In decades past, the otherwise healthy patient for coronary bypass surgery was the “ideal” patient for cardiac surgery/anesthesia teams. Such patients often presented with one or two vessel coronary artery disease in need of surgical revascularization. Perhaps the patient had suffered a myocardial infarction but overwhelmingly, ventricular function tended to be preserved. Free from both systolic and diastolic ventricular dysfunction, such patients tolerated anesthesia induction, maintenance, and emergence easily. Often these patients were relatively young, in their forties, fifties, and sixties and lacked other organ system diseases. Time on cardiopulmonary bypass tended to be short since the patients often required only one or two vessel revascularizations.

Today, patients presenting for coronary artery surgery are anything but “routine.” Frequently they will have already undergone numerous percutaneous coronary interventions (PCIs) prior to being referred for surgery. Many patients will have had a history of recurrent small myocardial infarctions, anginal episodes, and catheterizations. Over time myocardial damage accrues, leaving the patient with both systolic and diastolic dysfunction. Other patients are referred for coronary bypass surgery because they have complex coronary artery lesions not readily amenable to PCI or they have concurrent valvular heart disease.

Although few of today’s patients for coronary revascularization are “easy” to manage, review of the anesthesia management for this surgical procedure provides an overview of the anesthesia maneuvers necessary in the management of almost all cardiac surgical procedures. In other words, the skills and techniques applied in managing the “routine” coronary artery bypass (CAB) also apply when managing anesthesia for more complex procedures.

IMMEDIATE PREOPERATIVE ASSESSMENT AND ANTIBIOTIC PROPHYLAXIS

Increasingly, patients are admitted to hospital for elective CAB on the day of surgery. In that instance, the anesthesiologist may have very few moments to meet and to assess the patient for cardiac surgery. Most institutions operating a same day admission cardiac surgery program will have arranged for the patient to be evaluated in a preoperative anesthesia clinic well before the day of surgery. If that is the case, the anesthesiologist reviews the evaluative work completed in the outpatient clinic. Still, it is critically important that the anesthesiologist completes an immediate assessment prior to preparing the patient for surgery.

The patient should be questioned regarding any change in their overall health since their preoperative evaluation. They are asked if they are currently experiencing any dyspnea or anginal pain. Patients should be monitored at this time with electrocardiogram, pulse oximeter, and automatic blood pressure cuff. Supplemental oxygen should be provided.

Most patients will have continued their medications on the morning of surgery as instructed including beta-blockers. Angiotensin converting enzyme inhibitors can lead to perioperative hypotension and many patients will have been instructed to discontinue these medications. Nevertheless, a review of the patient’s current medical regimen is warranted especially regarding beta blockade and any diabetes-related medications. Both hyper and hypoglycemia can occur perioperatively in diabetic patients. Close monitoring of blood sugar is critical throughout the entire perioperative period.

A brief neurological examination will establish an immediate preoperative baseline. The eyes should be examined to note pupillary responses and pupillary size. The patient’s lungs are auscultated to detect the presence of any wheezes or rales indicative of heart failure.

Patients reporting anxiety and assuming they are free of conditions likely to lead to imminent cardiac collapse (eg, tight stenotic valvular disease, severely impaired ventricular function) can be medicated in the holding area with intravenous midazolam 0.5 to 2 mg. Resuscitative equipment should be available and the anesthesiologist immediately at hand. Inpatients are occasionally given oral lorazepam as a preoperative medication. Although the authors tend to avoid all premedication except for that given intravenously under immediate anesthesiology supervision, individual institutions are likely to have their own accepted protocols for preoperative sedation.

Prior to administering any sedative or anxiolytic the patient should be correctly identified according to hospital policies and all consents should be in proper order.

Antibiotic prophylaxis is administered within 1 hour of surgery incision time. This is a frequent anesthesiology quality assurance indicator and must be dutifully administered and charted. In patients free of methicillin-resistant Staphylococcus aureus, a first-generation cephalosporin is indicated.¹ Later-generation cephalosporins have better gram-negative and less gram-positive coverage. Since gram-positive S. aureus is most frequently implicated in cardiac surgical infections, the earlier cephalosporins, such as cefazolin, are best for antibiotic prophylaxis. If the patient has a presumed, known, or anticipated colonization with methicillin-resistant S. aureus, use of both a cephalosporin (cefazolin) and a glycopeptide (vancomycin) has been suggested to expand prophylaxis.¹ Should a patient have a beta-lactam allergy, vancomycin is employed for antibiotic prophylaxis. However, since vancomycin provides no gram-negative coverage, administration of an aminoglycoside for one to two doses is suggested.¹ Mupirocin topical antibiotic eliminates nasal colonies of all types of S. aureus. Since the nose is considered a depository for bacteria that leads to infection following cardiac surgery, treatment with mupirocin is recommended to commence on the day before surgery and continue from 2 to 5 days following.¹

When indicated cefazolin 2 g (patient weight > 60 kg) should be administered within 1 hour of surgical incision. Assuming normal renal function a repeat dose of 1 g should be given every 3 to 4 hours while the chest is open.

Vancomycin (15 mg/kg) is administered as a slow IV infusion for more than 1-hour duration. When a beta-lactam antibiotic is contraindicated secondary to allergy, gentamicin is also given within 1 hour of surgery along with vancomycin.

MONITORING AND VASCULAR ACCESS

Chapter 2 discussed in detail the placement of invasive monitors and their use in managing perioperative hemodynamic instability.

Depending upon institutional protocols, both the types of monitors employed and the location where such monitors are placed varies. All patients should be provided with a large-bore intravenous catheter. Inpatients often arrive to the holding area with either a #22- or #20-gauge catheter in place. There is often temptation to use such small catheters for anesthesia induction. Although it may be acceptable to do so, if veins of sufficient size are available, placement of a large-bore catheter will facilitate rapid fluid delivery should that be needed and central access not yet established following induction.

Central venous access with or without the use of a pulmonary arterial (PA) flotation catheter can be accomplished either before or after the induction of general anesthesia. In the author’s practice central access is completed following anesthesia induction. In other institutions central access is done with the patient sedated. The utility of PA catheters perioperatively was discussed in detail in Chapter 2. Placement of a PA catheter remains the individual choice of the physicians involved. Once again, institutional norms are likely to determine whether all, some, or no patients are monitored using a PA catheter.

Arterial line monitoring is of course essential and is customarily placed prior to anesthetic induction. The anesthesiologist should confirm that the radial arteries are not to be harvested for bypass graft conduits. Additionally, the anesthesiologist should consider femoral artery cannulation if needed. Compared with the aortic pressure pulse waves, peripheral pulse waves are narrower with higher systolic pressures and lower diastolic pressures. The mean blood pressure obtained from either a central arterial pressure tracing or from a peripheral arterial line are usually quite similar.

Both transesophageal echocardiography (TEE) and epiaortic ultrasound are routinely used in all patients when not contraindicated. The intraoperative use of TEE dramatically reduces the utility of the PA catheter in managing patients intraoperatively. Nonetheless, the PA catheter is often employed in the ICU setting to aid in the management of postoperative hemodynamic instability. Bispectral index (BIS) although controversial may be useful as cardiac surgery patients have a high incidence of awareness.

Baseline laboratory values should be obtained including blood gas, activated clotting time, electrolytes, blood glucose concentration, and ionized calcium.

ANESTHETIC INDUCTION AND MAINTENANCE

Induction of patients undergoing cardiac surgery should be performed with the perfusionist and a member of the surgical team capable of performing sternotomy in the operating room, in case of the need for emergent institution of cardiopulmonary bypass (CPB) arises secondary to intractable hemodynamic instability.

All patients are preoxygenated. Choice of induction agents varies according to the individual practitioner and the particular anesthesia-related issues at play. There is no magic formula that can be universally applied that will ensure hemo-dynamic stability during anesthetic induction. Every possible combination of narcotics, inhalational agents, and intravenous anesthetics can be employed in the management of the cardiac surgical patient.

Determining which combination of agents to employ is of course the task of the attending anesthesiologist. In making this choice the following must be considered:

1. How will the induction affect the balance between myocardial oxygen supply and myocardial oxygen demand?

2. Does the patient have ventricular dysfunction to the degree that they will not be able to tolerate a decrease in venous return, myocardial depression, or vasodilatation at the time of induction?

3. What other anesthetic considerations might influence the choice of agents?

Imbalance between myocardial oxygen supply and myocardial oxygen demand can readily lead to post induction ischemia. Inadequate anesthesia and analgesia results in tachycardia and hypertension leading to increased myocardial wall tension, greater myocardial oxygen demand, and decreased myocardial oxygen delivery. Consequently, historically many anesthesiologists have used large doses of synthetic narcotics (e.g. fentanyl 50-100μg/kg) to blunt the hypertensive and tachycardic response to stimulation. Various amounts of intravenous midazolam (2-10mg) along with non-depolarizing muscle relaxants are also employed in the anesthetic induction.

Other anesthesiologists use a lower narcotic dose and manage peri-induction hypertension and tachycardia with inhalational anesthetics (eg, sevoflurane) and short-acting beta-blockers (eg, esmolol), assuming the patient has a relatively normal ventricular function. Should hypotension develop at the time of induction, it should be treated with phenylephrine (incremental boluses of 40-80 μg), volume administration, and the stimulation of direct laryngoscopy and intubation.

Ultimately, the anesthesiologist will attempt to prevent peri-induction myocardial ischemia by being both proactive and reactive. Proactive management implies that the anesthesiologist is prepared for and aware of the hemodynamic changes likely to occur with induction of any cardiac patient. In this way, the anesthesia team corrects hemodynamic instability as soon as pressures begin to drift downward and/or the patient’s heart rate increases. Predicting the hemodynamic course of the patient is a hallmark of a skilled cardiac anesthesiologist. Concurrently, the anesthesiologist is immediately reactive prepared to respond to changes during the induction through constant surveillance of the myriad monitors employed.

Should myocardial ischemia occur following induction, it can translate either as new wall motion abnormalities on TEE (Video 4–1), ST-segment elevation or depression on ECG, or as an increase in PA pressure. The anesthesiologist will respond accordingly by treating the triggering event thought to provoke ischemia. Inotropes (eg, epinephrine, milrinone) could be administered by infusion in order to improve ventricular function. The surgery and perfusion teams should be alerted that the patient has become acutely ischemic in the event that emergency institution of CPB becomes necessary. Fortunately, most inductions are conducted in such a manner that the balance of myocardial oxygen supply and demand is maintained. Nonetheless, acute coronary syndrome secondary to coronary artery thrombosis unrelated to transient imbalances in myocardial oxygen supply/demand can also occur perioperatively leading to large ST-segment elevations.

More than ever, patients with both diastolic and systolic dysfunction present for cardiac surgery and the cardiac anesthesiologist must often induce patients at risk for both myocardial ischemia and perioperative hemodynamic collapse.² Patients with systolic dysfunction maintain their stroke volume (SV) through several compensatory mechanisms: expansion of the circulating blood volume, increased sympathetic tone, and ventricular dilatation. Although the heart may contract poorly (Video 4–2), the adaptive responses mentioned above may maintain an adequate cardiac output for vital organ perfusion. Anesthetic induction reduces sympathetic tone, lowers blood pressure, and decreases venous return. Positive pressure ventilation similarly reduces venous return to the heart. Therefore, following induction, the cardiac output can decrease profoundly as the anesthesiologist perturbs the patient’s compensatory mechanisms. Coronary perfusion pressure may decrease and the patient may develop myocardial ischemia leading to further hypotension and circulatory collapse.

At times, concern for severe hemodynamic instability may prompt the placement of an intra-aortic balloon pump prior to induction.

Anesthesiologists planning the induction of the cardiac surgery patient must consider the routine anesthetic concerns found in all patients. With all anesthetics the fundamentals of ABC (airway, breathing, and circulation) apply. Patients with airway problems undergoing cardiac surgery require special consideration. The American Society of Anesthesiologists’ algorithm for the management of difficult airways³ is applicable to both cardiac surgery and noncardiac surgery populations. Awake intubation when needed should be undertaken in the cardiac surgery patient with the understanding that careful hemodynamic monitoring is necessary to prevent stress-induced tachycardias and myocardial ischemia. While the airway is being secured, one member of the anesthesia team should be constantly focused upon the patient’s hemodynamics to respond to any intubation-related perturbations. Nasal intubations should be avoided if possible, as many patients are treated with various anticoagulation regimens and all will be systemically heparinized if cardiopulmonary bypass is planned.

Maintenance of anesthesia consists of a combination of narcotics, nondepolarizing muscle relaxants, inhalational agents, and, possibly, propofol. Anesthetic agents are titrated to optimize blood pressure and heart rate and to respond to the needs of the surgery team. Blood pressure is generally reduced to less than 100 mm Hg at the time of aortic cannulation. During surgery, the heart is often lifted, compressed, or manipulated leading to transient periods of hypotension. Communication with the surgical team during times of heart manipulation and careful anesthetic titration will allow the patient to better tolerate hemodynamically these interventions.

For many years it was thought that there were no specific benefits of one anesthetic regimen over another as long as the patient’s hemodynamics were maintained. However, inhalational agents may provide a cardioprotective effect independent of their use in maintaining the balance between myocardial oxygen supply and demand.^4–8 Anesthetic preconditioning, similar to ischemic preconditioning, has been suggested as a mechanism by which the use of volatile anesthetics may permit the heart to better tolerate ischemic injury during surgery.

When myocardial ischemia occurs the muscle cells die if the blood flow is not restored. However, even after blood flow is restored, the myocyte may yet be impaired or die through reperfusion injury. Ischemic preconditioning is the protection conferred to the ischemic myocardium by preceding short periods of sublethal ischemia. In other words, when the myocardium is exposed to a brief period of ischemia, it adapts so that when subsequently presented with an ischemic insult it better tolerates the ischemic period. The mechanisms by which the cell adapts are multifactorial and well beyond the scope of this text. However, preservation of cellular mitochondrial function through the activation of the mitochondrial K-ATP channel may be central to the preconditioning effect.⁸ Anesthetic preconditioning is thought to offer a pharmacological equivalent to ischemic preconditioning ultimately preserving cellular mitochondrial function during periods of ischemic stress. Various clinical studies have attempted to demonstrate improved myocardial preservation or reduced biomarkers of perioperative myocardial injury; however, the overall impact of the use of inhalational agents on clinical outcomes such as mortality and morbidity remains unclear.⁷ Nonetheless, the inclusion of inhalational anesthetics in the management of patients at risk for myocardial ischemia may have a protective benefit.

Patient positioning is checked to make sure that the arms are padded and that the face is free of any pressure.

Prior to surgical incision a time-out is performed so that all healthcare staff in the room reidentify the patient and the surgical procedure. The surgeon completes the sternotomy while assistants harvest saphenous vein graft conduits or the radial arteries. During sternotomy, the anesthesia team deflates the lungs to reduce the potential for the sternal saw to create lung injury. The surgeon next dissects free from the sternum the left internal mammary artery (LIMA). This graft is usually anastomosed to the left anterior descending artery and has been shown to benefit the coronary artery disease patient greatly having a significantly lower rate of stenosis compared with vein grafts. The right internal mammary artery may also be harvested and used as a free conduit.

INSTITUTION OF CARDIOPULMONARY BYPASS

Having dissected the LIMA and perhaps the right internal mammary artery (RIMA), the surgeon next prepares for the initiation of CPB (assuming surgery is not performed off-pump). The anesthesiologist administers heparin 3 to 4 mg/kg into a central line. The patient’s activated clotting time is measured and an arterial blood gas is obtained. The surgeon will next examine the ascending aorta to identify a location for placement of the aortic perfusion cannula. Epiaortic ultra-sound is often used to identify areas free of atherosclerotic plaque build up. The aortic perfusion cannula is placed. At this time the anesthesiologist will lower the patient’s blood pressure to less than 100 mm Hg systolic. This can be done gradually through the use of increased inhalational agents, intravenous anesthetics, or antihypertensive agents (eg, nitroglycerin). Next the surgeon will place the venous cannula. A snare suture is placed in the right atria. Often manipulation of the heart leads to various atrial and/or ventricular dysrhythmias. In general, these abnormal rhythms stop when the heart is no longer being manipulated. However, occasionally a patient will become unstable with rapid atrial or ventricular fibrillation. Should this occur the patient can be placed on CPB emergently assuming the ACT is greater than 400 to 480 seconds or the patient can be cardioverted. Using internal paddles the surgeon can cardiovert or defibrillate the patient. At times, pressor support is necessary to maintain blood pressure following heparin administration. In the event of hypotension, the anesthesiologist can also request the perfusionist to administer volume, should the aortic perfusion cannula be already placed. This should be discussed with the surgeon who will confirm that all line clamps have been removed and that the cannula is correctly positioned in the aorta and free of air bubbles. Following placement of various cardioplegia cannulae, the surgeon will initiate cardiopulmonary bypass by releasing the clamps on the venous cannula. At this time the venous return is directed toward the bypass machine. Pulmonary artery blood flow decreases as noted by the fall in PA pressures. The heart deflates in the chest. When the perfusionist notes that they are at “full flow,” and the heart is no longer ejecting blood in the pulmonary and systemic circulation ventilation to the patient can be discontinued. At “full flow” all venous return from the patient is directed toward the bypass machine, therefore the lungs no longer oxygenate the venous blood. The patient’s face is checked for swelling to rule out inadequate drainage from the superior vena cava. The surgeon next places the aortic cross clamp thus isolating the coronary arteries from aortic blood flow. Potassium rich cardioplegia solution is next administered arresting the heart so that the surgical repair may proceed. Cardiopulmonary bypass (CPB) management is discussed in detail in Chapter 17.

SEPARATION FROM CPB

Having completed coronary revascularization (or other surgical intervention) the patient must be separated from the bypass machine. The process of separation begins when the surgeon removes the aortic cross clamp. Blood from the aorta now flows through the coronary arteries and the venous bypass grafts. The patient is gradually rewarmed until core temperature is greater than 36°C and peripheral temperature at least 35.5°C. During this time, the heart will begin to beat as the cardiac rhythm is restored either by epicardial pacing or the return of the heart’s intrinsic rhythm. After the aortic cross clamp is removed, the flow of arterial blood into the heart washes out the cardioplegia solution, a cardiac rhythm is restored, and the heart often starts contracting spontaneously. Arterial blood gases are checked to confirm that the heart’s metabolic environment is sufficiently normalized that it can be expected to function in a normal manner. The frequency of blood samples obtained for analysis during CPB and the laboratory values measured vary from institution to institution. Most frequently they include:

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