A successful outcome after cardiac surgery depends on many factors. Accurate recognition of the pathology and the judicial choice of methods to achieve cardiac repair are essential. Equally important are the physiologic consequences of the operation. Ventricular function must be preserved or improved during cardiac procedures. Myocardial protection is therefore the crucial component of success in cardiac surgery.

The mainstay of myocardial protection is cardioplegia. This chapter is a brief review of myocardial protection as currently applied in the vast majority of cardiac operations worldwide. We offer a brief review of the components of cardioplegia and their effects on cardiac metabolism and function, followed by a detailed description of “how to do it.”

Much has been written about cardioplegia regarding (1) route of delivery (antegrade vs retrograde or both), (2) method of delivery (continuous vs intermittent), and (3) temperature (warm vs cold). This has often led to confusion and adversarial positions. Surgeons appropriately want to keep things simple, but as Einstein once said: “Everything should be made as simple as possible, but not simpler.” In this chapter, we present a method of cardioplegia that has been extensively applied clinically. It is called the “integrated method” of protection because it combines the salient features of the above elements in a manner that suits the ongoing physiologic needs of the heart during the course of an operation and expedites the time phase of the procedure.

Cardioplegia markedly reduces oxygen demand in the arrested heart and must be delivered uniformly in sufficient quantity to match this low demand (Fig. 25-1). These requirements are met by antegrade and retrograde delivery, cold-blood cardioplegia to reduce oxygen demands, and warm cardioplegia perfusion for induction and resuscitation. “Integrated myocardial protection” is a strategy that addresses each of these requirements in a manner that allows the operation to be performed without interruption.¹ This method (1) provides a bloodless operative field, (2) avoids unnecessary ischemia and cardioplegia overdose, and (3) permits aortic unclamping and discontinuation of bypass shortly after cardiac repair.

Electromechanical activity of the heart raises oxygen demand during arrest. Hypothermia reduces this demand and ischemic damage when coronary flow is interrupted in the course of the revascularization procedure provided that the cardioplegic perfusate is distributed adequately with reinfusions. Hypothermia alone, however, does not completely avoid injury in chronically “energy-depleted” (ischemic) hearts (Fig. 25-2).

Blood cardioplegia consists of four parts of blood to one part crystalloid solution. It is a natural buffering agent, maintains oncotic pressure, has advantageous rheologic properties, and is a free-radical scavenger. Blood cardioplegia replenishes substrate in vulnerable hearts, limits reperfusion injury, and reverses ischemia/reperfusion changes in the acutely ischemic myocardium. Complete myocardial recovery occurs after 4 h of ischemia in normal hearts when protected with cold-blood cardioplegia. However, it is uncommon to address normal hearts. The sequences described below were developed experimentally and are now clinically used routinely in the jeopardized hearts that are currently commonplace in cardiac surgical practice.

Cold-crystalloid cardioplegia does not have the rheologic advantages of blood cardioplegia. When administered in multiple doses, it often results in systemic hemodilution. Crystalloid cardioplegia also shifts the oxyhemoglobin disassociation curve leftward, retarding Na⁺/K⁺ adenosine triphosphatase, and thereby produces edema and activation of platelets, leukocytes, and complement.²

Blood cardioplegia consists of four parts blood to one part crystalloid solution. The components (Table 25-1) of blood cardioplegia are reviewed briefly here and have been well described in detail previously.³ Other more concentrated constituent dilutions (1:8 to 1:50) may be used if the crystalloid component is appropriately varied to include the components described in this chapter (Tables 25-2, 25-3, and 25-4).

A high level of potassium maintains cardiac arrest and prevents sudden intracellular calcium accumulation and disruption of the sarcolemma, as observed when reoxygenation occurs. A low level of calcium is used to limit calcium loading during the conditions of impaired ionic balance in the early period of reperfusion. The amino acid substrates aspartate and glutamate increase the energy-depleted heart’s ability to use oxygen and hasten ionic recovery. Hyperosmolarity reduces edema. Tromethamine (THAM) is alkalotic to (1) limit the evolution of acidosis during ischemia and (2) hasten enzymatic recovery. It is used in preference to bicarbonate, which yields more CO₂ and acidosis.

We routinely use two formulations of cardioplegia (bags 1 and 2) during elective cardiac operations and switch between them based on the metabolic requirements of the heart during specific phases of the operation. Bag 1 is called “induction/terminal” cardioplegia and is a high-potassium (20 mEq/L), aspartate, and glutamate-enriched solution (Table 25-1). It is infused as a cold solution after aortic cross-clamping to arrest the heart and then infused as a warm solution just prior to the release of aortic cross-clamping after all cardiac repairs are completed to resuscitate the energy-depleted ischemic myocardium (“hot shot”). Bag 2 is called “maintenance” cardioplegia and consists of a low-potassium (7–10 mEq/L) mixture without the amino acid additives (Table 25-2). It is administered as a cold solution intermittently during the operation. A third cardioplegia (bag 3) is called “rescue” cardioplegia and is used following myocardial infarction as a controlled reperfusate (Table 25-3). Its rationale and use are described later in this chapter.

Cardioplegia is effective only if it is well distributed. Adding retrograde perfusion via transatrial cannulation of the coronary sinus improves subendocardial perfusion, avoids ostial cannulation during aortic valve procedures, limits the removal of retractors during mitral procedures, and permits flushing of air and atheromas during coronary reoperations. Experimentally, right ventricular nutritive flow is limited by retrograde perfusion. Antegrade or retrograde cardioplegia alone are each inhomogeneous in their distribution in animals with normal coronary arteries as shown by microsphere studies. Therefore, both are needed to insure a uniform distribution in the myocardium.⁴

Clinical studies show that switching from antegrade to retrograde perfusion raises oxygen uptake and lactate washout, indicating that each modality perfuses different areas.⁵ Therefore, both antegrade and retrograde perfusion is required for complete protection (Fig. 25-3). The clinical benefits of the addition retrograde cardioplegia after coronary surgery were seen in a controlled prospective randomized trial. Three months after surgery, there was an increase in resting and exercise ejection fraction in patients who had retrograde cardioplegia as compared to those who did not.⁶ Adding retrograde to antegrade cardioplegia also reduces troponin levels after induced ischemia in patients with reduced ejection fraction less than 36 percent.^7,8 In patients with left-main coronary disease, adding retrograde cardioplegia during coronary bypass reduces the incidence of postoperative atrial fibrillation and troponin levels.⁹

Recent studies have shown that combined benefits occur by simultaneous delivery of retrograde and antegrade cardioplegia in coronary bypass procedures.^10,11 After vein grafting to a coronary artery, cardioplegia may be given through the graft in an antegrade manner and simultaneously through the coronary sinus. Myocardial venous hypertension is prevented by drainage through the Thebesian veins.

Noncoronary collateral flow from mediastinal collaterals displaces cardioplegia with warmer systemic blood. Topical hypothermia slows rewarming but may cause pulmonary complications (phrenic palsy) without supplementing the cardioprotective effects. Hence, continuous or intermittent cardioplegia is required. Continuous cardioplegic perfusion has been advocated to avoid ischemia, but adequate protection may not be achieved at usual flow rates, and the surgeon’s vision becomes obscured during infusion. Intermittent cardioplegia, delivered at 10- to 20-min intervals, maintains arrest, slows rewarming, and restores substrates depleted during ischemia. In addition, it flushes accumulated metabolites and counteracts acidosis and edema.

Paradoxical septal motion, seen in as many as 40 percent of patients after cardiac surgery can lead to acute right ventricular failure.¹² This may be caused by inadequate distribution of cardioplegia. We recently evaluated septal function by a commonly used qualitative scoring system and reported septal function among 119 patients undergoing a variety of cardiac surgical procedures.¹³ By using the integrated method of myocardial protection, paradoxical septal motion was not seen in any patient, strongly suggesting that this phenomenon is an iatrogenic injury or stunning of the septum. A prospective randomized clinical trial is currently underway with newer echocardiographic data including spectral tracking and velocity vectors.