Cardiopulmonary bypass (CPB) is a form of extracorporeal circulation provided by a heart–lung machine that provides systemic perfusion of oxygenated blood during open‐heart surgery. It is utilized for “on‐pump” coronary bypass surgery and is required for all types of “surgical” valve and aortic procedures. Vascular access for the CPB circuit may vary, depending on the operative approach, but the technology and physiologic concepts remain virtually the same. Although there has been a significant trend toward “minimally invasive” approaches for many types of cardiac surgery, including transcatheter valve procedures, off‐pump bypass surgery, and endovascular procedures, CPB remains an essential element of cardiac surgical practice. Additional applications of CPB, such as extracorporeal membrane oxygenation (ECMO), have been invaluable in improving outcomes in patients with cardiogenic shock after surgery and other clinical situations requiring cardiac or respiratory support.
I. General Comments
CPB (the “pump”) involves an extracorporeal circuit that drains blood from the venous system and returns oxygenated blood to the systemic circulation when the heart and lungs are not functional. CPB is accompanied by normovolemic hemodilution and nonpulsatile flow.1
The contact of blood with the extracorporeal circuit generates a systemic inflammatory response that is related to a multitude of pathophysiologic factors. CPB results in the activation of numerous cascades, including the kallikrein, coagulation, and complement systems.2,3 These may cause thrombin generation, the release of proinflammatory cytokines, and a systemic inflammatory response. Endothelial‐based reactions, including platelet adhesion, aggregation, and activation, as well as leukocyte adhesion and activation, have been implicated in myocardial reperfusion damage, pulmonary and renal dysfunction, neurocognitive changes, and a generalized capillary leak.
Use of membrane oxygenators, biocompatible circuits and centrifugal pumps, adopting a restrictive transfusion threshold, avoiding cardiotomy suction, and equivocally use of leukocyte filters and steroids may reduce some of these inflammatory responses to CPB.4–9 Most patients will experience few adverse effects from the systemic inflammatory response, but those with long pump runs or with significant hemodynamic issues following surgery may experience significant tissue edema and organ system dysfunction that may persist for days.
II. The Cardiopulmonary Bypass Circuit
The extracorporeal circuit consists of polyvinylchloride tubing and polycarbonate connectors. Circuits with biocompatible coatings (most commonly the Medtronic Cortiva BioActive Surface and Trillium Biosurface polymer coating circuits) have been shown to improve biocompatibility, which reduces complement, leukocyte, and platelet activation, and lessens the release of proinflammatory mediators.8,9 Although biocompatible circuits may reduce bleeding, atrial fibrillation, tissue edema, and the degree of pulmonary dysfunction, other clinical benefits of their anti‐inflammatory properties are modest. Studies have not shown that these circuits decrease thrombin generation, which is a marker of coagulation system activation and a trigger of endothelial cell dysfunction.
The bypass circuit is a potent activator of the coagulation system with generation of factor Xa and thrombin, which may contribute to a systemic inflammatory response and ischemia/reperfusion injury.10 Anticoagulation, generally with heparin, is essential during CPB to minimize activation of the coagulation system, thrombus formation, and fibrinolysis.11 Use of heparin‐coated circuits allows for the safe use of lower doses of heparin, which might be associated with less bleeding.12,13 A number of factors associated with the use of CPB, including hemodilution of clotting factors and platelets, platelet dysfunction, and fibrinolysis, may contribute to a coagulopathy.
The pump is primed with a balanced electrolyte solution, such as Lactated Ringer’s, Normosol, or Plasmalyte, although normal saline may be used in patients with chronic kidney disease to reduce the potassium load associated with the use of cardioplegia solutions. The average priming volume is about 1000–1500 mL. A colloid, usually albumin, is usually not added to the pump prime, but it may be given during the pump run to increase oncotic pressure and reduce fluid requirements, thus decreasing extravascular lung water. It may also ameliorate bleeding by delaying fibrinogen absorption and reducing platelet activation.14 The use of acute normovolemic hemodilution reduces blood loss and the number of blood transfusions required.15
Miniaturized circuits with lower priming volumes (500–800 mL) minimize hemodilution and reduce the blood–artificial surface interface, possibly minimizing the inflammatory response. These systems also allow for centrifugation of shed blood for retransfusion to reduce blood activation and lipid embolism. Studies using these circuits have demonstrated improved clinical outcomes, with decreased transfusion rates, lower troponin release, a reduced incidence of neurologic damage and atrial fibrillation, and a shorter duration of ventilation. The decrease in the inflammatory response may be equivalent to that seen during off‐pump surgery.16,17 However, these circuits do lower the safety margins for volume loss and air emboli, and make weaning and termination of bypass more difficult because of low volume reserve in the system.
The establishment of CPB involves the drainage of venous blood from the right atrium or venae cavae into a hardshell cardiotomy reservoir or bag. This usually occurs by gravity, but it may also occur by vacuum‐assisted drainage. The blood then passes through an antifoam and sock filter into the oxygenator attached to a heater/cooler unit, and is returned to the arterial system through a filter using either a roller or, preferably, a centrifugal pump.
In a closed reservoir system, which contains a collapsible bag, air passing through the venous lines can be vented through ports at the top of the bag. In a hardshell open system, air can potentially get entrained into the oxygenator if the cardiotomy volume is too low, so low‐volume alarms must be utilized and keen attention paid to reservoir volumes.
Active venous drainage using vacuum assist or kinetic assist (with a centrifugal pump) can be used to augment venous drainage.18,19 This is valuable during minimally invasive procedures or when small venous catheters are utilized. The least amount of negative pressure necessary to augment drainage should be used, although a pressure up to −60 mm Hg is acceptable. Vacuum assist causes an insignificant degree of hemolysis and may reduce hemodilution and transfusion requirements. However, one must always consider the possibility of venous air entrainment and undetected air microembolism when this technique is utilized. Excessive vacuum may pull air retrograde through the oxygenator membrane, causing depriming of a centrifugal pump. Monitoring for gaseous emboli on both the venous and arterial side should be utilized to minimize these risks.
Centrifugal pumps have replaced roller pumps to provide systemic flow in most current systems. Both provide nonpulsatile flow, unless additional technology is utilized to provide pulsatile flow. Roller pumps are pressure‐insensitive and can pressurize the arterial line in the face of outflow obstruction. Centrifugal pumps are afterload‐sensitive, such that they will reduce flow if outflow is obstructed. Centrifugal pumps cause less blood trauma than roller pumps, but the inflammatory response and effects on perioperative bleeding are fairly similar with both types of pumps.20,21 Roller pumps are used, however, for suction lines and cardioplegia delivery (Figure 5.1).
Oxygenators have integral heater–cooler coils which are located proximal to the oxygenator to minimize gas embolization. A separate heater–cooler unit is utilized to control the temperature of the arterial inflow to provide systemic warming and cooling. In 2015, the FDA published an alert that contamination occurring during manufacturing of the Sorin 3T heater–cooler units caused delayed sternal wound infections with Mycoplasma chimaera, leading to recommendations for strict adherence to instructions about the maintenance and cleaning of these units.
Suction lines return extravasated blood from the surgical field to the cardiotomy reservoir to conserve blood and blood elements and to maintain pump volume.
Despite the nearly universal use of these suction lines, the benefits of blood salvage into the pump may be offset by the adverse effects of the aspirated blood. Studies have shown that blood in contact with tissue factor in the pericardium is replete with fat and procoagulant and proinflammatory mediators, such as complement and cytokines.22–25 Thus, aspirated blood is a significant activator of coagulation, causing increased generation of thrombin and complement that promote inflammation, and is a major cause of hemolysis. Cytokines may contribute to increased perioperative bleeding and neurologic sequelae. Elimination of cardiotomy suction may reduce thrombin generation, platelet activation, and the systemic inflammatory response.25 Notably, return of cardiotomy suction into the circuit usually causes systemic hypotension, most likely because of the high levels of inflammatory mediators present.
The routine use of cell‐saving devices to aspirate and wash shed blood can preserve red cells while eliminating many of these inflammatory mediators while also removing fat from the blood. However, centrifugation of shed blood does remove coagulation factors and platelets from the blood. Most surgeons continue to use cardiotomy suction while still using cell‐saving devices.26
An additional suction line can be connected to an intracardiac vent, draining blood from the left ventricle (LV) or other cardiac chamber into the reservoir by active suctioning by a roller pump head. These lines are useful in providing ventricular decompression and/or improving surgical exposure. Active root venting should be used in all valve cases upon weaning from CPB to evacuate ejected air.
Oxygen and compressed air pass into the oxygenator from a blender which regulates oxygen concentration by adjusting the FiO2 and determines the gas flow by adjusting a “sweep rate”. The sweep rate is generally maintained at slightly less than the systemic flow rate to eliminate CO2 from the blood to achieve a desired value (generally around 40–50 mm Hg). To minimize blood activation, the oxygenator may be coated with heparin or Trillium to improve biocompatibility.27
The pump setup includes a separate heat exchanger for cardioplegia delivery. Tubes of differing diameters are passed through the same roller pump head, delivering a preselected ratio of pump volume to cardioplegia solution (such as 4:1). The final mixture then passes through this heat exchanger for the delivery of cold or warm cardioplegia. Monitoring of infusion pressure is essential, especially for retrograde delivery, which generally provides about 200 mL/min of flow at a pressure that should not exceed 40 mm Hg to prevent coronary sinus rupture. Very high line pressures indicate obstruction to flow, either because the line is clamped or kinked or because the cardioplegia catheter is obstructed. A low line pressure generally indicates misplacement of the catheter, either back into the right atrium or from perforation of the coronary sinus. Microplegia systems (such as the Quest MPS system) minimize the volume of crystalloid vehicle required during cardioplegia delivery. They mix the essential cardioplegia contents (primarily potassium and magnesium) with the blood in a specified ratio that is then delivered to the heart. This allows for a large amount of cardioplegia to be delivered with minimal hemodilution.
Additional features of the CPB circuit usually include the following:
In‐line monitoring of arterial and venous blood gases, electrolytes, hematocrit, and temperatures at multiple sites simultaneously. The last of these is useful during deep hypothermia cases.
An arterial line filter (usually 40 μm), which is essential to remove microemboli before blood is returned to the patient. Microemboli may consist of air, blood, or platelet microaggregates, or other particulate matter. Fat microemboli are found in abundance in cardiotomy suction and can be removed by 20 μm filters. Large emboli may become fractionated before reaching the arterial line filter, and then may not be completely removed.
Recirculation lines to allow for venting of air and to prevent stagnation of blood. This is essential during circulatory arrest cases and when direct thrombin inhibitors are used for anticoagulation in patients with heparin‐induced thrombocytopenia.
Hemofilters or hemoconcentrators, which can be placed in the circuit to remove excessive volume in patients with preexisting fluid overload or renal dysfunction. Modified ultrafiltration (MUF) at the end of the pump run can hemoconcentrate the pump contents by pumping blood from the arterial cannula through the concentrator for retransfusion through the venous cannula into the right atrium.28
A cell‐saving device into which blood is scavenged from the operative field to be centrifuged, washed, and collected in a bag. This can then be drained into the cardiotomy device for transfusion during CPB or after CPB is terminated, or placed in a transfer bag and given to the anesthesiologist for infusion. This has been shown to decrease blood transfusion requirements during cardiac surgical procedures.26
A detailed checklist must be utilized by the perfusionist before every case to make sure that no detail is overlooked. The patient’s life depends on the perfusionist and proper function of the heart–lung machine. Accurate record keeping during bypass is essential (Figure 5.2 and 5.3).
Figure 5.1The basics of a “closed” extracorporeal circuit. Blood drains through the venous line (A) into a venous reservoir bag (B), while blood from vent lines and the cardiotomy sucker (C) are actively suctioned using a roller pump (D) into a cardiotomy reservoir (E), which drains into the venous reservoir. The blood is then pumped by a centrifugal pump (F) through an integrated oxygenator–heat exchanger unit (G) and returned through an arterial filter (H) to the arterial circulation (I). For blood cardioplegia setups, a mixture of blood from the oxygenator and a stock cardioplegia solution is pumped through a roller pump head (J) using different size tubing (depending on the mixture ratio) and returned to the ascending aorta for antegrade cardioplegia delivery (K) and the coronary sinus for retrograde cardioplegia. The heater–cooler system is used for systemic and cardioplegia temperature management (L).
Anticoagulation. Prior to cannulation, achievement of adequate anticoagulation is essential to minimize thrombus formation on the cannulas and within the extracorporeal circuit (see also pages 250–251).1
Unfractionated heparin may be administered in a dose of 3–4 mg/kg for uncoated circuits with monitoring of its anticoagulant effect by the activated clotting time (ACT).11 A blood sample is drawn 3–5 minutes after heparin administration and should achieve an ACT >480 seconds in non‐heparin‐coated circuits and an ACT >400 seconds in heparin‐coated circuits. Patients with heparin resistance may require more heparin or administration of other blood products (2–4 units of fresh frozen plasma, antithrombin (AT) 500–1000 units) or even bivalirudin to achieve adequate anticoagulation (see page 251).29–32 Common systems to measure ACTs include the Hepcon (Medtronic), Hemochron (Accriva Diagnostics), and i‐STAT (Abbott) devices.
Because of patient variability in response to heparin and the effects of hypothermia and hemodilution on the ACT, the correlation between ACTs and the level of thrombin markers is imprecise. Using the Medtronic Heparin Hemostasis Management System (HMS), an individual dose–response curve can be generated which calculates the precise amount of heparin necessary to achieve a specified ACT. Monitoring of heparin concentrations is important during CPB as this may reduce heparin over‐ or underdosing and has been shown to reduce thrombin generation, fibrinolysis, and neutrophil activation.33 A level of ≥2.0 units/mL is recommended. During off‐pump surgery, the ACT should reach 250 seconds because the coronary artery being bypassed is occluded during the procedure.
In a patient with documented heparin‐induced thrombocytopenia (HIT), an alternative means of anticoagulation must be sought. Although one can give an antiplatelet medication (glycoprotein IIb/IIIa inhibitor or a prostaglandin analog) with heparin during bypass, the preferred approach is to use bivalirudin, a short‐acting direct thrombin inhibitor, to avoid heparin entirely.34,35 This issue is discussed in more detail on pages 251–253.
Antifibrinolytic drugs. CPB is associated with a variety of abnormalities in coagulation, among which is fibrinolysis. ε‐aminocaproic acid (Amicar) and tranexamic acid decrease fibrinolysis by inhibiting plasminogen activation and through antiplasmin activity. When given prior to going on bypass and during the pump run, they have both been demonstrated to reduce perioperative bleeding. Although a variety of different dosing regimens are used, ε‐aminocaproic acid is usually given in a dose of 10 g intravenously (IV) with 5–10 g in the pump prime. A common dose of tranexamic acid is 10 mg/kg with 1 mg/kg/h infusion during surgery (see page 249).36,37 Although many groups give the initial dose of antifibrinolytic medication prior to skin incision, it may be best to defer the bolus dose until after heparinization, to avoid a transient procoagulant state.38
Arterial cannulation is usually accomplished by placement of a cannula in the ascending aorta just proximal to the innominate artery (Figure 5.4). Cannula size is determined by the anticipated flow rate for the patient based on body surface area, so as to minimize line pressure and shear forces (Table 5.1).
Cannula designs have been modified in a variety of ways to minimize shear forces and jet effects on the aortic wall (Figure 5.5). Most commonly used are those with end holes and/or multiple side holes through which blood exits at lower velocity (the Medtronic EOPA and Soft‐flow cannulas).39
Steps to prevent systemic embolization, primarily to the brain, are imperative when CPB is used during surgery. Although gaseous microembolization can be addressed by improvements in CPB technology, cannulation and clamping are the primary causes of atheroembolism and stroke. Although most surgeons palpate the proposed cannulation site in the ascending aorta to assess for the presence of atherosclerotic plaque and calcification, this is a very insensitive means of detecting plaque. Transesophageal echocardiography (TEE) may identify protruding atheromas, but epiaortic imaging is the gold standard for identifying plaque and may lead to modification of the surgical approach.40–42 Cannulas with attached intra‐aortic filtration devices (Embol‐X catheter) and suction‐based extraction devices have been devised to trap embolic material upon unclamping with equivocal benefits.43–45
If ascending aortic cannulation is not feasible, an alternative cannulation site must be sought. Femoral artery cannulation, either percutaneously or via cutdown, is feasible if aortoiliac atherosclerosis is not severe and the TEE does not demonstrate significant descending aortic atherosclerosis which could produce retrograde cerebral embolization and stroke. In fact, one study of reoperative mitral valve surgery demonstrated a greater than fourfold incidence of stroke comparing retrograde arterial perfusion to central cannulation.46 Femoral cannulation also runs the risk of a retrograde dissection. Satisfactory flow into the cannula must be assured before connecting the cannula to the CPB circuit. After decannulation, distal flow must be confirmed after the femoral access site has been repaired.
Although central aortic cannulation can be accomplished in many types of minimally invasive surgery, femoral arterial cannulation is commonly used. In these patients, it is important to assess the patient’s iliofemoral system prior to surgery to identify whether femoral artery cannulation will be feasible. Furthermore, when a long duration of CPB is anticipated (complex minimally invasive or robotic surgery), there is an increased risk of a lower‐extremity compartment syndrome from ischemia/reperfusion injury.47–50 In these situations, options include placing the cannula percutaneously, placing it using the Seldinger technique to allow some distal flow, placing it through a sidearm graft sewn to the femoral artery to ensure distal flow, or placing an additional small cannula to provide distal perfusion.
If femoral cannulation is not feasible, or for surgery of the ascending aorta and arch, cannulation of the distal subclavian/axillary artery is an excellent alternative (Figure 5.6).51 This may be performed directly through an arteriotomy or preferably through an 8 mm sidearm graft anastomosed to the vessel, which provides distal arm circulation during bypass. With snaring of the proximal innominate artery, axillary cannulation allows for selective antegrade brain perfusion during deep hypothermic circulatory arrest (DHCA). In these cases, additional cannulation of the left carotid artery may also be considered.52–54
Either femoral or axillary arterial cannulation should be immediately available when there is concern about potential cardiac, aortic, or graft damage during resternotomy or for patients with ruptured ascending aortic aneurysms or aortic dissections with hemopericardium. The artery should be exposed and occasionally may need to be cannulated, either for immediate initiation of bypass if problems are encountered after sternotomy or, on occasion, to initiate bypass and systemic cooling before the sternotomy is performed, depending on the patient’s clinical condition.
In patients developing hemodynamic instability during transcatheter aortic valve replacement (TAVR) despite pharmacologic management, an intra‐aortic balloon pump is usually placed first for additional support. If the patient remains unstable, develops refractory arrhythmias, or has a cardiac arrest or life‐threatening tamponade, institution of CPB may be life‐saving. Use of 15 Fr arterial and 17 Fr venous cannulas placed through a percutaneous transfemoral approach can allow for systemic flow rates of up to 2.5 L/min while problems are rectified.
Venous drainage for most open‐heart surgery is accomplished with a double‐ or triple‐stage cavoatrial cannula (Figure 5.7). This is placed through the right atrial appendage or right atrial free wall with the distal end situated in the inferior vena cava (IVC) (Figure 5.8A). Blood drains from the IVC through several apertures near the end and from the right atrium through additional side holes. These catheters are used for most procedures that do not require opening of the right heart. The triple‐stage cannula provides excellent flow and allows for use of a smaller outer‐diameter cannula, especially with vacuum‐assisted drainage.
Mitral valve surgery may be accomplished using a double‐ or triple‐staged cannula or with bicaval cannulation, the latter being required if a biatrial transseptal approach is planned. Tricuspid valve surgery through a sternotomy incision is performed using bicaval cannulation with placement of caval snares around the cannulas to prevent air entry into the venous lines. A cannula may be placed directly into the superior vena cava (SVC) or passed through the right atrial appendage into the SVC. The IVC cannula is placed through a pursestring suture low in the right atrial free wall (Figure 5.8B).
Femoral venous cannulation is used in robotic and minimally invasive cases and may be supplemented by a 15 or 17 Fr venous line placed into the internal jugular vein. The femoral catheter is 50 cm long and is passed through the femoral vein to lie within the right atrium to ensure adequate venous drainage. Shorter venous catheters can be used, if necessary. Exposure of the femoral vein or even cannulation and establishment of CPB may also be used in high‐risk situations of hemodynamic instability or redo surgery. Minimally invasive tricuspid valve surgery can also be performed using femoral venous drainage. The transfemoral catheter is withdrawn into the IVC and the IVC is snared. An additional drainage catheter is placed in the SVC either directly or through the right atrium and the SVC is snared to eliminate air entry into the venous line. This is usually supplemented with vacuum‐assisted drainage. In redo cases, the cannula may be left in the SVC and snares are not necessary.55
Femoral arterial and venous cannulation have been used to systemically warm patients presenting with profound accidental hypothermia and can be used in emergency situations, such as cardiac arrest, to establish an ECMO circuit (see pages 312–315 and 563–565).
Cannulation for cardioplegia administration. Antegrade cardioplegia is delivered through a catheter placed in the aortic root just proximal to the position of the aortic cross‐clamp. This should provide the best myocardial protection in the absence of coronary disease. A retrograde catheter is routinely used to augment protection and ease the flow of an operation. It is very useful in patients with coronary disease and those with severe aortic regurgitation in whom antegrade cardioplegia cannot be delivered into the root (it can subsequently be given directly into the coronary ostia). The catheter is placed through a pursestring suture in the right atrial free wall, although some surgeons open the right atrium to place the catheter under direct vision, and place a suture around the coronary sinus ostium to optimize flow. Cannulas are held in position within the sinus with a balloon which may be self‐inflating or manually inflated which allows for pressure measurements near the tip of the catheter to prevent overpressurization and potential coronary sinus rupture.56
Figure 5.9 provides an illustration of cannulation and clamping for a routine on‐pump coronary bypass operation.
Figure 5.4Arterial cannulation. The arterial cannula is placed amidst two pursestrings in the ascending aorta just proximal to the innominate artery. The outflow should be directed into the arch, not into the innominate artery.
Note that smaller venous cannulas can be used when vacuum‐assisted drainage is employed BSA, body surface area (m2)
Figure 5.5Arterial cannulas include (top to bottom): Medtronic DLP 20 Fr curved metal cannula, Sarns Terumo 7 Fr Soft‐Flow cannula with multiple side holes, Medtronic 20 Fr EOPA cannula with end and side holes, Medtronic DLP 22 Fr straight arch cannula, and Medtronic 22 mm three‐dimensional select cannula.
Figure 5.6Axillary artery cannulation. An 8 mm side graft is sewn to the distal subclavian/axillary artery, into which the cannula is placed and secured in position.
Figure 5.7Venous cannulas include (top to bottom): Medtronic 32/40 double‐stage cavoatrial cannula, RMI 29/37/37 triple‐stage cannula, RMI 30 Fr straight “lighthouse” tipped cannula, and short DLP 32 Fr and long RMI 36 Fr right‐angle cannulas.
Figure 5.8Venous cannulation. (A) The cavoatrial catheter is placed through a pursestring in the right atrial appendage. The tip consists of multiple side holes and is placed into the IVC. The “basket” lies in the mid‐atrium and drains blood from the SVC and coronary sinus through multiple holes 9 cm back from the tip for dual‐stage cannulas and 6 and 11 cm from the tip for triple‐stage cannulas. (B) Bicaval cannulation. The SVC cannula may be placed into the SVC directly or via the right atrial appendage. The IVC cannula is placed through a pursestring low on the right atrial free wall.
Figure 5.9Cannulation and clamping during a routine on‐pump coronary bypass operation. Note aortic and venous cannulation, antegrade and retrograde cardioplegia catheters, and the aortic cross‐clamp just proximal to the aortic cannulation site.
IV. Initiation and Conduct of Cardiopulmonary Bypass (Table 5.2)
Retrograde autologous priming (RAP) along with venous antegrade priming (VAP) can be used to reduce the hemodilutional effects of the priming solution and maintain a higher hematocrit on pump. The process involves back‐draining the arterial line, then the venous reservoir and oxygenator, and then the venous line to remove about 1100 mL of crystalloid from the pump setup prior to initiating bypass. Simultaneously, an α‐agent may be given to maintain systemic pressure. RAP does maintain a higher oncotic pressure during the pump run and has been shown to minimize the accumulation of extravascular lung water and postoperative weight gain. It may also improve tissue perfusion on pump leading to lower lactate levels. It is probably most beneficial in small patients with low blood volumes and low hematocrits, and might be considered in patients who refuse transfusions (Jehovah Witnesses). Although the impact of RAP on clinical outcomes is not significant, it may reduce the overall number of transfusions required.57–61
Systemic pressures and flows. When pump flow is initiated, the patient’s pulsatile perfusion is replaced by nonpulsatile flow. The blood pressure initially decreases from hemodilution with a reduction in blood viscosity. The mean arterial pressure should then be maintained between 50 and 70 mm Hg during the pump run. It may transiently decrease during cardioplegia delivery (probably from potassium delivery into the systemic circulation), from return of large volumes of cardiotomy suction (from inflammatory mediators), and during rewarming (from vasodilation). Blood pressure may rise due to vasoconstriction from hypothermia, and from dilution of narcotics by the pump prime.
The systemic flow rate is calculated based on the patient’s body surface area and is modified by the degree of hypothermia and the venous oxygen saturation (SvO2). It should also take into account the degree of anemia, which can influence whole‐body oxygen delivery. The flow rate should exceed 2 L/min/m2 at normothermia and can be reduced to 1.5–1.7 L/min/m2 at 30 °C with “low flow” bypass. Flow needs to be increased during rewarming, when increased metabolism usually decreases the SvO2. Low‐flow bypass during moderate hypothermia has been shown to improve myocardial protection, reduce collateral flow improving exposure, reduce hemolysis, and reduce fluid requirements without any compromise in tissue perfusion.62
The optimal flow rate should be based on an assessment of adequate oxygen delivery. Means of assessing this include the SvO2, blood lactate levels, and in‐line monitoring of CO2 production.63 The latter two together may be the best way of predicting anaerobic metabolism, which is not assessed by the SvO2. Nonetheless, in most practices, as long as the SvO2 exceeds 65%, the flow rate is considered adequate, although this may not reflect regional flow.64,65
For example, at normothermia, the brain and kidney autoregulate to maintain perfusion as the flow rate is reduced at the expense of skeletal muscle and splanchnic flow. Due to concerns that the combination of hemodilution and a lower flow rate may reduce the mean arterial pressure below the autoregulatory threshold and compromise organ system function, there are proponents of using “high flow” (2–2.4 L/min/m2) rather than “low flow” bypass during hypothermia. Hypothermia may cause more regional variation in flow.65
CPB has significant adverse effects on renal perfusion, filtration, and oxygenation.66–68 Renal blood flow is determined primarily by the systemic flow rate, but hypothermia impairs renal autoregulation and induces renal vasoconstriction. This results in blood being shunted away from the kidneys while the glomerular filtrate rate and renal oxygen consumption remain unchanged. Thus, renal oxygen extraction increases significantly as there is a significant mismatch between oxygen supply and demand that is exacerbated by the anemia of hemodilution. One study demonstrated that renal function was not affected by using lower target blood pressures on CPB (<60 mm Hg vs. 60–69 mm Hg vs. >70 mm Hg), although urine output was less at the lower pressures.69 It does appear, however, that lower systemic flow rates and low hematocrits do adversely affect renal function, so in older patients, those with known chronic kidney disease, and with longer pump runs, maintenance of higher flow rates and a hematocrit above 21% may minimize the risk of acute kidney injury.67–73
One of the primary concerns with CPB is maintenance of adequate cerebral oxygenation, which is determined by the blood pressure, the systemic flow rate, and the pCO2. Cerebral autoregulation allows for maintenance of cerebral blood flow down to a mean arterial pressure as low as 40–50 mm Hg, but autoregulation may be inadequate in hypertensive or diabetic patients, in whom it may be desirable to maintain a higher pressure.74 In fact, some studies have shown that cerebral oxygenation is impaired at this level even if the flow rate is satisfactory, so the blood pressure must be maintained at an adequate level regardless of the flow rate, usually using vasopressors, such as phenylephrine, norepinephrine, or vasopressin.75 This may improve cerebral oxygenation but reduce flow to other regions, specifically the kidneys and splanchnic viscera.
The adequacy of cerebral oxygenation during CPB is usually assessed by cerebral oximetry using bifrontal sensors with near‐infrared spectroscopy. Numerous products are available, including the INVOS (Medtronic), Equanox (NONIN Medical), and ForeSight (Edwards) cerebral oximeters (see Figure 4.9, page 255). The regional cerebral oxygen saturation (rSO2) tends to fall during initiation of bypass and during rewarming, even with an increase in systemic flow. The rSO2 promptly detects problems with arterial desaturation even before it is evident by pulse oximetry.76 Studies have demonstrated that oxygen desaturation is associated with an increased incidence of neurocognitive changes.77 If the oxygen saturation falls more than 20% below baseline or below 40%, an intervention is recommended to restore cerebral blood flow. Before initiating bypass, an increase in blood pressure or an elevation in PCO2 will be effective in increasing cerebral blood flow. Once on bypass, modifications of flow rate, blood pressure, PCO2, or the hematocrit are beneficial. This technology may also alert the cardiac surgical team to potential catastrophes associated with brain malperfusion from cannula malplacement, dissections, oxygenator or other pump‐related failures, air embolism, anaphylactic reactions (such as from protamine), and monitoring problems. Although interventions to improve rSO2 should intuitively reduce the adverse effects of cerebral oxygen desaturation, few studies have documented improvements in clinical outcome.78
Both the hematocrit (HCT) on pump and the systemic flow rate determine the amount of oxygen delivery to the body. Hemodilution from the pump prime commonly reduces oxygen delivery by 25% as estimated from the following equation:
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