Chapter 13 Anesthesia for Myocardial Revascularization
Cardiac anesthesiologists who have been in practice for the past several decades have seen a variety of anesthetic and surgical practices come into vogue and fall out of favor based on new research and economic pressures. Perhaps the most striking example is the rise and fall of high-dose opioid anesthesia, which was initially driven by concern about excessive cardiovascular depression by volatile anesthetics in the 1970s and further accelerated in the mid-1980s by concerns about potential coronary steal with isoflurane. The prolonged postoperative mechanical ventilation resulting from the shift to high-dose opioids was also thought important to reduce stress on the recently revascularized myocardium. However, during the following decade, this approach was completely reversed by new basic and clinical research, such as lack of evidence for adverse effects of volatile agents, particularly as related to potential effects of coronary vasodilation on coronary steal, and by strong evidence of their benefits via rapid preconditioning; by social and economic factors (i.e., safety and efficacy of fast-tracking for most patients and recognition that time on the ventilator for many patients is an uncomfortable experience); and by the rapid rise in off-pump coronary artery bypass grafting (OPCAB), which by avoiding adverse physiologic effects of cardiopulmonary bypass (CPB) facilitates more rapid emergence and recovery in many patients.1,2 Given the increasing emphasis on pain control in all surgical patients and its reported association with enhanced postoperative outcome in a variety of surgical subgroups, there has been a resurgence in the use of neuraxial techniques in cardiac surgery, particularly in European and Asian countries.3 Although not commonly used in the United States because of logistical issues and liability concerns, the rapidly growing literature base mandates that clinicians familiarize themselves with their potential benefits and risks.
EPIDEMIOLOGY AND RISK ASSESSMENT
The Society of Thoracic Surgeons (STS) instituted a voluntary clinical database system with this approach in the early 1990s that has continued to grow rapidly as cardiac surgical groups are increasingly interested in benchmarking their practices against others.4 Many tertiary centers (e.g., Cleveland Clinic) and regional consortiums of hospitals (e.g., Northern New England Cardiovascular Disease Study Group) maintain databases, and some publish statistical models. Many states have established and maintain risk-adjusted mandatory reporting systems for hospital and individual surgeon performance (with New York State being an early and influential pioneer). A new scoring system (EuroSCORE) based on outcomes in 128 centers in eight European countries has received increasing attention. It appears to compare favorably with the STS model in North American patients.5 It is freely accessible by means of an interactive web-based calculator (www.euroscore.org) and is decidedly simpler and faster to use than the STS’s scoring system, which is now also freely accessible to the public at http://www.sts.org/sections/stsnationaldatabase/riskcalculator/index.html.
PATHOPHYSIOLOGY OF CORONARY ARTERY DISEASE
Anatomy
The anesthesiologist should be familiar with coronary anatomy if only to interpret the significance of angiographic findings. The coronary circulation and common sites for placement of distal anastomoses during CABG are shown in Figures 13-1 to 13-3.
The vertical and superior orientation of the RCA ostium allows easy passage of air bubbles during aortic cannulation, CPB, or open valve surgery. In sufficient concentration (e.g., coronary air embolus), myocardial ischemia involving the inferior LV wall segments and the right ventricle may occur (Fig. 13-4). In contrast, the nearperpendicular orientation of the left main coronary ostium makes air embolization much less common.
(Image courtesy of Martin J. London, MD, University of California, San Francisco, CA [www.ucsf.edu/teeecho].)
Venous drainage of the myocardium is primarily to the coronary sinus, which drains 96% of the LV free wall and septum, and the remainder of the venous return goes directly into the right atrium.6 A small fraction may enter other cardiac chambers directly through the anterior-sinusoidal, anterior-luminal, and thebesian veins.
Myocardial Ischemia and Infarction
In patients with CAD, myocardial ischemia usually results from increases in myocardial oxygen demand (Fig. 13-5) that exceed the capacity of the stenosed coronary arteries to increase their oxygen supply. However, the determinants of myocardial oxygen balance are complex, and alterations may have several effects. For example, an increase in blood pressure (i.e., increased afterload) increases wall tension and oxygen demand while also increasing coronary blood flow (CBF). It is now appreciated that myocardial ischemia may occur without changes in systemic hemodynamics and in awake patients may occur in the absence of chest pain (i.e., silent ischemia), particularly in diabetic patients.
In atherosclerotic heart disease, the fundamental lesion is an intimal lipid plaque that causes chronic stenosis and episodic thrombosis, occurring most often in an epicardial coronary artery, thereby reducing myocardial blood supply. Characteristics of the vulnerable plaque include high lipid content, a thin fibrous cap, a reduced number of smooth muscle cells, and increased macrophage activity. The lipid core is the most thrombogenic component of the plaque. Fuster described five phases in the progression of CAD by plaque morphology. Phase 1 is a small plaque present in many people younger than 30 years and usually progresses very slowly depending on the presence of risk factors associated with CAD (i.e., elevated low-density lipoprotein cholesterol). Phase 2 is a plaque with a high lipid content that has the potential to rupture. If it ruptures, it will lead to thrombosis and increased stenosis (phase 5), possibly producing unstable angina or an acute coronary syndrome. The phase 2 plaque usually does not rupture; it instead progresses onto phases 3 and 4, with enlargement and fibrous tissue organization, which may ultimately produce an occlusive plaque at phase 5.7
ANESTHESIA FOR CORONARY ARTERY BYPASS GRAFTING
Conventional CABG with CPB is still the most commonly performed cardiac surgical procedure (Box 13-1). Fast-track management with early extubation (4 to 8 hours postoperatively) has become the standard of care in nearly all centers. OPCAB is increasing steadily, although its use tends to be very frequent in some centers or infrequent in others as various surgeons have become “early adopters” or are waiting for firm evidence-based recommendations from future randomized, controlled trials. However, anesthetic management of the sickest patients undergoing multivessel operations combined with valve repair or replacement, repeat operations, and other complex procedures (e.g., ventricular septal defect repairs along with CABG after acute myocardial infarction) has changed relatively little over the past decade as the long duration of surgery usually mandates greater cumulative doses of fixed anesthetic agents with overnight or even prolonged postoperative mechanical ventilation. However, many clinicians have adopted use of infusions of shorter-acting agents (e.g., sufentanil, propofol, remifentanil), avoided large cumulative dosing of fixed agents with potentially long half-lives (e.g., midazolam), and now rely on a volatile anesthesia “base,” taking a “wait and see” attitude toward early extubation if surgery is “smooth” and physiologic parameters remain within acceptable limits (e.g., good urine output, normothermic, adequate hematocrit).
BOX 13-1 Management Strategies for Anesthesia for Myocardial Revascularization