The anesthetic management of patients undergoing coronary artery bypass graft surgery (CABG) requires an understanding of myocardial oxygen supply and demand, patient monitoring, and the anesthetic techniques that provide myocardial protection and favor oxygen delivery over consumption. Myocardial ischemia results when there is an imbalance between the oxygen supply of the coronary circulation and the metabolic demand of myocardial tissue. Ischemia initially leads to contractile dysfunction. However, if ischemia is severe or prolonged, it can lead to cell death, tissue necrosis, and permanent loss of contractile function of the affected myocardial region. This section reviews the basic pathophysiology of myocardial ischemia, the anesthetic management of patients at risk for developing myocardial ischemia, and anesthetic considerations during CABG surgery.
Coronary artery anatomy is particularly relevant to the anesthesiologist caring for patients with coronary artery disease. The severity of the coronary obstruction correlates with the margin of reserve for tolerating tachycardia and hypotension. Patients with coronary lesions obstructing 99% of the lumen (subtotal occlusion) may not tolerate even mild degrees of tachycardia and hypotension, whereas patients with lesions in the 70% to 75% range may tolerate some degree of hemodynamic compromise before developing ischemia. Knowledge of specific coronary lesions also allows for focused monitoring of targeted myocardial regions at increased risk for myocardial ischemia.
The 2 major coronary arteries are the first arterial branches of the aorta, which arise from 2 of the 3 sinuses of Valsalva in the aortic root (Fig. 52-1). The right coronary sinus is anteriorly located, and the left coronary sinus is located laterally and slightly posterior. The left coronary artery (LCA) divides into the left anterior descending coronary artery (LAD) and left circumflex artery (LCx). The LAD gives rise to the diagonal branches and supplies the anterior wall of the right ventricle (RV), the anterior two-thirds of the interventricular septum, the anterior wall of the left ventricle (LV), and the ventricular apex. The LCx gives rise to the obtuse marginal branches and supplies the left atrium (LA), and the posterior and lateral walls of the LV. Patients are described as having "a left main" if they have a significant lesion in the LCA. These patients are at particular risk for developing myocardial ischemia that affects a large portion of the LV, which would cause rapid hemodynamic compromise and cardiac arrest. Patients described as having a "left main equivalent" have high-grade obstructions in both the LAD and LCx arteries. These patients potentially have the same risk of coronary ischemia and rapid hemodynamic compromise as patients with left main disease.
The right coronary artery (RCA) supplies blood to the lateral and posterior walls of the RV, the inferior wall of the LV, and the posterior third of the interventricular septum. The RCA terminates as the posterior descending artery (PDA) in 85% to 90% of the population. The blood supply of the PDA determines the pattern of coronary dominance: RCA for right dominant and LCx for left dominant. Most patients have an RCA-dominant or balanced pattern of blood supply to the PDA. A balanced pattern is used to describe coronary anatomy with no particular dominance in terms of the blood supply to the PDA. The presence of a right-dominant or balanced system during OPCABG frequently leads to bradycardia and hypotension during RCA occlusion because it supplies blood to the sinoatrial node in 55% of patients, whereas the PDA supplies the atrioventricular node in right-dominant patients.
Myocardial blood collects in the coronary veins, which drain into the coronary sinus, and subsequently the right atrium (RA). The coronary sinus is often used as a conduit for the delivery of cardioplegia to the myocardium in a retrograde fashion. This is possible because the coronary veins lack valves, allowing blood to flow in either direction. Retrograde cardioplegia is used in patients with aortic insufficiency (AI), during aortic valve (AV) surgery, in the presence of high-grade coronary obstructions, and in patients with previous CABG who have a patent internal mammary artery graft. All of these situations limit the antegrade delivery of cardioplegia to the myocardium from the aortic root. Retrograde delivery of cardioplegia via the coronary sinus also has limitations. A coronary sinus catheter inserted beyond the small cardiac vein will prevent delivery of cardioplegia to the RV. Subsequently, the right heart may be poorly protected from myocardial ischemia during aortic cross-clamping.40 Coronary sinus catheters that are directed into the small or middle cardiac vein may cause coronary sinus rupture.
The LAD is positioned on the anterior aspect of the heart. The obtuse marginal branches of the LCx and diagonal branches of the LAD are located on the lateral or posterior aspect of the heart (see Fig. 52-1). The surgeon must rotate or lift the heart to gain access to these vessels, causing hemodynamic compromise if the cardiac chambers are compressed. The pulmonary outflow tract also may be compressed with cardiac rotation, again resulting in severe hypotension by dramatically reducing preload. Additionally, the electrocardiographic (ECG) axis changes during cardiac manipulation and may change the ECG–coronary artery anatomic relationship, limiting the ability to use ECG for ischemia monitoring. Use of TEE for ischemia and ventricular function monitoring may be compromised when the heart is lifted or manipulated within the surgical field. The PAC may be malpositioned during these maneuvers, providing erroneous data regarding cardiac output and filling pressures.
Coronary Blood Flow Physiology
The physiology of coronary blood flow is based on the assumption that coronary arteries are nondistensible tubes, and that blood is a homogeneous fluid. Blood flows from a region of higher pressure (aorta) to one of lower pressure (capillaries). The rate of flow is dependent on the pressure gradient that moves red blood cells through the coronary arteries in a laminar flow pattern. Flow is most dependent on the radius of the blood vessel, which is why coronary arterioles maximally dilate in response to coronary arterial stenosis.41 Coronary stenosis causes the vessel to maximally dilate distal to the stenosis, creating a vessel with a fixed radius. Manipulation of the coronary perfusion pressure then becomes the most important factor that determines coronary blood flow and the most important physiologic parameter manipulated by the anesthesia provider in the setting of coronary ischemia. Exercise-induced ischemia causes a compensatory increase in heart rate, α1-adrenergic–induced vasoconstriction, and increased LV filling pressure, all of which reduce coronary blood flow.42 Adequate coronary perfusion pressure is the most important factor in the prevention and treatment of myocardial ischemia, both in the operating room and during exercise.
A second important factor is blood viscosity, determined rheologically as the concentration or suspension of erythrocytes within the blood. Patients with coronary artery disease (CAD) have disturbed blood flow patterns that create an increased tendency for coronary arterial thrombosis.43 These abnormal flow patterns underscore the importance of aspirin therapy in the medical management of patients with CAD by reducing platelet adhesion and aggregation at the site of coronary stenoses.
Coronary blood flow has a characteristic phasic perfusion pattern, 70% to 80% of which occurs during the diastolic phase of the cardiac cycle. Cardiac contraction during systole impedes myocardial perfusion by increasing intraventricular cavitary pressure and coronary artery resistance, thus producing a nonlinear relationship between heart rate and diastolic time.44 β-Blockade is a very effective medical therapy for patients with CAD by preventing even small increases in heart rate during the perioperative period, reducing mortality with heart rate reduction, and improving outcome.45
Heart rate reduction improves subendocardial coronary artery blood flow,46,47 allowing for better matching of myocardial oxygen supply and demand (myocardial perfusion–contraction coupling), thus preserving regional myocardial contractility.48 Recovery of stunned or hibernating myocardium in patients with ischemic heart disease occurs with restoration of myocardial perfusion–contraction coupling.
Myocardial Oxygen Delivery
Myocardial oxygen delivery depends on the oxygen content in the blood and is composed of hemoglobin-bound oxygen and dissolved oxygen. Hemoglobin-bound oxygen composes most of the blood's carrying capacity. However, delivery of oxygen to myocardial cells is dependent on release of oxygen from hemoglobin and is represented by the oxygen–hemoglobin dissociation curve. A leftward shift of this curve from normal indicates a greater affinity of oxygen by hemoglobin, which has the effect of drawing more oxygen into the blood as it passes through the lungs but reducing oxygen release at the cellular level. A leftward shift is caused by alkalosis (both metabolic and respiratory), hypothermia, carboxyhemoglobinemia, methemoglobinemia, and decreased red blood cell 2,3-diphosphoglycerate (DPG), which may be observed after transfusion of a large volume of old blood stored in acid-citrate-dextrose. A rightward shift indicates less affinity of the red cells for oxygen, which has the effect of greater oxygen release to the tissues but at the expense of drawing less oxygen into the blood as it passes through the lungs. A rightward shift is caused by acidosis (both metabolic and respiratory), hyperthermia, and increased 2,3-DPG in the red blood cells.
Although anemia clearly reduces the oxygen-carrying capacity of blood, clinical studies have not determined the lowest acceptable level of anemia that does not produce myocardial ischemia. The degree of anemia that produces myocardial ischemia is dependent on factors that are specific for each patient and the loading conditions of the ventricle. Factors include the severity of CAD, myocardial wall thickness and tension, heart rate, and perfusion pressure. Isovolemic reduction in hemoglobin to 4.6 to 5.3 mg/dL in healthy volunteers produced ST-segment changes on Holter monitoring in 2 of 11 subjects, whereas hemoglobin levels of 5.0 mg/dL led to myocardial ischemia infrequently.49 In another investigation, ECG ST-segment changes suggestive of ischemia occurred in only 3 of 55 subjects during acute reduction in hemoglobin concentrations to 5 g/dL. These authors attributed the imbalance of myocardial oxygen supply and demand to tachycardia.50 Although excessive hemodilution (median lowest hematocrit below 25%) during CPB is a risk factor for major morbidity even in the absence of blood transfusion, preoperative anemia may not be associated with an increased risk of morbidity, provided that the lowest hematocrit during cardiopulmonary bypass is maintained above 28%.12
Patients with ischemic heart disease require a higher hemoglobin concentration to minimize perioperative complications. A higher incidence of postoperative mortality was found in cardiac surgical patients older than 75 years whose preoperative systemic oxygen delivery was less than 320 mL/min/m2 and who had anemia on the second postoperative day.51 Bracey et al found no increase in morbidity, mortality, or patient self-assessment of fatigue when the hemoglobin threshold for red cell transfusion was lowered to 8.0 g/dL after CABG.52 Therefore, the lower limit of hemoglobin concentration depends on multiple factors, such as the patient's age, heart rate, perfusion pressure, clinical evidence of myocardial ischemia, and success of coronary revascularization. Moderate exposure to allogenic blood products is not associated with reduced long-term survival after coronary artery bypass surgery.53
Myocardial oxygen demand is primarily determined by heart rate, ventricular wall tension, and myocardial contractility. Acting on the myocardial β receptors, β-blockers decrease heart rate and reduce contractility and thus are the primary treatment for patients with CAD at risk for myocardial ischemia. Although treatment with atenolol in the perioperative period does not significantly alter the neuroendocrine stress response,54 perioperative β-blockade reduces mortality and myocardial infarction (MI) among patients undergoing noncardiac surgery.55-57 Patients treated with metoprolol for whom ventricular filling pressures were unchanged had an up to 40% reduction in myocardial oxygen consumption.45 Metoprolol also improves survival, patient well-being, and New York Heart Association (NYHA) functional class in patients with congestive heart failure (CHF).58,59 β-Blockade and subsequent heart rate reduction clearly decrease myocardial oxygen consumption and increase oxygen supply in patients with CHF. Although most anesthesiologists recognize the benefits of perioperative β-blockade, few institutions have formalized protocols for administering β-blockers to surgical patients.60
Preload is the ventricular volume at end-diastole that determines myocardial fiber length, which in part determines the force of ventricular contraction. Manipulation of preload is an important therapeutic option in the care of patients with myocardial ischemia. Nitroglycerin is commonly used for treatment of myocardial ischemia, primarily exhibiting its antianginal effect by preload reduction through venodilation and coronary vasodilation. Morphine is useful for treating myocardial ischemia by causing vasodilation (preload reduction) and providing pain relief, thereby leading to reduced heart rate. Furosemide reduces preload through both its diuretic action and venodilation.61
Determination of end-diastolic volume is problematic in the clinical arena. Pulmonary artery occlusion pressure (PAOP) is commonly used for approximating LV end-diastolic volume (LVEDV), but multiple assumptions must be made in order to use PAOP to estimate preload. Use of a pressure measurement to estimate volume must take into account LV compliance, which is the change in unit pressure for each change of unit volume. Both LVEDV and the compliance of the myocardium determine the LV end-diastolic pressure (LVEDP). Myocardial ischemia decreases ventricular compliance, thereby increasing LVEDP for the same LVEDV. This change may be reflected in PAOP measurements, allowing the use of PAOP as an ischemia monitor.
Other factors that affect the relationship between PAOP and LVEDP are mitral stenosis (MS), LA compliance, and intrathoracic pressure. Although the severity of MS does not change over the course of an anesthetic or surgical procedure, the pressure gradient between the LA and LV is dynamic, dependent on the cardiac output, heart rate, and flow though the mitral valve (MV) during the diastolic phase of the cardiac cycle. Tachycardia decreases diastolic time, thereby increasing flow through the MV during diastole and thus increasing the pressure gradient between the LA and LV. An increase in PAOP in this circumstance is due to an increase in the pressure gradient across the MV rather than an increase in preload. Actual LV preload may be reduced because tachycardia impedes LV filling in patients with MS. When PAOP is used for ischemia monitoring, trends in pressure changes must be taken in the context of these other hemodynamic variables in patients with MS.
Figure 52-2 shows a normal central venous pressure waveform and the relationship of the waveform with the ECG. PAOP appears similar but reflects LA pressure rather than RA pressure. The presence of large, prominent V waves is indicative of mitral regurgitation (MR), which can occur with ischemic papillary muscle dysfunction. This acute increase in LA volume decreases the compliance of the LA and pulmonary veins.
A normal central venous pressure (CVP) waveform consists of 3 systolic components (c wave, x descent, and v wave) and 2 diastolic components (y descent, a wave). ECG, electrocardiogram. [Reprinted and modified from Mark JB. Central venous pressure monitoring: clinical insights beyond the numbers. J Cardiothorac Vasc Anesth. 1991;5:163-173. Copyright 1991 Elsevier.]
Large changes in intrathoracic pressure also affect PAOP.62 During spontaneous inspiration, mean PAOP declines because of the decrease in intrathoracic pressure. Positive-pressure ventilation causes increased intrathoracic pressure, which is reflected in the pulmonary venous pressure. Measurement of PAOP is made at the end of expiration to minimize the effects of inspiration on intrathoracic pressure and the pulmonary vasculature.
Afterload is impedance to ventricular ejection and is best described with pressure–volume loops. The ratio of end-systolic pressure to stroke volume defines the elastance of the arterial tree. In the absence of aortic stenosis (AS), this is primarily determined by arterial vasculature tone. Afterload conditions that allow more fiber shortening allow greater metabolic efficiency and reduced oxygen consumption.63 The clinician can manipulate afterload by changing the size or radius of the LV through preload manipulation or more commonly by affecting systemic vascular resistance or blood viscosity. Although systemic vascular resistance is only 1 component of afterload, it is the only factor that is easily measured and readily changed clinically.
Inotropy describes the contractile state of the ventricle and is measured using either the ejection or isovolumic phase of ventricular contraction. Pressure–volume loops consisting of ejection, relaxation, and isovolemic pressure are drawn under different loading conditions. The slope of the serial end-systolic pressure–volume relationship describes the myofibril contractile state independently from preload or afterload (Fig. 52-3). Simple clinical tools for measuring contractility independent of preload and afterload do not exist; however, some investigators have used simultaneous pressure and echocardiography area relationships to provide measurements of contractility.64
Example of end-systolic pressure–volume relations (ESPVRs) derived by caval vein occlusion before and after cardiopulmonary bypass (CPB). The ESPVRs (left) show the increased contractile performance after CPB in this patient. Although the slope of the ESPVR (Ees) is slightly decreased, the position of all end-systolic pressure–volume points to the left and above the pre-CPB ESPVR suggests higher contractility. Dotted lines indicate the position of the ESPVR at 75 mm Hg. The same holds for the preload recruited stroke work (PRSW) relation (upper right) and the dP/dtmax–end-diastolic volume (EDV) relation (lower right), although the differences are much less pronounced. The EDPVRs (left panel) provide clear evidence for a substantial increase in chamber stiffness after CPB, as observed in all patients. [From Tulner SA, Klautz RJ, van Rijk-Zwikker GL, et al. Perioperative assessment of left ventricular function by pressure–volume loops using the conductance catheter method. Anesth Analg. 2003;97:950-957, with permission.]
Anesthetic Considerations for Patients Undergoing CABG
Patients with CAD presenting for CABG require special considerations in their anesthetic management. First and foremost are techniques that minimize myocardial oxygen demand while maximizing myocardial oxygen delivery, as described in previous sections. These considerations include preoperative preparation, intraoperative monitoring, and the use of anesthetic agents with hemodynamic effects that favor oxygen supply over demand and allow for myocardial protection. Postoperative management that provides particular attention to pain management, temperature control, and attentive hemodynamic monitoring to prevent tachycardia, hypotension, and hypertension, must also be considered. Many of these considerations apply to patients undergoing CABG, with or without CPB. However, certain considerations apply to patients who undergo CABG with CPB, although others apply if coronary revascularization is performed without CPB (ie, OPCABG).
Most patients presenting for CABG undergo extensive preoperative testing of their cardiac disease and other medical problems. Medical conditions that predispose patients to the development of CAD also affect other organ systems. They include smoking, hypertension, hypercholesterolemia, diabetes, obesity, and advanced age. It is particularly important to identify comorbidities that may prolong or complicate the patient's postoperative course. One comorbidity that deserves particular attention is respiratory insufficiency. Patients with CAD often complain of dyspnea due to ventricular dysfunction caused by myocardial ischemia. Dyspnea related to myocardial ischemia should resolve with adequate revascularization. However, patients with a long-standing smoking history who develop underlying pulmonary disease may not derive the same benefit after CABG, but instead experience exacerbation of their pulmonary disease and require prolonged postoperative mechanical ventilation and suffer pulmonary complications after surgery.
Diabetes is a progressive metabolic disorder that leads to the development of CAD, cerebral vascular disease, neuropathy, nephropathy, and retinopathy. An important aspect of diabetes in the patient with CAD is that myocardial ischemia may occur in the absence of classic symptoms. Patients may suffer from ischemic episodes without therapy, leading to potentially irreversible cardiac damage. They may have prolonged recovery from CABG surgery because of the increased need for inotropic support. Tight control of glycemic blood levels during the perioperative period is important for reducing the incidence of wound infection following cardiac surgery.
Hypertension is another medical condition common in patients with CAD. It also is a risk factor for cerebral vascular disease, renal failure, and CHF. This condition may be asymptomatic, yet it carries the risk of end-organ damage if untreated for prolonged periods. Patients with uncontrolled hypertension often are more difficult to manage because of wide swings in blood pressure associated with events such as sternotomy and pericardotomy. Their vasculature is more responsive to catecholamines causing an exaggerated response, and the relatively volume contracted state leads to exaggerated hypotension in response to vasodilator therapy. Intraoperative blood pressure variability is associated with 30-day postoperative mortality in patients undergoing coronary bypass surgery,65 and an increased perioperative pulse pressure is associated with poor long-term survival after CABG.66
Renal disease is associated with cardiac surgical patients, especially in those with hypertension and diabetes. Development of renal failure after cardiac surgery is a concern, which occurs in 0.9% of CABG patients and 2.0% of patients undergoing valve procedures. More importantly, operative mortality has been reported to be 63.7% in patients who develop acute renal failure versus 4.3% for patients who do not develop renal failure.67 The risk of postoperative MI, reoperation for bleeding, and mediastinitis is higher in patients who develop postoperative renal failure.68
Continuous ECG monitoring, along with blood pressure measurement, pulse oximetry, and end-tidal carbon dioxide (CO2) analysis are standard monitors for all anesthetized patients. It is preferred that cardiac surgical patients have a display monitor that allows viewing of 2 ECG leads simultaneously with automated ST-segment analysis. ECG limb leads II and V5 allow for monitoring of myocardial regions supplied by the RCA and LAD coronary arteries, respectively. Automated ST-segment trending has only moderate sensitivity and specificity (75% for both) in detecting changes found by off-line Holter monitoring69 but is a marked improvement over mere observation by the clinician, whose attention must also be directed at providing anesthetic care. Monitoring 2 ECG leads simultaneously increases the sensitivity of detecting ischemia to 80% if leads II and V5 are monitored, 82% if leads II and V4 are monitored, and 90% if leads V4 and V5 are monitored (Fig. 52-4).70 Factors such as LV hypertrophy, cardiac conduction changes, electrolytes, and drugs such as digitalis all can affect the interpretation of ST segments,71 but the primary concern is acute ST-segment changes that occur during the perioperative period (Fig. 52-5).
Distribution of ischemic ST-segment changes in each of the 12 ECG leads of 105 patients with known or suspected coronary artery disease undergoing noncardiac surgery with general anesthesia. Sensitivity was calculated from the number of changes in a single lead as a percentage of the total number of episodes obtained with continuous intraoperative recording. [From London MJ, Hollenberg M, Wong MG, et al. Intraoperative myocardial ischemia: localization by continuous 12-lead electrocardiography. Anesthesiology. 1988;69:232-241, with permission.]
Electrocardiogram with ST-segment depression indicating myocardial ischemia.
All cardiac surgical patients require invasive arterial blood pressure monitoring. Although the radial artery is used at many institutions, consideration must be given to the possibility of harvesting the radial artery as a conduit for CABG. When used for this purpose, the radial artery is harvested from the patient's nondominant hand, so radial artery cannulation should be performed in the dominant hand. Femoral artery cannulation can be used and is preferred by some clinicians and institutions. The benefits of using femoral artery cannulation include a better correlation with mean arterial pressure in the immediate post-CPB period and access to the femoral artery if an IABP must be inserted. The intra-arterial catheter can be placed prior to or immediately after induction, but preinduction placement allows the clinician to respond more rapidly to the changing hemodynamic conditions that often occur during induction of anesthesia. Preinduction placement of the arterial catheter is preferred in the setting of a potentially difficult airway and for patients with a greater risk of rapidly changing hemodynamics (left main disease or severe ventricular dysfunction).
All cardiac surgical patients should have central venous access for the purpose of administering important vasoactive medications into the central circulation and for assessing volume status. The issue of whether to place a central venous pressure (CVP) catheter versus a PAC is controversial. A PAC measures pulmonary artery (PA) pressure and provides a means for sampling mixed venous oxygen saturation (SvO2). PA pressure is not easily determined with TEE, and SvO2 cannot be obtained with a CVP catheter or by TEE. Some studies have not demonstrated improved cardiac surgical outcomes with the use of a PAC.72 However, prolonged pre-CPB pulmonary hypertension and post-CPB elevation of PA diastolic pressure are predictors for the development of perioperative MI.73 Early treatment of pulmonary hypertension is presumed to improve outcome.
The American Society of Anesthesiologists (ASA) Task Force on Pulmonary Artery Catheterization has provided practice guidelines for PAC insertion (Table 52-2).74 PA pressure monitoring is indicated based on the medical condition of the patient or the nature of the surgery (Table 52-3) but is not recommended when the patient, procedure, and practice setting each poses a low risk for hemodynamic complications.74 Cardiac surgical patients with unstable angina, recent MI, active CHF, severe CAD or valvular heart disease, and severe pulmonary or renal disease should have PA pressure monitoring. However, routine PA catheterization is not necessary in all patients undergoing CABG. Outcome after CABG is not influenced by routine use of a PAC, suggesting its use can be delayed until a clinical need develops.72
Table 52-2 American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization Practice Guidelines ||Download (.pdf)
Table 52-2 American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization Practice Guidelines
Indications Related to the Patient
- Clinical evidence of significant cardiovascular disease
- Pulmonary dysfunction
- Renal insufficiency
- Other conditions associated with hemodynamic instability (eg, advanced age, endocrine disorders, sepsis, trauma, burns)
Indications Related to Surgery
- Surgical procedures associated with an increased risk of hemodynamic changes, including damage to the heart, kidneys, lungs, or brain
Indications Related to Practice Setting
- Physician skills
- Duration of procedure
- Technical support
- Training and experience of nursing staff
- Ability to manage potential complications
Table 52-3 Indications for Pulmonary Arterial Pressure Monitoring ||Download (.pdf)
Table 52-3 Indications for Pulmonary Arterial Pressure Monitoring
Indications Related to the Patient
- Right heart failure
- Pulmonary hypertension
- Pulmonary embolism
- Unstable angina
- Recent myocardial infarction
- Acute congestive heart failure
- Severe coronary artery disease
- Shock (cardiogenic, septic, or hemorrhagic)
- Massive trauma
- Severe lung disease
- Severe renal disease
Indications Related to Surgery
- Major organ transplantation
- Aortic cross-clamping procedures
- Large fluid shifts
- Massive blood loss
- Implantation/explantation of ventricular assist devices
Right bundle-branch block occurs in approximately 3% of patients undergoing PA catheterization.75 For this reason, placement of a PAC in patients with a previous left bundle-branch block is not recommended unless precautions are taken for managing the patient should complete heart block occur. A decision-making algorithm for inserting a PAC in patients with a preexisting left bundle-branch block is shown in Fig. 52-6.
Algorithm for pulmonary artery (PA) catheter insertion in patients with left bundle-branch block (LBBB). CVP, central venous pressure; TEE, transesophageal echocardiography. [Reprinted from Troianos CA. Intraoperative monitoring. In: Anesthesia for the Cardiac Patient. St. Louis, MO: Mosby; 2002:106, with permission from Elsevier.]
TEE can be used to assess global and regional myocardial contractility, volume status, and valvular function during cardiac surgery. Although TEE has revolutionized the intraoperative assessment and management of patients undergoing cardiac surgery, few data suggest that routine use of TEE for all patients with normal ventricular function undergoing elective CABG improves outcome. Regional wall-motion assessment by qualitative inspection of radial shortening and wall thickening is subjective. Accurate diagnosis is dependent on observer experience and having the ischemic myocardial segment in the imaging plane during the ischemic episode. More sophisticated techniques such as computerized digitations, color kinesis, and tissue Doppler imaging may allow for better assessment, but these techniques are not readily available or familiar to all users. Nonetheless, information obtained from TEE is far superior in quality and quantity to that obtained from a PAC and may be very helpful in guiding therapy toward optimizing hemodynamics in the perioperative period. Furthermore, TEE has proven invaluable for assessing the quality of the surgical procedure following separation from CPB, especially among patients undergoing CABG surgery who have significant ventricular dysfunction and those undergoing concurrent valve procedures, congenital heart surgery, and/or aortic surgery.35-39
Near-infrared reflectance spectroscopy has been used to demonstrate a correlation between low bifrontal regional cortical oxygen saturation and cognitive dysfunction, prolonged hospital stay, and perioperative stroke. Intraoperative cerebral oxygen desaturation is associated with an increased risk of cognitive decline and prolonged hospital stay after coronary artery bypass surgery.76 Thus some clinicians have advocated monitoring of cerebral oximetry in CABG patients as a technique for preventing profound cerebral desaturation and associated morbidity.77
Induction of general anesthesia for CABG patients can be accomplished using a variety of medications, provided the goals of preventing tachycardia, hypotension, and hypertension are achieved. The worst combination of hemodynamic perturbations is tachycardia with hypotension. Although hypertension increases ventricular wall tension and therefore myocardial oxygen demand, it also increases coronary perfusion pressure. Myocardial depression and the vasodilating effects of the anesthetic agents are the most important considerations in patients with severely impaired ventricular function or valvular heart disease. Laryngoscopy and intubation are the first intraoperative events after induction of anesthesia that test the effects of the anesthetic technique used. Coincident with these events is the institution of positive-pressure ventilation, which may result in hypotension among hypovolemic patients or in patients with air trapping due to pulmonary disease.
Patients with CAD benefit from a narcotic-based technique because of the lack of myocardial depression, a tendency for decreased heart rate, and an attenuated response to laryngoscopy and intubation. Fentanyl probably is the most frequently used opioid in cardiac surgery, although sufentanil is also a reasonable choice. The pre-bypass addition of remifentanil to a fentanil and propofol anesthetic reduces the release of biochemical markers of myocardial damage to patients undergoing elective on-pump coronary artery bypass grafting. This benefit may be attributed to either remifentanil itself or to an overall increased opioid dose.78 Use of remifentanil and sufentanil during induction has been associated with a high incidence of bradycardic/asystolic complications in patients who have been treated with β-blockers and calcium channel blockers.79,80 Many patients with CAD are likely to be taking 1 or both types of drugs. A nondepolarizing muscle relaxant devoid of cardiovascular side effects is used to facilitate intubation. Pancuronium can be used with a large dose of narcotic because the tachycardic side effects of pancuronium are balanced by the bradycardic side effects of the large-dose narcotic. Use of vecuronium or rocuronium is prudent when the initial narcotic dose is smaller because the bradycardic effects of the narcotic are not as pronounced. Pancuronium use with only a small narcotic bolus may result in undesirable tachycardia.
Modern practices that focus on early extubation and "fast-tracking" the patients through the postoperative period use smaller narcotic doses, with supplementation by short-acting hypnotic agents such as midazolam. Dexmedetomidine can also be used as an adjunct to anesthetic induction to attenuate the hemodynamic response to tracheal intubation, which is particularly important when low-dose fentanyl is used for induction.81 An intraoperative awareness protocol should be used to minimize the incidence of intraoperative recall, which is more of a concern with a low-dose narcotic-based anesthetic technique. A low concentration of a potent inhalational agent or intravenous propofol is used for hypnosis and amnesia. Reduced doses of opioids often are administered with small doses of hypnotic drugs such as benzodiazepines, thiopental, propofol, or etomidate to promote early postoperative extubation. Care must be taken when hypnotics are administered concomitantly with opioids. Mean arterial pressure can drop precipitously in hypovolemic patients. Midazolam significantly decreases blood pressure and increases heart rate when used as an induction agent.82 Propofol causes venodilation and can profoundly decrease blood pressure.83 A vasoactive drug such as ephedrine or phenylephrine should be readily available to treat hypotensive episodes during the induction of anesthesia. Although regional anesthesia for cardiac surgery may provide superior postoperative analgesia, shorter postoperative ventilation, reduced incidence of supraventricular dysrhythmias, and lower rates of perioperative MI, most clinicians use general anesthesia during CABG procedures.84
The same hemodynamic goals must be achieved for the patient with a difficult airway who requires an awake/sedated fiberoptic intubation prior to general anesthesia. The patient's airway should be well anesthetized with local anesthetics and the patient sedated with short-acting intravenous agents that blunt the response to laryngoscopy and intubation. An inhalational induction also might be considered in some patients. Alternatively, an intubating laryngeal mask airway can be used to secure the difficult airway under general anesthesia. The particular technique or approach is individualized to the patient's anatomy and medical condition, and the experience of the clinician in using 1 or more of these techniques.
Once the airway is secured and general anesthesia induced, anesthesia care is directed toward maintaining a stable blood pressure and heart rate. If access to the central circulation was not obtained before induction of anesthesia, cannulation of the internal jugular or subclavian vein is performed, and a PAC is inserted if indicated. The right internal jugular vein is often used because of its predictable location, accessibility, and direct route into the RA. The patient is placed in the Trendelenburg position during central venous cannulation, which increases preload and helps maintain blood pressure at an acceptable range following the induction of anesthesia, in the absence of surgical stimulation. Use of surface ultrasound for guiding the insertion and placement of a central venous cannula has become more popular.85 Blood pressure frequently declines as the operating room table is leveled following central venous cannulation. A fluid bolus or small doses of vasoactive drugs may be required.
Additional tasks for the anesthesia provider before surgical incision include placement of a TEE probe, antibiotic administration, determination of a baseline ACT, and infusion of antifibrinolytic drugs. Although many studies have demonstrated the beneficial effects of antifibrinolytic agents in reducing perioperative bleeding and morbidity,30 others have reported adverse side effects associated with multiorgan dysfunction and prothrombotic outcomes,31,32 especially among patients with a genetic predisposition to a hypercoagulable state.33 Thus, similar to all pharmacologic agents, the decision to administer any antifibrinolytic should include a thorough risk-to-benefit consideration that is individualized to each patient.
Patients must be anesthetized to a depth that avoids a tachycardic and hypertensive response to surgical incision. Small doses of short-acting agents such as esmolol (50-100 mg) or nitroglycerin (50-100 mcg) can be administered, or the anesthetic depth can be deepened with additional narcotic or potent inhalational agent. The patient's response to skin incision is a gauge to his or her subsequent response to the more stimulating event of median sternotomy. If the anesthetic depth was not adequate for skin incision, then additional narcotic or a bolus of esmolol should be administered before sternotomy. The lungs typically are deflated during sternotomy to prevent the sternal saw from cutting the lung parenchyma. Another complication that can occur during sternotomy is accidental tearing of the innominate vein or the RV. Sternotomy is especially hazardous during repeat CABG, where adhesions from previous surgery placed the heart immediately posterior to the sternum. Banked packed red blood cells must be immediately available at the time of sternotomy, particularly for patients at increased risk for this complication.
Maintenance of anesthesia during the pre-CPB period can be accomplished with a variety of techniques. Isoflurane–fentanyl anesthesia and propofol–fentanyl anesthesia both are acceptable techniques for maintaining anesthesia during CABG.86 Postoperative troponin release, cardiac morbidity, and mortality were similar between anesthetic regimens consisting of propofol-opioid versus isoflurane-opioid in patients undergoing CABG surgery.87 Use of sevoflurane and desflurane has been shown to result in shorter intensive care unit (ICU) and hospital length of stay.88 This finding seemed to be related to better preservation of early postoperative myocardial function. Considerable research has recently focused on the myocardial protective effects of potent inhalational anesthetics. Isoflurane protected the myocardium during ischemic episodes in an experimental model.89,90 Isoflurane and other volatile anesthetics may mimic the protective effects of a process called ischemic preconditioning.91 Brief periods of ischemia activate the protein kinase C–mediated pathway that confers cardioprotection during subsequently longer periods of ischemia.92 Sevoflurane decreases the inflammatory response after CPB, as measured by the release of IL-6, neutrophil β-integrins (CD11b/CD18), and TNF-α. Myocardial function after CPB, as assessed by regional wall motion and LV stroke work index, also is improved with sevoflurane.93 Both halothane and isoflurane have been shown to provide significant preservation of adenosine triphosphate (ATP) levels during ischemia, but this preservation did not improve hemodynamic recovery.94 In a comparative study in which patients received either propofol or inhalational anesthesia during CABG surgery, patients who received inhalational anesthesia (sevoflurane or desflurane) but not propofol had preserved LV function after CPB, with less evidence of postoperative myocardial injury.95 The cardioprotective effects are clinically most apparent when the inhalational agent is administered throughout the operation.96 Although recent evidence suggests that remifentanil may play a similar role in protective preconditioning, the effect may be attributable to an overall increased opioid dose rather than to remifentanil itself.79
Important activities that occur during the pre-CPB period include surgical dissection of the left internal mammary artery, opening of the pericardium, and placement of the aortic and venous cannulas in preparation for CPB. Sternal retraction that exposes the internal mammary artery may affect the function of intravenous and arterial catheters placed in the ipsilateral arm. This most commonly affects the left arm with harvesting of the left internal mammary artery. Papaverine is commonly injected into the ligated internal mammary artery to prevent vasospasm but may cause hypotension. This decrease in blood pressure usually is brief but may require treatment with a small dose of phenylephrine. Hypertension may develop during surgical manipulation of the pericardium and aorta as a result of sympathetic activation. A small bolus of narcotic or esmolol can blunt this hypertensive response.
Heparin is administered prior to ligation of the internal mammary artery (if used) and cannulation of the aorta to prevent thrombus formation. Heparin is a polyanionic mucopolysaccharide that increases the rate of anticoagulant effect of antithrombin III on factors II, X, XI, XII, and XIII. It usually is given in a dose range of 300 to 400 U/kg to achieve ACT greater than 400 seconds. The adequacy of anticoagulation must be determined prior to initiating CPB. For patients undergoing OPCABG, some surgeons administer a smaller dose of heparin, with the goals of achieving ACT greater than 300 seconds.
CABG without CPB (OPCABG) was first reported during the 1960s and 1970s.97,98 Advancements in the safety of CPB with better equipment and techniques allowed surgical access to more distal coronary target sites and a quiet surgical field, thereby eliminating the need for CABG without CPB.1,2 Developments in mechanical stabilization devices during the 1990s renewed the interest among surgeons to return to this technique in order to avoid the deleterious effects of CPB, particularly as the age of the surgical population increased to include more elderly patients with calcified aortas. OPCABG also allows faster recovery and fewer ICU days, providing an economic incentive to using this technique.
The anesthetic management of patients undergoing OPCABG encompasses the same hemodynamic goals as the pre-CPB management of patients undergoing CABG with CPB, but the goals are more difficult to achieve, particularly when distal coronary anastomoses are being performed. Myocardial protection with the use of inhalational agents remains an important consideration. Compared to patients who receive propofol, patients receiving sevoflurane have less myocardial injury in the first 24 postoperative hours.99 Similarly, patients who received isoflurane during OPCABG had lower troponin-T leakage than patients who received a propofol infusion.100 OPCABG requires more attention, vigilance, and intervention on the part of the anesthesia provider while the surgeon is performing the distal coronary anastomoses. Maintenance of perfusion pressure, cardiac output, and normothermia, while avoiding profound myocardial ischemia, is challenging during surgical manipulation that produces ventricular compression and temporary coronary occlusion. Ischemia monitoring is compromised by cardiac displacement that alters ECG polarization and affects the anatomic relation with a TEE probe. Vasoactive medications and the Trendelenburg position are used to maintain blood pressure and cardiac output. Despite the best efforts, however, decreases in cardiac output with elevations in central venous pressure and PAOP are commonly observed during surgical manipulation. Cardiac dysrhythmias are not uncommon and are treated by increasing the perfusion pressure and using medications such as lidocaine, amiodarone, and magnesium. Sevoflurane anesthesia is associated with less atrial fibrillation or supraventricular arrhythmias after OPCABG surgery than an equivalent dose of desflurane.101 Malignant dysrhythmias that are not corrected by medications or electrical cardioversion may prompt the need for CPB. Temporary cardiac pacing may be required in patients with right coronary dominant anatomy because of bradycardia or cardiac arrest during right coronary occlusion. Upon successful completion of all distal coronary anastomoses, the blood pressure is lowered before application of the partial aortic clamp for the proximal anastomoses. Release of this clamp after all of the proximal grafts are completed may produce reperfusion dysrhythmias or send air through the coronary grafts, if they were not adequately de-aired by the surgeon.
Anticoagulation is reversed with protamine after the surgeon is satisfied with the grafts and the absence of surgical bleeding. The surgical wound is closed, and the patient is transported to the ICU. Some patients may be candidates for extubation immediately after surgery, but this should be individualized according to the patient's temperature, need for inotropic and mechanical support of the circulation, coexisting medical problems, and degree of mediastinal bleeding.102 Although extubation within 2 to 4 hours after surgery is a reasonable goal for most patients, immediate extubation is possible after OPCABG using either opioid-based or thoracic epidural-based anesthesia.103 Thoracic epidural analgesia may be of particular benefit in obese patients (>30 kg/m2 body mass index) by providing early tracheal extubation and shorter ICU stays.104 The benefits of thoracic epidural analgesia must obviously be weighed heavily against the risks associated with anticoagulation and appropriate management of the epidural catheter.
For patients undergoing CABG with CPB, a 2-stage cannula is placed in the RA to direct blood away from the patient to the CPB circuit, and a cannula is placed in the aorta to return oxygenated blood to the patient's circulatory system. The patient must be fully heparinized before cannulation to avoid thrombus formation. The arterial blood pressure is lowered to 85 to 90 mm Hg systolic pressure prior to aortic cannulation to reduce aortic wall tension and minimize the risk of aortic dissection as the aortic wall is punctured. The surgeon may request hand-bag ventilation to provide better visualization of the RA for insertion of the venous cannula. Atrial fibrillation may develop during placement of the venous or coronary sinus catheters. Cardioversion with internal paddles may be required if the patient becomes hypotensive prior to CPB.
Some institutions "retrograde prime" the CPB circuit by allowing the patient's blood to displace the clear fluid priming volume from the aortic and venous lines to the CPB machine. This process nearly always causes hypotension due to volume depletion and requires vigilance and treatment by the anesthesia provider to avoid profound hypotension. Small boluses of phenylephrine are effective for raising blood pressure during this process. Once the retrograde priming is complete, pump volume is infused through the aortic cannula and the venous cannula is unclamped, thereby initiating CPB.
Mechanical ventilation of the lungs is no longer necessary for oxygenation and ventilation during CPB because the bypass machine provides these physiologic functions. Mechanical ventilation of the lungs is usually discontinued when a calculated circulation flow through the bypass machine is achieved. Although some have suggested that continued pulmonary ventilation during CPB might mitigate reperfusion injury to the lungs, recent evidence in humans did not demonstrate a significant difference in pulmonary vascular resistance between patients mechanically ventilated during CPB versus those who were not.105 Dexamethasone may have a beneficial effect on A-a oxygen gradient, respiratory index, and PaO2/FiO2 ratio at 12 and 24 hours, but no effect on extubation time or lung compliance following CPB.106
The surgical field is observed for complications related to cannulation such as venous obstruction, aortic dissection, bleeding, and cardiac distension. Anesthesia is maintained by volatile anesthetics administered through a vaporizer on the CPB machine or by continuous infusion of hypnotic drugs such as propofol, titrated according to mean arterial blood pressure and readings on the awareness monitor. Some clinicians routinely administer hypnotics with initiation of CPB and during rewarming to reduce the incidence of intraoperative awareness. Additional muscle relaxation helps reduce oxygen consumption by minimizing shivering as the patient is cooled. ECG, systemic and pulmonary pressures, urine output, and temperature are monitored. PA pressure may increase with cardiac distension or because the PAC has migrated to more peripheral regions in the lung during cardiac manipulation. In the absence of cardiac distension, the PAC should be withdrawn until the pressure measured in the distal port decreases.
The clinician should use the CPB time to prepare for post-CPB events. Most patients with good ventricular function do not require inotropic support following successful coronary revascularization. However, patients with poor preoperative ventricular function and those who undergo complicated surgical procedures and prolonged prebypass ischemia often require inotropic or IABP support in the postbypass period. Prior to termination of CPB, the surgeon places epicardial atrial and ventricular pacing leads, to be used as needed to establish an adequate cardiac rhythm and rate.
The patient is rewarmed to normothermia with CPB as the surgeon completes the coronary anastomoses. The rewarming process may take longer in patients with a higher body mass index and more profound hypothermia. Mechanical ventilation is resumed upon the surgeon's request, after inspection of the anastomotic sites reveals the absence of a surgical cause for bleeding. If inhaled anesthetics are being used in the CPB circuit, their delivery should be continued via the anesthesia machine. The dose of the potent inhalational agent used should be minimal to avoid myocardial depression. Vasoactive infusions should be started or maintained. Communication between the surgeon and the anesthesiologist is paramount to confirm that both are ready to begin the process to separate the patient from CPB. Venous drainage to the pump is reduced, and the patient's heart begins to receive more blood from the circulation. Preload is adjusted by observing mean arterial pressure, cardiac distension, and PA or central venous pressure. The physician performing TEE provides information to the surgeon regarding volume status and contractility, which also aids the separation from CPB. A cardiac index is determined if a PAC is used. The venous cannula is removed from the RA with satisfactory separation from CPB. The surgeon, perfusionist, and anesthesiologist all must be aware when protamine is administered to reverse the anticoagulant effects of heparin. CPB must not be reinitiated once protamine administration has started without administering another dose of heparin. Once it is determined that the patient will not return to cardiopulmonary bypass, the administration of protamine is completed. With adequate neutralization of the heparin, the surgeon inspects the surgical field for bleeding and closes the surgical wound with adequate hemostasis. The patient is transported to the ICU for postoperative care.
Postoperative Outcome after CABG
Postoperative myocardial ischemia occurs in up to 48% of cardiac surgical patients and is associated with adverse cardiac outcomes.107 Thirty-eight percent of ischemic episodes occur during the first 2 postoperative days and peak within the first 2 hours of revascularization. These findings have important implications for monitoring, diagnosis, and treatment. Treatment of myocardial ischemia is directed toward adjusting the factors that determine myocardial oxygen supply and demand. Ischemia that develops immediately upon termination of CPB usually is related to air or particulate emboli in the bypass grafts. Elevation of mean arterial pressure and incremental increases in boluses of nitroglycerin are effective for treating ischemia caused by air in the venous grafts. The surgeon should confirm graft patency with Doppler flow probes or palpation. Persistent myocardial ischemia is treated with placement of an IABP. "Stunned myocardium" may be the result of reperfusion injury or intraoperative MI. These patients will require support of cardiac function until myocardial function improves.
Patients at risk for increased mortality after CABG are identified by several factors that evolve and are more prevalent or less over time. For example, patients undergoing myocardial revascularization between 1999 and 2004 were older and more likely to have metabolic syndrome or diabetes and peripheral vascular disease but fewer were smokers, compared with patients undergoing myocardial revascularization between 1993 and 1998. In terms of complications, the latter cohort had a higher rate of postoperative infarction and renal insufficiency, but a lower incidence of stroke and shorter duration of mechanical ventilation and hospital stays.108 Preoperative risk factors that increase mortality include age older than 80 years, emergent surgery, prior cardiac surgery, and renal failure.68,108 Mediastinitis is more common among patients with chronic obstructive lung disease, severe obesity, diabetes, renal failure, emergent surgery, and preoperative ejection fraction less than 40%.68,109 Renal failure is associated with advanced age, history of CHF, and preexisting renal disease.68,109
Growing areas of development are genomic predictors and other proteins that can be used to identify patients at risk for complications. For example, noncoding single-nucleotide polymorphisms within the chromosome 4q25 region are independently associated with atrial fibrillation after CABG.110 Preoperative C-reactive protein levels as low as 3 mg/L are associated with increased long-term mortality and extended hospital length of stay in patients undergoing primary CABG.111 Similarly, heart-type fatty acid–binding protein peaks earlier and is a superior independent predictor of postoperative mortality and ventricular dysfunction after CABG.112