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6 Myocardial Management in Arterial Revascularization 53 Provide Optimal Protection at These Levels [11, 12]

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6 Myocardial Management in Arterial Revascularization 53 Provide Optimal Protection at These Levels [11, 12] Chapter 6 Myocardial Management in Arterial 6 Revascularization B.S. Allen, G.D. Buckberg The objectives of every cardiac operation must be a Table 6.1. Myocardial supply/demand balance during aortic technically perfect anatomic result and avoidance of in- cross-clamping traoperative damage in pursuit of this goal. Neverthe- Supply Demand less, perioperative myocardial damage remains the most common cause of morbidity and death following Noncoronary collaterals Electromechanical activity technically successful coronary bypass operation. This Intrinsic substrate stores Wall tension (glycogen) occurs whether the conduits are arterial or venous. Temperature (metabolic rate) Cardiac damage from inadequate myocardial protec- tion leading to low output syndrome can prolong hos- principles are directly applicable to use of all arterial pital stay, and may also result in delayed myocardial fi- conduits during coronary revascularization. Issues of brosis leading to cardiac dysfunction months to years protection are important here, due to potential conduit later [1, 2]. Cardioprotective strategies, like cardiac op- discrepancy between arterial grafts and the coronary erations, have evolved to the point that it is essential to artery. Clearly, the long-term patency of arterial grafts understand various techniques in order to limit intrao- must be matched by absence of intraoperative damage perative damage during a complicated operation. Sur- whiletheyareconstructed. geons must refrain from using simplistic cardioplegic Table 6.1 lists the factors affecting the myocardial en- protection strategies for the very reason that simplicity ergy supply/demand balance during aortic clamping. and safety are not synonymous. As with technical as- The two factors affecting supply include oxygenated pects of the surgical repair, the primary object of pro- blood coming from noncoronary collateral blood flow, tection techniques is the use of the best strategy. Inte- and intrinsic or extrinsic substrate stores. All surgeons gration of surgical techniques is usually required to have noted noncoronary collateral flow during aortic perform the best technical operation. Similarly, opti- clamping, as blood appears in the coronary arteriotomy mal myocardial protection also requires integration of site during coronary revascularization despite a flaccid various techniques to achieve the best results. Most sur- aorta. The second determinant of supply is myocardial geons would not abandon a complex surgical proce- glycogen or exogenous glucose to provide anaerobic dure (like all arterial revascularization) that was metabolism to generate some energy during ischemia proved superior solely because of its lack of simplicity. to maintain cell membrane viability. Anaerobic glycoly- Likewise, we should not choose a protection strategy sis requires the presence of substrate (i.e., glucose or for simplicity, unless it provides optimal and complete glycogen), and a metabolic environment (i.e., buffer- myocardial protection. Optimal myocardial protection ing) to allow anaerobic energy production. Myocardial is as important as an excellent technical repair in oxygen demands are determined principally by electro- achieving the best long-term outcome with surgical mechanicalactivity.Cardiacarrestisusedbecausethe correction. Although, the surgeon might desire simplic- fibrillating or beating ischemic heart has a much higher ity,thepatientisonlyconcernedwithsuccess. energy requirement. The second determinant of de- This chapter describes how oxygenated cardioplegia mand is the wall tension within the myocardium, that is solutions can be delivered warm to allow their use for minimizedbyasystole,andthethirdthemyocardial active resuscitation before ischemia is imposed, cold to temperaturethatgovernsmetabolicratedirectly. limit damage, and again warm to avoid and reverse is- chemic and reperfusion damage before and after aortic unclamping [1, 2]. It focuses primarily on the princi- 6.1 ples that form the basis for clinical strategies for cardio- Cardioplegic Prerequisites plegic delivery that can ensure that the selected cardio- plegic solution can exert its desired effect, and it de- Essential clinical prerequisites for cardioplegia include scribes how these can be implemented. The described (1) a solution that is shown to be safe through testing 52 III Myocardial Protection During Coronary Bypass Surgery Using Arterial Grafts under experimental conditions, in ischemic models, These solutions should be delivered according to estab- (2) the distribution of flow to all cardiac regions, (3) pe- lished experimental protocols, and, most importantly, riodic replenishment to counteract noncoronary collat- the aim must be complete preservation of metabolic eral washout, and (4) strategies for protection in vari- and functional parameters. A failure to reconstitute ous clinical conditions. creatine phosphate or other metabolic levels following aortic unclamping should be looked at as a protection failure, in the same way that a residual ventricular sep- 6.2 tal defect (VSD) or AVvalve regurgitation is a technical Cardioplegic Composition failure. Optimal protection is as important as the tech- nical aspects of the repair in achieving the best long- The cardioplegic objectives are to stop the heart safely, term outcome for the patient. Using arterial grafts will allow continued energy production, and counteract not improve long-term survival if the patient is left deleterious effects of ischemia. The principles which with myocardial dysfunction as a result of poor protec- underlie the composition of any cardioplegic solution tion. are enumerated in Table 6.2. First, immediate arrest lowers energy demands to avoid depletion by ischemic electromechanical work, and high-energy stores are 6.3 enhanced with oxygenated solutions compared to crys- Blood Cardioplegia (Table 6.3) talloid solutions, that deplete adenosine triphosphate (ATP) before arrest [1, 2]. Second, reducing myocardial We have selected blood as the cardioplegic vehicle, temperature during perfusion lowers metabolic rate sincethisphysiologicsourceofoxygenisavailable duringischemia.Third,substrate(i.e.,glucoseorgly- readily in the extracorporeal circuit, and its use limits cogen) and Krebs cycle intermediates (i.e., glutamate or hemodilution when large volumes of cardioplegia are aspartate) [3] enhance anaerobic or aerobic energy needed. An additional advantage of a blood cardiople- production (or both) during aortic clamping. Fourth a gic vehicle is to ensure the buffering capacity of blood buffer such as TRIS (hydroxymethyl) aminoethane proteins, especially histidine imidazole groups [8]. Fur- (THAM), bicarbonate, phosphate, or perhaps some thermore, the rheologic benefits on the microvascula- other buffer optimizes the small energy output of an- ture afforded by erythrocytes enhance papillary mus- aerobic glycolysis during ischemia [1, 4]. Fifth, there cle perfusion compared with oxygenated crystalloid must be some degree of membrane stabilization with cardioplegia and reduce coronary vascular resistance exogenous additives or hypocalcemia [1, 5, 6]. Magne- and edema formation [9]. The erythrocytes of blood sium enrichment improves protection by preventing cardioplegia also contain abundant endogenous oxy- calcium influx, even in the presence of hypocalcemia. gen free radical scavengers (i.e., superoxide dismutase, The role of steroids, calcium channel blockers, and pro- catalase, and glutathione) [10], which may reduce oxy- caine is uncertain at this time. Oxygen radical scaven- gen-mediated injury during reperfusion. Their benefits gers (i.e., superoxide dismutase [5], catalase, allopuri- enumerate only the known benefits of using blood as nol, coenzyme Q10 [CoQ10], [6]) may counteract the cy- the vehicle for delivering oxygenated cardioplegia. We totoxic oxygen metabolites during ischemia and reper- are confident that further studies will reveal other nat- fusion [7]. Sixth, myocardial edema is limited by alter- urallyoccurringbloodcomponents(i.e.,enzymes,co- ing the osmolarity and colloid osmotic pressure of the factors, substrates, and electrolytes) that are important cardioplegic solution during infusions [7]. and would otherwise need to be added to any artificial- It is essential that only cardioplegic solutions de- ly constructed solution. signed and tested for a specific purpose be utilized. Blood cardioplegia is not just any crystalloid solu- tion added to blood. Solutions like Plegisol (St. Thomas solution) were specifically developed to work best as a Table 6.2. Pharmacologic cardioplegia crystalloid solution, with the constituents adjusted to Principle Method Immediate arrest K+,Mg2+,procaine Table 6.3. Blood cardioplegia Hypothermia 10°–20°C Oxygenation during arrest Substrate Oxygen, glucose, glutamate, Reoxygenation during replenishment aspartate Avoids reperfusion injury Avoids hemodilution Appropriate pH (buffer) THAM, bicarb., phosphate Endogenous Membrane stabilization Ca2+,steroids,procaine Oxygen radical scavengers Ca2+ antagonist, magnesium Buffers O2 radical scavenger Onconicity 6 Myocardial Management in Arterial Revascularization 53 provide optimal protection at these levels [11, 12]. Mix- 6.4 ing Plegisol (or other crystalloid cardioplegia solu- Operative Strategy tions) with blood alters the final (delivered) composi- tion, and, as such, may not provide the same level of The strategies for clinical cardioplegia may be separat- protection. These solutions must be tested and com- ed into the phases
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