modifications may include insertion of a vent to decompress the LV, or delivery of cardioplegia via a retrograde approach into the coronary sinus, or directly into the coronary ostia. Inotropic support of the LV is typically necessary during weaning from CPB. (See 'Aortic regurgitation' above.)
●Cerebrovascular disease – Considerations for patients with known cerebrovascular disease include avoiding hyperthermia >37°C and considering use of epiaortic or transesophageal echocardiography to guide insertion of the aortic cannula since cerebrovascular disease is frequently associated with aortic atherosclerosis. (See 'Cerebrovascular disease' above.)
●Renal insufficiency – Considerations for patients with pre-existing renal insufficiency include (see 'Pre-existing renal insufficiency' above):
•Reduce doses of tranexamic acid because of increased risk for seizures
•We suggest maintaining oxygen delivery >300 mL/minute/m2 to ensure optimal renal perfusion (Grade 2C)
•Avoid nephrotoxic fluids and drugs
•Avoid hyperthermia >37°C
●Patients on dialysis – Patients typically undergo routine scheduled dialysis before elective cardiac surgery. For emergency surgery or if additional fluid removal is needed, hemoconcentration by continuous ultrafiltration (CUF) may be performed during CPB, or zero-balance ultrafiltration may be employed for removal of toxins or drugs. (See 'Dialysis-dependent end-stage renal disease' above.)
●Cold agglutinin disease – (See 'Cold agglutinin disease' above.)
•Preoperative optimization – To reduce cold agglutinin autoantibody titers in the preoperative period, strategies include use of glucocorticoids, rituximab, cyclophosphamide, chlorambucil, intravenous immunoglobulin (IVIG), or plasma exchange.
•Intraoperative management – If cold agglutination is discovered during CPB, the patient is rewarmed and maintained at 36 to 37°C. Cardioplegia delivery is modified so that either continuous warm blood cardioplegia, or only intermittent cold crystalloid cardioplegia is administered, rather than cold (2 to 4°C) blood cardioplegia. Intravenous (IV) fluids and blood products are warmed and a whole body warmer is used.
●Sickle cell disease or trait – (See 'Sickle cell disease and sickle cell trait' above.)
•Preoperative optimization – Adequate hydration is necessary to avoid hemolysis, sickling of red blood cells (RBCs), hypercoagulability, and vaso-occlusion. We suggest preoperative exchange transfusion to reduce the circulating HbS fraction in patients with circulating HbS >30 percent (Grade 2C). If necessary, the perfusionist can perform an exchange transfusion during initiation of CPB.
•We suggest the following intraoperative management strategies:
-Use a centrifugal CPB pump, rather than a roller pump, to decrease damage to RBCs (Grade 2C).
-Maintain higher than normal CPB flow (ie, cardiac index ≥2.4 L/minute/m2) (Grade 2C).
-Maintain mean arterial pressure (MAP) target >60 mmHg target using CPB flow rather high doses of vasopressor support (Grade 2C).
-Maintain higher than normal arterial oxygen tension sufficient to target a mixed venous oxygen saturation >80 percent (Grade 2C).
-Administer sodium bicarbonate as necessary to keep pH 7.40 to 7.45 (Grade 2C).
-Avoid systemic hypothermia (Grade 2C).
-Avoid cold blood cardioplegia (Grade 2C); use cold crystalloid cardioplegia exclusively, or before switching to warm blood cardioplegia.
-Avoid hemoconcentration (Grade 2C).
-Avoid cell saver use (Grade 2C).
-Avoid sodium nitroprusside; free hemoglobin in the plasma can catalyze release of cyanide from this agent (Grade 2C).
●Thalassemia
•Preoperative optimization may involve allogeneic transfusion.
•Intraoperative management strategies include (see 'Thalassemia' above):
-Use a centrifugal CPB pump to decrease risk of hemolysis (Grade 2C).
-Monitor for delayed hemolytic transfusion reaction. (See "Hemolytic transfusion reactions".)
-Monitor for hemolysis and for hemoglobinuria. If necessary, plasma transfusion may be used to supplement haptoglobin.
●Bleeding disorders – Management of inherited bleeding disorders is discussed in separate topics. (See 'Inherited bleeding disorders' above.)
