COMPONENTS Venous Cannulation and Drainage PRINCIPLES OF VENOUS DRAINAGE VENOUS CANNULAS AND CANNULATION PERSISTENT LEFT SUPERIOR VENA CAVA AUGMENTED OR ASSISTED VENOUS RETURN COMPLICATIONS ASSOCIATED WITH VENOUS CANNULATION AND DRAINAGE CAUSES OF LOW VENOUS RETURN Arterial Cannulation ARTERIAL CANNULAS CONNECTION TO THE PATIENT ATHEROSCLEROSIS OF THE ASCENDING AORTA ASCENDING AORTIC CANNULATION CANNULATION OF THE FEMORAL OR ILIAC ARTERY OTHER SITES FOR ARTERIAL CANNULATION Venous Reservoir Oxygenators Heat Exchangers Pumps Filters and Bubble Traps MICROEMBOLI LEUKOCYTE-DEPLETING FILTERS Tubing and Connectors Heparin-Coated Circuits Cardiotomy Reservoir and Field Suction Venting the Heart Cardioplegia Delivery Systems Hemoconcentrators (Hemofiltration/Ultrafiltration) Perfusion Monitors and Safety Devices CONDUCT OF CARDIOPULMONARY BYPASS The Perfusion Team Assembly of Heart-Lung Machine PRIMING Anticoagulation and Reversal Starting Cardiopulmonary Bypass Cardioplegia Key Determinants of Safe Perfusion BLOOD FLOW RATE PULSATILE FLOW ARTERIAL PRESSURE HEMATOCRIT TEMPERATURE pH/Pco2 MANAGEMENT ARTERIAL Pao2 GLUCOSE Patient Monitors TRANSESOPHAGEAL ECHOCARDIOGRAPHY TEMPERATURE NEUROPHYSIOLOGIC MONITORING ADEQUACY OF PERFUSION URINE OUTPUT GASTRIC TONOMETRY AND MUCOSAL FLOW Stopping Cardiopulmonary Bypass SPECIAL TOPICS Special Applications of Extracorporeal Perfusion RIGHT THORACOTOMY LEFT THORACOTOMY LEFT HEART BYPASS PARTIAL CARDIOPULMONARY BYPASS FULL CARDIOPULMONARY BYPASS FEMORAL VEIN TO FEMORAL ARTERY BYPASS CANNULATION FOR MINIMALLY INVASIVE (LIMITED ACCESS) SURGERY Deep Hypothermic Circulatory Arrest Antegrade and Retrograde Cerebral Perfusion Complications and Risk Management MASSIVE AIR EMBOLISM RISK MANAGEMENT REFERENCES
Venous Cannulation and Drainage
PRINCIPLES OF VENOUS DRAINAGE
Venous blood usually enters the circuit by gravity or siphonage into a venous reservoir placed 40 to 70 cm below the level of the heart. The amount of drainage is determined by central venous pressure; the height differential; resistance in cannulas, tubing, and connectors; and absence of air within the system. Central venous pressure is determined by intravascular volume and venous compliance, which is influenced by medications, sympathetic tone, and anesthesia. Inadequate blood volume or excessive siphon pressure may cause compliant venous or atrial walls to collapse against cannular intake openings to produce "chattering" or "fluttering." This phenomenon is corrected by adding volume to the patient.
VENOUS CANNULAS AND CANNULATION
Venous cannulas are usually made out of flexible plastic, which may be stiffened against kinking by wire reinforcement. Tips are straight or angled and often are constructed of thin, rigid plastic or metal. Size is determined by patient size, anticipated flow rate, and an index of catheter flow characteristics and resistance (provided by the manufacturer). For an average adult with 60-cm negative siphon pressure, a 30F cannula in the superior vena cava (SVC) and 34F in the IVC or a single 42F cavoatrial catheter suffices. Catheters are typically inserted through purse-string guarded incisions in the right atrial appendage, lateral atrial wall, or directly in the SVC and IVC.
Three basic approaches for central venous cannulation are used: bicaval, single atrial, or cavoatrial ("two stage") (Fig. 11-3). Bicaval cannulation and caval tourniquets are necessary to prevent bleeding and air entry into the system when the right heart is entered during CPB. Because of coronary sinus return, caval tourniquets should not be tightened without decompressing the right atrium. Bicaval cannulation without caval tapes is often preferred to facilitate venous return during exposure of the left atrium and mitral valve.
At times, venous cannulation is accomplished via the femoral or iliac vein. This either open or percutaneous cannulation is used for emergency closed cardiopulmonary assist, for support of particularly ill patients before induction of anesthesia, for prevention or management of bleeding complications during sternotomy, for reoperations,3 for certain types of aortic and thoracic surgery, and for applications of CPB that do not require thoracotomy. Adequate flow rates require using a cannula that is as large as possible and advancing the catheter into the right atrium guided by transesophageal echocardiography (TEE). Specially designed commercially manufactured long, ultrathin, wire-reinforced catheters are available for this purpose.
PERSISTENT LEFT SUPERIOR VENA CAVA
A persistent left superior vena cava (PLSVC) is present in 0.3% to 0.5% of the general population and usually drains into the coronary sinus; however, in about 10% of cases it drains into the left atrium.4–6 The presence of a PLSVC should be suspected when the (left) innominate vein is small or absent and when a large coronary sinus or the PLSVC itself is seen on baseline TEE.7,8
A PLSVC may complicate retrograde cardioplegia or entry into the right heart.9 If an adequate-sized innominate vein is present (30% of patients), the PLSVC can simply be occluded during CPB, if the ostium of the coronary sinus is present.10 If the right SVC is not present (approximately 20% of patients with PLSVC), the left cava cannot be occluded. If the innominate vein is absent (40% of patients) or small (about 33%), occlusion of the PLSVC may cause venous hypertension and possible cerebral injury. In these patients a cannula is passed retrograde into the PLSVC through the coronary sinus ostium and secured. Alternatively, a cuffed endotracheal tube may be used as a cannula.11
AUGMENTED OR ASSISTED VENOUS RETURN
Negative pressure is sometimes applied to the venous lines to provide assisted venous drainage using a roller pump or centrifugal pump,12 or by applying a regulated vacuum to a closed hard-shell venous reservoir (vacuum-assisted venous drainage, VAVD).13 This may permit use of smaller diameter catheters14 and may be helpful when long, peripheral catheters are used. Augmented negative pressure in the venous line increases the risk of aspirating gross or microscopic air and causing cerebral injury,15–18 hemolysis, or aspiration of air into the blood compartment of membrane oxygenators. Positive pressure in the venous reservoir can cause air to enter the venous lines and right heart.19 These potential complications require special safety monitors and devices and adherence to detailed protocols.19,20
COMPLICATIONS ASSOCIATED WITH VENOUS CANNULATION AND DRAINAGE
These include atrial arrhythmias, atrial or caval tears and bleeding, air embolization, injury or obstruction due to catheter malposition, reversing arterial and venous lines, and unexpected decannulation. Placing tapes around the cavae may lacerate branches, nearby vessels (e.g., right pulmonary artery), or the cava itself. Before or after CPB, catheters may compromise venous return to the right atrium from the body. Venous catheters and/or caval tapes may displace or compromise central venous or pulmonary arterial monitoring catheters; conversely, monitoring catheters may compromise the function of caval tapes.
Any intracardiac catheter may be trapped by sutures, which may impede removal before or after the wound is closed. Any connection between the atmosphere and cannula intake ports may entrain air to produce an air lock or gaseous microembolism. Assisted venous drainage (AVD) increases the risk of air entrainment.21,22 Finally, improperly placed purse-string sutures may obstruct a cava when tied.23
CAUSES OF LOW VENOUS RETURN
Low venous pressure, hypovolemia, drug- or anesthetic-induced venous dilatation, inadequate differential height between heart and reservoir, too small cannula size, cannula obstruction from any cause, air locks, or excessive flow resistance in the drainage system are possible causes of reduced venous return. Partial obstruction of the venous line may distend the right ventricle and impair later contractility.
The tip of the arterial cannula is usually the narrowest part of the perfusion system and at required flows small aortic and arterial catheters produce high pressure differentials, jets, turbulence, and cavitation. Most arterial catheters are rated by a performance index, which relates external diameter, flow, and pressure differential.24 High-velocity jets may damage the aortic wall, dislodge atheroemboli, produce dissections, disturb flow to nearby vessels, and cause cavitation and hemolysis. Pressure differences that exceed 100 mm Hg cause excessive hemolysis and protein denaturation.25 Weinstein26 attributed a predominance of left-sided stroke following cardiac surgery to the sand-blasting effect of end-hole aortic cannulas directing debris into the left carotid artery. Aortic catheters with only side ports27 are designed to minimize jet effects and better distribute arch vessel perfusion and pressure28 and may be associated with fewer strokes.26
Recently a dual-stream aortic perfusion catheter has been developed that features an inflatable horizontal streaming baffle that is designed to protect the arch vessels from atherosclerotic and other emboli and permits selective cerebral hypothermia.29,30 Another novel aortic cannula features a side port that deploys a 120-µm mesh filter to remove particulate emboli beyond the ascending aorta.31 Although this catheter increased the pressure gradient by 50%,32 it removed an average of 8 emboli in 99% of 243 patients and cerebral injuries were less than expected.33
CONNECTION TO THE PATIENT
Anatomic sites available for arterial inflow include the proximal aorta, innominate artery and distal arch, and femoral, external iliac, axillary, and subclavian arteries. The choice is influenced by the planned operation34 and distribution of atherosclerotic disease.35
ATHEROSCLEROSIS OF THE ASCENDING AORTA
Dislodgement of atheromatous debris from the aortic wall from manipulation,36 cross-clamping, or the sand-blasting effect of the cannula jet is a major cause of perioperative stroke37,38 and a risk factor for aortic dissection39 and postoperative renal dysfunction.40 Simple palpation during transient hypotension or transesophageal echocardiography (TEE) is less sensitive and accurate for detecting severe atherosclerosis than epiaortic ultrasonic scanning.36,41,42 TEE views of the middle and distal ascending aorta are often inadequate,41–44 but some recommend this method for screening.44,45 Epiaortic scanning is preferred for all patients who have a history of transient ischemic attack, stroke, severe peripheral vascular disease, palpable calcification in the ascending aorta, calcified aortic knob on chest radiograph, age older than 50 to 60 years, or TEE findings of moderate aortic atherosclerosis.36 Calcified aorta ("porcelain aorta"), which occurs in 1.2% to 4.3% of patients,46,47 is another indication for changing the location of the aortic cannula.48,49 Alternative sites include the distal aortic arch46,50 and innominate, axillary-subclavian, or femoral arteries.
ASCENDING AORTIC CANNULATION
The distal ascending aorta is the preferred cannulation site because of ease and fewest complications. Most surgeons place two purse-string sutures (1.0–1.3 cm diameter) partially through the aortic wall, followed by a 4- to 5-mm, full-thickness stab wound, and insert the cannula under a finger while the mean arterial pressure is approximately 60 to 80 mm Hg. Usually the cannula is inserted 1 to 2 cm with a whiff of back bleeding, rotated to ensure that the tip is completely within the lumen, and positioned to direct flow to the mid transverse aorta. A few surgeons prefer a long catheter with the tip placed beyond the left subclavian artery.51 Proper cannula placement is critical28 and is confirmed by noting pulsatile pressure in the aortic line monitor and equivalent pressure in the radial artery. Once inserted the cannula must be adequately secured in place.
Complications of ascending aorta cannulation Complications include difficult insertion; bleeding; tear in the aortic wall; intramural or malposition of the cannula tip (in or against the aortic wall, toward the valve, or in an arch vessel)52; atheromatous emboli; failure to remove all air from the arterial line after connection; injury to the aortic back wall; high line pressure indicating obstruction to flow; inadequate or excessive cerebral perfusion53; inadvertent decannulation; and aortic dissection.54,55 It is essential to monitor aortic line and radial artery pressures and to carefully observe the aorta for possible cannula-related complications during onset of CPB and during placement of aortic clamps. Asymmetric cooling of the face or neck may suggest a problem with cerebral perfusion. Late bleeding and infected or noninfected false aneurysms are delayed complications of aortic cannulation.
Aortic dissection occurs in 0.01% to 0.09% of aortic cannulations39,55–58 and is more common in patients with aortic root disease. The first clues may be discoloration beneath the adventia near the cannula site, an increase in arterial line pressure, or a sharp reduction in return to the venous reservoir. TEE may be helpful in confirming the diagnosis,59 but prompt action is necessary to limit the dissection and maintain perfusion. The cannula must be promptly transferred to a peripheral artery or uninvolved distal aorta. Blood pressure should be controlled pharmacologically and perfusion cooling to temperatures less than 20°C initiated. During hypothermic circulatory arrest, the aorta is opened at the original site of cannulation and repaired by direct suture, patch, or circumferential graft.57,58 When recognized early, survival rates range from 66% to 85%, but when discovered after operation survival is approximately 50%.
CANNULATION OF THE FEMORAL OR ILIAC ARTERY
These vessels are usually the first alternative to aortic cannulation, but are also indicated for initiating cardiopulmonary bypass quickly for severe bleeding, cardiac arrest, acute intraoperative dissection or severe shock, limited access cardiac surgery, and selected reoperative patients.3 Femoral or iliac cannulation limits cannula size but the retrograde distribution of blood flow is similar to antegrade flow.60
Femoral cannulation is associated with many complications3,61 that include tears, dissection, late stenosis or thrombosis, bleeding, lymph fistula, infection in the groin, or cerebral and coronary atheroembolism. In patients with prior aortic dissections femoral perfusion may cause malperfusion; thus some surgeons recommend alternative cannulation sites for these patients.62,63 Ischemic complications of the distal leg may occur during prolonged (3–6 hours) retrograde perfusions64,65 unless perfusion is provided to the distal vessel. This may be provided by a small Y catheter in the distal vessel65 or a side graft sutured to the artery.66
Retrograde arterial dissection is the most serious complication of femoral or iliac arterial cannulation and may extend to the aortic root and/or cause retroperitoneal hemorrhage. The incidence is between 0.2% and 1.3%67–70 and is associated with a mortality of about 50%. This complication is more likely in diseased arteries and in patients over 40 years old. The diagnosis is similar for an aortic cannula dissection and may be confirmed by TEE of the descending thoracic aorta.59 Antegrade perfusion in the true lumen must be immediately resumed by either the heart itself or by cannulation in the distal aorta or axillary-subclavian artery. It is not always necessary to repair the dissected ascending aorta unless it affects the aortic root.67–69
OTHER SITES FOR ARTERIAL CANNULATION
The axillary-subclavian artery is increasingly used for cannulation.71–75 Advantages include freedom from atherosclerosis, antegrade flow into the arch vessels, and protection of the arm and hand by collateral flow. Because of these advantages and the dangers of retrograde perfusion in patients with aortic dissection, some surgeons prefer this cannulation site for these patients.63,75,76 Brachial plexus injury and axillary artery thrombosis are reported complications.71 The axillary artery is approached through a subclavicular incision; the intrathoracic subclavian artery may be cannulated through a left thoracotomy.77
Occasionally the innominate artery may be cannulated through a purse-string suture without obstructing flow around a 7F to 8F cannula to the right carotid artery.34,49 The ascending aorta can also be cannulated by passing a cannula through the aortic valve from the left ventricular apex.78,79 Coselli and Crawford80 also describe retrograde perfusion through a graft sewn to the abdominal aorta.
The venous reservoir serves as volume reservoir and is placed immediately before the arterial pump when a membrane oxygenator is used (see Fig. 11-1). This reservoir serves as a high-capacitance (i.e., low-pressure) receiving chamber for venous return, facilitates gravity drainage, is a venous bubble trap, provides a convenient place to add drugs, fluids, or blood, and adds storage capacity for the perfusion system. As much as 1 to 3 L of blood may be translocated from patient to circuit when full CPB is initiated. The venous reservoir also provides several seconds of reaction time if venous return is suddenly decreased or stopped during perfusion.
Reservoirs may be rigid (hard) plastic canisters ("open" types) or soft, collapsible plastic bags ("closed" types). The rigid canisters facilitate volume measurements and management of venous air, often have larger capacity, are easier to prime, permit suction for vacuum-assisted venous drainage, and may be less expensive. Some hard-shell venous reservoirs incorporate macrofilters and microfilters and can serve as cardiotomy reservoirs and to receive vented blood.
Disadvantages include the use of silicon antifoam compounds, which may produce microemboli,81,82 risk of microembolism, and increased activation of blood elements.83 Soft bag reservoirs eliminate the blood-gas interface and by collapsing reduce the risk of pumping massive air emboli.
Membrane oxygenators imitate the natural lung by interspersing a thin membrane of either microporous polypropylene (0.3- to 0.8- µm pores) or silicone rubber between the gas and blood phases. Compared to bubble oxygenators, membrane oxygenators are safer, produce less particulate and gaseous microemboli,84,85 are less reactive to blood elements, and allow superior control of blood gases.86,87 With microporous membranes, plasma-filled pores prevent gas entering blood but facilitate transfer of both oxygen and CO2. Because oxygen is poorly diffusible in plasma, blood must be spread as a thin film (approximately 100 µm) over a large area with high differential gas pressures between compartments to achieve oxygenation. Areas of turbulence and secondary flow enhance diffusion of oxygen within blood and thereby improve oxyhemoglobin saturation.88 Carbon dioxide is highly diffusible in plasma and easily exits the blood compartment despite small differential pressures across the membrane.
The most popular design uses sheaves of hollow fibers (120–200 µm) connected to inlet and outlet manifolds within a hard-shell jacket (Fig. 11-4). The most efficient configuration creates turbulence by passing blood between fibers and oxygen within fibers. Arterial PCO2 is controlled by gas flow, and PO2is controlled by the fraction of inspired oxygen (FIO2) produced by an air-oxygen blender. Modern membrane oxygenators add up to 470 mL of O2 and remove up to 350 mL CO2 per minute at 1 to 7 liters of flow with priming volumes of 220 to 560 mL and resistances of 12 to 15 mm Hg per liter blood flow. Most units combine a venous reservoir, heat exchanger, and hollow fiber membrane oxygenator into one compact unit.
A new membrane oxygenator features a very thin (0.05 µm), solid membrane on the blood side of a highly porous support matrix. This membrane reduces the risk of gas emboli and plasma leakage during prolonged CPB, but may impair transfer of volatile anesthetics.89
Flow regulators, flow meters, gas blender, oxygen analyzer, gas filter, and moisture trap are parts of the oxygenator gas supply system used to control the ventilating gases within membrane oxygenators. Often an anesthetic vaporizer is added, but care must be taken to prevent volatile anesthetic liquids from destroying plastic components of the perfusion circuit.
Bubble oxygenators are obsolete in the United States, but are used elsewhere for short-term CPB because of cost and efficiency. Because each bubble presents a new foreign surface to which blood elements react, bubble oxygenators cause progressive injury to blood elements and entrain more gaseous microemboli.90,91 In bubble oxygenators, venous blood drains directly into a chamber into which oxygen is infused through a diffusion plate (sparger). The sparger produces thousands of small (approximately 36 µm) oxygen bubbles within blood. Gas exchange occurs across a thin film at the blood-gas interface around each bubble. Carbon dioxide diffuses into the bubble and oxygen diffuses outward into blood. Small bubbles improve oxygen exchange by effectively increasing the surface area of the gas-blood interface,92 but are difficult to remove. Large bubbles facilitate CO2 removal. Bubbles and blood are separated by settling, filtration, and defoaming surfactants in a reservoir. Bubble oxygenators add 350 to 400 mL oxygen to blood and remove 300 to 330 mL CO2 per minute at flow rates from 1 to 7 L min.86,93 Priming volumes are less than 500 mL. Commercial bubble oxygenators incorporate a reservoir and heat exchanger within the same unit and are placed upstream to the arterial pump.
Oxygenator malfunction requiring change during CPB occurs in 0.02% to 0.26% of cases,94–96 but the incidence varies between membrane oxygenator designs.97 Development of abnormal resistant areas in the blood path is the most common cause,96 but other problems include leaks, loss of gas supply, rupture of connections, failure of the blender, and deteriorating gas exchange. Blood gases need to be monitored to ensure adequate CO2 removal and oxygenation. Heparin coating may reduce development of abnormally high resistance areas.95
Heat exchangers control body temperature by heating or cooling blood passing through the perfusion circuit. Hypothermia is frequently used during cardiac surgery to reduce oxygen demand or to facilitate operative exposure by temporary circulatory arrest. Gases are more soluble in cold than in warm blood; therefore, rapid rewarming of cold blood in the circuit or body may cause formation of bubble emboli.98 Most membrane oxygenator units incorporate a heat exchanger upstream to the oxygenator to minimize bubble emboli. Blood is not heated above 40°C to prevent denaturation of plasma proteins, and temperature differences within the body and perfusion circuit are limited to 5°C to 10°C to prevent bubble emboli. The heat exchanger may be supplied by hot and cold tap water, but separate heater/cooler units with convenient temperature-regulating controls are preferred. Leakage of water into the blood path can cause hemolysis and malfunction of heater/cooler units may occur.94
Separate heat exchangers are needed for cardioplegia. The simplest system is to use bags of precooled cardioplegia solution. More often cardioplegia fluid is circulated through through a dedicated heat exchanger or tubing coils placed in an ice or warm water bath.
Most heart-lung machines use two types of pumps, although roller pumps can be used exclusively (Table 11-1). Centrifugal pumps are usually used for the primary perfusion circuit for safety reasons and for a possible reduction in injury to blood elements. However, this latter reason remains highly controversial and unproven.99–104
Centrifugal pumps produce pulseless blood flow and standard roller pumps produce a sine wave pulse around 5 mm Hg. The arterial cannula dampens the pulse of pulsatile pumps, and it is difficult to generate pulse pressures above 20 mm Hg within the body during full CPB.112,113 To date no one has conclusively demonstrated the need for pulsatile perfusion during short-term or long-term CPB or circulatory assistance.114–117
Complications that may occur during operation of either type of pump include loss of electricity; loss of the ability to control pump speed, which produces "runaway pump" or "pump creep" when turned off; loss of the flow meter or RPM indicator; rupture of tubing in the roller pump raceway; and reversal of flow by improper tubing in the raceway. A means to manually provide pumping in case of electrical failure should always be available.
Filters and Bubble Traps
During clinical cardiac surgery with CPB the wound and the perfusion circuit generate gaseous and biologic and nonbiologic particulate microemboli (<500 µM diameter).31,118–123 Microemboli produce much of the morbidity associated with cardiac operations using CPB (see section 11D). Gaseous emboli contain oxygen or nitrogen and may enter the perfusate from multiple sources and pass through other components of the system.18,21 Potential sources of gas entry include stopcocks, sampling and injection sites,122 priming solutions, priming procedures, intravenous fluids, vents, the cardiotomy reservoir, tears or breaks in the perfusion circuit, loose purse-string sutures (especially during augmented venous return),18 rapid warming of cold blood,98 cavitation, oxygenators, venous reservoirs with low perfusate levels,21,82 and the heart and great vessels. Bubble oxygenators produce many gaseous emboli; membrane oxygenators produce very few.84–86 Aside from mistakes (open stopcocks, empty venous reservoir, air in the heart) the cardiotomy reservoir is the largest source of gaseous emboli in membrane oxygenator perfusion systems.
Blood produces a large number of particulate emboli related to thrombus formation (clots), fibrin, platelet and platelet-leukocyte aggregation, hemolyzed red cells, cellular debris, and generation of chylomicrons, fat particles, and denatured proteins.124 Stored donor blood is also an important source of blood-generated particles.125 Other biologic emboli include atherosclerotic debris and cholesterol crystals and calcium particles dislodged by cannulation, manipulation for exposure, or the surgery itself. Both biologic and nonbiologic particulate emboli are aspirated from the wound. Bits of muscle, bone, and fat are mixed with suture material, talc, glue, and dust and aspirated into the cardiotomy reservoir.125,126 Materials used in manufacture, spallated material, and dust may also enter the perfusate from the perfusion circuit125 if it is not first rinsed by recirculating saline through a prebypass microfilter, which is discarded.
In vivo microemboli are detected by transcranial Doppler ultrasound,127 fluorescein angiography,84 TEE, and retinal inspection. In the circuit, microemboli are monitored by arterial line ultrasound128 or monitoring screen filtration pressure. Microfilter weights and examination, histology of autopsy tissues, and electron particle size counters of blood samples125 verify microemboli beyond the circuit.
Prevention and control of microemboli Table 11-2 outlines methods to reduce microembolism. Major methods include using a membrane oxygenator and cardiotomy reservoir filter; minimizing and washing blood aspirated from the field129; and preventing air entry into the circuit and using left ventricular vents when the heart is opened.130,131
Two types of blood microfilters are available for use within the perfusion circuit: depth and screen.135–137 Depth filters consist of packed fibers or porous foam, have no defined pore size, present a large, tortuous, wetted surface, and remove microemboli by impaction and absorption. Screen filters are usually made of woven polyester or nylon thread, have a defined pore size, and filter by interception. Screen filters vary in pore size and configuration and block most air emboli; however, as pore size decreases, resistance increases. As compared to no filter, studies indicate that all commercial filters effectively remove gaseous and particulate emboli.138–141 Most investigations find that the Dacron wool depth filter is most effective, particularly in removing micro- and macroscopic air. Pressure differences across filters vary between 24 and 36 mm Hg at 5 L/min flow. Filters cause slight hemolysis and tend to trap some platelets; nylon filters may activate complement.135,136
The need for microfilters in the cardiotomy suction reservoir is universally accepted,126 and most commercial units contain an integrated micropore filter. The need for a filter in the cardioplegia delivery system, however, is questionable,142 and the need for an arterial line filter is unsettled.137 In vitro studies demonstrate that an arterial filter reduces circulating microemboli139–141 and clinical studies are confirmatory.140,141 However, these filters do not remove all microemboli generated by the extracorporeal circuit.18,122,126,143 When bubble oxygenators are used, studies show equivocal or modest reductions in microemboli84,144–146 and neurologic outcome markers.146–150 In contrast, membrane oxygenators produce far fewer microemboli and when used without an arterial filter, the numbers of microemboli are similar to those found with bubble oxygenators plus arterial line filters.85,137
Although efficacy of arterial line microfilters remains unsettled, use is almost universal.151 Filters are effective bubble traps, but increase costs, occasionally obstruct during use, are difficult to de-air during priming, and should be used with a bypass line and valved purge line to remove air.
Other sources of biologic microemboli may be more important. Cerebral microemboli are most numerous during aortic cannulation,152–154 application and release of aortic clamps,153,154 and at the beginning of cardiac ejection after open heart procedures.155 Furthermore, as compared to perfusion microemboli, surgically induced emboli are more likely to cause postoperative neurologic deficits.156
Leukocyte-depleting filters are discussed in section 11C and have been recently reviewed.157–160 These filters reduce circulating leukocyte counts in most studies,161–163 but fail to produce convincing evidence of clinical benefit.164–166
Tubing and Connectors
The various components of the heart-lung machine are connected by polyvinyl tubing and fluted polycarbonate connectors. Medical grade polyvinyl chloride (PVC) tubing is universally used because it is flexible, compatible with blood, inert, nontoxic, smooth, nonwettable, tough, transparent, resistant to kinking and collapse, and can be heat sterilized. To reduce priming volume, tubing connections should be short; to reduce turbulence, cavitation, and stagnant areas, the flow path should be smooth and uniform without areas of constriction or expansion. Wide tubing improves flow rheology, but also increases priming volume. In practice 1/2- to 5/8-inch (internal diameter) tubing is used for most adults, but until a compact, integrated, complete heart-lung machine can be designed and produced as a unit, the flow path produces some turbulence. Careless tubing connections are sources of air intake or blood leakage and all connections must be secure. For convenience and safety, most tubing and connectors are prepackaged and disposable.
Heparin can be attached to blood surfaces of all components of the extracorporeal circuit by ionic or covalent bonds. The Duraflo II heparin coating ionically attaches heparin to a quaternary ammonium carrier (alkylbenzyl dimethyl-ammonium chloride), which binds to plastic surfaces (Edwards Lifesciences, Irvine, CA). Covalent attachment is produced by first depositing a polyethylenimine polymer spacer onto the plastic surface, to which heparin fragments bind (Carmeda Bioactive Surface, Medtronic Inc., Minneapolis, MN). Ionic-bound heparin slowly leaches, but this is irrelevant in clinical cardiac surgery. The use of heparin-coated circuits during CPB has spawned an enormous literature167–172 and remains controversial largely because studies are contaminated by patient selection, reduced doses of systemic heparin, and washing or discarding field-aspirated blood.172 There is no credible evidence that heparin-coated perfusion circuits reduce the need for systemic heparin or reduce bleeding or thrombotic problems associated with CPB (see section 11B). Although the majority of studies indicate that heparin coatings reduce concentrations of C3a and C5b-9,173 the inflammatory response to CPB is not reduced (see section 11C) and the evidence for clinical benefit is not convincing.174,175
Other surface modifications and coatings in development168 include a phosphorylcholine coating,176 surface-modifying additives,179 a trillium biopassive surface,177,178 and a synthetic protein coating180 (see also section 11C).
Cardiotomy Reservoir and Field Suction
Blood aspirated from the surgical wound may be directed to the cardiotomy reservoir for defoaming, filtration, and storage before it is added directly to the perfusate. A sponge impregnated with a surfactant removes bubbles by reducing surface tension at the blood interface and macro, micro, or combined filters remove particulate emboli. Negative pressure is generated by either a roller pump or by vacuum applied to the rigid outer shell of the reservoir. The degree of negative pressure and blood level must be monitored to avoid excessive suction or introducing air into the perfusate.
The cardiotomy suction and reservoir are major sources of hemolysis, particulate and gaseous microemboli, fat globules, cellular aggregates, platelet injury and loss, thrombin generation, and fibrinolysis.82,118,126,181,182 Air aspirated with wound blood contributes to blood activation and destruction and is difficult to remove because of the high proportion of nitrogen, which is poorly soluble in blood. High suction volumes and admixture of air are particularly destructive of platelets and red cells.181,183 Commercial reservoirs are designed to minimize air entrainment and excessive injury to blood elements. Air and microemboli removal are also facilitated by allowing aspirated blood to settle within the reservoir before it is added to the perfusate.
An alternative method for recovering field-aspirated blood is to dilute the blood with saline and then remove the saline to return only packed red cells to the perfusate. Centrifugal cell washers (e.g., Haemonetics Cell Saver, Meomonetics Corp., Braintree, MA) automate this process, which has the advantage of removing air, thrombin, and nearly all biologic and nonbiologic microemboli from the aspirate at the cost of discarding plasma. A third alternative is to discard all field-aspirated blood.184 Increasingly, field-aspirated blood is recognized as a major contributor to the thrombotic, bleeding, and inflammatory complications of CPB (see sections 11B and 11C).
Venting the Heart
If the heart is unable to contract, distention of either ventricle is detrimental to subsequent contractility.185 Right ventricular distention during cardiac arrest or ventricular fibrillation is rarely a problem, but left ventricular distention can be insidious in that blood can enter the flaccid, thick-walled chamber from multiple sources during this period. During CPB blood escaping atrial or venous cannulas and from the coronary sinus and thebesian veins may pass through the unopened right heart into the pulmonary circulation. This blood plus bronchial venous blood, blood regurgitating through the aortic valve, and blood from undiagnosed abnormal sources (patent foramen ovale, patent ductus, etc.) may distend the left ventricle unless a vent catheter is used (Fig. 11-6). During CPB bronchial venous blood and noncoronary collateral flow average approximately 140 ± 182 and 48 ± 74 mL/min, respectively.186
The most common and serious complication of left heart venting is residual air when the heart is filled and begins to contract. De-airing maneuvers and TEE are important methods for ensuring removal of all residual air. In addition, many surgeons aspirate the ascending aorta via a small metal or plastic cannula to detect and remove any escaping air as the heart begins to eject.194,195 Bleeding problems or direct injury to the myocardium are other complications associated with left ventricular vents.
Cardioplegia Delivery Systems
Cardioplegic solutions contain 8 to 20 mEq/L potassium, magnesium, and often other components and are infused into the aortic root proximal to the aortic cross clamp or retrograde into the coronary sinus to arrest the heart in diastole. The carrier may be crystalloid or preferably blood and is infused at temperatures around 4°C or 37°C, depending upon surgeon's preference. Normothermic cardioplegia must be delivered almost continuously to keep the heart arrested; cold cardioplegia is infused intermittently. Cardioplegic solutions are delivered through a separate perfusion system that includes a reservoir, heat exchanger, roller pump, bubble trap, and perhaps microfilter (see Fig. 11-2). Temperature and infusion pressure are monitored. The system may be completely independent of the main perfusion circuit or branch from the arterial line. The system also may be configured to vent the aortic root when between infusions.
Antegrade cardioplegia is delivered through a small cannula in the aortic root or via handheld cannulas directly into the coronary ostia when the aortic valve is exposed. Retrograde cardioplegia is delivered through a cuffed catheter inserted blindly into the coronary sinus.196 Proper placement of the retrograde catheter is critical, but not difficult, and is verified by palpation, TEE, color of the aspirated blood, or pressure waveform of a catheter pressure sensor.197 Complications of retrograde cardioplegia include rupture or perforation of the sinus, hematoma, and rupture of the catheter cuff.198,199
Hemoconcentrators, like oxygenators, contain one of several available semipermeable membranes (typically hollow fibers) that transfer water, electrolytes (e.g., potassium), and molecules up to 20 kD out of the blood compartment.200 Hemoconcentrators may be connected to either venous or arterial lines or a reservoir in the main perfusion circuit, but require high pressure in the blood compartment to effect fluid removal. Thus a roller pump is needed unless connected to the arterial line. Suction may or may not be applied to the air side of the membrane to facilitate filtration. Up to 180mL/min of fluid can be removed at flows of 500 mL min.201 Hemoconcentrators conserve platelets and most plasma proteins as compared to centrifugal cell washers and may allow greater control of potassium concentrations than diuretics.202 Aside from cost, disadvantages are few and adverse effects are rare.201
Perfusion Monitors and Safety Devices
Table 11-3 lists monitors and safety devices that are commonly used during CPB. Pressure in the arterial line between pump and arterial line filter is monitored continuously to instantly detect any increased resistance to arterial inflow into the patient. This pressure should be higher than radial arterial pressure because of resistance of the filter (if used) and cannula. The arterial pressure monitor may be connected to an audible alarm or the pump switch to alert the perfusionist of abrupt increases.
Flow-through devices are available to continuously measure blood gases, hemoglobin/hematocrit, and some electrolytes.203 These devices in the venous line permit rapid assessment of oxygen supply and demand.204–206 In the arterial line the devices offer better control of blood gases.207 The need for these devices is unproven and because reliability is still uncertain, use may distract operative personnel and spawn unnecessary laboratory measurements.208–211 The use of automated analyzers by the perfusion team in the operating room is an alternative if frequent measurement of blood gases, hematocrit, and electrolytes is desirable.203
The flow and concentration of oxygen entering the oxygenator should be monitored.212 Some teams also monitor exit gases to indirectly estimate metabolic activity and depth of anesthesia.212 Some manufacturers recommend monitoring the pressure gradient across membrane oxygenators, which may be an early indication of oxygenator failure.95–97
Temperatures of the water entering heat exchangers must be monitored and carefully controlled to prevent blood protein denaturation and gaseous microemboli.98 During operations using deep hypothermia changes in venous line temperatures reflect rates of temperature change in the patient and arterial line temperatures help protect against brain hyperthermia during rewarming.
A low-level sensor with alarms on the venous reservoir and a bubble detector on the arterial line are desirable safety devices. A one-way valve is recommended in the purge line between an arterial filter/bubble trap and cardiotomy reservoir to prevent air embolism. Some perfusionists also use these valves in the venous and vent lines to protect against retrograde air entry into the circulation or in the arterial line to prevent inadvertent exsanguination.106
Automatic data collection systems are available for preoperative calculations and to process and store data during CPB.213,214 Computer systems for operating CPB are in development.215
|CONDUCT OF CARDIOPULMONARY BYPASS|
Although the surgeon is directly responsible to the patient for the outcome of the operation, he or she needs a close working relationship with the anesthesiologist and perfusionist. These three principals must communicate freely, often, and candidly. Their overlapping and independent responsibilities relevant to CPB are best defined by written policies that include protocols for various types of operations and emergencies and by periodic multidisciplinary conferences.
The surgeon determines the planned operation, target perfusion temperatures, methods of cardioplegia, cannulations, and anticipated special procedures. During operation the surgeon communicates the procedural steps involved in connecting and disconnecting the patient to CPB and interacts with the other principals to coordinate perfusion management with surgical exposure and working conditions. The perfusionist is responsible for setting up and priming the heart-lung machine, performing safety checks, operating the heart-lung machine, monitoring the conduct of bypass, monitoring anticoagulation, adding prescribed drugs, and maintaining a written perfusion record.
The anesthesiologist monitors the operative field, anesthetic state and ventilation of the patient, the patient's physiology, and conduct of perfusion. A vigilant anesthesiologist is the safety officer and often "troubleshooter" of these complex procedures and is in the best position to anticipate, detect, and correct deviations from desired conditions. In addition the anesthesiologist provides TEE observations before, during, and immediately after bypass. While the surgeon corrects the anatomic pathology, the anesthesiologist and perfusionist maintain the patient's life and expectation of recovery
Assembly of Heart-Lung Machine
The perfusionist is responsible for setting up and preparing the heart-lung machine and all components necessary for the proposed operation. Most perfusionists use commercial, sterile, pre-prepared customized tubing packs that are connected to the various components that constitute the heart-lung machine. This dry assembly takes about 10 to 15 minutes, and the system can be kept in standby for up to 7 days. Once the system is primed with fluid, which takes about 15 minutes, it should be used within 8 hours. After assembly the perfusionist conducts a safety inspection and completes a written prebypass checklist.
Adult extracorporeal perfusion circuits require 1.5 to 2.0 L of balanced electrolyte solution (lactated Ringer's solution, Normosol-A, Plasma-Lyte). Before connections are made to the patient, the prime is recirculated through a micropore filter to remove particulate and air emboli. The priming volume represents approximately 30% to 35% of the patient's blood volume and reduces the hematocrit to about two-thirds of the preoperative value. The addition of crystalloid cardioplegia causes further dilution. Thus sometimes a unit of banked blood is added to raise the perfusate hematocrit to a predetermined minimum (e.g., 25% or more). Porcine heparin (2000 units) is added to each unit of banked whole blood to ensure anticoagulation. There is no consensus regarding the optimal hematocrit during CPB; most perfusates have hematocrits between 20% and 25% when used with moderate hypothermia (25°C-32°C). Dilution reduces perfusate viscosity, which is not a problem during clinical CPB, but also reduces oxygen-carrying capacity; mixed venous oxygen saturations below 60% usually prompt either transfusion or increased pump flow.204,205 Sometimes 12.5 to 50 g of mannitol is added to stimulate diuresis and possibly minimize postoperative renal dysfunction.
Efforts to avoid the use of autologous blood include reducing the priming requirement of the machine by using smaller-diameter and shorter tubing lengths and operating the machine with minimal perfusate in the venous and cardiotomy reservoirs. This latter practice increases the risk of air embolism, the risk of which can be reduced by using collapsible reservoirs and reservoir level sensors that stop the pump. Autologous blood prime is another method, which displaces and then removes crystalloid prime by bleeding the patient into the circuit just before beginning CPB.216,217 This method reduces perfusate volume, but phenylephrine may be required to maintain stable hemodynamics.216,217 The method reduces transfusions and does not affect clinical outcome.
The use of colloids (albumin, gelatins, dextrans, and hetastarches) in the priming volume is controversial.218 Colloids reduce the fall in colloid osmotic pressure219,220 and may reduce the amount of fluid entering the extracellular space. The question is whether or not clinical outcome is improved. Prospective clinical studies have failed to document significant clinical benefits with albumin,219–224 which is expensive and may have adverse effects.225,226 Hetastarch may contribute to postoperative bleeding.227 McKnight et al found no influence of prime composition on postoperative nitrogen balance.228 Because of possible adverse effects, including neurologic deficits, the addition of glucose and/or lactate to the prime is avoided.229,230
Anticoagulation and Reversal
Porcine heparin (300–400 units/kg IV) is given before arterial or venous cannulas are inserted. CPB is not started until anticoagulation is confirmed by either an activated clotting time (ACT) or the Hepcon test. Although widely used, bovine heparin is more antigenic in inducing antiplatelet IgG antibodies than is porcine heparin.231 The anticoagulation effect is measured about 3 minutes after heparin administration. However, groups differ in the minimum ACT that is considered safe for CPB. The minimum ACT is 400 seconds; many groups recommend 480 seconds232 because heparin only partially inhibits thrombin formation during CPB (see section 11B). In patients who have received aprotinin, ACT should be measured using kaolin as opposed to celite, because celite artifactually and erroneously increases ACT. Failure to achieve a satisfactory ACT may be due to inadequate heparin or to low concentrations of antithrombin. If a total of 500 units/kg of heparin fails to adequately prolong ACT, fresh frozen plasma (or recombinant antithrombin when available233 is needed to increase antithrombin concentrations to overcome "heparin resistance." Antithrombin is a necessary cofactor that binds circulating thrombin; heparin accelerates this reaction a thousandfold. See section 11B for mangagement of patients with suspected or proven heparin-induced antiplatelet IgG antibodies and alternative anticoagulants to heparin.
During CPB, ACT or the Hepcon test is measured every 30 minutes. If ACT goes below the target level, more heparin is given. Usually one third of the initial heparin bolus is given every hour even when the ACT is within the normal range. The Hepcon test titrates the heparin concentration and is more reproducible than ACT, but ACT provides satisfactory monitoring of anticoagulation. Although excessively high concentrations of heparin (ACT >1000 sec) may cause remote bleeding away from operative sites, low concentrations increase circulating thrombin concentrations and risk clotting within the extracorporeal perfusion circuit.
One mg of protamine (not to exceed 3 mg/kg) is given for each 100 units of heparin injected in the initial bolus dose. The heparin-protamine complex activates complement and often causes acute hypotension, which may be attenuated by adding calcium (2 mg/1 mg protamine). After a third of the planned protamine dose, blood must not be returned to the cardiotomy reservoir from the surgical field. Rarely, protamine may cause an anaphylactic reaction in patients with antibodies to protamine insulin.234 Neutralization of heparin is usually confirmed by an ACT or Hepcon test and more protamine (50 mg) is given if either test remains prolonged and bleeding is a problem. Heparin rebound is the term used to describe a delayed heparin effect due to release of tissue heparin after protamine is cleared from the circulation. Although protamine is a mild anticoagulant, one or two supplemental 25- to 50-mg doses can be given empirically if heparin rebound is suspected. In most instances the heart-lung machine should be available for immediate use until the patient leaves the operating room.
Starting Cardiopulmonary Bypass
CPB is started at the surgeon's request with concurrence of the anesthesiologist and perfusionist. As venous return enters the machine, the perfusionist progressively increases arterial flow while monitoring the patient's blood pressure and volume levels in all reservoirs. Six observations are critical:
Once full stable cardiopulmonary bypass is established for at least 2 minutes, lung ventilation is discontinued, perfusion cooling may begin, and the aorta may be clamped for arresting the heart.
Antegrade blood or crystalloid cardioplegia is administered directly into the aortic root at 60 to 100 mm Hg pressure proximal to the aortic cross-clamp by a dedicated cardioplegia roller pump (see Fig. 11-2). Blood entering the coronary sinus is captured by the right atrial or unsnared caval catheters; right ventricular distention is prevented. Usually the heart is cooled to a prespecified myocardial temperature range. The heart usually arrests within 30 to 60 seconds; delay indicates problems with delivery of the solution or unrecognized aortic regurgitation. Some surgeons monitor myocardial temperature or pH via direct needle sensors.235
The usual flow of retrograde cardioplegia is 200 to 400 mL/min at coronary sinus pressures between 30 and 50 mm Hg.236 Higher pressures may injure the coronary venous system198; low pressures usually indicate inadequate delivery due to malposition of the catheter or leakage around the catheter cuff, but may indicate a tear in the coronary sinus.199 Induction of electrical arrest is slower (2 to 4 minutes) than with antegrade, and retrograde cardioplegia may provide incomplete protection of the right ventricle.196,237
Key Determinants of Safe Perfusion
The following offers rational guidelines for management of CPB, which uses manipulation of temperature, hematocrit, pressure, and flow rate to adequately support cellular metabolism during nonphysiologic conditions.
BLOOD FLOW RATE
Normally, basal cardiac output is determined by oxygen consumption, which is approximately 250 mL/min. It is impractical to measure oxygen consumption during cardiac surgery; therefore, the generally accepted flow rate at 35° to 37°C and hematocrit of 25% is approximately 2.4 L/min m2 in deeply anesthetized and muscle-relaxed patients. Hemodilution reduces blood oxygen content from approximately 20 mL dL to 10 to 12 mL dL; consequently flow rate must increase over resting normal cardiac output or oxygen demand must decrease. The resistance of venous catheters, turbulence, and loss of physiologic controls of the vasculature are reasons venous return and maximum pump flows are limited.
Hypothermia reduces oxygen consumption by a factor of 0.5 for
every 10°C decrease in temperature. However, at both normothermia
and hypothermia maximal oxygen consumption falls with decreasing
flow as described in the following equation:
This relationship at various temperatures is depicted in Figure 11-7. For this reason Kirklin and Barratt-Boyes238 recommend that flows be reduced only to levels which permit at least 85% of maximal an oxygen consumption. At 30°C this flow rate is approximately 1.8 L/min/m2; at 25°C, 1.6 L/min/m2; and at 18°C, 1.0 L/min/m2.
Theoretical benefits of pulsatile blood flow include transmission of more energy to the microcirculation, which reduces critical capillary closing pressure, augments lymph flow, and improves tissue perfusion and cellular metabolism. Pulsatile flow, theoretically, also reduces vasocontrictive reflexes and neuroendocrine responses and may increase oxygen consumption, reduce acidosis, and improve organ perfusion. However, despite extensive investigation no one has convincingly demonstrated a benefit of pulsatile blood flow over nonpulsatile blood flow for short- or long-term CPB.112,115,116,239–243 Two studies reported the association of pulsatile flow with lower rates of mortality, myocardial infarction, and low cardiac output syndrome,244,245 but others failed to detect clinical benefits.246–251
Pulsatile CPB, which actually reproduces the normal pulse pressure within the body, is expensive, complicated, and requires a large-diameter aortic cannula. Higher nozzle velocities increase trauma to blood elements,252 and pulsations may damage micromembrane oxygenators.253 Thus for clinical CPB, nonpulsatile blood flow is an acceptable, nonphysiologic compromise with few disadvantages.
Systemic arterial blood pressure is a function of flow rate, blood viscosity (hematocrit), and vascular tone. Perfusion of the brain is normally protected by autoregulation, but autoregulation appears to be lost somewhere between 55 and 60 mm Hg during CPB at moderate hypothermia and a hematocrit of 24%.133,254–256 Cerebral blood flow may still be adequate at lower arterial pressures,257,258 but the only prospective randomized study found a lower combined major morbidity/mortality rate when mean arterial pressure was maintained near 70 mm Hg (average 69 ± 7) rather than below 60 (average 52).259 In older patients, who may have vascular disease260 and/or hypertension, mean arterial blood pressure is generally maintained between 70 and 80 mm Hg at 37°C. Higher pressures are undesirable because collateral blood flow to the heart and lungs increases blood in the operative field.
Hypotension during CPB may be due to low pump flow, aortic dissection, measurement error, or vasodilatation. Phenylephrine is most often used to elevate blood pressure, but arginine vasopressin (0.05–0.1 unit/min) has recently been introduced. If anesthesia is adequate, hypertension is preferably treated with nitroprusside instead of nitroglycerin, which predominately dilates veins.
The ideal hematocrit during CPB remains controversial because of competing advantages and disadvantages. Low hematocrits reduce blood viscosity and hemolysis, reduce oxygen-carrying capacity, and reduce the need for autologous blood transfusion. In general, viscosity remains stable when percent hematocrit and blood temperature (in °C) are equal (i.e., viscosity is constant at hematocrit 37%, temperature 37°C, or at hematocrit 20%, temperature 20°C). Hypothermia reduces oxygen consumption and permits perfusion at 26°C to 28°C with hematocrits between 18% and 22%, but at higher temperatures limits on pump flow may not satisfy oxygen demand.261–263 Hill264 found that hematocrit during CPB did not affect either hospital mortality or neurologic outcome, but DeFoe observed265 increasing hospital mortality with hematocrits below 23% during CPB; thus the issue remains unresolved.266 However, higher hematocrits (25%–30%) during CPB appear justified263 in view of the increasing safety of autologous blood transfusion, improved neurologic outcomes with higher hematocrits in infant cardiac surgery,267 and more frequent operations near normothermia in older sicker patients.
The ideal temperature for uncomplicated adult cardiac surgery is also an unsettled question.263 Until recently nearly all operations reduced body temperature to 25° to 30°C during CPB to protect the brain, support hypothermic cardioplegia, permit perfusion at lower flows and hematocrits, and increase the safe duration of circulatory arrest in case of emergency. Hypothermia, however, interferes with enzyme and organ function, aggravates bleeding, increases systemic vascular resistance, delays cardiac recovery, lengthens duration of bypass, increases the risk of cerebral hyperthermia, and is associated with higher levels of depression and anxiety postoperatively.268 Since the embolic risk of cerebral injury often is greater than perfusion risk, perfusion at higher temperatures (33°C-35°C), or "tepid" CPB, is recommended, in part because detrimental high blood temperatures are avoided during rewarming.269 Increasingly, efforts are made to avoid cerebral hyperthermia during and after operation, and one study suggests improved neuropsychometric outcomes if patients are rewarmed to only 34°C.270
There are two strategies for managing pH/Pco2 during hypothermia: pH stat and alpha stat. During deep hypothermia and circulatory arrest (see below) there is increasing evidence that pH-stat management may produce better neurologic outcomes during pediatric cardiac surgery.267 Alpha stat may be better in adults.248,271,272 pH stat maintains temperature-corrected pH 7.40 at all temperatures and requires the addition of CO2 as the patient is cooled. Alpha stat allows the pH to increase during cooling so that blood becomes alkalotic. Cerebral blood flow is higher, and pressure is passive and uncoupled from cerebral oxygen demand with pH stat. With alpha stat, cerebral blood flow is lower, autoregulated, and coupled to cerebral oxygen demand.273
Pao2 should probably be kept above 150 mm Hg to assure complete arterial saturation. Whether or not high levels (i.e., >200 mm Hg) are detrimental has not been determined.
Although Hill264 found no relationship between blood glucose concentrations during CPB and adverse neurologic outcome, others are concerned that hyperglycemia (>180 mg/dL) aggravates neurologic injury230 and other morbidity/mortality.274
Systemic arterial pressure is typically monitored by radial, brachial, or femoral arterial catheter; central venous pressure is routinely monitored by a jugular venous catheter. Routine use of a Swan-Ganz pulmonary arterial catheter is controversial and not necessary for uncomplicated operations in low-risk patients.275 During CPB the pulmonary artery catheter should be withdrawn into the main pulmonary artery to prevent lung perforation and suture ensnarement.
A comprehensive transesophageal echocardiography (TEE) examination276 is an important monitor during most applications of CPB277 to assess catheter and vent insertion and location196,278,279; severity of regional atherosclerosis43,44; myocardial injury, infarction, dilatation, contractility, thrombi, and residual air; undiagnosed anatomic abnormalities276; valve function after repair or replacement; diagnosis of dissection59,280; and adequacy of de-airing at the end of CPB.281
Bladder or rectal temperature is usually used to estimate temperature of the main body mass, but does not reflect brain temperature.282 Esophageal and pulmonary artery temperatures may be affected by local cooling associated with cardioplegia. The jugular venous bulb temperature is considered the best surrogate for brain temperature, but is difficult to obtain.283 Nasopharyngeal or tympanic membrane temperatures are more commonly used, but tend to underestimate jugular venous bulb temperature during rewarming by 3° to 5°C.284 During rewarming, arterial line temperature correlates best with jugular venous bulb temperature.285
The efficacy of neurophysiologic monitoring during CPB is under investigation and not yet established as necessary. Techniques being investigated include jugular venous bulb temperature and saturation, transcranial Doppler ultrasound, near-infrared transcranial reflectance spectroscopy (NIRS), and the raw or processed electroencephalogram (EEG).286,287
ADEQUACY OF PERFUSION
During CPB oxygen consumption (VO2) equals pump flow rate times the difference in arterial (CaO2) and venous oxygen content (CvO2). For a given temperature, maintaining VO2 at 85% predicted maximum during CPB assures adequate oxygen delivery (see Fig. 11-7). 238 Oxygen delivery (DO2) equals pump flow times CaO2 and should be above 250 mL/min/m2 during normothermic perfusion.261 Mixed venous oxygen saturation (SvO2) assesses the relationship between DO2 and VO2; values below 60% indicate inadequate oxygen delivery. Because of differences in regional vascular tone, higher SvO2 does not assure adequate oxygen delivery to all vascular beds.210,288 Metabolic acidosis (base deficit) or elevated lactic acid levels also indicate inadequate perfusion.
Urine output is usually monitored but varies with renal perfusion, temperature, composition of the pump prime, diuretics, absent pulsatility, and hemoconcentration. Urine production is reassuring during CPB and oliguria requires investigation.
GASTRIC TONOMETRY AND MUCOSAL FLOW
These Doppler and laser measurements gauge splanchnic perfusion but are rarely used clinically.
Stopping Cardiopulmonary Bypass
Prior to stopping CPB the patient is rewarmed to 34°C to 36°C, the heart is defibrillated, and the lungs are reexpanded (40 cm H2O pressure) and ventilated. Cardiac rhythm is monitored, and hematocrit, blood gases, acid-base status, and plasma electrolytes are reviewed. If the heart has been opened, TEE is recommended for detection and removal of trapped air before ejection begins. Caval catheters are adjusted to ensure unobstructed venous return to the heart. If inotropic drugs are anticipated, these are started at low flow rates. Vent catheters are removed, although sometimes an aortic root vent is placed on gentle suction to remove undiscovered air.
Once preparations are completed, the surgeon, anesthesiologist, and perfusionist begin to wean the patient off CPB. The perfusionist gradually occludes the venous line and simultaneously reduces pump input as cardiac rate and rhythm, arterial pressure and pulse, and central venous pressure are monitored and adjusted. Initially blood volume within the pump is kept constant, but as pump flow approaches zero, volume is added or removed from the patient to produce arterial and venous pressures within the physiologic ranges. During weaning, cardiac filling and contractility is often monitored by TEE, and intracardiac repairs and regional myocardial contractility are assessed. Pulse oximetry saturation near 100%, end-tidal CO2 greather than 25 mm Hg, and mixed venous oxygen saturation higher than 65% confirm satisfactory ventilation and circulation. When cardiac performance is satisfactory and stable, all catheters and cannulas are removed, protamine is given to reverse heparin, and blood return from the surgical field is discontinued.
Once the patient is hemodynamically stable, as determined by surgeon and anesthesiologist, and after starting wound closure, the perfusate may be returned to the patient in several ways. The entire perfusate may be washed and returned as packed cells. Excess fluid may be removed by a hemoconcentrator. More often the perfusate, which still contains heparin, is gradually pumped into the patient for hemoconcentration by the kidneys. Occasionally some of the perfusate must be bagged and given later. The heart-lung machine should not be completely disassembled until the chest is closed and the patient is ready for transfer.
Reoperations, surgery of the descending thoracic aorta, and minimally invasive procedures may be facilitated by surgical incisions other than midline sternotomy. These alternative incisions often require alternative methods for connecting the patient to the heart-lung machine. Some alternative applications of CPB are presented below.
Anterolateral incisions through the 4th or 5th interspaces provide easy access to the cavae and right atrium, adequate access to the ascending aorta, and no direct access to the left ventricle. Adequate exposure of the ascending aorta is available for cross-clamping, aortotomy, and administration of cardioplegia by retracting the right atrial appendage. De-airing the left ventricle (e.g., after mitral valve repair) is more difficult. External pads facilitate defibrillation.
Lateral or posterolateral incisions in the left chest are used for a variety of operations. Venous return may be captured by cannulating the pulmonary artery via a stab wound in the right ventricle, or by retrograde cannulation of the left pulmonary artery or cannulation of the left iliac or femoral vein. With iliac or femoral cannulation, venous return is augmented by threading the cannula into the right atrium using TEE guidance.289 The descending thoracic aorta or left subclavian, iliac, or femoral arteries are accessible for arterial cannulation.
LEFT HEART BYPASS
Left heart bypass utilizes the beating right heart to pump blood through the lungs to provide gas exchange.290 An oxygenator is not used and intake cannulation sites are exposed through a left thoracotomy. The left superior pulmonary vein–left atrial junction is an excellent cannulation site for capturing blood. The left atrial appendage can also be used, but is more friable and difficult. The apex of the left ventricle is infrequently used because of myocardial injury. The tip of the intake catheter must be free in the left atrium and careful technique is required to avoid air entry during cannulation and perfusion. The extracorporeal circuit typically consists only of tubing and a centrifugal pump and does not include a reservoir, heat exchanger, or bubble trap. This reduces the thrombin burden (see section 11B) and may permit reduced or no heparin, if anticoagulation poses an additional risk (e.g., in acute head injury). Otherwise, full heparin doses are recommended. The reduced perfusion circuit precludes the ability to add or sequester fluid, adjust temperature, or intercept systemic air emboli. Intravenous volume expanders may be needed to maintain adequate flows; temperature can usually be maintained without a heat exchanger.291
Full left heart bypass may be employed for left-sided coronary artery surgery by draining all of the pulmonary venous return out of the left atrium and leaving no blood for left ventricular ejection. If the heart fibrillates, blood can still passively pass through the right heart and lungs, but often an elevated central venous pressure is required.292
Partial left heart bypass is identical in configuration and cannulation to full left heart bypass and is used to facilitate surgery on the descending thoracic aorta. The patient's left ventricle supplies blood to the aorta proximal to aortic clamps, and the circuit supplies blood to the distal body. Typically about two-thirds normal basal cardiac output (i.e., 1.6 L/min/m2) is pumped to the lower body. Arterial pressure is monitored proximal (radial or brachial) and distal (right femoral, pedal) to the aortic clamps. Blood volume in the body and circuit is assessed by central venous pressure and TEE monitoring of chamber dimensions. Management is more complicated because of the single venous circulation and separated arterial circulations.290,293
PARTIAL CARDIOPULMONARY BYPASS
Partial CPB with an oxygenator is also used to facilitate surgery of the descending thoracic aorta. After left thoracotomy, systemic venous and arterial cannulas are placed as described above. The perfusion circuit includes a reservoir, pump, oxygenator, heat exchanger, and bubble trap. The beating left ventricle supplies the upper body and heart, so lungs must be ventilated and upper body oxygen saturation should be independently monitored. Blood flow to the separate upper and lower circulations must be balanced as described for partial left heart bypass above.
FULL CARDIOPULMONARY BYPASS
Full CPB with peripheral cannulation is used when access to the chest is dangerous because of proximity of the heart, vital vessels (e.g., mammary arterial graft), or pathologic condition (e.g., ascending aortic mycotic aneurysm) abutting the anterior chest wall.3 The patient is supine and a complete extracorporeal perfusion circuit is prepared and primed. Venous cannulas may be inserted into the right atrium via the iliac or femoral vessels and/or the right jugular vein. The iliac, femoral, or axillary-subclavian arteries may be used for arterial cannulation. Initiation of CPB decompresses the heart, but cooling is usually deferred to keep the heart beating and decompressed until the surgeon can insert a vent catheter.
FEMORAL VEIN TO FEMORAL ARTERY BYPASS
Femoral vein to femoral artery bypass with full CPB is used to initiate bypass outside the operating room for emergency circulatory assistance,3 supportive angioplasty,294 or accidental hypothermia. Femoral vessel cannulation is occasionally used during other operations to facilitate control of bleeding (e.g., cranial aneurysm, tumor invading the inferior vena cava) or ensure oxygenation (e.g., lung transplantation, upper airway reconstruction).
CANNULATION FOR MINIMALLY INVASIVE (LIMITED ACCESS) SURGERY
Off-pump coronary artery bypass (OP-CAB) describes construction of coronary arterial bypass grafts on the beating heart without CPB. Minimally invasive direct coronary artery bypass (MID-CAB) refers to coronary arterial bypass grafting with or without CPB through small, strategically placed incisions. Peripheral cannulation sites, described above, may be used, but often central cannulation of the aorta, atrium, or central veins is accomplished using specially designed or smaller cannulas placed through the operative incision or through a separate small incisions in the chest wall.295,296 Venous return may be augmented by applying negative pressure (see discussion of venous cannulation above); often soft tipped arterial catheters are used to minimize arterial wall trauma.27
The Port-Access System provides a means for full CPB, cardioplegia administration, and aortic cross-clamping without exposing the heart and can be used for both valvular and coronary arterial operations.70,279 Through the right internal jugular vein separate transcutaneous catheters are inserted into the coronary sinus for retrograde cardioplegia and the pulmonary artery for left heart venting. A multilumen catheter is inserted through the femoral artery and using TEE and/or fluoroscopy is positioned in the ascending aorta for arterial pump inflow, for balloon occlusion of the ascending aorta, and for administration of antegrade cardioplegia into the aortic root. Venous return is captured by a femoral venous catheter advanced into the right atrium. The system allows placement of small skin incisions directly over the parts of the heart that require surgical attention.
Minimally invasive surgery using CPB is associated with potential complications that include perforation of vessels or cardiac chambers, aortic dissection, incomplete de-airing, systemic air embolism, and failure of the balloon aortic clamp. Because CO2 is heavier than air and more soluble in blood, the surgical field is sometimes flooded with CO2 at 5- to 10-L/min flow to displace air when the heart is open. The balloon aortic clamp can leak, prolapse through the aortic valve, or move distally to occlude arch vessels. For safety the position of the occluding balloon is closely monitored by TEE, bilateral radial arterial pressures, and one of the following: transcranial Doppler ultrasound, cerebral near-infrared spectroscopy, or electroencephalogram.296a
Deep Hypothermic Circulatory Arrest
Deep hypothermic circulatory arrest (DHCA) is used for operations involving the aortic arch, porcelain aorta, thoracoabdominal aneurysms, pulmonary thromboendarterectomy, selected uncommon cardiovascular and neurologic procedures,297,298 and certain complex congenital heart procedures. The technology involves reducing body temperature to less than 20°C, arresting the circulation for a short period, and then rewarming to 37°C. Deep hypothermia reduces cerebral oxygen consumption (Fig. 11-8), and attenuates release of toxic neurotransmitters and reactive oxidants during ischemia and reperfusion.299
Changes in temperature affect acid-base balance, which must be monitored and managed during deep hypothermia. The pH-stat protocol (CO2 is added to maintain temperature corrected blood pH at 7.4) may be preferred over the alpha-stat protocol, which allows cold blood to become alkalotic. Compared to alpha-stat, pH-stat increases the rate and uniformity of brain cooling,300,301 slows the rate of brain oxygen consumption by 30% to 40% at 17°C,301–303 and improves neurologic outcomes in animal models267,304,305 and perhaps in infants,306–308 but not necessarily in adults.309 Hyperglycemia appears to increase brain injury and is avoided during deep hypothermia.310 The value of high-dose corticosteroids or barbiturates remains unproven.
The safe duration of circulatory arrest during deep hypothermia is unknown. In adults arrest times as short as 25 minutes are associated with poor performance on neuropsychologic tests of fine motor function and memory.311 Ergin312 found duration of arrest was a predictor of temporary neurologic dysfunction, which correlated with long-term neuropsychologic deficits.313 At 18°C, cerebral metabolism and oxygen consumption are 17% to 40% of normothermia314–316 and abnormal encephalographic patterns and cerebrovascular responses can be detected after 30 minutes of circulatory arrest.314,317 Most investigators,318–322 but not all323 report increased mortality and adverse neurologic outcomes after 40 to 65 minutes of circulatory arrest. Most surgeons try to keep the period of arrest at less than 45 minutes and, if the operation allows, many perfuse for 10 to 15 minutes between serial arrest periods of 10 to 20 minutes.
Antegrade and Retrograde Cerebral Perfusion
Antegrade cerebral perfusion is used in lieu of DHCA or as a supplement. The cerebral vessels can be cannulated separately and perfused together by a single pump324 or perfused collectively after a graft with a side branch is sewn to the top of the aortic arch from which the innominate, left carotid, and left subclavian arteries originate. Separate perfusion of separately cannulated vessels is rarely done. Perfusion is usually provided by a separate roller pump that receives blood from the arterial line. Line pressure is monitored and a microfilter may or may not be used. The cerebral vessels are collectively perfused with cold blood between 10° and 18°C and at approximate flows of 10 mL/kg/min; perfusion pressures are restricted to 30 to 70 mm Hg. At the present time each individual surgeon seems to have a preferred protocol between these broad ranges.325–332 The adequacy of cerebral perfusion can be assessed by monitoring jugular venous saturation or near-infrared spectroscopy. Selective antegrade cerebral perfusion risks dislodging atheromatous emboli or causing air embolism, cerebral edema, or injury from excessive perfusion pressure.
Retrograde cerebral perfusion (RCP) was introduced in 1980 as emergency treatment for massive air embolism.333 Ueda introduced continuous RCP for cerebral protection as an adjunct to deep hypothermic circulatory arrest during aortic surgery.334 During RCP and DHCA the superior vena cava is perfused at blood pressures usually between 25 and 40 mm Hg, temperatures between 8°C and 18°C, and flows between 250 and 400 mL/min from a spur off the arterial line, which is clamped downstream to the spur. Some surgeons advocate much higher pressures and flows to compensate for runoff and have not shown detrimental effects.335 A snare is usually placed around the superior caval catheter cephalad to the azygous vein to reduce runoff. The IVC may or may not be occluded.322,336–339
Retrograde cerebral perfusion has been widely and safely used,321,335,339–347 but its effectiveness in protecting the brain is not clear.322,328,348 The method can wash out some particulate emboli entering from arteries, which is a major cause of brain injury after aortic surgery.337,349 However, it is not clear how adequately and completely all regions of the brain are perfused.322,339,348,350 Lin342 found cortical flows to be only 10% of control values. RCP slows but does not arrest the decrease in cerebral oxygen saturation324,335 and the decay in amplitude of somatosensory evoked potentials.351 Others from clinical comparisons and animal studies believe RCP provides some cerebral protection over DHCA alone.321,335,339,341,342,344,345,347,352 A few studies report that antegrade cerebral perfusion provides better protection than retrograde.324,338,353
Complications and Risk Management
Life-threatening incidents occur in 0.4% to 2.7% of operations with CPB and the incidence of serious injury or death is between 0.06% and 0.08% (Table 11-4).94,151,354 Massive air embolism, aortic dissection, dislodgement of cannulas, and clotting within the circuit during perfusion are the principal causes of serious injury or death. Malfunctions of the heater-cooler, oxygenator, pumps, and electrical supply are the most common threatening incidents related to equipment. Other threatening incidents include premature takedown or clotting within the perfusion circuit. Complications related to connections to and from the heart-lung machine and perfusion during operation are described above with descriptions of the various components of the perfusion circuit.
The incidence of massive air embolism is between 0.003% to 0.007% with 50% of outcomes adverse.94,151 Air can enter any component of the perfusion circuit at anytime during operation if the integrity of the circuit is broken.355 Stopcocks, connections, vent catheters, empty reservoirs, purse-string sutures, cardioplegia infusion catheters, and unremoved air in opened cardiac chambers are the most common sources of air emboli. Uncommon sources include oxygenator membrane leaks, residual air in the circuit after priming, reversal of flow in venous or arterial lines, and unexpected inspiration by the patient during cannula removal.
Massive air embolism during perfusion is a catastrophe and management guidelines are evolving.20,333,355–358 Perfusion should stop immediately and clamps should be placed on both venous and arterial lines. Air in the circuit should be rapidly removed by recirculation and entrapment of all air in a reservoir or bubble trap. The patient should be immediately placed in steep Trendelenburg position and blood and air at the site of entry should be aspirated until no air is retrieved. TEE should be rapidly employed to search for air, but perfusion must resume promptly depending upon body temperature to prevent ischemic brain damage. Cooling to deep hypothermia should be considered to protect the brain and other organs while air is located and removed. As soon as possible, retrograde perfusion of the brain should be undertaken while the aortic arch is simultaneously aspirated with the patient in steep Trendelenburg position. Corticosteroids and/or barbiturates may be considered. Depending upon circumstances and availability, hyperbaric oxygen therapy may be helpful if patients can be treated within 5 hours of operation.357,359
Minimizing risks of extracorporeal perfusion requires strict attention to personnel training, preparation and training for emergencies, equipment function, and record keeping.20 All members of the operative team must be trained, certified, and recertified in their respective roles and participate in continuing education programs. A policy manual for the perfusion team and written protocols should be developed and continuously updated for various types of operations and emergencies. Emergency kits are prepared for out-of-operating-room crises. Adequate supplies are stocked in designated locations with sufficient inventory to support any operation or emergency for a specified period. An inventory of supplies is taken and recorded at regular intervals. Checklists are prepared and used for setting up the perfusion system and connecting to the patient. Equipment is inspected at regular intervals; worn, loose, or outdated parts are replaced; and preventive maintenance is provided and documented. New equipment is thoroughly checked before use and instructions are thoroughly digested by all user personnel. Safety alarms are optional; none replace the vigilance and attention of all OR personnel during an operation. Complete, signed written records are required for every perfusion; adverse events are recorded in a separate log and reviewed by the entire OR team. A continuous quality assurance program is desirable.360
During the procedure communication must be open between the surgeon, anesthetist, and perfusionist to coordinate activites. Statements are verbally acknowledged. Distractive conversations are discouraged. The entire OR team is committed to a zero-error policy, which can only be achieved by discipline and attention to details.354,361,362